Problem-Based Feline Medicine

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First published 2006
ISBN - 10 0 7020 2488 0

ISBN - 13 978 0 7020 2488 7
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Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our knowledge, changes in practice, treatment and drug therapy
may become necessary or appropriate. Readers are advised to check the most current
information provided (i) on procedures featured or (ii) by the manufacturer of each
product to be administered, to verify the recommended dose or formula, the method
and duration of administration, and contraindications. It is the responsibility of the
practitioner, relying on their own experience and knowledge of the patient, to make
diagnoses, to determine dosages and the best treatment for each individual patient, and
to take all appropriate safety precautions. To the fullest extent of the law, neither the
publisher nor the author assumes any liability for any injury and/or damage.
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20 – THE CAT WITH ENLARGED LYMPH NODES ixix
CONTENTS
Contributors
Abrams-Ogg, A – Department of Clinical Studies, Sciences, Colorado State University, Fort Collins,
Ontario Veterinary College, University of Guelph, CO, USA
Guelph, Ontario, Canada Filippich, L.J. – School of Veterinary Science,
Arrington, K.A. – Beltway Emergency Animal University of Queensland, Brisbane, Queensland,
Hospital, Glenn Dale, MD, USA Australia
Bagley, R.S – Associate Professor, Department of Gunn-Moore, D. – Senior Lecturer, Head of Feline
Veterinary Clinical Sciences, College of Veterinary Clinic, University of Edinburgh Hospital for Small
Medicine, Washington State University, Pullman, Animals, Easter Bush Veterinary Centre, Roslin,
WA, USA Midlothian, UK
Barber P.† – Formerly Lecturer, Department of Jergens, A.E. – Associate Professor, CVMBS-VTH
Veterinary Clinical Studies, University of Veterinary Clinical Sciences, Iowa State University,
Edinburgh Hospital for Small Animals, Roslin, Ames IA, USA
Midlothian, UK Johnstone, I.P. – Adjunct Associate Professor,
Bartges, J.W. – Professor of Medicine and Nutrition, Veterinary Teaching Hospital, School of Veterinary
and The Acree Endowed Chair of Small Animal Science, University of Queensland, Brisbane,
Research, College of Veterinary Medicine, Queensland, Australia
University of Tennessee, Knoxville, Tennessee, Jones, B.R. – Professor of Small Animal Clinical
USA. Studies and Dean, School of Agriculture, Food
Bernays, M. – Staff Veterinary Ophthalmologist, Science and Veterinary Medicine, University
Animal Eye Services, MacGregor, Queensland, College Dublin, Belfield, Dublin, Ireland
Australia King, T. – Veterinary Specialist Services, Underwood,
Boothe, D.M. – Anatomy, Physiology and Queensland, Australia
Pharmacology, College of Veterinary Medicine, Lappin, M.R. – Professor, CVMBS-VTH, Clinical
Auburn University, Auburn, Alabama, USA Sciences, Colorado State University, Fort Collins,
Braz-Ruivo, L.A.H. – Beltway Emergency Animal CO, USA
Hospital, Glenn Dale, MD, USA Levy, J. – Department of Small Animal Clinical
Breathnach, R.M.S – School of Agriculture, Food Sciences, College of Veterinary Medicine,
Science and Veterinary Medicine, University University of Florida, Gainesville, FL, USA
College Dublin, Belfield, Dublin, Ireland Litster, A.L. – School of Veterinary Science,
Burton, G. – Animal Allergy and Dermatology University of Queensland, Brisbane, Queensland,
Service, Springwood, Queensland, Australia Australia
Campbell, F. – Veterinary Medical Teaching Hospital, Maddison, J.E. – Royal Veterinary College, North
University of California, Davis CA, USA Mymms, Hatfield Hertfordshire, UK
Cuddon, P.A. – Neurological Center for Animals, Mason, R.A. – Oceanview Veterinary Specialists
Lakewood, CO, USA Nikken Wellness Consultant, Healthy
Dowers, K.L. – Department of Clinical Sciences, Achievements International, Mill Creek,
College of Veterinary Medicine & Biomedical WA, USA
ix
x CONTRIBUTORS
McCarthy, G.M. – School of Agriculture, Food Shipstone, M. – Dermatology for Animals, Stafford
Science and Veterinary Medicine, University Heights, Queensland, Australia
College Dublin, Belfield, Dublin, Ireland Smith, R.I.E. – Veterinary Ophthalmologist, Animal
Menrath, V.H. – Adjunct Associate Professor, Creek Eye Services, MacGregor, Queensland, Australia
Road Cat Clinic Pty Ltd, Mount Gravatt, Straw, R.C. – Director, Animal Cancer Care and
Queensland, Australia Brisbane Veterinary Specialist Centre, Albany
Miller, J.B. – Professor, Department of Companion Creek, Queensland, Australia
Animals, Atlantic Veterinary College, University of Thomson, M. – Animal Cancer Care, School of
Prince Edward Island, Charlottetown PE, Canada. Veterinary Science, The University of Queensland,
Parent, J. M.– Professor, Department of Veterinary Brisbane, Queensland, Australia
Clinical Studies, Ontario Veterinary College, Wilson, G.J. – Animal Dental & Oral Care,
University of Guelph, Guelph, Ontario, Canada Wellington Pt, Queensland, Australia
Quesnel A.D.† – Formerly Professeure agrégée, Zoran, D. – Small Animal Medicine and Surgery,
Département de sciences cliniques, Université de CVM, Texas A & M University, College Station,
Montréal, Faculté de médecine vétérinaire, Quebec, TX, USA
Canada
Rand, J.S. – School of Veterinary Science, University † Deceased.
of Queensland, Brisbane, Queensland, Australia
Seksel, K. – Sydney Animal Behaviour Service,
Seaforth, New South Wales, Australia
20 – THE CAT WITH ENLARGED LYMPH NODES xixi
CONTENTS
Preface
Problem-based feline medicine was inspired by teach- the signs are not organ-specific, and to help them
ing students in the clinic, and from consulting to walk through the thought processes, they were first
veterinarians in practice. It was apparent that the encouraged to answer the question “What mecha-
way veterinary medicine was traditionally taught nisms can be responsible for these signs?” Hence the
often caused problems when the students were in first section in the summary table and introduction
the clinic. Many times they did very well in written answers the questions: “What mechanism/s causes
examinations, but could not utilize the material this problem?” (MECHANISM?), “Which organs or
taught to make a diagnosis in the clinic. Traditional body systems cause this problem?” (WHERE?),
disease-based text books, divided into sections based “What diseases/s cause this problem?” (WHAT?)
on aetiology, assumed the clinician knew whether The format for each chapter is the same. The chap-
the disease was viral or bacterial, fungal or metabol- ter title is based on a presenting sign. A summary
ic. Clients usually do not say “my cat has feline page lists the answers to “MECHANISM?”,
leukaemia and what is the most appropriate treat- “WHERE?”, and “WHAT?” This is followed by a quick
ment”. They say “my cat is losing weight and is not reference guide to the diseases that should be consid-
as active as normal”. The dilemma for students is, ered as potential rule-outs. They are starred with 0-3
which page of a text-book do I to turn to? Making a stars to indicate how important the disease is as a
diagnosis is the most important part of being a vet- cause of the problem. Some diseases are common but
erinarian, because without a diagnosis, determin- rarely cause the sign (problem), and they did not get
ing appropriate treatment is problematic.
My hope is that this book will support students
and veterinarians in practice, and assist them in
turning to the “right page” for the information they
need to make a diagnosis. A challenge in writing a
book like this, is the duplication of material, and dif-
ferences between authors when writing about the
same disease in different chapters. I think this con-
tributes to the richness of information in the book,
and reflects that life it is not black and white, and
there are different opinions based on different expe-
riences.
One difficulty students had using the acronym
DAMNPIT, was that in formulating a list of likely
diseases causing the problem, they often omitted
obvious diseases. When they first listed the organs
or body systems that could cause the signs, and
then used DAMNPIT, it increased their score rate.
Sometimes the organ system is not evident when
xi
xii PREFACE
a frequency star. Next is the introduction, which in utilize VIN to check new developments, particularly
more detail describes “MECHANISM?”, “WHERE?”, in diagnostic tests and treatment.
and “WHAT?”. This is followed by the diseases, Strive for excellence and enjoy. Remember, mak-
roughly listed in order of likelihood of causing the ing a diagnosis is one of the most important things
sign. Therefore, diseases with 3 stars are listed before you do as a veterinarian.
those with no stars, that are rare causes of the signs. If you have suggestions for the next edition of the
Some suggested reading lists are included if the read- book, I would love to hear them (contact me by
er wants to delve further. Although Veterinary email: [email protected]).
Information Network (VIN) is not referenced specifi-
Jacquie
cally for most chapters, the reader is encouraged to
This book is dedicated to those who shaped my life:
To my dad who taught me that “if a job is worth doing, it is worth doing well”, and that
“a job is not done until it is finished”.
To my mum who has always been a cheerful supporter in all the twists and turns in my life.
To the students who inspired, taught and challenged me.
To my husband Tom, my rock, my safe and welcoming harbor, and my sanctuary in stormy seas.
To my daughter Lisette, who reminded me when it was time to play, and the
importance of having a balanced life.
Thank you all and bless you
xiv CONTENTS
Acknowledgments
There are many people I would like to thank who information. Although sometimes the information
have helped turn my vision of a problem-based text sourced from VIN is not referenced in the text,
into a reality. Firstly, the contributing authors, who I would especially like to acknowledge the useful-
helped make this text happen when it became ness and great support that this database provides
apparent that it was expanding into too big a vision to veterinarians in practice and academia.
for one person to accomplish. Secondly, to Annette I would also like to acknowledge the veterinary
Litster who proof read many chapters, and joined as class of ‘95 at the University of Queensland, who
a contributing author late in the project, respond- inspired me to embark on this project, and all the stu-
ing cheerfully to urgent requests to write and sube- dents, before and after, who reinforced the belief that
dit the gastrointestinal tract section. Thirdly, to the this format would help veterinarians in practice.
many staff and students who helped with format- In the early mornings, Merlin our Burmese cat
ting the manuscript and editing, including Heidi provided me with company and inspiration while
Farrow, Joanne Chapel, Philippa Williams, Sarah I worked on the manuscript, by sitting on the
Gestier and Desley Badrick. keyboard, on pages I was reading, or on my lap
I would like to acknowledge the invaluable purring.
resource of the Veterinary Information Network Lastly, but most importantly, this book would not
(VIN), which greatly assisted in my commitment to have been possible without the support and love of
include the most recent material and practical my husband Tom and daughter Lisette.
xiv
1. How to make a problem-based
diagnosis
Jacquie Rand
● Competence at making a diagnosis is the most important part of being a

veterinarian. Therefore, it is the most important skill learnt in veterinary
education. High-level surgery skills and in-depth knowledge of drugs may be
useless if the wrong diagnosis is made.
● Making a diagnosis involves problem-solving. If clinical signs are treated
without first making a diagnosis, it is likely that corticosteroids, antibiotics and
euthanasia will be over-prescribed.
There are two ways to make a diagnosis. Firstly 1. Obtain detailed data from a complete history and
there is the “expert method”. This is the way physical examination.
many veterinarians make a diagnosis, and it Take an exact and detailed history. It is critical
involves pattern recognition. that questions are asked to cover a detailed
The disadvantages of the “expert method” are that it history in all areas of the pet’s health, not just
requires a lot of experience to be accurate, and there is for the problem presented. To get the correct
a greater chance of being wrong, especially for the less- information it may be necessary to ask the
experienced practitioner, because the same signs may same question in different ways.
occur for many diseases. For example, diarrhea may be
Complete a thorough physical examination.
caused by many diseases including intestinal parasites,
food intolerance, intussusception, lymphoma and The history and physical examination are the most
inflammatory bowel disease. The appropriate treatment critical parts of making a diagnosis.
varies depending on the diagnosis. Diagnostic tests may not overcome deficiencies in
the history and physical examination. For example, if
The second method of making a diagnosis is by hematology and biochemistry analyses were performed
using a problem-based approach. This leads to but a chest radiograph was not taken because increased
fewer mistakes and facilitates better veterinary frequency of coughing was missed in the history, or
practice. dyspnea was missed on the physical examination, a pri-
mary lung tumor may be missed despite performing
many other tests to determine the cause of lethargy.
KEY ELEMENTS FOR MAKING ● Normal physical examination findings need to be
A PROBLEM-BASED DIAGNOSIS appreciated before abnormal findings can be identi-
To make a problem-based diagnosis, the signs exhibit- fied. Veterinary students are encouraged to take
ed are separated out into individual problems, and each every opportunity to practice physical examinations
problem is considered separately. so the range of normal is recognized.
The individual steps in making a problem-based 2. List the problems identified based on the history
diagnosis are as follows. and physical examination.
1
2 HOW TO MAKE A PROBLEM-BASED DIAGNOSIS
It is important to only list the problem at the level “WHERE?” for an abdominal mass includes liver,
that it is understood. For example, if the cat has an GIT, spleen, urinary tract, omentum, reproductive tract,
abdominal mass, the problem is initially listed as an etc. “WHERE?” for alopecia is skin; “WHERE?” for
abdominal mass and not a neoplasm, because it may be PU/PD is kidney, which is the end organ influencing
caused by a number of other conditions including reac- water intake and urine output. It is usually better to
tive lymphadenomegaly, feces, abscess, etc. simplify the answer in this way, rather than listing all
Characterize each problem listed based on duration, the organs that can cause polyuria/polydipsia, although
character and severity. this can also be done, e.g. kidney, liver, brain, kidney,
Characterize each problem by the 3 Cs: adrenal, bladder, etc.
● Chronicity (duration) To answer “WHERE?”, you may have to answer the
● Character question what is the “MECHANISM?” that results in
● Concern (severity/frequency/size). this problem, and use your knowledge of pathophysio-
– For example, the problem “sneezing and nasal logic principles to answer “WHERE”?
discharge” may be characterized as 2 months ● For example, abdominal effusion can be due to:
duration (chronicity), purulent (character), – Decreased oncotic pressure as a consequence of
occurring approximately six times/day (i.e. mod- hypoalbuminemia resulting from liver, GIT or
erate severity). kidney dysfunction.
– Increased hydrostatic pressure resulting from
Select the problem/s to consider first. Choose those
cardiac disease or vascular obstruction.
that are most likely to provide a diagnosis.
– Increased permeability of blood vessel walls.
Choose problems for consideration first that are:
– Lymphatic obstruction involving abdominal
● Severe or frequent problems. Problems that are
lymphatics.
infrequent or mild may not lead to the main definitive
diagnosis as quickly, or may be independent problems. If the answer to “WHERE?” is more than one organ
● Represent the problem the owner was concerned system, then diagnostic tests are usually required to
about. localize the problem. For example, for an abdominal
● Problems that are most specific for an organ or mass, results of diagnostic tests such as a serum bio-
body system. Avoid using non-specific problems chemistry profile (showing increased liver enzymes),
such as lethargy or anorexia. These problems indi- radiography (indicating hepatomegaly), and/or ultra-
cate severity of the problem, but are not organ-spe- sound (revealing a mass in area of liver), may be
cific and can be caused by almost any disease in the required to answer the question WHERE? (liver).
body. They are not useful diagnostically because
Once the organ systems involved have been identified,
they require a wide range of diagnostic tests to be
you can move on to answering the question
performed in an attempt to detect an organ-specific
“WHAT?”. That is, for each organ or body system
abnormality.
identified as potentially being involved, what diseases
are potential causes of the problem?
3. List the differential diagnoses (likely diseases)
for each problem. To formulate a list of differen- ● To assist in listing the diseases that can cause
tials, it helps to ask two questions, “WHERE?” and the problem, it helps to use an acronym such
“WHAT?”. as DAMNPIT to aid the memory.
To answer “WHERE?”, ask yourself which organs
or body systems can cause the problem? D : * degenerative
If possible, try to first categorize the answer to A : * anomaly (congenital)
“WHERE?” into sub-headings. For example, for * accident (e.g. volvulus, intussusception)
seizures, the problem could have extra-cranial or intra-
M : * metabolic (e.g. electrolyte, hormonal)
cranial causes. Similarly, for vomiting, there could be
* mechanical (e.g. foreign body, urolith)
extra-gastrointestinal or gastrointestinal causes; and for
jaundice, the sub-headings pre-hepatic, hepatic, and N : * neoplastic
post-hepatic are appropriate. * nutritional
1 – HOW TO MAKE A PROBLEM-BASED DIAGNOSIS 3
P : * physical (e.g. heat, cold, water, fire) To rank diseases as likely, possible, or unlikely, cross-
* psychological match the patient’s signalment (breed, age, gender),
* pharmacological (drug effect) clinical signs, and physical examination findings with
I: * infectious (viral, bacterial, mycoplasma, the known characteristics of the disease including
rickettsial, protozoal, fungal, parasitic) typical signalment, signs and physical examination
* immune findings of the disease and frequency of disease (how
* iatrogenic (caused by you) common it is).
* idiopathic (unknown) ● For the differential diagnosis “diabetes mellitus”, con-
* infarct sider whether the typical signalment, history and

physical examination findings of this disease fit the
T : * trauma
patients findings. An example of the thought process-
* toxic/adverse drug
es are the following: Diabetes mellitus is a very like-
For example, the answer to “WHAT?” diseases could ly cause of the problem because it occurs in older cats,
cause polyuria/polydipsia in a 10-year-old male castrated male cats are more often affected, and the patient has
domestic shorthair cat that has a history of losing weight all the expected signs, including signs of chronic dis-
for 2 months, a good appetite until the last couple of days, ease, polydipsia and polyuria, weight loss and a good
frequently urinating in the litter box, and drinking appetite until recently. The high volume of water
1 liter/day include: drunk by this cat can occur with diabetes mellitus.
● For the differential diagnosis, “chronic renal failure”
D: Chronic renal failure an example of the thought processes is: Chronic renal
A: failure is a possible cause of the problem because the
expected signs include evidence of a chronic disease,
M: Diabetes mellitus with weight loss and recent inappetence. However, cats
Diabetes insipidus with renal failure that have marked polydipsia often
Hyperthyroidism have a more picky appetite once weight loss is appar-
Hyperadrenocorticism ent, and the volume of water drunk is usually less.
Hepatic failure ● For the differential diagnosis “hepatic failure”, an
Hypercalcemia example of the thought processes is: Hepatic failure
Acromegaly is an unlikely cause of this cat’s problem because
Hypoadrenocorticism although this cat has some of the clinical signs
Hypercalcemia expected with hepatic failure, it does not have all of
N: Renal neoplasia the typical signs. The signs of this patient that fit
Lymphoma and include: chronic disease with lethargy, inappetence
pseudohyperparathyroidism and weight loss. Polydipsia can occasionally occur if
Polycythemia vera there is liver failure. However, cats with hepatic fail-
P: ure sufficient to cause weight loss and affect renal
concentrating mechanisms are usually inappetent
I : Infectious Pyelonephritis and jaundiced. In addition, hepatic failure is a rare
Cystic endometrial hyperplasia/ cause of polydipsia in cats.
pyometra ● It helps to know 1–5 lines of information for each
Immune Glomerulonephritis/renal disease on your list of differential diagnoses. You
amyloidosis should know more about the common diseases
T: Vitamin D toxicity than uncommon diseases. Learn the typical signal-
Drugs such as ment, clinical signs, physical examination findings,
corticosteroids and frequency of diseases that occur in your area.
After listing the diseases, rank the diseases as likely, 4. Formulate a diagnostic plan to prove or disprove
possible or unlikely based on cross-matching the each possible disease. Choose the initial diagnos-
patient’s data with the characteristics of the disease. tic tests based on:
4 HOW TO MAKE A PROBLEM-BASED DIAGNOSIS
● Prioritizing, ruling in or out the most likely update the problem list, differential diagnoses,
diseases diagnostic plan and treatment plan.
● Choose tests initially that are least invasive,
and to some extent easiest and/or cheapest to
perform
● Choose the tests that have the best Summary of the steps in making a
combination of specificity and sensitivity. problem-based diagnosis
Remember that each negative or normal test result 1. Obtain data from a detailed history and
makes the list shorter. physical examination.
For example, for the problem “liver mass” that was
2. List the problems identified based on the
identified based on ultrasound, radiology and biochem-
history and physical examination.
istry profile, the following is an example of a diagnos-
tic plan. 3. List the differential diagnoses for the
● Following ultrasound identification of the mass, major and most organ-specific problems.
fine-needle biopsy and cytological examination will Use your answers to “WHERE?” and
be performed, with culture requested if no neoplastic “WHAT?” to formulate a logical list of
cells are obvious. Although the sensitivity and speci- differential diagnoses. Cross-match the
ficity are not as high as with a wedge biopsy or patient and disease characteristics to
laparotomy, it is balanced by the less-invasive identify the most likely diseases.
nature, ease and cost. These diagnostic decisions 4. Formulate a diagnostic plan to rule-in or
need to be made in conjunction with the owner. rule-out the likely differential diagnoses.
● If a definitive diagnosis is not possible from the results
5. Formulate a treatment plan.
of the fine-needle biopsy, the next diagnostic tests that
could be considered would be a needle biopsy suitable 6. Update points 2–5 as diagnostic data
for histological examination, or laparotomy and become available and the response to
wedge biopsy. The decision will require balanced therapy is observed.
consideration of many factors including input from
the owner regarding cost, invasiveness, etc.
5. Formulate a rational treatment plan based on
the diagnoses identified.
USING THE BOOK
● Treatment may either be specific for a disease process,
This book is set out to facilitate making a problem-
such as antibiotics and drainage of an abscess, or be
based diagnosis. At the start of each chapter there is
non-specific, for example, IV fluids for dehydration.
a summary of the answers to the questions
Initial treatment plans will often be formulated in par-
‘Mechanism?’, ‘Where?’, and ‘What?’ for each prob-
allel with diagnostic plans, because some problems
lem. A quick reference summary lists the diseases that
such as dehydration or cyanosis need addressing early.
can be associated with that problem. Stars after each
6. As diagnostic data are received and the response disease denote the importance of the disease as a cause
to initial therapy is observed, it is important to of the problem.
CHAPTER NUMBER - CHAPTER TITLE 5
PART 1
Cat with upper respiratory tract
signs
2. The cat with acute sneezing or nasal

discharge
Jacquie Rand
KEY SIGNS
● Serous, mucoid, purulent or bloody nasal discharge less than 2 weeks’ duration.
● Acute sneezing or snuffling.
MECHANISM?
● Signs of acute sneezing or nasal discharge usually result from viral, chlamydophilial or
mycoplasmal infection.
WHERE?
● Nose (nasal cavity, paranasal sinuses).
WHAT?
● Most cats (80%) with acute onset of sneezing or nasal discharge have calicivirus or
herpesvirus.
5
6 PART 1 CAT WITH UPPER RESPIRATORY TRACT SIGNS
QUICK REFERENCE SUMMARY

Diseases causing acute sneezing or nasal discharge
MECHANICAL
● Foreign body (p 15)
Acute onset of sneezing and rubbing face, progressing to chronic discharge, often unilateral, no
systemic signs.
NEOPLASIA
● Bleeding ulcer on external nares (p 16)
Acute sneezing and bleeding may occur with a bleeding ulcer on the external nares, particularly the
nasal septum. Usually caused by squamous cell carcinoma (SCC), but occurs occasionally with
eosinophilic granuloma or associated with acute calicivirus infection. Signs are often episodic with squa-
mous cell carcinoma.
●Intranasal tumors (p 17)
Occasionally present with acute sneezing, ± nasal discharge and bleeding.
INFECTIOUS
Bacterial:
● Bordetella bronchiseptica (p 14)
Pyrexia, sneezing, nasal discharge, mandibular lymphadenopathy, coughing and dyspnea.
Viral:
● Feline rhinotracheitis virus (herpesvirus-1)*** (p 7)
Paroxysms of sneezing, severe serous to mucopurulent oculonasal discharge, usually bilateral
severe conjunctivitis with tearing, photophobia and chemosis, ± corneal lesions.
● Feline calicivirus*** (p 11)
Fever, mild upper respiratory tract signs, oral ulcers.
Chlamydophila, Mycoplasma:
●Chlamydophila felis (Chlamydophila felis) **(p 13)
Mainly conjunctivitis, initially unilateral, later bilateral and often chronic.
● Mycoplasma (p 14)
Mainly conjunctivitis, usually without systemic illness; often occurs as secondary infection in viral
upper respiratory tract disease.
Fungal:
●Cryptococcus (p 16)
Usually chronic signs, but occasionally acute onset of sneezing and nasal discharge.
Immune:
● Allergic (p 17)
Serous or mucoid ocular and/or nasal discharge, without systemic signs. Signs may be seasonal in
occurrence.
2 – THE CAT WITH ACUTE SNEEZING OR NASAL DISCHARGE 7
Necrosis of epithelium occurs within 24–48 h of viral

INTRODUCTION contact.
Signs occur 2 to 6 days after infection.
MECHANISM?
Secondary bacterial infection of lesions usually
Signs of acute sneezing or nasal discharge indicate
occurs, producing purulent ocular-nasal discharges.
inflammation of the nasal cavity, which in cats is
almost always the result of infection, usually viral or Osteolysis of the turbinate bones may occur.
associated with chlamydophilia or mycoplasma.
Virus may cause corneal necrosis resulting in keratitis,
ulceration, and occasionally corneal rupture and loss of
WHERE? the eye.
Nose (nasal cavity, paranasal sinuses). Concurrent infections with calicivirus, Chlamy-
dophila, Mycoplasma or Bordetella bronchiseptica are
common, and may alter the clinical signs.
WHAT?
Most cats (80%) with acute onset of sneezing or nasal
Clinical signs
discharge have calicivirus or herpesvirus.
Earliest sign is paroxysms of sneezing.
DISEASES CAUSING ACUTE Severe conjunctivitis occurs, with tearing, photophobia
SNEEZING OR NASAL DISCHARGE and chemosis.
Severe ocular and nasal discharges occur which are ini-
FELINE RHINOTRACHEITIS VIRUS (FELINE tially serous, but progress rapidly to mucopurulent.
HERPESVIRUS-1), “RHINO” OR Discharge is typically more marked than with calicivirus.
“SNUFFLES”***
Later, discharge and crusting of nares and conjunctiva
may produce nasal obstruction and sealing of the eyelids.
Classical signs
Anorexia, depression and pyrexia are common; dehy-
● Acute onset of sneezing, pyrexia, depression.
dration may occur.
● Marked discharge from eyes and nose, initially
serous but progressing to mucopurulent. Tracheal and bronchial inflammation may result in
● Severe conjunctivitis with chemosis and coughing and dyspnea, and occasionally bacterial
photophobia. pneumonia occurs in kittens.
● Corneal keratitis or ulcers in some cats.
Very rarely, ulceration on the nose or tongue occurs, but
● Generally less than 10–14 days duration.
this is much more frequent with calicivirus infection.
For more details of ocular changes see page 1212 (The Corneal involvement resulting in keratitis may occur 1–2
Cat With Ocular Discharge or Changed Conjunctival weeks later. Keratitis is visible as corneal cloudiness
Appearance) and page 1237 (The Cat With (edema and inflammation), and punctate or branching
Abnormalities Confined to the Cornea). ulcers, which may coalesce to large ulcers.
Corneal perforation and secondary bacterial infection
may result in destruction of the eye; this occurs more
Pathogenesis often in young kittens (ophthalmia neonatorium).
Herpesvirus causes an acute infection of the upper Herpesvirus keratitis often occurs in the absence of
respiratory tract, conjunctiva and cornea. signs of active upper respiratory tract infection.
Virus multiplication is temperature restricted, and Infection of the pregnant queen may lead to fetal
most lesions occur on cooler mucosal-epithelial sur- absorption, abortion, or kittens either born infected or
faces, e.g. nasopharynx, conjunctiva, turbinates. developing signs shortly after birth.
Signs in newborn kittens include continuous crying, Differential diagnoses

nasal discharge, sneezing and dyspnea.
Calicivirus usually has milder upper respiratory signs;
Signs are worse in: oral ulcers are classical; no keratitis or corneal ulcera-
● Young kittens once maternal antibody levels tion; occasionally viral pneumonia occurs.
decrease.
● Conditions of crowding, e.g. animal shelters,
Chlamydophila generally has milder signs, although
breeding colonies and pet shops. young kittens can have severe conjunctivitis and ocu-
● Stress factors or other intercurrent disease, e.g.
lar-nasal discharge; typically conjunctivitis lasts longer
FIV, FeLV, renal failure. (weeks) with Chlamydophila.
Signs of rhinotracheitis usually resolve in 2 weeks, Cryptococcosis or nasal tumors may occasionally
but purulent rhinitis and sinusitis may persist longer. present with an acute onset of sneezing; however, signs
do not resolve, but become chronic and progressive.
Superficial ulcerative dermatitis occasionally
occurs on the face, trunk and footpads. The lesions are Concurrent FeLV or FIV should be suspected in cats
usually more severe on the face and occur on the nasal with very severe, prolonged signs, or in adult vacci-
planum or haired skin. They consist of vesicles, ulcers nated cats with severe signs, and in cats with recurrent
and crusts, and may be pruritic. Upper respiratory upper respiratory disease.
tract signs may or may not be present, and signs See page 1213 for more details of differential diagnoses
appear to occur in situations of reactivation of latent in The Cat With Ocular Discharge or Changed
infection. Conjunctival Appearance.
Stomatitis may be associated with latent herpesvirus
infection, and may or may not occur with dermatitis. Treatment
Minimize hospital contamination. Cats should be
Diagnosis treated as outpatients, unless dehydrated or requiring
oxygen.
A definitive diagnosis is usually not made, and a pre-
sumptive diagnosis is based on clinical signs. Use broad-spectrum antibiotics if nasal discharge is
mucopurulent, indicating secondary bacterial infection.
The following diagnostic tests are offered by some lab-
● Antibiotics also help prevent chronic rhinitis.
oratories: fluorescent antibody staining of conjuncti-
● Amoxicillin, cephalosporin, doxycycline or
val or nasal mucosal scrapings or biopsy, antibody
trimethaprim-sulfadiazine are indicated.
titers (measured initially and after convalescence),
● Doxycycline is useful if concurrent infections
virus isolation or polymerase chain reaction (PCR).
of Chlamydophila, Mycoplasma or Bordetella are
● These are infrequently performed for individual
suspected.
cats with signs of upper respiratory tract disease,
because the result rarely changes the treatment. Correct dehydration and maintain optimum hydration
● Obtaining a definitive diagnosis is more useful if a using subcutaneous or intravenous fluids.
cattery problem persists despite vaccination. ● Dehydration is common, because cats will not eat
● Diagnostic tests are indicated to confirm her- or drink, and marked fluid loss may occur from the
pesvirus infection if corneal ulceration is poorly ocular-nasal discharge and salivation.
responsive to treatment, but false-negative results
Improve airflow through the respiratory tract.
are common.
● Clean crusted discharge from the nose three times
Histopathological examination of the skin lesions daily.
indicates ulcerative dermatitis with epithelial cell ● Use a protective agent such as vaseline on the nose
necrosis and eosinophilic inflammation. Epidermal to prevent excoriation.
cells may contain basophilic intranuclear inclusion ● Use a vaporizer or nebulizer to provide airway
bodies. PCR indicates the presence of herpesvirus in humidification, or have the owners put the cat in a
skin samples. steamy bathroom.
● Nasal decongestants (intranasal or oral) are gener- front of cat, or oxazepam (Serax; 2–2.5 mg/cat, PO
ally not well tolerated by cats, but can be tried. q 12 h) or cyproheptadiene (Periactin, 1–2 mg/cat
– Intranasal decongestants (e.g. pedi- PO q 12 h) just before feeding.
atric preparations of phenylephrine, neo- ● Multivitamins (A, B and C) but especially thiamine
synephrine or oxymethazoline, 1 drop in one and vitamin A.
nostril) may be useful, but do not use longer than ● Tempt to eat with strong smelling foods, e.g. fried
a couple of days. chicken or sardines. Warming food to body temper-
– Oral decongestants, e.g. ephedrine or pseu- ature increases palatability.
doephedrine (e.g. Sudafed) can be tried, but are ● Handfeed or force feed initially.
unpalatable to cats, and may induce severe sali- ● Tube feed via a naso-osophageal, esphageal or gas-
vation. trostomy tube if the cat is still depressed and
anorexic after 3 days.
Treat eyes with topical therapy. For more treatment
details see page 1214 (The Cat With Ocular Discharge or Warmth enhances recovery because the virus is tem-
Changed Conjunctival Appearance) and page 1239 (The perature sensitive (e.g. use incubator or heating pad).
Cat With Abnormalities Confined to the Cornea).
● Clean discharges from eyes three times daily.
Prognosis
● Antibiotic eye ointment (without steroids), e.g.
tetracycline or tobramycin. Avoid use of baci- Mortality is usually low, although may be higher (up
tracin-neomycin-polymyxin ointment because of to 30%) in young kittens.
reports of acute death associated with its use.
Persistent or recurrent chronic bacterial rhinitis and
● Antiviral eye drops or ointment should be used if
sinusitis occurs in some cats as a result of nasal epithe-
herpetic keratitis is present; they may also help
lium damage and osteolysis.
conjunctivitis.
● Chronic rhinitis is evident as recurrent sneezing,
– Idoxuridine q 4–5 h (Dendrid, Herplex, IDU,
and mucopurulent nasal discharge, which responds
Stoxil), vidarabine q 5 h (Vira-A), trifluo-
temporarily to antibiotics.
rothymidine q 2–4 h for 3 weeks (Viroptic).
Viroptic was the most effective of the viricidal Scarring and occlusion of the lacrimal ducts may
agents in vitro, but it is expensive, and may be produce chronic wetting of the face from tears.
very irritating to the eye.
Rarely, chronic keratitis, poorly healing corneal ulcers,
Acyclovir (100–200 mg/cat q 8–12 h, per os; conjunctival adhesions (symblephron), and keratocon-
Zovirax) may be useful in resistant ulcers. If using junctivitis sicca occur.
this drug monitor white and red cell counts for evi-
Herpesvirus ulcerative facial dermatitis or stomatitis
dence of bone marrow suppression. The efficacy is
syndrome appears to occur in some cats in situations
controversial in FHV-1 infection because the enzyme
associated with reactivation of latent infection.
involved in conversion to the active form has low
activity in cats compared to humans, and the drug is Carrier state is common (up to 80% of recovered
100 times less active. cats), and may last years.
● Virus is shed intermittently, often following stress;
L-lysine (500 mg/cat q 24 h, per os) is recommended,
shedding may or may not be associated with mild
and may help to reduce signs and viral shedding. It
clinical signs.
competes with arginine which is essential for viral
● Glucocorticoid administration or environmental
replication.
stress such as from overcrowding or relocation may
Interferon (30 IU α-interferon) orally and topically predispose to reactivation of infection.
(30 u/ml in artificial tears q 6 h) daily until lesions have
resolved and then taper. Transmission
Support nutrition Herpesvirus is highly contagious with rapid spread
● Appetite stimulants. Use diazepam (Valium; in catteries, veterinary hospitals and multicat house-
0.1–0.2 mg/kg, IV) and immediately place food in holds.
● Infection rates may reach 100% in unvaccinated – If a cattery problem occurs, vaccinate litters as
cats and kittens. early as 4 weeks of age, and repeat every 3–4
● Young kittens (5–8 weeks of age) are most suscep- weeks until 14 weeks of age.
tible. ● Intranasal vaccine is a modified live vaccine,
● Occasionally kittens are born with infection. which produces rapid immunity (1–4 days). Some
cats have transient mild sneezing and naso-ocular
Most infections occur via direct close contact with
discharge after vaccination.
infected cats.
– Vaccinate with a single dose. If less than 10
● Fomites are also important in spread, especially
weeks of age at the first dose, give second dose
unwashed hands, food, bowels and contaminated
3–4 weeks later.
cages.
– If a cattery problem occurs, divide the dose
● Airborne transmission occurs over short distances
amongst the litter and give at 2 weeks of age, and
(approximately 1.2 m (4 feet)). Virus is present in
follow with a parenteral vaccination every 4
the droplets formed by sneezing.
weeks until 14 weeks of age.
● Virus is shed in secretions (ocular, nasal and oral)
● The combination of intranasal and subcuta-
for 1–3 weeks after infection.
neous vaccination reduced the incidence of upper
Spread in boarding catteries, shelters and veterinary respiratory tract disease (31% of cats developed
hospitals is facilitated by the high frequency of car- signs) in a shelter compared with subcutaneous
rier cats in the population that shed virus at times of vaccination alone (51% of cats developed signs),
stress or glucocorticoid treatment and may show no and was cost-effective.
signs of infection.
The frequency of booster vaccinations is controver-
Vertical transmission occasionally occurs from a sial. Annual boosters are typically recommended, par-
carrier queen, resulting in kittens born with disease. ticularly because occurrence of upper respiratory tract
● More usually, carrier queens shed virus 4–6 weeks signs is common in vaccinated cats, especially when
after queening, infecting kittens at the time mater- exposed to stress. However, measurement of serum
nal immunity is waning. titers suggests that humoral immunity lasts for 48
months or more. Serological titers are not equivalent
Feline herpesvirus is relatively fragile, and is stabile
to protection from challenge, although the predictive
for less than 24 h outside the host.
value for resistance to challenge for a positive serum
● The virus is susceptible to most disinfectants.
antibody titer was 70% for herpesvirus and 92% for
calicivirus. Additional boosters are recommended
before a heavy challenge, e.g. boarding in a cattery.
Prevention
Live parenteral vaccine can produce signs of upper res-
Vaccination piratory tract disease if aerosolized or spilt on the cat’s
Parenteral and intranasal vaccines are available in hair, so take care with administration.
combination with feline calicivirus vaccine.
Maternal antibodies can block the effect of the vaccine.
Combinations with feline parvovirus, chlamy- ● Antibody levels vary between kittens, and may last
dophila, rabies and/or feline leukemia vaccines are 5–6 weeks with herpesvirus (7–8 weeks with cali-
also available. civirus).
● Parenteral vaccines for subcutaneous administra-
Vaccinating queens 1–4 weeks before partum increases
tion are available as modified live or inactivated
colostrum-derived maternal immunity.
vaccines.
● DO NOT USE WITH LIVE PANLEUKOPENIA
– Administer twice with a 3–4-week interval
VACCINE in pregnant queens.
between doses.
– If the kitten is less than 8 weeks old at the first Localized viral infection can occur in vaccinated cats,
dose, give a third dose 3–4 weeks after the sec- and may produce mild ocular and nasal discharge, and
ond dose. viral shedding.
Disease control in the cattery or shelter ● Signs are often milder than feline herpesvirus
Vaccinate kittens early, and vaccinate all cats regu- infection.
larly to maintain immunity. Early signs are often non-specific, and typical of a sick
Isolate sick cats, and pregnant and nursing queens from cat, i.e. lethargy, anorexia and pyrexia.
the main cattery. Nasal and ocular discharge is often only mild and
Vaccinate and isolate incoming cats for 3 weeks. serous or mucoid, or may be absent.
● Avoid introducing cats that are likely carriers, i.e.
Sneezing is less prominent than in herpesvirus and is
from catteries with known infection problems. not paroxysmal.
Carrier queens shed virus and infect nursing kittens, Oral ulcers are characteristic and present in 70% of
therefore, remove queens that repeatedly have infected cats.
litters, or wean kittens early. ● Oral ulcers may occur either as small ulcers (2–5
Avoid overcrowding and other causes of stress. mm in diameter) or as a large ulcer.

● Typically ulcers are located on the anterior or lat-
Clean and disinfect cages daily and bowels with eral margin of the tongue. Less frequently they
sodium hypochlorite (0.175%, i.e. 1:32 dilution of occur at the angle of the jaws, on the hard palate,
household bleach) added to detergent. nasal philtrum or lips.
● Footpad ulcers occur occasionally, hence the name
FELINE CALICIVIRUS (FCV)*** “paw and mouth disease”.

Salivation may be profuse in the first few days after
Classical signs ulcers form.
● Lethargy, anorexia, fever. Conjunctiva are generally only mildly hyperemic, and
● Oral ulcers of less than 1 week duration. are not chemotic, as occurs with herpesvirus or chlamy-
● Mild upper respiratory tract signs dophila.
(sneezing, discharges).
Viral pneumonia occurs occasionally with certain
See other reference on page 1137 for details (The Fading strains, and may produce significant mortality. Death is
Kitten and Neonate). often sudden and preceded by labored respiration.
Rarely, vomiting and diarrhea occur as a result of
Pathogenesis enteritis.
Calicivirus replicates in epithelial cells of the upper res- “Limping kitten syndrome” occurs occasionally with
piratory tract, conjunctiva, tongue and in pneumocytes some strains of virus.
of the lung alveoli. ● Acute viral arthritis results in reluctance to move,
and acute swelling and pain on palpation of the
Multiple antigenic subtypes occur with differing path-
joints.
ogenicity.
● Most isolates cause low mortality. A rare variant strain (FCV-Ari) reported from
● Some very pathogenic isolates cause severe pneu- California, USA, produces a high fever, facial and
monia and significant mortality. paw edema (50% of cats), ocular and nasal discharge,
● Other isolates cause “limping kitten syndrome”. conjunctivitis and ulcerative stomatitis (50% of cats),
● FCV-Ari isolate produces high mortality. hemorrhage from the nose, GIT, etc. (30–40% of
cats), icterus (20% of cats) and rapid death.
Mortality is high (30–50%).
Clinical signs ● Swelling of the feet and face is a combination of
Clinical signs vary from mild to severe, depending on edema and hemorrhage, which is thought to result
viral subtype and immune status of the cat. from vasculitis. Hemostatic abnormalities have
been attributed to vasculitis and disseminated tularensis (tularemia), all may be difficult to differen-
intravascular coagulation (DIC). tiate pre-mortem if the illness progresses rapidly to
● Some cats also had pneumonia, pleural effusion, death.
pancreatitis and abdominal effusion.
Pancreatitis does not usually produce such a high fever
as FCV-Ari.
Diagnosis
Treatment
Presumptive diagnosis of calicivirus infection is based
on clinical signs Treatment for calicivirus infection including the hem-
orrhagic form involves supportive therapy (see treat-
A definitive diagnosis is usually not made except where
ment of herpesvirus for details, page 8).
there is an ongoing cattery problem, and is based on
● Maintain good hydration.
demonstrating a rising antibody titer, or on PCR or
● Humidify airways using a vaporizer or nebulizer.
viral isolation. These tests are available through some
● Use broad-spectrum antibiotics for secondary
laboratories.
infections.
Identification of FCV-Ari is based on the clinical syn- ● Clean discharges from face.
drome, pathology and culture of virus from blood, ● Provide oxygen if dyspneic.
nasal or ocular discharge, spleen or lungs. ● Analgesics (e.g. buprenorphine) may help make the
Thrombocytopenia and prolonged PT and aPTT may be cat more comfortable if there is severe ulceration.
evident in some cats.
No specific therapy is available, and no antiviral
drug is effective.
Differential diagnosis
Herpesvirus generally has more pronounced ocular- Prognosis
nasal discharge and paroxysms of sneezing. Corneal Signs generally resolve within 5–7 days.
lesions in herpesvirus infection are usually diagnostic,
and mouth ulcers rarely occur. Rarely, mortality is high with strains causing severe
viral pneumonia or vasculitis (FCV-Ari), and kittens
Mycoplasma often occurs as a secondary infection may die suddenly.
in viral upper respiratory tract disease, rather than a
primary disease, and is not associated with mouth Chronic gingivitis and stomatitis occurs in some carriers.
ulcers. Persistent mild conjunctivitis or ulcerative keratitis
Chlamydia generally has mild upper respiratory tract may be a problem.
signs, but no mouth ulcers; conjunctivitis often persists
longer and is more severe than with calicivirus. Transmission
Caustic stomatitis generally does not cause fever. Calicivirus is highly contagious, with nearly 100%
Ocular-nasal discharge is usually absent, or if present, morbidity in susceptible cats.
is a mild, serous discharge.
Infection spreads rapidly when multiple cats are housed
Concurrent infection with herpesvirus, mycoplasma together.
or Bordetella may confuse the clinical picture. ● Young unvaccinated kittens 2–6 months of age are
Acetaminophen (paracetamol) toxicity produces simi- most susceptible.

lar facial and paw swelling in an acutely ill cat as does Incubation period is 2–4 days. First signs generally
FCV-Ari, but cats are not febrile. occur 3 days after exposure, but this varies with dose
Other acute infectious illnesses may appear similar and virulence of virus.
to FCV-Ari, for example Yersinia pestis (feline Transmission is primarily via direct contact with
plague), Salmonella spp. (song-bird fever), Francisella infected cats.
● Fomite transmission occurs, e.g. food and water Clinical signs

bowls, cages, human hands, shoes and clothing.
● Virus can survive several days, and in some situa- Conjunctivitis is often initially unilateral, but pro-
tions up to 8–10 days, on contaminated objects. gresses to bilateral involvement.
● Conjunctiva are hyperemic, which is usually mild
Virus is shed in secretions from the mouth and nose of but can be severe, and are occasionally edematous
sick cats. and chemotic.
● Ocular discharge is initially seromucous, but rap-
The carrier state is common, and may last years.
Carrier cats provide a source of infection, and shed idly becomes mucopurulent.
virus continuously, mainly from the tonsils. Sneezing and nasal discharge result from ocular dis-
Virus is resistant to lipotrophic disinfectants, and charge draining through the nasolacrimal duct.
sodium hypochlorite (1:32 dilution of household Pneumonia occasionally occurs in kittens.
bleach) is efficacious.
Chlamydophila may cause abortion and infertility,
although this is controversial and poorly documented in
Prevention cats.
Vaccines are available combined with feline
herpesvirus vaccine (see herpesvirus (page 10) for
administration details). Diagnosis
Vaccination decreases severity and duration of signs. Visualization of inclusion bodies in epithelial cells
● Vaccination may not afford 100% protection if
obtained from conjunctival scraping (Diff-Quick stain)
challenged by a subtype that is different from the is diagnostic.
● Inclusion bodies are visible as groups or clusters of
vaccine strain.
organisms in the cytoplasm (in the same plane as
Cattery control involves vaccination, isolation of incom- the nucleus).
ing cats and good hygiene (see herpesvirus, page 11). ● Inclusions are most often visible in the first 2 weeks
of infection, and numbers decrease with chronicity.
CHLAMYDOPHILA FELIS Antibody-based detection in conjunctival scrapings
(CHLAMYDOPHILA FELIS PSITTACI)** using ELISA or latex agglutination is available. False
positives occur with both tests if many bacteria are
Classical signs present.
● Conjunctivitis, initially acute but ● Use a dry swab, and roll well to get sufficient tissue
progressing to chronic inflammation. for the test.
● Sneezing and nasal discharge is usually PCR is becoming more commonly available from
mild and often becomes chronic. diagnostic laboratories, and is the technique now used
predominantly for studies involving chlamydophila.
See other reference on page 1215 for details (The Cat
With Ocular Discharge or Changed Conjunctival
Appearance). Differential diagnosis
Herpesvirus generally produces more severe ocular-nasal
Pathogenesis discharge and systemic signs. If ulcerative keratitis is pres-
ent, it is usually diagnostic for herpesvirus.
Chlamydophilosis causes approximately 20% of upper
respiratory tract disease in cats, but is a frequent cause Calicivirus typically causes oral ulcers, which are not
of conjunctivitis. present with chlamydophila.
Infection may occur concurrently with herpes or cali- Mycoplasma may not be clinically distinguishable
civirus infection. from chlamydophila.
Treatment Clinical signs

Use tetracycline ophthalmic ointment. Continue for Conjunctivitis is initially unilateral, progressing to
10 days after clinical remission (usually 2–4 weeks of bilateral involvement.
treatment 3–4 times daily). Avoid use of bacitracin- ● Conjunctiva may be normal, hyperemic or edema-
neomycin-polymyxin ointment because of reports of tous.
acute death associated with its use. ● In severe infections, conjunctiva may be covered in
a gray pseudomembrane (diptheritic membrane).
Oral doxycycline therapy may also be required in
resistant cases. It is excreted in tears, and is also effec- Nasal discharge is mild, and results from ocular dis-
tive as a sole agent. Treat for 21 days, although up to 6–8 charge draining into the nose.
weeks treatment may be required in refractory cases.
Oral azithromycin (Zithromax, Pfizer, 5 mg/kg q 24 h Diagnosis
PO for 14 days) is an alternative treatment to tetracy- Diagnosis is based on visualization of clusters of coc-
cline. coid or coccobacillary organisms in the periphery of
Some chronic cases may require long-term systemic epithelium cells from stained (e.g. Diff-Quik stain)
therapy. conjunctival scrapings.
Isolation of the organism can be done in most labora-
Prognosis tories from clean conjunctival swabs. Remove ocular
discharges with sterile normal saline solution prior to
Chlamydophilosis frequently progresses to chronic taking the sample, to reduce contamination from sec-
signs, with conjunctival thickening and prominent con- ondary bacterial infections.
junctival lymphoid follicles.
Untreated cats frequently relapse after apparent recovery. Differential diagnosis
Chlamydophila has similar clinical signs, but is more
Transmission common.
Transmission is by direct contact with an infected cat.
Treatment
Chloramphenicol or doxycycline ophthalmic oint-
MYCOPLASMA ment (6 mm (1/4 inch) strip q 6 h).
Classical signs
BORDETELLA
● Conjunctivitis with purulent ocular
discharge; unilateral progressing to Classical signs
bilateral.
● Pyrexia.
● Sneezing and nasal discharge.
See main reference on page 1218 for details (The Cat
● Mandibular lymphadenopathy.
With Ocular Discharge or Changed Conjunctival
● Coughing.
Appearance).
● Dyspnea, cyanosis, pneumonia.
Pathogenesis
Pathogenesis
Causal agents are Mycoplasma felis and M. gatae.
Bordetella bronchiseptica may act as a primary
Mycoplama more often plays a secondary role to pathogen, or play a secondary role to herpesvirus or
herpesvirus or calicivirus infections. calicivirus infection.
Infection appears widespread in the feline popula- Differential diagnosis

tion. B. bronchiseptica may be a normal commensal in
the respiratory tract of cats, because it can be isolated Herpesvirus and calicivirus can have similar signs, and
from many healthy cats. It can be isolated from as many mixed infections are common, making definitive diag-
as 20% of cats in rescue catteries. The lowest rates of nosis impossible based solely on signs.
isolation are from one- and two-cat households.
Treatment
Overgrowth of the organism may produce upper res-
piratory tract inflammation or pneumonia. Use appropriate antibiotics based on susceptibility
data and the ability to reach therapeutic concentra-
Severe cases with bronchopneumonia have occurred tions in respiratory secretions such as oxytetracy-
in situations of overcrowding and other stress factors. cline, doxycycline or enrofloxacin. Beware of
The incidence in cats is reported to be higher in house- sudden retinal degeneration if using enrofloxacin.
holds where signs were present in dogs. Montelukast (Singulaire, 0.25–1 mg/kg SID) is a
In most cats, signs resolve after approximately leukotriene receptor blocker. Although the cat has insuf-
10 days. Occasionally, coughing persists longer. ficient leukotriene receptors for cysteinyl leukotrienes to
cause bronchoconstriction, anecdotal evidence suggests
that montelukast may reduce sneezing and nasal dis-
charge associated with Bordetella. This effect may be
Clinical signs mediated through blockage of leukotriene-mediated
Signs are most likely to occur in cats from multi-cat attraction of inflammatory cells such as eosinophils and
environments, especially rescue or shelter catteries, neutrophils, and their subsequent release of inflamma-
where calicivirus and herpesvirus are also a problem. tory cytokines and other chemicals.
Typically there is an acute onset of pyrexia, and Prevention

sneezing and nasal discharge.
An intranasal modified live vaccine is available which
Mandibular lymphadenopathy may be palpable. does not prevent or eliminate infection with Bordetella,
Coughing may be spontaneous, or only evident on tra- but usually prevents severe overgrowth and clinical signs.
cheal pressure. Generally, coughing is not as pro- It is most useful in catteries or shelters with culture-
nounced as in dogs. proven outbreaks of disease. It is effective in 3–5 days.
Dyspnea, cyanosis, crackles and wheezes may be aus- The rate of adverse signs (e.g. sneezing) associated
cultated over lung fields in some cats. Death from with Bordetella vaccination probably exceeds the fre-
pneumonia may occur, especially in young kittens less quency of disease caused by the organism in cats living
than 8 weeks old. in one- or two-cat households.
Improve cattery/shelter conditions to decrease over-
crowding if the organism appears to be causing recur-
Diagnosis rent problems.
Bacteria can be isolated from the nasal discharge,

oropharyngeal secretions, tonsillar swabs, or a transtra- FOREIGN BODY
cheal wash.
● Samples should be transported in special medium Classical signs
(e.g. charcoal Amies transport medium), and need ● Acute onset of sneezing and face rubbing,
special media for culture. progressing to chronic signs.
● Although B. bronchiseptica is a normal commensal
● Unilateral discharge.
in many cats, in cats with disease from the organism, ● Gagging.
large numbers of organisms are often isolated.
See main reference on page 28 for details (The Cat Upper respiratory tract signs are most common, and
With Chronic Nasal Disease). include sneezing, snuffling and chronic nasal dis-
charge.
Grass or seeds may occasionally enter the nose of
Nasal discharge may be unilateral or bilateral, and
cats. Other foreign bodies such as gun pellets are less
serous, mucopurulent or hemorrhagic.
common.
Distortion and swelling over the bridge of nose, or a
polyp-like mass projecting from the nasal cavity are
Clinical signs
present in 70% of cats with the respiratory form.
Typically there is an acute onset of sneezing and dis-
Depression, anorexia or inappetence and weight loss are
tress, and rubbing at the face.
often present with nasal or CNS involvement.
Signs may progress to chronic gagging, or sneezing and
Submandibular lymph nodes are often enlarged.
discharge.
A unilateral serosanguinous discharge is typically Diagnosis
present.
Diagnosis is based on cytological identification of the
organism in nasal discharge, exudate from skin lesions,
lymph node aspirate, cerebrospinal fluid (CSF), or ocu-
Diagnosis
lar aspirate. Cryptococcus appears as yeast-like organ-
Visualize foreign body using an otoscope, fiberoptic isms (5–15 μm) surrounded by a wide, clear capsule.
scope, or with a dental mirror in the nasopharynx. Use
Serology to detect cryptococcal capsular antigen in
a spay hook to retract the soft palate for better visuali-
blood, CSF, or urine is sensitive and specific.
zation.
Tissue biopsy of the granulomatous mass or skin lesion,
Flushing the nose using a naso-esophageal feeding
and histological identification of the organism may be
catheter may remove parts or all of the whole foreign
required if cytology is negative.
body for diagnosis.
Fungal isolation with culture is rarely required for
diagnosis, but is useful for sensitivity testing.
CRYPTOCOCCOSIS
BLEEDING ULCER ON EXTERNAL NARES
Classical signs
Classical signs
● Chronic nasal discharge and sneezing,
progressing in severity. ● Bleeding ulcer on external nares.
● Soft tissue swelling over the nasal bones ● ± Sneezing.
(Roman nose), or polyp-like mass in nasal
cavity. See main reference on page 27 for details (The Cat
● Facial distortion. With Signs of Chronic Nasal Disease).
See main reference on page 25 for details (The Cat With Clinical signs
Signs of Chronic Nasal Disease).
Acute sneezing and/or discharge may occasionally
occur associated with a bleeding ulcer on the external
nares, particularly the nasal septum. It is usually asso-
Clinical signs
ciated with squamous cell carcinoma (SCC), but
Occasionally, the initial signs of cryptococcosis are occasionally with eosinophilic granuloma or with
acute in onset. acute calicivirus infection.
Diagnosis ● Radiography demonstrates increased opacity of

the nasal cavity and often destruction of the
Cytological examination of an impression smear, or turbinates, nasal septum, lateral bone and loss of
biopsy and histological examination of the lesion is teeth adjacent to the lesion. Radiographic changes
usually diagnostic for squamous cell carcinoma of the are often unilateral or asymmetrical.
external nares. ● A traumatic flush using a stiff catheter and
Eosinophilic granuloma requires biopsy for diagnosis. syringe (e.g. cut-off dog urinary catheter) yields
better results than an atraumatic flush.
Acute calicivirus infection is diagnosed based on clini- ● A biopsy is often required to obtain tissue for a his-
cal signs, and in some cases PCR. tological diagnosis. Tissue may be obtained using
biopsy forceps through the external nares or via a
INTRANASAL TUMORS rhinotomy.
Classical signs ALLERGIC RHINITIS

● Chronic nasal discharge and sneezing,
progressing in severity. Classical signs
● Facial distortion. ● Acute or chronic serous or mucoid nasal
discharge, often seasonal.
With Signs of Chronic Nasal Disease).
Clinical signs
Clinical signs
Allergic rhinitis appears to be a rare and poorly docu-
Acute sneezing and/or discharge may occasionally mented condition in cats.
occur associated with an intranasal tumor. Suspect
this disease when signs do not resolve over 2–3 weeks, It presents as serous or mucoid ocular and/or nasal dis-
and instead progress with worsening discharge, and charge without systemic signs, and may be seasonal in
often nasal distortion. occurrence.
Intranasal tumors are associated with chronic sneez- It has been reported associated with allergy to
ing and snuffling, which progressively worsen with Japanese cedar (Cryptomeria japonica).
time and a purulent or bloody nasal discharge, which
may temporarily respond to antibiotics. The dis- Diagnosis
charge may initially be unilateral and progress to bilat- Diagnosis is based on exclusion of all other causes of
eral involvement. nasal discharge, and biopsy results indicating rhinitis
Snoring, snorting, inspiratory stridor, stertor or with no evidence of underlying pathogens. A mixed
dyspnea may result from nasal obstruction. neutrophilic and eosinophilic rhinitis has been reported.
Facial distortion, e.g. elevation of bridge of nose Most cases with similar signs are the result of viral
(Roman nose) or facial swelling may occur. upper respiratory disease, often with chronic bacterial
rhinitis cases.
Diagnosis Treatment
Intranasal tumors usually require an invasive approach A combination of antihistamine and steroid may work
for diagnosis. Cytological examination of the discharge well in some cats. For example, trimeprazine tartrate (5
or atraumatic nasal flush usually reveals evidence of mg) and prednisolone (2 mg) in Temaril-P (1/4 to 1/2
inflammation (neutrophils and bacteria) but no tumor. tablet PO q 12–24 h).
RECOMMENDED READING
Binns SH, Dawson S, Speakman AJ, et al. A study of feline upper respiratory tract disease with reference to preva-
lence and risk factors for infection with feline calicivirus and feline herpesvirus. J Feline Med Surg 2000; 2(3):
123–133.
Gaskell R, Dawson S. Feline respiratory disease. In: Greene CE (ed.) Infectious Diseases of the Dog and Cat, 2nd
edn. Philadelphia, PA: WB Saunders Co., 1998, pp 97–106.
Jacobs GJ, Medleau L, Calvert C, et al. Cryptococcal infection in cats: factors influencing treatment outcome, and
results of sequential serum antigen titers in 35 cats. J Vet Int Med 1997; 11: 1–4.
Kate F, Hurley KF, Pesavento PA, et al. An outbreak of virulent systemic feline calicivirus disease. J Am Vet Med
Assoc 2004; 224(2): 241–249.
Lappin MR. Sneezing and nasal discharge; viral diseases. In: Lappin MR (ed.) Feline Internal Medicine Secrets, 1st
edn. Philadelphia, PA: Hanley and Belfus, 2001, pp 8–11.
Ramsey DT. Feline chlamydophila felis and calicivirus infections. Vet Clin North Am Small Anim Pract 2000; 30(5):
1015–1028.
Stein JE. Sneezing and nasal discharge; bacterial diseases. In: Lappin MR (ed.) Feline Internal Medicine Secrets, 1st
edn. Philadelphia, PA: Hanley and Belfus, 2001, pp 4–8.
Stein JE, Lappin MR. Bacterial culture results in cats with upper or lower respiratory disease. J Vet Int Med 2001;
15: 320.
Sykes JE. Feline upper respiratory tract pathogens: herpesvirus-1 and calicivirus. Compend Contin Educ Pract Vet
2001; 23(2): 166–175.
Sykes JE, Allen JL, Studdert VP, et al. Detection of feline calicivirus, feline herpesvirus 1 and Chlamydophila felis psittaci
mucosal swabs by multiplex RT-PCR/PCR. Vet Microbiol 2001; 81(2): 95–108.
3. The cat with signs of chronic nasal
disease. (chronic > 3 weeks duration)
Jacquie Rand
KEY SIGNS
● Chronic mucoid, purulent and/or bloody nasal discharge.
● Chronic sneezing or snuffling.
● Stertorous respiration, snoring, dyspnea or mouth breathing.
● Facial distortion or nasopharyngeal distortion.
● Gagging.
MECHANISM?
● Signs of chronic disease result from chronic inflammation or obstruction of the nasal struc-
tures or its junction with the pharynx.
WHERE?
● External nares, nasal cavity, frontal sinuses and nasopharynx
WHAT?
● Most cats with signs of chronic nasal disease have secondary bacterial infection following her-
pes or calicivirus infection; less common causes are Cryptococcus and neoplasia.

Diseases causing signs of chronic nasal disease
ANOMALY
● Congenital anomaly of the nose or hard palate**(p 27)
Breed-related obstruction of the external nares (e.g. Persian cats) causes chronic snuffling and ster-
torous respiration.
Cleft palate, and congenital anomalies of the nasal cavity cause signs in young kittens which
depend on the type and severity of the anomaly, e.g. nasal discharge and inability to suckle associ-
ated with a cleft palate.
MECHANICAL
● Foreign body (p 28)
Acute onset of sneezing and rubbing face or gagging, followed by chronic unilateral nasal dis-
charge and sneezing, or gagging. Often associated with a blade of grass, a grass seed or awn.
continued
19
continued
NEOPLASTIC
● Neoplasia**(p 23)
Chronic mucopurulent or hemorrhagic nasal discharge, often unilateral initially, but progressing to
bilateral; sneezing, stertorous respiration ± facial distortion.
● Nasopharyngeal polyp (p 30)
Chronic snuffling, stertorous respiration and dyspnea from nasal obstruction; retching or gagging
with eating, ± mucopurulent nasal discharge.
INFLAMMATION
●Secondary rhinitis associated with dental disease* (p 27)
Mild, chronic mucopurulent or hemorrhagic discharge and sneezing.
●Nasopharyngeal stenosis (p 30)
Chronic snuffling, partial nasal obstruction, retching or gagging with eating.
INFECTIOUS
Bacterial:
● Secondary bacterial rhinitis*** (p 21)
Occurs secondary to viral upper respiratory tract disease. Signs include chronic mucopurulent or
hemorrhagic nasal discharge, sneezing, stertorous respiration, occasionally nasal distortion.
Fungal:
● Cryptococcus*** (p 25)
Chronic mucopurulent or hemorrhagic nasal discharge, sneezing, stertorous respiration, distortion
over bridge of nose (Roman nose), polyp-like mass in nasal opening.
● Other fungi
Aspergillus, Penicillium, Sporothrix or other fungi are very rare causes of chronic nasal disease.
Chlamydophila felis and Mycoplasma:
● Chlamydophila felis (Chlamydophila felis psittaci) and mycoplasma (p 29)
Chronic ocular and nasal discharge, chronic conjunctivitis and sneezing.
Immune:
●Allergic rhinitis (p 31)
Acute or chronic serous or mucoid nasal discharge, which is often seasonal.
Trauma:
● Oronasal fistula or nasal fractures following trauma (p 29)
Chronic snuffling, sneezing and nasal discharge associated with cleft palate, oronasal fistula or
obstructed nasal cavity.
3 – THE CAT WITH SIGNS OF CHRONIC NASAL DISEASE 21
Careful history taking and physical examination help

INTRODUCTION localize the lesion.
Examination of the oropharynex under anesthesia and
MECHANISM? radiography aid localization and diagnosis.
Chronic nasal disease should be suspected when a cat
has any of the following signs for more than 3 weeks.
WHAT?
● Chronic sneezing or snuffling.
● Nasal discharge which may be mucoid, purulent The most common cause of chronic nasal disease is
or bloody. secondary bacterial infection following herpes or
● Signs of nasal obstruction, such as stertorous respi- calicivirus infection
ration (snoring), stridor (high-pitched whistling ● Less common causes are Cryptococcus and neoplasia.
indicating obstruction), dyspnea or mouth breathing. ● Foreign bodies are generally rare causes of
● Gagging. chronic nasal signs in cats.
● Facial distortion. – Grass in the nasopharyngnx is more common,
● Nasopharyngeal distortion or bulging of the soft and causes gagging.
palate into the oral cavity.
Diagnosis is based on history and physical examination
The nasal mucosa responds to chronic disease by findings, radiography, Cryptococcus titer, and cytolog-
increased mucoid discharge. ical or histopathological examination of tissue samples.
● A purulent discharge occurs with infection or
necrosis.
● Blood may be present if there is severe inflamma- DISEASES CAUSING SIGNS OF
tion or erosion. CHRONIC NASAL DISCHARGE
– Bleeding without other signs of nasal disease,
such as a purulent nasal discharge, may indicate
a systemic bleeding problem, rather than nasal
SECONDARY BACTERIAL RHINITIS***
disease.
Classical signs
Facial distortion occurs with neoplasia or chronic
● Chronic sneezing and snuffling following
infection.
acute upper respiratory tract signs.
● Fungal (usually Cryptococcus) more often causes
● Chronic mucopurulent nasal discharge.
nasal distortion than chronic bacterial infection.
● Stertorous respiration.
Gagging occurs when there is nasopharyngeal stimu- ● Occasionally, nasal distortion.
lation from a mass lesion, a foreign body, or caudal
nasal discharge.
Ciliated columnar epithelium lining of the nasal cav-
Pathogenesis
ity undergoes squamous metaplasia after her-
pesvirus infection. Secondary bacterial infection of the nasal cavity and
● This decreases mucociliary clearance and predis- sinuses following feline herpesvirus or calicivirus
poses to secondary bacterial infection. infection is one of the most common causes of chronic
sneezing and nasal discharge in cats.
WHERE? Feline herpesvirus (feline rhinotracheitis virus) pre-
disposes to persistent or recurring bacterial infection
Signs of chronic nasal disease result from problems in
of the nose and sinuses.
any of the following sites:
● External nares, nasal cavity, frontal sinuses and Herpesvirus causes structural changes in the nose
nasopharynx. and sinuses.
These changes decrease mucociliary clearance from the misdiagnosed as bacterial infection, because of the
nose, and cause nasal and sinus obstruction. presence of neutrophils and bacteria.
● Structural changes include necrosis of the nasal ● To exclude neoplasia, material must be collected via a
epithelium, squamous metaplasia, osteolysis of traumatic flush using a stiff polypropylene catheter
the turbinates, and mucosal gland hypertrophy. attached to a syringe, or via a biopsy using a pinch
● The result is decreased density of cilia and biopsy technique through the nares, or a core biopsy
increased viscosity of mucus. This decreases via a trephine, or surgical biopsy via rhinotomy.
mucociliary clearance from the nose and ● Cytological examination of the nasal discharge or
sinuses. atraumatic nasal flush is inadequate to exclude
● Persistent thickening of the lining tissues of the neoplasia as a cause of the secondary bacterial
nasal cavity and sinuses leads to nasal and sinus infection.
obstruction, predisposing to chronic sinusitis. ● Surgical rhinotomy and biopsy may be necessary
● The normal opening between the nasal cavity and to exclude neoplasia when the history and radi-
frontal sinuses is small in cats, and is relatively eas- ographic findings are equivocal.
ily obstructed.
Negative Cryptococcus titer.
Organisms most frequently isolated are those that
Check FeLV and FIV status.
comprise the normal flora of the nose (e.g.
Staphylococcus, Streptococcus, Pseudomonas).
Cats with feline immunodeficiency virus (FIV) or
feline leukemia virus (FeLV) may be more susceptible. Neoplasia produces similar signs, but duration of signs
is usually less than 6 months, and cats are often older
than 10 years of age. Radiographic lesions are often
Clinical signs unilateral or asymmetric, whereas chronic rhinitis
tends to be bilaterally symmetrical.
Chronic sneezing, snuffling and mucopurulent nasal
discharge is often present for months or years. Cryptococcosis produces similar signs, although 70% of
cats with nasal involvement have distortion over the
Stertorous respiration, (snoring) or stridor (whistling), bridge of the nose, or a polyp-like mass visible in the
may be audible from the nasal area. nasal cavity.
● Only rarely do cats with chronic bacterial infec-
Occasionally, nasal distortion is present when signs
have been present for years. tion have nasal distortion, and this is usually only
after signs have been evident for years.
● Diagnosis of cryptococcosis is based on finding evi-
Diagnosis dence of the organism on cytology, histology or

serology.
History of chronic snuffling following acute upper res-
piratory tract infection.
Treatment
Radiographic findings
Treatment requires prolonged antibiotic therapy for
● Usually there is loss of lucency in the nasal cavity
1–4 months. Many cats cannot be cured, and nasal dis-
(fluid density) and often in the frontal sinuses.
charge and sneezing persist, requiring repeated therapy
● Radiographic changes are usually bilaterally sym-
when signs are exacerbated. Different combinations of
metrical.
therapy work better in individual cats.
● Osteolysis of the turbinates and/or nasal septum
● Use broad-spectrum antibiotics, or base choice
may be evident.
on culture and sensitivity. Because of the large
Cytology or histology reveals many neutrophils with number of normal flora in the nasal cavity, culture,
intra- and extracellular bacteria, and no evidence of and therefore sensitivity results, are hard to inter-
Cryptococcus neoformans or neoplastic cells. pret. The best antibiotics to use are broad spectrum
● Beware of similar cytologic findings with neopla- with efficacy against anaerobes, and that penetrate
sia, and sometimes cryptococcosis. Often neoplasia is bone and cartilage.
– Commonly used antibiotics include doxycy- ● Leukotriene antagonists like zafirlukast

cline, cephalexin, amoxicillin-clavulanic acid, (Accolade; 0.5–1.0 mg/kg PO q 12–24 h) or mon-
clindamycin, enrofloxacin and azithromycin. telukast (Singulaire, 0.25–1.0 mg/kg SID) help by
Amoxicillin-clavulanic acid, metronidazole, clin- reducing pain and inflammation, and may be effec-
damycin and azithromycin are good first choices. tive in some cats.
– Doxycycline and metronidazole may be advanta-
If signs persist despite antibiotics, surgical removal of
geous because they have an immunomodulating
chronically inflamed tissue via a rhinotomy is some-
effect which may help reduce inflammation.
times successful.
– Azithromycin is attractive because of the alter-
● Surgery is generally more successful for chronic
nate day dosing, and in cattery and breeder situ-
sinusitis with radiographic evidence of fluid in the
ations the pharmacokinetics allow twice weekly
sinuses, than for chronic rhinitis. Opening the fora-
dosing (q 72 h).
men between the sinus and nasal passages facili-
● One regime that is effective in many cats is
tates drainage of the sinus.
enrofloxacin (Baytril; 2.5 mg/kg q 12 h for 30
● Surgery involves turbinectomy and/or ablation
days) together with azithromycin (Zithromax;
of the frontal sinuses. For frontal sinus ablation,
20 mg QD for 30–45 days).
the sinuses are curetted out, the periosteum
– Fluroquinolones, particularly enrofloxacin may
removed, and the cavity filled with subcutaneous
be associated with retinal degeneration and
abdominal fat or methylmethacrylic.
blindness, especially at high doses, and many
ophthalmologists avoid using these drugs. Interferon alone or with ATZ (zidovudine) or PMEA
● Cats with Pseudomonas cultured from the sinuses (phosphonomethoxyethyl adenine) may help in FeLV-
may respond to a long course of carbenicillin. and FIV-infected cats to stimulate immunity and
● If signs return rapidly after stopping antibiotics, improve signs.
long-term antibiotics administered once daily at
half the total daily dose may help control signs in
Prognosis
some cats. However, resistance to antibacterial
action commonly occurs, and a better strategy is a Most cats have a good quality of life, although
longer course of antibiotics based on culture and signs often persist and must be controlled with
sensitivity using dosages suitable for osteomyelitis, antibiotics.
followed by a course of antibiotics when signs
relapse.
Prevention
● Intranasally administered antibiotics such as
gentomicin ophthalmic drops sprayed into each Regular vaccination to prevent feline calicivirus and
nostril twice daily for 30 days may help, if the cat herpesvirus infection is recommended, because most
will tolerate them. chronic bacterial rhinitis occurs secondary to upper res-
● Acetylcysteine (Mucomyst) helps to liquefy piratory viral infection.
nasal secretions when used with nebulization, but
may be expensive for long-term use.
NEOPLASIA**
● In some cats, intermittent flushing of the nasal
cavity under anesthesia (with tracheal intubation)
Classical signs
can be useful in controlling clinical signs.
● Occasionally, cats will tolerate local instillation of ● Progressively worsening chronic sneezing
saline drops in the nasal cavity. This stimulates a and snuffling.
sneeze response and encourages evacuation of ● Purulent or blood-tinged nasal discharge,
mucus. which may temporarily respond to antibiotics.
● Individual cats may show improvement with anti- ● Epiphora, ± signs of retrobulbar pressure,
histamines especially second-generation antihista- e.g. exophthalmos.
mines such as loratidine (Claritin; 2.5 mg/day) ● Nasal obstruction, and occasionally facial
because of their anti-inflammatory effects as well distortion.
as their ability to dry up excessive mucus.
Pathogenesis ● Occasionally, central nervous system signs occur,

e.g. seizures, circling, ataxia, behavioral change.
Neoplasia may involve primarily the external nares, – Signs may be present for days, or in rare cases,
the nasal cavity or the paranasal sinuses. for as long as 2 years. Usually, signs are present
● Neoplasia typically causes purulent nasal dis-
for less than 6 months prior to diagnosis.
charge, bleeding, sneezing and/or obstruction.
Neoplasia involving primarily the external nares is Diagnosis
most commonly squamous cell carcinoma. Less fre-
quently fibrosarcoma or fibroma are involved. Cytological examination of an impression smear, or
● Squamous cell carcinoma usually occurs in older biopsy and histological examination of the lesion is
cats with a non-pigmented nose, that live in a sunny usually diagnostic for squamous cell carcinoma of the
climate and are outside during the day. external nares.
Neoplasia primarily involving the nasal cavity or the Intranasal tumors require a more invasive approach.
frontal sinuses is most commonly adenocarcinoma Cytological examination of the discharge or atraumatic
and lymphoma. nasal flush usually reveals evidence of inflammation
● Less common tumors are undifferentiated carci- (neutrophils and bacteria) but no tumor.
● Radiography demonstrates increased opacity of
noma or sarcoma, olfactory neuroblastoma,
fibrosarcoma, chondrosarcoma, chondroma, the nasal cavity and often destruction of the
osteosarcoma and squamous cell carcinoma. turbinates, nasal septum, lateral bone and loss
of teeth adjacent to the lesion. Radiographic
Neoplasia usually occurs in older cats (> 8–10 years). changes are often unilateral or asymmetrical.
● A traumatic flush using a stiff catheter and
Most occur in the caudal third of the nasal passage.
syringe (e.g. cut-off dog urinary catheter) yields
better results than an atraumatic flush.
Clinical signs ● A biopsy is often required to obtain tissue for a
Squamous cell carcinoma involving the external nares histological diagnosis. Tissue may be obtained
may cause sneezing and a bloody nasal discharge. using biopsy forceps through the external nares or
● Lesions causing signs of nasal disease many consist via a rhinotomy.
of a bleeding ulcer on the nasal septum, or an
advanced erosive lesion on the external nares. Differential diagnosis
– Signs may be present for months or years.
Cryptococcosis can produce very similar signs to
Intranasal tumors are associated with the following intranasal tumors. However, 70% of cats with crypto-
signs: coccosis have either distortion of the bridge of the
● Chronic sneezing and snuffling, which progres- nose or a polyp-like mass visible projecting from the
sively worsen with time. nasal cavity.
● Purulent or bloody nasal discharge, which may ● Most have a positive Cryptococcus titer.
temporarily respond to antibiotics. ● Cats with cryptococcosis tend to be younger than
– The discharge may initially be unilateral and cats with neoplasia.
progress to bilateral involvement. ● Chronic bacterial infection of the nasal cavity sec-
● Snoring, snorting, inspiratory stridor, stertor or ondary to viral upper respiratory disease may produce
dyspnea from nasal obstruction. similar signs. However, signs are typically present for
● Facial distortion, e.g. elevation of bridge of nose longer, and only very rarely is there nasal distortion.
(Roman nose) or facial swelling.
● Epiphora (associated with obstruction of the
Treatment
lacrimal duct), or a bloody ocular discharge.
● Signs of retrobulbar pressure may be present, e.g. Treatment of squamous cell carcinoma involving the
exophthalmos and ocular deviation. external nares depends on the extent of local invasion.
● Radiotherapy, cryotherapy, intralesional chemo- found in soil contaminated by pigeon droppings, and in
therapy, or resection of the nasal planum are the debris of pigeon roosts.
indicated depending on the lesion.
Cryptococcus neoformans gattii is found in the develop-
● If ulcerated and erosive, radical resection of the
ing flower of Red River gums and forest red gums; high
nasal planum yields best results.
concentrations of organisms are found in the bark and the
Lymphoma is best treated with radiotherapy and/or accumulated debris surrounding the base of the tree.
chemotherapy. ● These trees have been widely exported around the
world from Australia.
Other tumors of the nasal cavity have a guarded to poor
prognosis. At the time of diagnosis, there is usually Organisms are viable for at least 2 years, if protected
extensive local invasion, and the recurrence rate after from direct sunlight and drying.
radiotherapy and/or surgery is high.
Nasal infection occurs via inhalation of airborne
organisms or contamination of the wound with organ-
Prognosis isms.
● There are no reports of transmission between ani-
Squamous cell carcinoma of the external nares can
mals or people; infection is from the environment.
have a good prognosis if the lesion is small, or if radi-
● Cell-mediated immunity may be compromised in
cal resection of the nasal planum totally removes the
infected animals; there are some reports of a
tumor. Local recurrence may occur, but the tumor is
higher incidence of FIV infection in cats with
slow to metastasize.
Cryptococcus.
Lymphoma has a guarded prognosis, but may respond ● Cats are more susceptible than dogs or humans.
to chemotherapy or radiotherapy. ● Any age of cat can be infected, but the average age
is 5 years (younger than cats with neoplasia).
Other intranasal tumors have a very poor prognosis,
● Following inhalation, the organism deposits in the
especially if destruction of the turbinates is evident
upper respiratory tract producing nasal granu-
radiographically.
lomas, or deposits in the alveoli producing pul-
monary granulomas, which are usually subclinical.
● The organism may disseminate through the crib-
CRYPTOCOCCOSIS*–**
riform plate or via the blood to the central nervous
system (CNS).
Classical signs
● If CNS signs develop, cats may or may not have con-
● Chronic nasal discharge and sneezing, current signs of respiratory infection.
progressing in severity.
In cats with cryptococcosis, 50–80% have respiratory
● Soft-tissue swelling over the nasal bones
disease involving mainly the nasal cavity, and 10–40%
have cutaneous or subcutaneous lesions. Central
cavity.
nervous system (CNS) involvement and ocular dis-
ease are less common.
Pathogenesis
Clinical signs
Cryptococcus neoformans most commonly produces
Upper respiratory tract signs are most common, and
granulomatous lesions in the nasal cavity or paranasal
include sneezing, snuffling and chronic nasal discharge.
sinuses.
● Nasal discharge may be unilateral or bilateral, and
Disease is caused by Cryptococcus neoformans neofor- serous, mucopurulent or hemorrhagic.
mans or Cryptococcus neoformans gattii.
Distortion and swelling over the bridge of the nose,
Cryptococcus neoformans neoformans is shed in or a polyp-like mass projecting from the nasal cavity
pigeon feces; high concentrations of organisms are are present in 70% of cats with the respiratory form.
Depression, anorexia or inappetence and weight loss are Differential diagnosis

often present with nasal or CNS involvement.
Neoplasia may have similar signs. The presence of a
Submandibular lymph nodes are often enlarged. polyp-like mass in the nose, or swelling over the bridge
Skin lesions consist of papules or nodules varying of the nose suggest cryptococcosis rather than neopla-
from 0.1–1 cm in diameter. sia. Cats with neoplasia are on average older than cats
● Lesions may ulcerate and exude serous fluid, or
with cryptococcosis.
remain as intact nodules. Chronic bacterial infection of the nasal cavity sec-
● Skin lesions may be single or multiple, and occur ondary to viral upper respiratory disease has similar
alone, or with involvement of other organs. signs. However, it is only rarely associated with nasal
Central nervous system signs result from inflamma- distortion.
tion of the brain and meninges or a mass lesion (granu-
loma). Treatment
● Signs reported are referable to the cerebrum Best success occurs using a multi-drug regime
(seizures, circling, ataxia, behavioral change, head comprising of amphotericin (fungicidal) plus 5-fluo-
pressing, blindness), or brainstem (head tilt, nys- rocytosine (flucytosine), combined with or followed by
tagmus, facial paralysis, paresis, ataxia, circling). fluconazole or itraconazole (fungistatic).
● Occasionally, signs are referable to the spinal cord. ● Amphotericin B is very nephrotoxic, so use
Ocular signs include epiphora, dilated unresponsive diuresis to protect the kidneys. Liposomal or lipid-
pupils, blindness and anterior uveitis. encapsulated amphotericin B are safer than regular
amphotericin B but are expensive.
Occasionally, other organs are involved, e.g. bone, – Amphotericin B can be given IV (see standard texts)
kidney. or SC (0.5–0.8 mg/kg) in 400 ml of 0.45% saline
containing 2.5% dextrose. Administer subcuta-
Diagnosis neously two or three times a week for 1–3 months,
Diagnosis is based on cytological identification of the until a total cumulative dose of 12–26 mg/kg is
organism in nasal discharge, exudate from skin reached. Monitor serum creatinine, urea (more sen-
lesions, lymph node aspirate, cerebrospinal fluid (CSF) sitive, but influenced by many non-renal factors)
or ocular aspirate. and urine specific gravity and sediment for casts. If
● Stain sample with new methylene blue, Indian ink
azotemia develops, discontinue amphotericin until
or Diff-Quick. it resolves and reduce dose (Malik et al. 1996).
● Cryptococcus appears as yeast-like organisms Sensitivity to amphotericin toxicity varies consider-
(5–15 μm) surrounded by a wide, clear capsule. ably between cats, and some cats develop acute renal
● Organism buds from a narrow base, in contrast to failure with relatively small doses. It is imperative that
Blastomyces which has broad-based budding and serum urea concentration and urine are checked prior
thinner capsule. to each dose. The client should be instructed to return
Serology to detect cryptococcal capsular antigen in immediately if the cat becomes lethargic, inappetent or
blood, CSF, or urine is sensitive and specific. is vomiting.
Tissue biopsy of the granulomatous mass or skin lesion, Combine with 5-fluorocytosine 50 mg/kg q 8 h PO.
and histological identification of the organism may be Either during or after the course of amphotericin is
required if cytology is negative. completed, use an imadizole/triazole to mop up infec-
Fungal isolation with culture is rarely required for tion (fungistatic):
● Ketaconazole is cheapest, but has most side effects
diagnosis, but is useful for sensitivity testing.
(anorexia, vomiting, hepatic disease) and is perhaps
Radiographs often reveal turbinate lysis and opacity least potent (10 mg/kg PO q 12–24 h).
of the nasal cavity (soft-tissue density). Sinus involve- ● Itraconazole may work better than ketaconazole,
ment is common. and has fewer side effects (5 mg/kg PO q 12–24 h).
● Fluconazole is better for CNS infection, but is Clinical signs

expensive (2.5–10 mg/kg PO q 12 h).
Typically, there is chronic snuffling and stertorous
Approximately 3 weeks of treatment are required respiration from the nasal region. Signs may be evi-
before there is an improvement in clinical signs. dent most or all of the time if the stenosis is severe.
A decreasing serum Cryptococcus titer is predic- Dyspnea or mouth breathing occurs with stress.
tive of recovery, but depending on the laboratory, it
may be expensive to get the actual titer measured. Narrow external nares are visible on physical examination.
Clinical signs return if treatment is stopped too early. Diagnosis

Ideally, treat until titer is negative, which may be
longer than 1 year. However, some healthy cats remain The diagnosis is usually based on clinical signs (nasal
antibody positive. If the cat is clinically healthy and the stridor) and physical examination (stenotic nares).
titer drops 16–32-fold, it is unlikely to relapse.
Alternatively treat for 4 weeks after resolution of all signs, Differential diagnosis
with a minimum treatment period of 8 weeks. Relapses The features of stenotic nares (signs since the cat was a
are more common with these shorter treatment periods. young adult, cranial nasal stertor and narrow external
nares) make most other diseases unlikely.
Prognosis Treatment
Prognosis is variable. A falling titer in response to ther- Treatment involves surgical removal of the wing of the
apy suggests optimistic prognosis for cure. Prognosis is nostril.
guarded if there is CNS involvement.
Prognosis
CONGENITAL ANOMALY OF THE NOSE Prognosis is good with surgery, provided there is not
OR HARD PALATE** concurrent marked narrowing of the nasal cavity.
Classical signs SECONDARY RHINITIS ASSOCIATED WITH

● Chronic snuffling and stertorous DENTAL DISEASE*
respiration.
● Dyspnea or mouth breathing. Classical signs
● Narrow external nares. ● Chronic sneezing.
● Chronic unilateral or bilateral
mucopurulent nasal discharge, which may
Pathogenesis be bloody.
● Oronasal fistula.
Congenital stenosis of the external nares is common
in some breeds, e.g. Persians, Himalayans.
● The combined effects of stenosis of the external Pathogenesis
nares and reduced nasal air space cause respiratory
obstruction. An oronasal fistula may result in low-grade chronic
● Partial obstruction results in increased respiratory
rhinitis, because food and fluids enter the nose from
effort and stertorous respiration. the mouth.
● With stress (e.g. visit to veterinarian or cat show), An oronasal fistula usually results from advanced
stridor becomes more pronounced, and cats may periodontal disease of the canine teeth, with or with-
become severely dyspneic and mouth breath. out loss of the tooth.
● Often, the tooth is still present, and a deep peri-

FOREIGN BODY
odontal pocket extends into the nasal cavity or
maxillary sinus.
Classical signs
● Occasionally, a periapical abscess from a dental
fracture or caries results in rhinitis. ● Acute onset of sneezing and rubbing face,
● Iatrogenic oronasal fistula may result from poor progressing to chronic signs.
dental extraction technique. ● Unilateral discharge.
● Gagging.
Clinical signs
Chronic sneezing, and mucopurulent nasal dis- Pathogenesis
charge, which may be blood-tinged.
Most foreign bodies are of plant origin, and are either
Presence of an oronasal fistula associated with tooth grass, grass seeds or awns.
loss or advanced periodontal disease, or a tooth fracture
suggesting a periapical abscess. Shotgun or airgun pellets, wood or bone are less fre-
● Examination under deep sedation or general anes- quent.
thesia is often required for diagnosis.
Clinical signs
Diagnosis
Signs depend on where the foreign body lodges.
Diagnosis is based on signs of chronic nasal disease Foreign bodies lodging in the nasal cavity cause
and the presence of an oronasal fistula. sneezing and nasal discharge. Blades of grass tend to
Rarely, a periapical abscess is the cause. This is visible lodge in the nasopharynx and produce gagging.
on radiograph. Typically, there is a sudden onset of:
● Sneezing, which initially is marked and paroxys-
Differential diagnosis mal, and then becomes chronic.

● Rubbing or pawing at the nose.
Visualization of the oronasal fistula is diagnostic. ● Unilateral nasal discharge, which is initially
● Very rarely another disease process is also present, serous or blood-tinged, but progresses to mucopu-
and is responsible for the signs of chronic nasal dis- rulent and may be bloody.
ease, e.g. oronasal fistula with concurrent neoplasia ● Gagging occurs when the foreign body lodges in the
or chronic bacterial infection secondary to viral nasopharynx, or discharge drains into the pharynx
upper respiratory tract disease. from a foreign body in the posterior nasal cavity.
● Radiograph the nose prior to surgery. Evidence
of turbinate lysis suggests tumor, cryptococcosis or
chronic bacterial rhinitis secondary to herpesvirus. Diagnosis
● Failure to respond to surgery suggests another dis-
Diagnosis is based on visualizing the foreign body using:
ease process. ● An otoscope or rhinoscope for foreign bodies in
the anterior nasal cavity.
Treatment ● A dental mirror (warmed and sprayed with
defogging agent) for foreign bodies in the caudal
Seal oronasal fistula surgically using a mucoperiosteal
nasal cavity and nasopharynx. Pull the soft palate
pedicle flap.
rostrally to improve the view.
● A nasal flush may remove all or parts of the foreign
Prognosis body for diagnosis.
● Rhinotomy, when all else fails.
Prognosis is excellent, if the fistula is successfully
closed, but some fistulas may be difficult to close. Radiographs are rarely diagnostic, except for gun pellets.
Differential diagnosis Clinical signs

Chronic bacterial rhinitis secondary to viral upper Typically there is chronic snuffling, sneezing and nasal
respiratory infection may produce similar laboratory discharge in a cat that sustained facial injuries in a fall
findings with neutrophils and bacteria, and no neoplas- or car accident.
tic or fungal elements. However, the discharge is typi-
Examination reveals a split hard palate either cen-
cally bilateral, whereas with a foreign body it is
trally along the palatine symphysis, or laterally
typically unilateral.
adjacent to the teeth along the maxillary symphysis.
Neoplasia and cryptococcosis may have similar
Signs often resolve spontaneously with spontaneous
signs, and the discharge is initially often unilateral.
healing of the cleft.
Positive diagnosis can be difficult with neoplasia and
foreign bodies, and may require a rhinotomy.
Diagnosis
Diagnosis is based on a history of trauma, signs of
Treatment nasal disease and visual evidence of the cleft.
Treatment involves removing the foreign body by
flushing, or grasping with forceps via the nares, Differential diagnosis
nasopharynx or rhinotomy.
Congenital cleft palate may look similar, but usually
signs are present from a few weeks of age, rather than
a recent onset following trauma.
Prognosis
Oronasal fistula associated with dental disease may
The prognosis is excellent if the foreign body can be
produce similar signs; evidence of advanced peri-
entirely removed.
odontal disease and lack of history or evidence of
facial trauma should allow differentiation.
ORONASAL FISTULA OR NASAL Treatment

FRACTURES FOLLOWING TRAUMA
If spontaneous resolution does not occur in 2–3 weeks,
Classical signs surgical repair is necessary.
● Chronic snuffling, sneezing and nasal

discharge. Prognosis
● Cleft hard palate (lateral or midline). Good.
CHLAMYDOPHILA FELIS
(CHLAMYDOPHILA FELIS PSITTACI) AND
Pathogenesis
MYCOPLASMA
Cats that have been hit by a car, or have jumped out
of a high-rise building often have splitting of the Classical signs
hard palate along the symphyses.
● Chronic ocular-nasal discharge.
Signs of chronic nasal discharge and sneezing result ● Chronic conjunctivitis.
when food and water enter the nasal cavity. ● Chronic sneezing.
Spontaneous healing of the cleft often occurs within
See main references on page 13 for details (The Cat
2–3 weeks.
With Acute Sneezing or Nasal Discharge) and Page
If the hard palate is shattered into several pieces, necrosis 1215 (The Cat With Ocular Discharge or Changed
of a fragment may occur, forming an oronasal fistula. Conjunctival Appearance).
Clinical signs Stertorous respiration (snoring) or stridor (whistling

noise) may be evident, and results from partial nasal
Chlamydophilia and mycoplasma infection may result in obstruction. Dyspnea may occur, particularly when the
chronic mucopurulent ocular and nasal discharge. cat is stressed.
Typically there is chronic conjunctivitis. Follicular Retching or gagging may occur on eating.
hyperplasia of lymphoid tissue in the conjunctiva and
nictitating membrane is often visible as multiple, small No or minimal nasal discharge is present.
white nodules.
Chronic sneezing may occur.
Diagnosis
Diagnosis With the cat under general anesthesia, visualize the
stenosis with a dental mirror. Pull the soft palate ros-
A presumptive diagnosis is often made based on trally for an improved view.
signs. A definitive diagnosis is based on identification ● Stenosis is visible as a pin-point opening in the
of the organism. nasopharynx. The normal opening is approxi-
● Examine a stained (e.g. Diff-Quick) preparation of
mately 5 mm in diameter.
a conjunctival scraping or smear obtained with a
dry cotton bud. Chlamydophila felis infection is Radiographs are generally normal.
associated with inclusion bodies in epithelial cells
but they are difficult to identify in chronic disease. NASOPHARYNGEAL POLYP
Mycoplasma is seen as clusters of coccoid or coc-
cobacillary organisms in the periphery of epithe- Classical signs
lium cells.
● Stertorous respiration from nasal area, or
Antibody-based detection in conjunctival scrapings dyspnea.
using ELISA or latex agglutination may be useful for ● ± Nasal discharge.
Chlamydophila felis, but false positives occur with
both tests if many bacteria are present. See main reference on page 37 for details (The Cat
Polymerase chain reaction (PCR) and IFA tech- With Stridor).
niques for detection of the organisms are also available
from some laboratories. Clinical signs
Stertorous respiration is audible from the nasal area.
If the obstruction is severe, there may be dyspnea, and
NASOPHARYNGEAL STENOSIS
open mouth breathing may occur with stress.
Classical signs There may be no nasal discharge, or a mucopurulent
discharge may be evident.
● Stertorous respiration from nasal area,
± dyspnea. Discharge from ear and signs of otitis media may also
● No nasal discharge. be present.

Diagnosis
With Stridor).
With the cat under general anesthesia, visualize the
polyp directly or with a dental mirror. Pull the soft
Clinical signs
palate rostrally for an improved view. The rostral soft
Chronic snuffling is typically present for 3 months to palate may bulge down into the oral cavity with pres-
2 years. sure from the polyp.
Radiography reveals a rounded density in the Diagnosis

nasopharynx, just caudal to the hard palate.
Diagnosis is based on exclusion of all other causes
of nasal discharge and biopsy results indicating rhini-
ALLERGIC RHINITIS tis with no evidence of underlying pathogens.
A mixed neutrophilic and eosinophilic rhinitis has
Classical signs been reported.
● Acute or chronic serous or mucoid nasal Most cases with similar signs are the result of viral
discharge, often seasonal. upper respiratory disease often with chronic bacterial
rhinitis cases.
Clinical signs Treatment

Allergic rhinitis appears to be a rare and poorly docu- A combination of antihistamine and steroid may work
mented condition in cats. well in some cats. For example, Temaril-P (1/4 to 1/2
It presents as serous or mucoid ocular and/or nasal dis- tablet PO q 12–24 h).
charge, with no systemic signs and is typically seasonal
in occurrence.
It has been reported associated with allergy to
Japanese cedar (Cryptomeria japonica).
RECOMMENDED READING
Disorders of the nasal cavity In: Nelson RW, Couto CG (eds) Small Animal Internal Medicine, 2nd edition. St Louis,
Mosby, 1998, pp 225–237.
Gaskell R, Dawson S. Feline respiratory disease. In: Greene CE (ed) Infectious Diseases of the Dog and Cat, 2nd edi-
tion. Philadelphia, WB Saunders Co., 1998, pp 97–106.
Jacobs GJ, Medleau L, Calvert C, et al. Cryptococcal infection in cats: factors influencing treatment outcome, and
results of sequential serum antigen titers in 35 cats. J Vet Int Med 1997; 11: 1–4.
Lappin MR. Sneezing and nasal discharge; viral diseases. In: Lappin MR (ed) Feline Internal Medicine Secrets, 1st
edition, Hanley and Belfus, Philadelphia, 2001, pp 8–11.
Malik R, Craig AJ, Wigney DI, et al. Combination chemotherapy of canine and feline cryptococcosis using subcu-
taneous administered amphotericin B. Aust Vet J 1996; 73: 124–128.
O’Brien RT, Evans SM, Wortman JA, Hendrick MJ. Radiographic findings in cats with intranasal neoplasia or
chronic rhinitis: 29 cases (1982–1988). J Am Vet Med Assoc 1996; 208: 385–389.
Stein JE. Sneezing and nasal discharge; bacterial diseases. In: Lappin MR (ed) Feline Internal Medicine Secrets, 1st
edition. Hanley and Belfus, Philadelphia, 2001, pp 4–8.
Stein JE, Lappin MR. Bacterial culture results in cats with upper or lower respiratory disease. J Vet Int Med 2001;
15: 320.
4. The cat with stridor or stertor
Jacquie Rand and Robert Allen Mason
KEY SIGNS
● Stridor.
● Snuffling.
● Snoring.
MECHANISM?
● Stridor is a harsh, high-pitched respiratory sound and stertor is a snoring sound created by upper
airway obstructive diseases, such as laryngeal obstruction. Airflow through a narrowed upper
airway has increased resistance and becomes more turbulent.
● With dynamic obstructions, such as laryngeal paralysis and tracheal collapse, the airflow
limitation occurs mainly during inspiration. Fixed obstructions, such as foreign objects and
mass lesions, affect airflow during both inspiration and expiration.
WHERE?
● Stridor or stertor arise from luminal narrowing in the upper airways, generally involving the
pharynx, soft palate, laryngeal structures and the upper trachea. Nasal stridor may also be
encountered.
WHAT?
● Most cats with respiratory stridor have nasal disease. Persians and Himalayans frequently have
respiratory stridor from stenotic nares. Chronic bacterial rhinitis following viral upper respiratory
tract infection, neoplasia or Cryptococcus infections are the most common acquired causes of stridor.
NASAL STRIDOR
Diseases causing stridor or stertor
ANOMALY
● Stenosis of the external nares** (p 35)
Breed-related obstruction of the external nares (e.g. Persian cats) causes chronic snuffling and ster-
torous respiration.
32
4 – THE CAT WITH STRIDOR OR STERTOR 33
MECHANICAL
● Foreign body (grass, grass seed, awn) (p 40)
Acute onset of sneezing and rubbing face or gagging followed by chronic unilateral nasal dis-
charge and sneezing. Occasionally stridor.
NEOPLASTIC
● Neoplasia** (p 36)
Chronic mucopurulent or hemorrhagic nasal discharge, often initially unilateral progressing to
bilateral, sneezing, stertorous respiration ± facial distortion.
● Nasopharyngeal polyp (p 37)
Chronic snuffling, stertorous respiration and dyspnea from nasal obstruction, retching or gagging
with eating ± mucropurulent nasal discharge.
INFLAMMATION
● Nasopharyngeal stenosis (p 38)
Chronic snuffling, partial nasal obstruction, retching or gagging with eating.
INFECTIOUS
Bacterial:
● Secondary bacterial rhinitis*** (p 35)
Typically there is a history of signs of chronic bacterial rhinitis occurring following acute viral
upper respiratory tract disease. Signs include chronic mucopurulent or hemorrhagic nasal dis-
charge, sneezing, stertorous respiration and occasionally nasal distortion.
Fungal:
● Cryptococcosis and other fungi** (p 36)
Cryptococcosis typically results in chronic mucopurulent or hemorrhagic nasal discharge, sneez-
ing, stertorous respiration and distortion over bridge of nose (Roman nose), or a polyp-like mass in
the nasal opening. Occasionally there are signs of a nasopharyngeal mass only. Other fungi such as
Aspergillus, Penicillium, Sporothrix and some other fungi are very rare causes of chronic nasal
disease.
Chlamydophila and Mycoplasma spp:
● Chlamydophila and Mycoplasma spp (p 38)
Chronic ocular and nasal discharge, and chronic conjunctivitis. Sneezing and occasionally stridor.
Trauma:
● Oronasal fistula or nasal fractures following trauma (p 39)
Chronic snuffling, sneezing, stridor or stertor and nasal discharge associated with cleft palate or
obstructed nasal cavity.
continued
continued
STRIDOR FROM PHARYNGEAL, LARYNGEAL OR TRACHEAL AREA
Degenerative:
● Laryngeal paralysis (p 43)
Generally neurogenic paresis/paralysis of the abductor muscles of the arytenoid cartilages of the
larynx. Often idiopathic, although traumatic causes are reported. Inspiratory dyspnea with stertor
(snoring sounds) or stridor (whistling obstructive sounds) is the hallmark of laryngeal paralysis.
Changes in voice and character of purring are often reported by owner.
● Tracheobronchial collapse (p 44)
Harsh, “honking” cough caused by degeneration of the cartilage support of the large airway walls.
If upper cervical trachea is involved, stridor may be present. Rare in cats.
Anomaly:
● Congenital anomalies of the upper respiratory tract* (p 39)
Dyspnea usually indicates fixed obstruction (inspiratory and expiratory) because of the stenotic
nature of most defects. Inspiratory dyspnea, stertor and stridor occur with the brachycephalic syn-
drome.
Mechanical:
● Airway foreign bodies (p 40)
Harsh, productive cough and acute dyspnea occur with foreign objects that have been inhaled,
regurgitated or aspirated into the nasopharynx, trachea or bronchi. Stridor is noted when the foreign
body is lodged in the larynx or trachea. Nasal foreign bodies create a form of stridor that has a more
whistling character than laryngeal stridor. Sneezing and nasal discharge are common with nasal
foreign bodies.
Neoplastic:
● Airway tumors (p 41)
Signs depend on the site of the tumor. Nasal tumors causing obstruction may produce stridor and
open-mouth breathing. Pharyngeal tumors causing obstruction may result in dysphagia, stridor,
stertor and voice changes. Tracheal tumors result in a fixed obstruction, and inspiratory and expira-
tory dyspnea, stridor and commonly a cough.
Inflammation:
● Laryngeal edema (p 42)
Usually occur secondary to an allergic reaction, following alphaxalone/alphdolone anesthesia or
laryngeal trauma. Signs include inspiratory dyspnea and stertorous breathing or stridor.
● Laryngeal stenosis (p 42)
Common in cats after laryngeal trauma or surgery. Results in dyspnea and stridor on inspiration.
● Laryngeal eosinophilic granuloma (p 45)
Occurs weeks or months after signs of viral upper respiratory tract infection. Signs include stridor
from the laryngeal region and swollen, edematous arytenoid cartilages of larynx.
INTRODUCTION DISEASES CAUSING NASAL STRIDOR
MECHANISM? SECONDARY BACTERIAL RHINITIS***

Airflow through a narrowed upper airway has increased
Classical signs
resistance and becomes more turbulent. This resistance
is a function of the diminished luminal diameter of the ● Chronic sneezing and snuffling.
tube, the resistance increasing to the fourth power of ● Chronic mucopurulent nasal discharge.
the radius. ● Stertorous respiration or stridor.
● Occasionally, nasal distortion.
With dynamic obstructions, dyspnea occurs during
inspiration, because the negative intraluminal airway
pressure creates a vacuum, pulling the walls inwardly.
Any weakened area of the airway wall will tend to
move into the lumen, decrease the luminal diameter,
Clinical signs
and create an obstruction.
Chronic secondary bacterial rhinitis occurs in some
Fixed obstructions cause both inspiratory or expira-
cats following viral upper respiratory tract disease.
tory stridor, although inspiratory noises are more
prominent. Typically there is a history of chronic sneezing and snuf-
fling following acute upper respiratory tract signs.
Stertor are snoring sounds. Stridor is a harsh,
high-pitched whistling respiratory sound created Chronic mucopurulent nasal discharge.
by upper airway obstructive diseases, such as the
Stertorous respiration (snoring) or stridor (high pitched
inspiratory sound of acute laryngeal obstruction.
whistling respiration).
Occasionally, nasal distortion.
WHERE?
Diagnosis
Stridor or stertor arise from luminal narrowing in the
upper airways, generally involving the pharynx, soft Diagnosis is based on a history of chronic signs of long
palate, laryngeal structures and the upper trachea. duration (>6 months), especially if the history includes
Nasal stridor or stertor may also be encountered. acute upper respiratory tract signs preceding the
chronic problem. Diagnosis is based on exclusion of
neoplasia and cryptococcosis.
WHAT?
With dynamic obstructions, the airflow limitation STENOSIS OF THE EXTERNAL NARES**
occurs mainly during inspiration. Dynamic obstruc-
tions include laryngeal paralysis, tracheal collapse Classical signs
and epiglottic entrapment.
● Chronic snuffling and stertorous
Fixed obstructions, such as foreign objects and mass respiration or stridor.
lesions, affect airflow during both inspiration and expi- ● Dyspnea or mouth breathing.
ration, although inspiratory noises are generally more ● Narrow external nares.
prominent.
Pathogenesis The discharge may initially be unilateral and

progress to bilateral involvement.
Congenital stenosis of the external nares is common in
some breeds, e.g. Persians, Himalayans. Snoring, snorting, inspiratory stridor, stertor or dyspnea
from nasal obstruction are common.
The combined effects of stenosis of the external
nares and reduced nasal air space cause respiratory Facial distortion, e.g. elevation of bridge of nose
obstruction. (Roman nose) or facial swelling may be evident.
Partial obstruction results in increased respiratory effort Epiphora (associated with obstruction of the lacrimal
and stertorous respiration or stridor. duct), or a bloody ocular discharge may occur.
With stress (e.g. visit to veterinarian or cat show), stri- Signs of retrobulbar pressure may be present, e.g.
dor becomes more pronounced, and cats may become exophthalmos and ocular deviation.
severely dyspneic and mouth breath. Occasionally, central nervous system signs, e.g.
seizures, circling, ataxia, behavioral change occur.
Clinical signs
Nasal signs may be present for days, or in rare cases,
Chronic snuffling and stertorous respiration or stridor. for as long as 2 years. Usually, signs are present for less
Dyspnea or mouth breathing. than 6 months prior to diagnosis.
Narrow external nares in a brachycephalic cat. Diagnosis

Diagnosis Radiography demonstrates increased opacity of the
nasal cavity and often destruction of the turbinates,
Based on clinical signs and physical examination. nasal septum, lateral bone and loss of teeth adjacent to
the lesion. Radiographic changes are often unilateral
Treatment or asymmetrical.
Surgical removal of the wing of the nostril. Cytological examination of the discharge or atraumatic
nasal flush usually reveals evidence of inflammation
NEOPLASIA ** (neutrophils and bacteria) but no tumor.
A traumatic flush using a stiff catheter and syringe (e.g.
Classical signs cut-off dog urinary catheter) yields better results than
● Progressively worsening chronic sneezing an atraumatic flush.
and snuffling. A biopsy is often required to obtain tissue for a histo-
● Purulent or blood-tinged nasal discharge, logical diagnosis. Tissue may be obtained using biopsy
which may temporarily respond to forceps through the external nares or via a rhinotomy.
antibiotics.
● Nasal obstruction and epiphora.
● Occasionally facial distortion ± signs of
retrobulbar pressure, e.g. exophthalmos. CRYPTOCOCCOSIS AND OTHER FUNGI**
See main reference on page 23 for details (The Cat Classical signs
With Signs of Chronic Nasal Disease). ● Chronic nasal discharge, stridor and
sneezing, progressing in severity.
Clinical signs ● Soft tissue swelling over the nasal bones
Chronic sneezing and snuffling, which progressively
cavity.
worsen with time.
Purulent or bloody nasal discharge, which may tem- See main reference on page 25 for details (The Cat
porarily respond to antibiotics. With Signs of Chronic Nasal Disease).
Clinical signs Classical signs—Cont’d

Sneezing, snuffling, stridor or stertor and chronic nasal ● Chronic non-responsive otitis, head tilt and
discharge are most common with cryptococcosis. Horner’s syndrome.
Nasal discharge may be unilateral or bilateral, and
serous, mucopurulent or hemorrhagic.
Distortion and swelling over the bridge of nose, or a Clinical signs
polyp-like mass projecting from the nasal cavity are Nasopharyngeal polyps are thought to occur second-
present in 70% of cats with the respiratory form of ary to chronic upper respiratory tract inflammation
cryptococcosis. as they consist of inflammatory tissue covered by
Depression, anorexia or inappetence and weight loss are epithelium. They are thought to arise from the
often present with nasal or CNS involvement. Eustachian tube or bulla.
Mandibular lymph nodes are often enlarged. They are a relatively common cause of stridor and
dyspnea, and typically occur in young cats (average
Vestibular disease has been reported associated with age 11⁄2 years old), and most begin to exhibit signs
cryptococcal infection. before they are 1 year of age. Abyssinians may be pre-
Aspergillus, Penicillium, Sporothrix and some other disposed.
fungi are very rare causes of chronic nasal disease. Chronic mucopurulent nasal discharge and congestion
is common, but may be absent.
Diagnosis
Inspiratory noises, usually stridor, but sometimes ster-
Cytological identification of the organism in nasal tor, along with dyspnea and open-mouth breathing have
discharge, exudate from skin lesions, lymph node aspi- been reported.
rate, cerebrospinal fluid (CSF), or ocular aspirate is
diagnostic. Note that very occasionally small numbers Signs of ear disease, including chronic discharge, head
of organisms may be cultured from the nasal exudate of tilt and possibly Horner’s syndrome on the affected
normal cats. side, may be present.

blood, CSF, or urine is sensitive and specific.
Diagnosis
Tissue biopsy of the granulomatous mass or skin lesion,
and histological identification of the organism may be Radiographs or CT may show a soft tissue mass lesion
required if cytology is negative. in the nasopharynx
PCR (polymerase chain reaction) assays are now avail- Rhinoscopy and otoscopy are valuable in visualizing
able to detect cryptococcal antigens in biopsy material. the mass and obtaining biopsy material. The polyp may
be visualized directly or with a dental mirror. The ros-
Fungal isolation with culture is rarely required tral soft palate may bulge down into the oral cavity with
for diagnosis, but is useful for sensitivity testing. pressure from the polyp. Pull the soft palate rostrally
Radiographs often reveal turbinate lysis and opacity for an improved view.
of the nasal cavity (soft tissue density). Sinus involve-
ment is common.
NASOPHARYNGEAL POLYP
Tracheitis from feline rhinotracheitis virus is generally
Classical signs associated with other upper respiratory signs.
● Nasal discharge and congestion. Laryngeal paralysis or edema, tracheal foreign

● Inspiratory dyspnea and stridor. body, and tracheobronchial neoplasm can be differ-
entiated endoscopically.
Nasopharyngeal stenosis may have similar signs, and Stenosis is visible as a pin-point opening in the
caudal rhinoscopy is required to distinguish this from nasopharynx (normal opening is approximately
polyp formation. 5 mm).
Radiographs are generally normal.
Treatment
Surgical therapy to remove the polyp is required. Diagnosis
Concurrent bulla osteotomy may be needed to remove
Diagnosis is based on the history, signs and visual evi-
the entire source of the polyp and prevent recurrence.
dence of the stenosis.
Generally, removal is via the mouth. The soft palate is
retracted and the base of the polyp grasped with for-
ceps. Gentle traction should be applied until the polyp Treatment
detaches. Alternatively, the stalk may be cut. Bleeding
Treatment involves surgical removal of the stenosis.
may be profuse, but more often is minimal.
Prognosis
NASOPHARYNGEAL STENOSIS
Prognosis is good with surgery
Classical signs
● Stertorous respiration from nasal area. CHLAMYDOPHILIA AND MYCOPLASMA
● Dyspnea.
● No or minimal nasal discharge. Classical signs
● Chronic ocular-nasal discharge.
Pathogenesis ● Chronic conjunctivitis.
● Acute or chronic sneezing.
Rare condition thought to arise secondary to chronic ● Stertor and stridor
nasal inflammation or trauma.
A strong membrane forms across the nasopharynx. It See main references on page 13 for details (The Cat
may completely occlude the nasopharyngeal opening, With Acute Sneezing or Nasal Discharge) and pages
or more often it reduces the opening to pin-point size. 1215, 1218 (The Cat With Ocular Discharge or
Changed Conjunctival Appearance).
Clinical signs
Chronic snuffling of 3 months to 2 years duration is Clinical signs
reported. Chlamydophila felis and Mycoplasma spp. infection
Any age of cat from < 1 year to 10 years may be affected. may result in initial acute signs of upper respiratory
tract infection progressing to chronic conjunctivitis,
Stertorous respiration (snoring) or stridor (whistling chronic mucopurulent ocular and nasal discharge.
noise) occurs from partial nasal obstruction.
Sneezing and occasionally stridor or stertor may occur.
Dyspnea, or open-mouth breathing may occur.
Follicular hyperplasia of lymphoid tissue in the conjunc-
Retching or gagging may be evident on eating. tiva and nictitating membrane is often visible as multi-
No or minimal nasal discharge. ple, small white nodules in Chlamydophila infection.
Diagnosis Diagnosis
With the cat under general anesthesia, visualize the A presumptive diagnosis is often made based on
stenosis with a dental mirror. Pull the soft palate ros- signs. A definitive diagnosis is based on identification
trally for an improved view. of the organism.
Examine a stained (e.g. Diff-Quick) preparation of a

FOREIGN BODY (GRASS, GRASS SEED,
conjunctival scraping or smear obtained with a dry cot-
AWN)
ton bud. Chlamydophila felis infection is associated
with inclusion bodies in epithelial cells but they are dif-
Classical signs
ficult to identify in chronic disease. Mycoplasma is seen
as clusters of coccoid or coccobacillary organisms in the ● Acute onset of sneezing and rubbing face,
periphery of epithelium cells. progressing to chronic signs.
● Unilateral discharge.
Antibody-based detection in conjunctival scrapings
● Gagging.
using ELISA or latex agglutination may be useful for
Chlamydophila felis, but false positives occur with
both tests if many bacteria are present.
Polymerase chain reaction (PCR) and IFA techniques
Grass or seeds may occasionally enter the nose of cats.
for detection of the organisms are also available from
Other foreign bodies such as gun pellets are less common.
some laboratories.
Clinical signs
Typically there is an acute onset of sneezing and dis-
ORONASAL FISTULA OR NASAL tress, and rubbing at the face.
FRACTURES FOLLOWING TRAUMA
Signs may progress to chronic gagging, or sneezing and
discharge.
Classical signs
A unilateral serosanguineous discharge is typically
● Chronic snuffling, sneezing, stridor or
present.
stertor and nasal discharge .
● Cleft hard palate (lateral or midline).
Diagnosis
See main reference on page 29 for details (The Cat Visualize foreign body using an otoscope, fiber-optic
With Signs of Chronic Nasal Disease). scope, or with a dental mirror in the nasopharynx. Use a
spay hook to retract the soft palate for better visualization.
Flushing the nose using a naso-esophageal feeding
Clinical signs catheter may remove parts or all of the whole foreign
body for diagnosis.
Typically there is chronic snuffling, sneezing, stridor
or stertor, and nasal discharge in a cat that sustained
facial injuries in a fall or car accident. THE CAT WITH PHARYNGEAL,
LARYNGEAL OR TRACHEAL STRIDOR
Examination may reveal a split hard palate either OR STERTOR
centrally along the platine symphysis, or laterally
adjacent to the teeth along the maxillary symph-
ysis. CONGENITAL ANOMALIES OF THE UPPER
RESPIRATORY TRACT*
Signs often resolve spontaneously with spontaneous
healing of the cleft or nasal fracture. Classical signs
● Usually inspiratory and expiratory
dyspnea.
Diagnosis ● Inspiratory dyspnea with both stridor and
stertor occurs with the brachycephalic
Diagnosis is based on a history of trauma, signs of nasal
syndrome.
disease, visual evidence of the cleft and radiography.
Pathogenesis palatal resection, and resection of the everted lateral

ventricles.
Congenital anatomic anomalies characteristic of
brachycephalic breeds (Persians, Himalayans), are
related to the flat face and short neck. Stenotic nares is Prognosis
the most commonly evident anomaly.
The prognosis is excellent for nasal, palatal and laryn-
Brachycephalic syndrome includes stenotic nares, geal defects with surgical intervention, if indicated.
elongated soft palate, eversion of the lateral laryngeal Tracheal hypoplasia is currently not treatable.
ventricles, laryngeal collapse and hypoplastic trachea. Prevention or treatment of obesity is a major prog-
nostic factor, as lean cats tolerate this much better than
Clinical signs obese cats.
Stenotic nares, hypoplastic trachea, etc., create a non-

dynamic, fixed obstruction leading to inspiratory and Prevention
expiratory dyspnea.
Prevention is via selected breeding programs. Not using
Dynamic obstructions occur with an elongated soft severely affected cats for breeding will help to reduce
palate and create inspiratory dyspnea with stertor. the prevalence.
Stridor is present with laryngeal collapse or lateral ven-
tricular eversion.
AIRWAY FOREIGN BODIES
Collapse, exercise intolerance, dyspnea or dysphagia
may also be reported.
Classical signs
Oronasal reflux, especially with fluids, occurs with a
● Sneezing and stridor (nasal foreign
cleft palate.
bodies).
● Coughing and stridor (pharyngeal and
Diagnosis tracheobronchial foreign bodies).
Diagnosis is based mostly on clinical signs of stertor
and stridor in a brachycephalic cat. Nasal stenosis
Clinical signs
can be assessed visually. Pharyngoscopy and laryn-
goscopy are required to diagnose and stage the severity Grass is one of the most common foreign bodies. The
of palatal and laryngeal involvement. blade of grass becomes adherent to the roof of the pharynx
and extends into the nasopharyngeal region.
Lateral cervical and thoracic radiographs are needed to
assess tracheal hypoplasia. Cuterebra larvae may bury in the retropharyngeal
tissue or in the pharyngeal soft palate. A clue to
diagnosis is evidence of a hole in the mucosa or a mass
lesion.
Upper airway foreign bodies and masses may mimic
Bone fragments and sewing needles may become
brachycephalic syndrome in a brachycephalic breed,
embedded in the pharnx. Cotton, string and fishing
although careful history-taking will usually differentiate
line may get caught around the base of the tongue.
them based on time of onset. Laryngeal edema may
Grass seeds may cause nasal foreign bodies.
occur due to causes other than congenital malformation.
Acute onset of sneezing and nasal discharge are
common signs of nasal foreign bodies. The cat may
Treatment
be in sudden and severe distress attempting to dislodge
If possible, surgically correct the defect, if the signs the foreign body. Pawing at the face and mouth is com-
are severe. This includes wedge resection of the nares, monly observed.
Signs of fixed obstruction occur with nasal and tra- See reference on page 23 for details (The Cat With
cheobronchial foreign bodies because airflow is limited Signs of Chronic Nasal Disease).
during inspiration and expiration due to constant partial
obstruction of the airway. This may result in increased
Pathogenesis
breathing sounds, and often stridor and dyspnea during
inspiration and expiration. Nasal tumors are most commonly squamous cell carci-
noma (SCC) of the nasal planum, solid nasal carcino-
Typically nasal foreign bodies have sneezing, stridor
mas and nasal lymphoma.
and pawing or rubbing of the face, while pharyngeal
and tracheobronchial foreign bodies present with SCCs of the tonsil are common pharyngeal masses,
coughing, stridor, gagging or retching, pawing at the along with benign nasopharyngeal polyps.
mouth, salivation and dyspnea. Typically the signs are
Tracheal tumors consist of lymphoma, SCC, leiomyosar-
frequent, marked and have a sudden onset.
coma and osteochondral tumors from the tracheal rings.
Adenocarcinomas have increased prevalence in the
Diagnosis
Siamese.
Some nasal and most tracheal foreign bodies may be
Lymphosarcoma and squamous cell carcinomas are the
seen radiographically.
most frequent tumor types involving the larynx.
Rhinoscopy and tracheobronchoscopy can be both
diagnostic and therapeutic. Rigid tracheoscopy allows
Clinical signs
for larger retrieval instruments to be utilized than with
flexible endoscopy. Nasal obstruction produces stridor, open-mouth
breathing, unilateral nasal discharge and cough-
Differential diagnosis ing from post-nasal drip. Anosmia may lead to inappe-
tence.
Nasopharyngeal polyps may cause similar signs of
nasal obstruction and sneezing, but tend to have a more Pharyngeal masses produce dysphagia, stridor, ster-
chronic course. torous dyspnea and voice changes. Fetid halitosis is
also reported.
Tracheal or bronchial neoplasia may have similar
signs, but again are more chronic in nature and can be Tracheal tumors cause fixed obstruction, leading to
distinguished bronchoscopically. both inspiratory and expiratory dyspnea with stridor,
which is often louder on inspiration. A harsh, dry
Treatment cough is common.
Removal of the foreign body, either surgically or
endoscopically, is often curative. Nasal foreign bodies Diagnosis
may be endoscopically retrieved or hydropulsed, but
Diagnosis is made via rhinoscopy, pharyngoscopy or
occasionally require surgical rhinotomy.
tracheoscopy with biopsy. It is possible to image soft
tissue masses radiographically, but endoscopy is still
AIRWAY TUMORS advised for biopsy. Other imaging modalities (CT and
MRI) provide excellent images and aid in surgical and
Classical signs radiotherapy planning.
● Nasal obstruction: stridor, open-mouth
breathing. Differential diagnosis
● Pharyngeal obstruction: dysphagia, stridor,
stertor and voice changes. Inhaled and penetrating foreign bodies may produce
● Tracheal tumors: fixed obstruction, similar signs, but usually have a history of acute onset.
inspiratory and expiratory dyspnea and Benign or parasitic granulomas of the airways may
stridor. Cough is common. mimic neoplastic masses but can be differentiated on
biopsy.
Treatment Stertor occurs, which is worsened with excitement or

exercise.
Solid nasal tumors often respond well to external beam
radiotherapy, with survival times of 20–27 months. Diagnosis
Rhinotomy with turbinatectomy has been reported to
be successful. Acute onset of inspiratory dyspnea.
Often, there is extensive local invasion by the neo- Laryngoscopic inspection under heavy sedation or light
plasm, and the recurrence rate after radiotherapy with anesthesia with a rigid laryngoscope and blade reveals
or without surgery is high. erythema and edema of the laryngeal mucosa.
Nasal lymphoma responds well to standard chemother- Differential diagnosis

apy for lymphoma, with remission times of 16 months
reported. See page 676 for therapy. Laryngeal paralysis, laryngeal mass lesion or foreign
bodies may have similar signs, but are differentiated on
Pharyngeal and tracheal masses and nasopharyngeal history and visualization of the larynx.
polyps (see page 37) are best addressed with surgical
resection. Treatment
Laryngeal tumors are difficult to resect and generally Corticosteroids are indicated.
carry a poor prognosis. ● Dexamethasone (0.1–0.25 mg/kg IV or IM), or
prednisolone sodium succinate (10–30 mg/kg IV)
are good parenteral choices.
LARYNGEAL EDEMA Antihistamines may be useful, but histamine release has
generally already occurred at the time of presentation.
Classical signs
Intubation or tracheostomy may be indicated in
● Inspiratory dyspnea. severe situations.
● Stertorous breathing, stridor.
Prognosis
Pathogenesis Generally good, but severe obstruction, if untreated,
Usually occurs secondary to an allergic reaction can be fatal. Laryngeal edema can also be a harbinger
(type I hypersensitivity) from an insect sting, or fol- of systemic anaphylaxis.
lowing vaccination.
Prevention
Acute laryngeal edema occurs in some cats associated
with the intravenous anesthetic agent alfaxalone/alph- Avoidance of insect stings, access to poisonous plants
dolone (Saffan, Scherng-Plough) which is available in and caustic agents such as dishwashing powder and
Europe and other countries. The oil-based preparation cleaning agents.
causes histamine release. Use of the new formulation of alfaxalone (Alsaxon-
Edema may be the result of laryngeal trauma, either CD, Turox, Australia), which is water-based.
blunt trauma to the throat, penetrating trauma (cat-bite
wound), or from the ingestion of sharp objects or
caustic materials (phenols, alkalis, acids) or plants LARYNGEAL STENOSIS
(poinsettias, philodendrons, dieffenbachia).
Classical signs
Clinical signs ● Dyspnea and stridor on inspiration.

● Common in cats after laryngeal trauma or
Inspiratory dyspnea, which may be associated with surgery.
severe respiratory distress and cyanosis.
Pathogenesis lateralization) may be required (see Laryngeal

paralysis section).
The cat appears to be more prone to fibrosis and stricture
formation of the upper airway than is the dog. Trauma In emergency respiratory distress, temporary
from external penetrating wounds, aspirated foreign tracheostomy may be required below the stricture,
bodies, or from caustic chemical damage, or post- although this too can lead to future stricture
operative scarring can lead to excessive scar formation formation.
and stricture.
The narrowed lumen creates the airway resistance and Prognosis
stridor. A web of fibrosis may form across the larynx Depends upon the nature and location of the stricture.
and is especially dangerous.
Clinical signs Prevention

Laryngeal stenosis causes a dynamic airflow limitation, At the time of laryngeal trauma or surgery, corticos-
resulting in inspiratory stridor and dyspnea. teroids may help diminish scar formation.
Stridor is worse with excitement or exercise.
Occasional stertor is evident.
LARYNGEAL PARALYSIS
Voice changes (absent or whisper-like meow), or
harsh purring sounds may be reported. Classical signs
Diagnosis ● Inspiratory dyspnea and increased airway

noise.
Diagnosis is based on clinical signs and history of prior ● Stertorous breathing (snoring).
laryngeal damage or surgery. ● Stridor (high-pitched whistling =
Laryngoscopic inspection under heavy sedation or obstructive).
light anesthesia with a rigid laryngoscope and blade
● Voice changes, absence of purring.
reveals the stricture.
Low-dose ketamine (4–6 mg/kg IV), ketamine/ Pathogenesis
diazepam (3–5 mg/kg/0.1–0.2 mg/kg IV) or propofol
Exact pathomechanism is unclear in cats because of the
(4–6 mg/kg IV) allows visual inspection.
small numbers reported.
Differential diagnosis It may be congenital, although most cases appear in
middle-aged to older cats.
Other causes of fixed upper respiratory tract obstruc-
tion are considerations, but can usually be differenti- Peripheral neuropathies of recurrent laryngeal nerves
ated visually or on biopsy. They include the following: can cause laryngeal paralysis. In dogs they have been
● Oropharyngeal neoplasia (SCC, oral melanoma, associated with endocrinopathies (hypothyroidism –
nasopharyngeal polyp). but this is rare in cats), myasthenia gravis, immune-
● Laryngeal or tracheal neoplasia (intraluminal mediated or paraneoplastic peripheral neuropathies,
adenocarcinoma, extraluminal masses) or foreign but this association has not been documented in cats.
bodies.
Trauma, either to the recurrent laryngeal nerve (head,
cervical or thoracic trauma) or to the structure of the lar-
Treatment
ynx itself, can impair the laryngeal function. Temporary
Surgical intervention is generally required. or permanent damage to the recurrent laryngeal nerve
● Surgical resection of the stricture, if possible, is may occur following cervical surgery, for example fol-
indicated. Laryngeal tie-back surgery (arytenoid lowing thyroidectomy.
Neoplasia, affecting either the innervation of the larynx Dynamic causes of upper respiratory tract obstruction are:
(i.e., thyroid adenocarcinoma) or affecting the laryn- ● Brachycephalic airway syndrome (elongated soft
geal structures directly (i.e., squamous cell carcinoma) palate, lateral ventricle eversion).
can create laryngeal paralysis. ● Cervical tracheal collapse.
● Pyogranulomatous or lymphoplasmacytic laryngitis.
Parasitic involvement of the larynx and lead poisoning
are very rare associations. Other causes of fixed upper respiratory tract obstruc-
tion include:
Percutaneous ultrasound-guided radiofrequency heat
● Oropharyngeal neoplasia (SCC, oral melanoma,
ablation and ethanol injections for treatment of hyperthy-
nasopharyngeal polyp).
roidism in cats are both recent procedures, and laryngeal
● Tracheal neoplasia (intraluminal adenocarcinoma,
paralysis was a reported side effect of both.
extraluminal masses).
● Tracheal foreign bodies.
Clinical signs
Inspiratory dyspnea, tachypnea. Treatment
Stridor, worse with excitement or exercise. Correction of the underlying cause of the neuropathy is
rarely possible.
Occasional stertor.
Surgical intervention is generally required for bilat-
Voice changes (absent or whisper-like meow), harsh
eral disease.
purring sounds.
● Laryngeal tie-back surgery (arytenoid lateraliza-
Dysphagia and weight loss. tion) is recommended by most surgeons, although
other techniques are described. Success is directly
correlated with skill of the operator.
Diagnosis
In emergency respiratory distress, temporary tra-
Diagnosis is based on clinical signs of laryngeal stridor
cheostomy may be required.
and inspiratory dyspnea.
Laryngoscopic inspection under heavy sedation or Prognosis
Generally good to excellent long-term prognosis with
reveals absent or paradoxical motion of the arytenoid
successful surgery.
cartilages. Normally they should abduct on inspiration.
If they close on inspiration, it is paradoxical motion.
Prevention
One retrospective study of 16 cases revealed 12 to be
None known.
bilateral, and four to be unilateral.
Erythema and swelling of the arytenoid mucosa (“kiss-
TRACHEOBRONCHIAL COLLAPSE
ing lesions”) may be evident from the repetitive trauma
at the contact surfaces.
Classical signs
Low-dose ketamine (4–6 mg/kg IV), ketamine/
● Harsh, honking cough.
● Stridor on inspiration if cervical segment
(4–6 mg/kg IV) allows visual inspection without dimin-
involved.
ishing laryngeal function.
● Very rare in cats.
Clinical signs
Other causes of dynamic or fixed upper respiratory
tract obstruction are distinguished on laryngoscopic Tracheobronchial collapse is very rare in cats and
inspection. generally occurs secondary to trauma or to com-
pression caused by an extraluminal mass. It has Weight loss and avoidance of neck collars can be very
been reported associated with proximal tracheal beneficial in affected cats.
obstructions from a trachael granuloma or polyp.
The cough is often harsh, non-productive and parox- LARYNGEAL EOSINOPHILIC GRANULOMA
ysmal, ending in a gagging episode which may appear
to be productive. Classical signs
Cervical trachea collapse produces inspiratory dysp- ● Stridor from laryngeal region.
nea, while intrathoracic tracheal or bronchial collapse ● Swollen, edematous arytenoid cartilages
will lead to mostly expiratory dyspnea. Stridor is of larynx.
occasionally reported.
Clinical signs
Diagnosis
Syndrome often occurs weeks or months after signs of
Radiographs may show attenuation of the tracheal or
viral upper respiratory tract infection.
bronchial lumina. Fluoroscopy may be more sensitive
for dynamic collapse. Stridor from laryngeal region is evident.
Tracheobronchoscopy is valuable in both diagnosing The larynx appears edematous and swollen.
and grading the severity of the collapse.
With stress, cats become dyspneic and may mouth
breathe.
Tracheitis from feline rhinotracheitis virus is generally Diagnosis
associated with other upper respiratory signs.
Visual appearance and biopsy are diagnostic.
Laryngeal paralysis or edema, tracheal foreign body Biopsy reveals an eosinophilic granuloma.
and tracheobronchial neoplasm can be differentiated
endoscopically.
Small airway disease (feline asthma/bronchitis com-
plex) can worsen upper airway collapse, but generally Invasive squamous cell carcinoma may have a similar
diagnosis is based on the radiographic peribronchiolar appearance but can be differentiated on biopsy.
pattern and airway inflammation on lung wash cytology. Other inflammatory infiltrations of the larynx, for
example with lymphocyte, may appear similar, but are
Treatment differentiated on biopsy.
Medical treatment is indicated for a short and mini-
mally attenuated collapsing segment, and consists pri- Treatment
marily of antitussive therapy (butorphanol 1 mg/cat PO
Oral steroids such as prednisolone 2 mg/kg bid PO for
q 6–12 h as needed).
10 days, then taper dose.
Surgical therapy may be indicated with severe col-
If oral medication cannot be given, methylprednisolone
lapse due to trauma. This generally requires referral to
acetate (2–4 mg/kg 7 days for 2–6 treatments), can be
a specialist with experience in airway surgery.
used.
Extraluminal spiral ring prostheses made from a 3 ml
syringe case were successful in reducing signs in two Occasionally, refractory cases need chlorambucil
cats. (0.1–0.2 mg/kg q 24 h initially PO, IM, then q 48 h).
RECOMMENDED READING
Little CJL. Nasopharyngeal polyps. In: August J (ed) Consultations in Feline Internal Medicine. W.B Saunders,
Philadelphia, 1997, pp 310–316.
McKiernan BC. Respiratory diseases. In: Kirk R (ed) Current Veterinary Therapy. W.B Saunders, Philadelphia, 1983,
pp 191–261.
McKiernan C. Sneezing and nasal discharge. In: Ettinger S, Feldman E. (eds) Textbook of Veterinary Internal
Medicine. W.B Saunders, Philadephia, 2000, pp 194–197.
Schachter S, Norris CR. Laryngeal paralysis in cats: 16 cases (1990–1999). J Am Vet Med Assoc 2000; 216(7):
1100–1103.
Sherding R. The Cat: Diseases and Clinical Management. W.B Saunders, New York, 1994.
PART 2
Cat with lower respiratory tract
or cardiac signs
5. The dyspneic or tachypneic cat

Robert Allen Mason and Jacquie Rand
KEY SIGNS
Dyspnea
● Anxious, uncomfortable breathing.
● Increased respiratory effort.
● Respiratory distress.
Tachypnea
● Rapid breathing, not necessarily labored.
MECHANISM?
● Dyspnea can be caused by several mechanisms:
obstruction to airflow.
weakness of ventilatory muscles.
pleural space disease, inhibiting expansion of the lungs.
diminished oxygen-carrying capacity of the blood.
WHERE?
● Upper respiratory tract (nasal cavity, paranasal sinuses, pharynx, larynx, trachea).
● Lower respiratory tree (bronchial tree, small airways).
● Lung parenchyma, pleural space, chest wall and ventilatory muscles.
WHAT?
● Acute severe dyspnea in cats is often caused by an acute asthma attack, trauma or decompen-
sating congestive heart failure.
47
48 PART 2 CAT WITH LOWER RESPIRATORY TRACT OR CARDIAC SIGNS

Diseases causing a dyspneic or tachypneic cat
DEGENERATIVE
● Cardiomyopathy** (p 54)
Dilated cardiomyopathy (DCM), hypertrophic (HCM), intermediate (ICM) or restrictive (RCM)
often present as acute dyspnea. Abnormal heart sounds are often audible as mumurs, gallops and
arrhythmias. Advential lung sounds, such as crackles may be audible with pulmonary edema.
Occasionally, marked pleural effusion is present and heart and lung sounds are muffled ventrally.
Coughing is an uncommon presenting sign in the cat.
● Tracheobronchial collapse (p 69)
Very rare in cats. Degeneration of the cartilage support of the large airway walls results in tracheo-
bronchial collapse. Cervical collapse causes inspiratory dyspnea, while intrathoracic collapse
causes expiratory dyspnea. Harsh honking cough and stridor may be evident.
● Laryngeal paralysis (p 67)
Idiopathic laryngeal paralysis is reported in cats. Iatrogenic paralysis may occur after cervical sur-
gery or trauma. Inspiratory dyspnea, stridor and stertor are common signs.
ANOMALIES
● Congenital heart defects (p 67)
Atrioventricular valve dysplasia, septal defects, aortic and pulmonic stenosis (rare) and patent duc-
tus arteriosus all lead to pressure and/or volume overload on the heart and potentially result in con-
gestive heart failure. Dyspnea, open-mouth breathing, cyanosis, exaggerated chest excursions with
minimal airflow all may occur. Abnormal heart sounds are common.
● Congenital anomalies of the upper respiratory tract (p 68)
Stenotic nares, elongated soft palate, hypoplastic trachea (i.e., brachycephalic syndrome) create
variable upper airway resistance. Stertor and inspiratory dyspnea are common signs.
● Acquired or congenital diaphragmatic defects* (p 57)
Abdominal contents lie within the pleural or pericardial cavities, creating variable degrees of dysp-
nea. Signs include increased chest excursions with decreased airflow, muffled heart and lung
sounds, and reluctance to lie in lateral recumbency. Palpation of the abdomen has an empty feel.
MECHANICAL
● Grass awns, foreign bodies (p 65)
Foreign bodies may be inhaled into the nasal cavity, upper respiratory tract or lower airways. The
character of the dyspnea is dependent on location.
● Pleural effusion** (p 54)
Dyspnea characterized by excessive chest excursions with poor airflow, orthopnea, muffled heart
and lung sounds. Signs of chronic illness may be present such as weight loss.
METABOLIC
● Myopathy/neuropathy (p 61)
Hypokalemia, myasthenia gravis, polyradiculoneuritis (rare in cats), botulism, polymyositis and
other causes of weakness of the respiratory muscles cause poor ventilatory muscle excursions.
5 – THE DYSPNEIC OR TACHYPNEIC CAT 49
● Anemia/hypoxemia* (p 57)
Reduced oxygen-carrying capacity of the blood results from anemia (blood loss, hemolysis,
myelodysplastic disease) or altered hemoglobin (methoxyhemoglobinemia from acetaminophen
toxicity, carboxyhemoglobinemia from CO toxicity). Tachypnea, pallor, cyanosis or brick-red
mucous membranes may be seen.
● Pulmonary thromboembolism*
Secondary to hypercoagulable states, blood flow stasis, vascular injuries and heartworm disease.
Creates significant ventilation/perfusion mismatch, with sudden onset of severe dyspnea and
tachypnea. Cyanosis and collapse may occur. Lung parenchyma may appear normal radiographi-
cally.
● Aortic thromboembolism* (p 58)
Acute single-limb paresis or, with “saddle” thrombus, bilateral hindlimb paralysis. The affected
limb is cold, painful and the foot pads are cyanotic. Signs of congestive heart failure may be
severe, with marked worsening of dyspnea.
NEOPLASTIC
● Pleural/mediastinal masses*
Signs relate to the space-occupying nature of the mass. Dyspnea with muffled heart and lung
sounds or pleural effusion. Heart sounds are typically asymmetric because of displacement of the
heart by the mass. Compression of the chest wall may reveal decreased compliance.
● Airway tumors
Nasal, laryngeal and cervical tracheal masses create stertor, stridor and inspiratory dyspnea.
Thoracic tracheal and bronchial masses create expiratory dyspnea. Coughing may occur with tra-
cheal masses.
● Pulmonary neoplasia
Dyspnea may be subtle. Systemic signs such as weight loss and possibly coughing may be evident.
Inappetence, weight loss, fetid breath and reluctance to play may also be noted.
● Cardiac tumors
Extremely rare in cats. Space-occupying effect in chest or signs of congestive heart failure from
obstruction of blood flow may produce dyspnea.
INFLAMMATORY
INFECTIOUS
● Acute and chronic infectious upper respiratory tract disease**
Sneezing, acute or chronic oculonasal discharge, and sometimes conjunctivitis are present.
Inspiratory dyspnea occurs if there is marked nasal obstruction. Nasal distortion may be present
with cryptococcosis, neoplasia or rarely with secondary bacterial rhinitis.
Bacterial:
● Pyothorax**
Dyspnea characterized by excessive chest excursions with poor airflow, orthopnea, muffled heart
and lung sounds. Signs of chronic illness may be present such as weight loss. Signs of sepsis
such as hypothermia and hypoglycemia are occasionally present. Often signs of chronic illness
such as weight loss and inappetence were evident before presentation for dyspnea.
continued
continued
● Pneumonia
Uncommon in cats. Fever, fetid halitosis, crackles and wheezes heard over lung fields.
Parasitic:
● Parasites
Heartworm (Dirafilaris immitus), lung worm (Aleurostrongylus abstrusus, Capillaria aerophilia),
lung flukes (Paragonomus kellicoti), and migrating nematodes (Toxocara cati) are potential lung
pathogens. Coughing may be seen. Inappetence, weight loss and poor hair coat may be evident.
Vomiting is reported in feline heartworm disease along with dyspnea. Acute marked respiratory
distress and sudden death may also occur with heartworm.
Immune:
● Feline asthma/bronchitis complex)***
Acute dyspnea occurs with status asthmaticus. Cats are air-starved, and present with frantic, open-
mouth breathing, increased expiratory effort, and with possible wheezing and coughing.
● Laryngeal edema (p 64)
Laryngeal edema may follow a hypersensitivity reaction. Inspiratory dyspnea, stridor and stertor
are common signs.
● Acute systemic anaphylaxis (p 68)
Clinical signs include acute dyspnea, collapse, pale mucus membranes and other signs of hypoten-
sive shock. There may be a history of exposure to a foreign antigen, usually protein. Anaphylaxis
may occur on the first exposure to the inciting antigen.
Idiopathic:
● Pulmonary fibrosis (p 69)
Pulmonary fibrosis causes both inspiratory and expiratory dyspnea. It is a very rare condition and
may be associated with feline asthma/bronchitis complex. A syndrome consistent with usual inter-
stitial pneumonia in human beings has been reported in cats.
● Fibrosing pleuritis (p 70)
Restrictive fibrosing pleuritis cause both inspiratory and expiratory dyspnea. It is a rare sequel of
pyothorax and other chronic pleural effusions, especially chylothorax. Heart and lung sounds are
muffled ventrally.
Trauma:
● Upper airway/chest wall trauma***
Character of the dyspnea corresponds to the area of injury. Marked inspiratory dyspnea, stridor and
subcutaneous emphysema may be evident with laryngeal or trachea trauma. Chest wall trauma
may result in dyspnea, cyanosis, abnormal or decreased lung sounds and evidence of shock.
● Weakness of ventilatory, muscles or diseases

INTRODUCTION which restrict thoracic expansion (myopathies,
neuropathies, neuromuscular disease, obesity and
MECHANISM? organomegaly).
● Pulmonary vascular disease (pulmonary hyperten-
Dyspnea is the distressful feeling associated with diffi- sion, pulmonary thromboembolism, shock).
cult or labored breathing. In animals, the term dyspnea ● Diminished oxygen-carrying capacity (methemo-
is often applied to labored breathing that appears to be globinemia, anemia).
uncomfortable. ● Cardiac disease (congestive heart failure, cyanotic
Tachypnea is rapid breathing (not necessarily labored). heart disease with right-to-left shunting).
● Miscellaneous (pain, fever, anxiety, hyperthermia).
Hyperpnea is deep breathing.
Hyperventilation refers to increased air entering the
pulmonary alveoli, brought about by prolonged, rapid
WHERE?
and deep breathing.
Upper respiratory tract (nasal cavity, paranasal
Panting, however, refers to swift and shallow breath-
sinuses, pharynx, larynx, trachea). With upper respira-
ing, with a rapid respiratory frequency and a small tidal
tory tract obstructions, stertor and stridor may be evi-
volume.
dent. Stertor is a snoring sound. Stridor is a harsh,
Respiratory causes of dypsnea include upper and high-pitched whistling respiratory sound created by
lower airway obstruction. upper airway obstructive diseases. Stridor arises from
luminal narrowing in the upper airways, generally
Upper airway obstructions may be fixed or dynamic.
involving the pharynx, soft palate, laryngeal structures
Airflow through a narrowed upper airway has increased
and the upper trachea. Nasal stridor may also be
resistance and becomes more turbulent. This resistance
encountered.
is a function of the diminished luminal diameter of the
tube, the resistance increasing to the fourth power of Lower respiratory tree (bronchial tree, small airways).
the radius.
Lung parenchyma, pleural space, chest wall and venti-
● Fixed obstructions affect both inspiration and
latory muscles. Pleural space disease often has dyspnea
expiration.
with excessive chest wall excursions accompanied by
● With dynamic obstructions, dyspnea occurs dur-
minimal nasal airflow.
ing inspiration, because the negative intraluminal
airway pressure creates a vacuum, pulling the walls Oxygen delivery system (blood vessels, RBCs, heart).
inwardly. Any weakened area of the airway wall
will tend to move into the lumen, decrease the lumi-
nal diameter, and create an obstruction.
What?
Lower airway obstructions may be obstructive or
Acute severe dyspnea in cats is often caused by an
restrictive.
acute asthmatic attack, decompensating congestive
● Obstructions include intraluminal masses and for-
heart failure or trauma.
eign bodies, bronchoconstriction, extraluminal
compression by masses or left atrial enlargement, The dyspneic cat is extremely fragile, and needs to be
and rarely tracheobronchial collapse. handled very gently and with minimal restraint. Cats
● Restrictive obstructions include pleural space dis- with open-mouth breathing and cyanosis have very lit-
ease (pneumothorax, hydrothorax, pleural masses) tle respiratory reserve left, and the slightest additional
and primary pulmonary disease (pulmonary fibro- stress may be lethal.
sis, pneumonia) that restrict expansion of the lung.
In most cases, we need to resist the temptation to make
Non-respiratory causes of dyspnea are varied and a definitive diagnosis until our patient is more stable.
include: These cats are focusing on their next breath, and are
not in the least concerned with our welfare and well- Pyrexia often occurs within 24 hours of cat-bite
being. wounds.
These cats often require much less restraint than a
well cat. If there is the slightest resistance to restraint – Diagnosis
STOP RESTRAINING THEM – and proceed with
Diagnosis is based on the history and physical exam
supportive care in as least a stressful manner as
findings.
possible.
Radiographic assessment of the severity of lung trauma
may be misleading in the early stages. Often there is a
lag time of 12–18 hours from the time of blunt trauma
DISEASES CAUSING DYSPNEA
of the chest wall to appearance of interstitial fluid den-
OR TACHYPNEA
sities in the lung. This is analogous to deep bruising on
the skin and muscle after trauma – it takes time for the
UPPER AIRWAY/CHEST WALL TRAUMA*** bruise to fully develop.
Complete focal lung consolidation with severe contu-
Classical signs
sion may be evident radiographically after chest wall
● Inspiratory dyspnea (in upper airway trauma.
trauma).
● +/– Subcutaneous emphysema.
● +/– Paradoxical chest wall motion with flail
chest. Upper airway neoplasia or foreign body in some situa-
● Evidence of superficial trauma. tions may present similarity to trauma, but can be dif-
ferentiated on diagnostic findings such as radiography
or endoscopy.
Clinical signs Pleural space disease, pneumonia and pulmonary neo-
plasia can be differentiated based on history, physical
The character of the dyspnea corresponds to the area of
exam and diagnostic findings.
injury and whether the upper or lower respiratory tract
is involved.
Blunt (car injury, horse kick or fall) or penetrating Treatment
(bite or firearm wound) trauma to the larynx or tra-
Treatment involves supportive care, wound cleaning
chea, may cause inspiratory dyspnea.
and microbial therapy. Surgical repair of upper respira-
Air leakage from a wound to the upper or lower respiratory tract trauma may be required.
tory tract may lead to subcutaneous emphysema and
Flail chest is defined as a segment of the rib cage with
pneumomediastinum. Crepitus is evident on palpation
proximal and distal fractures, resulting in an unstable
with subcutaneous emphysema.
segment of the chest wall.
Dyspnea, cyanosis, abnormal or decreased lung ● Temporary stabilization may be provided with
sounds occur with severe pulmonary contusions, and techniques using Bachaus towel clamps, wooden
signs of shock may be evident. tongue depressors, etc.
● Rapid definitive surgical correction of the flail
Paradoxical chest wall motion of a flail chest segment
chest is not as important as stabilizing the patient
can occur, that is, inward motion during inspiration.
from the severe trauma, and treating the severe
Traumatic hemothorax may produce increased chest wall pulmonary contusion with oxygen supplementa-
motion with poor air movement. tion, antibiotics, analgesics, bronchodilators, etc.
Other signs of superficial trauma and shredded nails are Tube thoracostomy and intermittent or continu-
usually evident with automobile trauma. ous drainage of the pleural space is indicated when
significant pneumothorax requires that air be removed ● Transtracheal wash may be perfomed in the awake
more than three times within 24 h. cat.
● Bronchoscopy for bronchoalveolar lavage (BAL) or
Positive-pressure ventilation must be used with
unguided catheter BAL are performed in the anes-
extreme caution due to the fragility of the traumatized
thetized cat and are preferred by most clinicains over
lung and susceptibility to additional barotrauma.
a transtracheal wash.
Cytology reveals highly cellular samples with intact
FELINE ASTHMA/BRONCHITIS COMPLEX*** non-degenerative neutrophils as the primary cells.
● Eosinophils are not a reliable marker of inflamma-
Classical signs tion in the cat due to the increased prevalence (up to
● Expiratory dyspnea with wheezing. 24%) in normal airways.
● Cough is a prominent sign. Pulmonary function testing for increased airway resist-
● Status asthmaticus – severe acute ance includes spirometry, whole-body plethysmogra-
respiratory distress. phy, and tidal breathing flow–volume loops (TBFVL).
● Cyanosis, open-mouth breathing. These are rarely available outside of teaching institu-
tions.
See main reference on page 92 for details (The Coughing
Cat ).
Main differential for status asthmaticus is acute con-
Clinical signs gestive heart failure of cardiomyopathy.
Signs can occur at any age, although average is 2–8 Other respiratory diseases, such as parasitic pneumo-
years. nia, aspiration pneumonia, bronchopulmonary neopla-
Signs may be episodic (with asthma) or chronic (with sia and pleural space diseases may present with
bronchitis). dyspnea.
There may or may not be a history of coughing for

weeks or months preceding an episode of mild to Treatment
severe, life-threatening respiratory distress from bron- ● The cornerstone of therapy for cats with status
choconstriction. Cats may present severely air-starved,
asthmaticus is to minimize handling until signs
with cyanosis, open-mouth breathing and a significant
abate, and administer oxygen, bronchodilators and
expiratory push.
glucocorticoids.
● Oxygen supplementation is required during respi-
ratory distress and an oxygen chamber or tent
Diagnosis seems to be best tolerated by air-starved patients.
Adventitial lung sounds such as wheezing and crackles Oxygen hoods made with an Elizabethan collar and
are very common. cellophane, or oxygen delivery via a nasal canula
have proven useful in some cats, but may stress
Thoracic radiographs may be normal or have the fol-
other cats and exacerbate signs.
lowing changes: ● Minimal handling and restraint of acutely dysp-
● Hyperlucency, hyperinflation, and flattening of
neic patients is essential.
the diaphragm due to air trapping may be seen with ● For severe signs (dyspnea, open mouth breathing
asthma.
+/- cyanosis) which are a life-threatening emer-
● Diffuse prominent peribronchiolar pattern is the
gency, it is important not to stress the cat as this
hallmark of chronic bronchitis.
may precipitate death. Administer oxygen via oxygen
● Right heart enlargement may be present.
cage or nasal canula, methylprednisolone sodium
Lung wash for cytology and culture. succinate (100 mg/cat IV) or dexamethasone
(2 mg/kg IV) and terbutaline (0.01 mg/kg IV) q30 Differential diagnosis
minutes for up to 4 h until a response is observed.
● Once stabilized cats are discharged with fluticas- Acute marked dyspnea is most often associated with sta-
one (Flovent®) 220 mcg q 12 h and albuterol tus asthmaticus and is differentiated from cardiogenic
(Proventil, Ventolin) q 6 h as needed dyspnea on signs, expiratory push, wheezing, prior his-
● See page 94 The Coughing Cat for details of acute tory of coughing and radiographic findings.
and chronic therapy
Treatment
Oxygen therapy (O2 chamber or tents).
CARDIOMYOPATHY**
Furosemide (1–2 mg/kg IV or IM).
Classical signs Provide sedation if the cat is frantic (morphine 0.1
● Dyspnea – mild to acute and severe with mg/kg IM prn, or butorphanol 0.2–0.4 mg/kg IM q 4–6
cyanosis. h as needed).
● Abnormal heart sounds (murmurs, gallops, If there are signs of pleural effusion, emergency tho-
arrhythmias). racocentesis in cats with severe respiratory distress
● +/- Signs of pleural effusion or pulmonary may be life saving.
edema. ● A butterfly set on a 60 ml syringe is introduced at
the 5th–7th intercostal space (ICS) on the right,
See main reference on page 128 for details (The Cat just above the costochondral junction. Remove as
With Abnormal Heart Sounds and/or an Enlarged much fluid as possible, or until breathing
Heart). improves.
Definitive therapy is based on ultrasonographic charac-
Clinical signs terization of the type and severity of the cardiomyopathy
present. See page 130 for treatment details (The Cat
Dyspnea varies from mild and associated with reduced With Abnormal Heart Sounds and/or an Enlarged Heart).
activity levels and reluctance to play, to acute, fulminant
air-starvation with open-mouth breathing and cyanosis.
Abnormal heart sounds (murmurs, gallops, arrhyth- PLEURAL EFFUSION**
mias) may be present, or may be difficult to assess in
the distressed patient. Classical signs
Pleural effusion is occasionally present especially with

● Muffled heart and/or lung sounds ventrally.
DCM, and results in increased chest excursions with lit-
● Dyspnea characterized by excessive chest
tle airflow (can be detected by listening close to the excursions with poor airflow.
muzzle during breathing) and muffled ventral sounds.
● Orthopnea (positional dyspnea).
Pulmonary edema is more common especially with See main reference on page 71 for details (The Cat
hypertrophic and restrictive/intermediate cardiomy- With Hydrothorax).
opathies, and results in increased adventitial lung
sounds such as crackles.
Clinical signs
Diagnosis
Marked chest wall excursions and minimal airflow.
Definitive diagnosis is based on ultrasonographic char-
acterization of the type and severity of the cardiomy- Orthopnea (worsening dyspnea in lateral recumbency)
opathy present. and reluctance to lie in lateral recumbency.
Muffled heart and lung sounds ventrally, dull chest Clinical signs
percussion.
Pyothorax is more common in intact males and is likely
Depending on the etiology of the effusion, signs of associated with fight wounds.
chronic illness may be present such as weight loss.
Inappetence or anorexia and pyrexia may be present Dull or muffled heart and lung sounds are audible ven-
with pyothorax. trally.
Marked chest wall excursions with minimal airflow are
Diagnosis evident, and dyspnea is worsened by lateral recumbency
(orthopnea).
With mild to moderate clinical signs, thoracic radiogra-
phy may be diagnostic. Signs are evident when fluid The cat typically has a sick, septic, thin, unkempt
exceeds 50 ml/kg. appearance and may be febrile.
With severely affected cats in respiratory distress, radi- Diagnosis

ography should be delayed until after thoracocentesis.
● CATS WITH PLEURAL EFFUSIONS DIE IN
A thick, fetid, septic, suppurative exudate is obtained
RADIOLOGY! on thoracocentesis. Cytology and Gram stains reveal
many degenerate neutrophils, some with intracellular
Fluid analysis is essential to determine etiology. bacteria. Culture and sensitivity should be performed,
but may show no growth of organisms.
Hemothorax, transudation from increased hydrostatic
ACUTE AND CHRONIC INFECTIOUS UPPER
pressure (cardiac disease) or decreased oncotic pres-
RESPIRATORY TRACT DISEASE**
sure (protein-losing enteropathies, nephropathies or
hepatic disease), lymphatic obstruction (thoracic neo-
Classical signs
plasia), chylothorax and pyothorax are all forms of
hydrothorax that need to be differentiated. ● Acute or chronic nasal discharge (bilateral,
copious, mucopurulent).
● Open-mouth breathing.
Treatment ● Coughing.
Thoracocentesis is part of the universal therapy for all ● Ocular discharge.
forms of pleural effusion. ● +/- Nasal distortion.
Definitive therapy is based upon the underlying cause.
With Signs of Chronic Nasal Disease) and page 5 (The
Cat With Acute Sneezing or Nasal Discharge).
PYOTHORAX**
Classical signs Clinical signs

● Dyspnea related to pleural effusion. Upper respiratory tract disease may cause inspiratory
● Signs of chronic disease (weight loss, dyspnea as a result of nasal obstruction.
inappetence).
Signs may be acute and associated with calici or herpes
● +/- Fever.
virus infection or chronic associated with cryptococco-
● Turbid, flocculent and other fetid-smelling
sis, neoplasia or chronic secondary bacterial rhinitis
pleural fluid.
following calici or herpes viral infection.
See main reference on page 75 for details (The Cat When dyspnea is present, nasal discharge is usually
With Hydrothorax). bilateral, often mucopurulent and copious.
Open-mouth breathing may occur especially with stress. Clinical signs

Coughing may be present if Bordetella bronchiseptica Mediastinal masses are often thymomas, thymic lym-
or herpes virus are involved. phoma, or mediastinal lymphoma. Occasionally, ectopic
Ocular discharge, conjunctivitis and chemosis occur thyroid adenocarcinoma may create a space-occupying
with acute upper respiratory tract infection with calici mass of the mediastinum. Pleural masses include
or herpes virus and Chlamydophila felis. mesotheliomas, osteosarcoma or chondrosarcoma of
the ribs or sternabrae.
Stertorus respiration (snoring) may be evident.
Signs are related to the space-occupying nature of the
Nasal distortion may occur with cryptococcosis, neo- mass, or to obstruction of lymphatic drainage, leading
plasia or rarely with chronic secondary bacterial rhinitis. to pleural effusion.
Orthopnea (dyspnea worsened by lateral recumbency),
Diagnosis tachypnea, minimal airflow with increased chest excur-
Signalment, clinical signs and history are often sugges- sions, muffled heart and lung sounds, or asymmetrical
tive of the etiology. In acute upper respiratory tract sounds if the heart is displaced laterally.
infection, multiple cats in the home are often affected. Extraluminal compression of the trachea can cause dys-
Radiographic findings: pnea and cough.
● Usually there is loss of lucency in the nasal cavity Compression of the anterior chest wall may reveal
resulting from fluid (fluid density). In chronic nasal decreased compliance.
diseases causing dyspnea, there is often osteolysis
of the nasal turbinates. Lysis tends to be asymmet-
rical with neoplasia and is more often symmetrical Diagnosis
with cryptococcosis and chronic bacterial rhinitis
secondary to viral disease. Thoracic radiography may reveal the mass lesion or
the secondary pleural effusion.
Culture or PCR is now available for calicivirus, her-
pesvirus and Chlamydophila felis. Bacterial culture Thoracic ultrasound can be extremely useful.
● Small mediastinal masses surrounded by aerated
may be useful to identify bacteria in secondary bacter-
ial rhinitis so the most appropriate antibacterial therapy lung may not be visible from a paracostal approach,
can be selected, e.g. Pasteurella spp. and may require a thoracic inlet window.
● Transesophageal ultrasonography is excellent for
Cats with cryptococcosis frequently have nasal distor- demonstrating mediastinal masses, but requires
tion over the bridge of the nose or a polyp-like mass specialized equipment and general anesthesia.
visible in the nasal cavity. Diagnosis is based on cytol-
ogy, histology or a positive serology titer. Analysis of the thoracocentesis fluid may be diagnos-
tic on the rare occasions that the neoplasm has exfoli-
Neoplasia is most reliably diagnosed on histology, ated into the fluid. Pleural effusions associated with
although a cytological sample may be diagnostic. tumors are usually modified transudates, but may be
transudates, exudates or chylous. Surgical or ultra-
PLEURAL/MEDIASTINAL MASSES* sound-guided biopsy of the mass is usually required for
a definitive diagnosis.
Classical signs Mediastinal lymphoma occasionally has hypercalcemia
● Muffled heart and lung sounds ventrally or as a paraneoplastic syndrome.
asymmetrical sounds.
● Dyspnea characterized by excessive chest Differential diagnosis
excursions with poor airflow.
● Orthopnea (positional dyspnea). Other causes of pleural effusion need to be differenti-
ated. Chylothorax is more commonly idiopathic and
associated with lymphatic lymphangiectasia, although ● Bone marrow biopsy may be indicated if there is
cardiac disease and trauma need to be excluded. History, evidence of anemia of longer than 4–6 days duration
signs (evidence of murmurs, gallops and arrhythmias), without a regenerative response.
radiography and ultrasound help to differentiate these ● Measurement of carboxyhemoglobin concentration
causes from thoracic neoplasia. is required for diagnosis of CO toxicity. Routine
STAT assays are available in human hospitals.
Treatment
Lymphoma of the thymus or mediastinal lymph
ACQUIRED OR CONGENITAL
nodes is best handled with standard chemotherapy pro-
DIAPHRAGMATIC DEFECTS*
tocols for lymphoma (see page 676).
Classical signs
Surgical excision is the treatment of choice for thy-
● May or may not have clinical signs.
moma, and may be curative.
● Muffled heart and/or lung sounds.
Mesothelioma is an infiltrative disease that cannot be ● Occasionally dyspnea, cyanosis.
readily resected, and there are few reports in the litera- ● Vague gastrointestinal signs, gaunt
ture of effective chemotherapy. Local infusion of car- abdomen on palpation.
boplatin may be helpful with or without intravenous
doxirubicin. Prognosis is grave.
Clinical signs
Diaphragmatic hernia may occur as a congenital
ANEMIA/HYPOXEMIA* defect allowing abdominal organs to move into the
thoracic space or pericardium, or may follow trauma,
Classical signs especially a motor-car accident or fall from a
● Dyspnea, tachypnea and tachycardia. building.
● Pallor from anemia, cyanosis with With congenital hernias, signs may be evident as a kit-
methemoglobinemia. ten or there may be no signs until later in life, depend-
ing on the severity of the hernia.
Clinical signs With aquired hernias, signs may or may not be evident
Signs may be acute or chronic in onset depending on immediately following trauma, and worsen or
the underlying disease process. improve as adhesions form to limit movement of vis-
cera. In some cats, signs are only present with activity
Pale mucous membranes, tachycardia and tachyp- or stress.
nea occur with anemia.
Typically there are muffled heart and lung sounds, and
Cyanosis occurs with methemoglobinemia. occasionally borborygmus is audible in the chest.
Cherry red mucous membranes occur with carboxy- The severity of dyspnea is variable from mild, to acute
hemoglobinemia from carbon monoxide (CO) toxicity. and severe. Sudden worsening of signs may occur when
more abdominal viscera move into the chest.
Diagnosis Tachypnea, orthopnea (worsened dyspnea in lateral
recumbency) and cyanosis may occur depending on the
Diagnosis of anemia is based on finding a decreased
volume of abdominal organs in the thorax.
hematocrit on CBC.
● PCV < 10% may be associated with dyspnea, espe- On palpation, the abdomen has a gaunt or empty feel.
cially if the cat is stressed. Other ventral midline defects such as umbilical her-
● Evidence of blood loss or poor RBC production nias, pectus excavatum, etc., may be present with con-
may be evident. genital hernias.
Intermittent vomiting and inappetence are the most Typically, there is acute onset of single limb paresis
common gastrointestinal signs. or paralysis, which most often involves the hindlimbs.
Signs may be bilateral with a “saddle thrombus” at the
Diagnosis aortic trifurcation.
Thoracic radiographs demonstrate bowel loops, or On physical examination the limb is cool and pulse-
space-occupying soft tissue densities within the pleural less, with cyanotic foot pads or nail beds. The gas-
or pericardial space. Globose cardiomegaly is evident trocnemius muscle is firm and painful on palpation.
with peritoneopericardial diaphragmatic hernia.
Signs of congestive heart failure including cyanosis,
Other imaging modalities such as ultrasonography, pos- respiratory distress, or evidence of pleural effusion may
itive contrast upper GI series, pneumoperitoneography be present. Dyspnea and tachypnea may be acutely
or contrast injected into the abdomen (celiogram) may exacerbated. Heart murmurs, arrhythmias and gallops
be useful for diagnosis. are often evident.
Differential diagnosis Diagnosis

Pleural space disease (effusions, pneumothorax, mass Diagnosis is based on the clinical signs and confirmed
lesions), pericardial effusion and cardiomyopathy may by evidence of lack of blood flow in the distal limb
have similar signalment and signs to traumatic measured by a Doppler flow meter.
diaphragmatic hernia, but can usually be differentiated
Thoracic radiography and ultrasonography
on radiography and ultrasonography.
demonstrate underlying heart disease, often with sig-
nificant chamber enlargement, especially of the left
Treatment atrium.
Treatment consists of surgical repair after stabilizing Contrast arteriography of the affected limb is the
the patient. If dyspnea is the major clinical sign, stabi- “gold standard”, but not frequently used in clinical
lization may not be possible until the pericardial or cases.
pleural cavities are evacuated. Oxygen therapy is of lit-
tle value in a patient with severe pleural occupation.
PULMONARY THROMBOEMBOLISM*
AORTIC THROMBOEMBOLISM* Classical signs

● Sudden onset of severe dyspnea with
Classical signs
normal lung parenchyma radiographically.
● Acute single or bilateral limb paresis or ● Peracute dyspnea, orthopnea, tachypnea.
paralysis, most often involving hindlimbs. ● Cyanosis, collapse.
● Signs of congestive heart failure – ● Cough, with or without hemoptysis.
cyanosis, respiratory distress, pleural
effusion.
● Heart murmurs, arrhythmias and gallops.
Pathogenesis
Pulmonary thromboembolism involves embolic
See main reference on page 915 for details (The Weak showering of the pulmonary arterial tree, causing
and Ataxic Cat or Paralyzed Cat). obstruction of blood flow to that portion of the lung.
Thrombi may be produced locally (i.e., feline heart-
Clinical signs
worm disease), or may embolize from distant locations.
Cardiomyopathy in cats is sometimes associated with Thrombi may originate in the right atrium (cardiomy-
thrombus formation in the left atrium. The thrombus may opathy, advanced tricuspid valvular disease), caudal
be dislodged, and most commonly obstructs the aorta at vena cava, femoral veins, mesenteric venous system or
its trifurcation (saddle thrombus). jugular veins.
Hypercoagulable states such as protein-losing When lesions are evident radiographically, lung pat-
nephropathies (i.e., glomerulonephritis, renal amyloi- terns range from focal areas of hyperlucency to alveo-
dosis, hypertension) or enteropathies (i.e., IBD, lym- lar infiltration, and mild to moderate pleural effusion.
phangiectasia), stasis of blood flow, exposure of
Pulmonary arterial angiography is the “gold stan-
vascular subendothelial tissue (i.e., vasculitis, right
dard” for evaluation of pulmonary thromboembolism
atrial dilation, post-stenotic “jet lesions”, trauma and in-
(PTE) in people. This requires catheterization of the
dwelling jugular catheters) all predispose to thrombus
right heart and injection of contrast material into the
formation.
pulmonary arterial tree. Areas of obstruction or
Pulmonary arterial obstruction causes ventilation/ decreased blood flow may be detected.
perfusion (V/Q) mismatch, resulting in hypoxemia and
Scintigraphic ventilation/perfusion studies utilize
dyspnea.
both aerosolized and injected radioisotopes to identify
● Increased pulmonary arterial pressure may induce
areas of V/Q mismatch. Special facilities and expertise
cor pulmonale, or right-sided heart failure.
are required, which are generally unavailable outside of
Feline heartworm disease frequently presents as teaching institutions.
severe peracute pulmonary inflammation, edema and
Echocardiography may reveal right atrial enlarge-
pulmonary thromboembolism resulting in acute respi-
ment with thrombus formation, pulmonary arterial
ratory failure and death.
dilation, right ventricular enlargement, pulmonary
hypertension on Doppler studies of the tricuspid and
pulmonic valves, or evidence of heartworm in the
Clinical signs
right heart or pulmonary arteries.
Severity of signs is proportional to the degree of arterial
Tall P waves on ECG may indicate right atrial
obstruction.
enlargement, and right axis shift supports right ventric-
Acute onset of severe dyspnea and tachypnea is typi- ular enlargement consistent with cor pulmonale.
cal. Cyanosis or collapse may also occur. Massive dis-
ease may result in sudden death. Differential diagnosis
Orthopnea (positional dyspnea), especially in lateral Severe dyspnea and cyanosis with normal thoracic radi-
recumbency, and reluctance to lie in lateral recum- ographs may accompany upper airway obstruction or
bency, may be an early sign. feline asthma.
Coughing may be evident, and ranges from mild to
Treatment
severe, and may involve hemoptysis.
Oxygen therapy during the respiratory crisis is impor-
Signs of right-sided heart failure may occur, such as
tant, but limited in efficacy if the blood delivery to the
tachycardia, jugular venous distension and split second
lung is compromised.
heart sounds.
The primary disease condition, if identified, should
Often presenting signs relating to the primary condition
be addressed as a priority.
are also evident, i.e., weight loss and diarrhea with pro-
tein-losing enteropathy. Thrombolytic therapy is controversial. The use of tis-
sue plasminogen activator (TPA) has been advocated,
but requires local delivery into the pulmonary arterial
Diagnosis circulation. This requires cardiac catheterization under
fluoroscopy. There are inherent risks involved with the
Thoracic radiographs may be totally normal, and in
procedure, and the risk of inducing a bleeding diathesis.
the presence of severe dyspnea, increase the index of
suspicion of pulmonary thromboembolism. Anti-thrombotic therapy using heparin has been
● Enlarged or truncated pulmonary arteries may be advocated to prevent further thrombin formation.
seen. Various protocols ranging from low (100 IU/kg SQ q 8
hours) to moderate doses (300 IU/kg SQ q 8 h) have Clinical signs

been published, with no clear advantages of any one
protocol. Nasal tumors are most commonly squamous cell car-
cinoma of the nasal planum, solid nasal carcinomas and
Coumadin is a more potent anti-thrombotic agent in nasal lymphoma.
the cat. Having an oral liquid suspension compounded
makes the titration of the dosage much more reliable in Nasal obstruction produces stridor, stertor or open-
the cat. Doses of 0.1 mg/kg PO q 24 h are a recommended mouth breathing, uni- or bilateral nasal discharge and
starting point. Monitoring the prothrombin time (PT) and coughing from post-nasal drip. Anosmia may lead to
the INR (international normalization ratio), with a treat- inappetance.
ment endpoint of an INR of 2.0–3.0, may help to prevent Squamous cell carcinomas of the tonsil are common
overdosage, although trials in cats are lacking. pharyngeal masses, along with benign nasopharyngeal
Fluid therapy must be used judiciously, due to the polyps.
predisposition of right-sided heart failure. Pharyngeal masses produce dysphagia, stertorous
dyspnea and voice changes. Fetid halitosis is also
reported.
Prognosis
Tracheal tumors consist of lymphoma, squamous cell
Prognosis is directly proportionate to the severity carcinoma, leiomyosarcoma and osteochondral tumors
of the lesion, as well as to the underlying cause. from the tracheal rings. Adenocarcinomas have
Resolvable causes (i.e., trauma or catheter-induced) increased prevalence in Siamese cats.
have a better long-term prognosis that do patients
with irreversible causes (i.e., renal amyloidosis). Tracheal tumors cause fixed obstruction, leading to
both inspiratory and expiratory dyspnea. A harsh, dry
cough is common.
Prevention
Treat underlying risk factors early in the disease course,
for example, protein-losing nephropathies and Diagnosis
enteropathies. Diagnosis is by rhinoscopy, pharyngoscopy or tra-
Acetylsalicylic acid or heparin theoretically may help cheoscopy with biopsy. It is possible to image soft tis-
prevent further thrombus formation, although there are sue masses radiographically, but endoscopy is still
no studies demonstrating efficacy in cats. advised for biopsy.
AIRWAY TUMORS
Inhaled and penetrating foreign bodies, and benign or
Classical signs parasitic granulomas of the airways may mimic neo-
plastic masses. Foreign bodies result in acute onset of
● Nasal obstruction produces stridor and
signs and often distress, compared to chronic signs in
open-mouth breathing.
neoplasia and granulomas. Visualization and biopsy
● Pharyngeal obstruction results in
will differentiate these diseases.
dysphagia, stertor and voice changes.
● Tracheal tumors produce fixed obstruction
with inspiratory and expiratory dyspnea, Treatment
and often coughing.
Solid nasal tumors respond well to external beam
See main reference on pages 41 and 24 for details (The radiotherapy, with survival times of 20–27 months.
Cat With Stridor, and The Cat With Signs of Chronic Rhinotomy with turbinatectomy has been reported to
Nasal Disease). be successful.
● Often, there is extensive local invasion by the neo- heartworms on ultrasound. Occasionally peripheral
plasm, and the recurrence rate after radiotherapy basophilia is evident (see Feline heartworm page 104,
and/or surgery is high. The Coughing Cat).
Nasal lymphoma responds well to standard Lungworm infection with Capillaria aerophilia is
chemotherapy for lymphoma, with remission times of diagnosed by finding eggs in the stools or lung wash,
16 months reported. and with Aelurostrongylus abstrussus, by finding lar-
vae in the lung wash or fecal Baermann.
Pharyngeal and tracheal masses and nasopharyngeal
polyps are best treated with surgical resection. Lung flukes (Paragonimus kellicotti) produce opercu-
lated eggs in the stool.
PARASITIC DISEASE Toxoplasmosis rarely produces clinical disease in cats.

Mixed fluffy interstitial and alveolar patterns are
Classical signs typically evident on radiographs. Tachyzoites may be
recovered in the lung wash.
● Coughing.
● Reduced physical activity and reluctance to Differential diagnosis
play.
● Mild to severe dyspnea. Other forms of pneumonia, including bacterial, viral, fun-
● Weight loss, poor coat, inappetance. gal, inflammatory and neoplasia, need to be considered if
● Sudden marked respiratory distress (feline no larvae or ova are found in the stool or lungwash.
heartworm).
Treatment
See main reference on page 104 for details (The Cough- Feline heartworm disease therapy is usually sympto-
ing Cat). matic, as adulticide therapy is associated with a high
mortality rate (see Feline heartworm disease, page 105,
The Coughing Cat).
Clinical signs
Lungworm – Capillaria aerophilia and Aeluro-
Heartworm (Dirafilaria immitis), lungworm (Aeluro-
strongylus abstrussus – fenbendazole (50 mg/kg PO q
strongylus abstrusus, Capillaria aerophilia), lung
24 h for 3 days) or ivermectin (400 μg/kg PO, SQ).
flukes (Paragonomus kellicoti), migrating nematodes
(Toxocara cati) and toxoplasmosis all may cause respi- Lung flukes – Paragonimus kellicotti, fenbendazole
ratory signs. (50 mg/kg PO q 24 h for 3 days), or praziquantel
(25 mg/kg PO q 8 h for 2 days).
Coughing may be present and is typically harsh, pro-
ductive and paroxysmal. Toxoplasmosis – clindamycin, 12.5 mg/kg PO q 12 h,
potentiated sulfa (trimethoprim or ormetoprim) or
Mild to marked dyspnea and reduced activity may be
azithromycin.
observed, depending on the severity of the lung disease.
Weight loss, poor coat and ill-thrift may be evident. MYOPATHY/NEUROPATHY
Vomiting is a common sign with feline heartworm dis-
ease. Sudden death or sudden extreme respiratory distress Classical signs
and generalized respiratory failure occur in approxi- ● Dyspnea characterized by weakened chest
mately 30% of symptomatic cats with heartworm disease. excursions.
● Weakened gait, ventroflexion of the head.
Diagnosis ● Regurgitation may lead to aspiration
pneumonia.
Feline heartworm disease is suggested by a positive
heartworm antibody test, radiographic changes of See main reference on page 941 for details (The Cat
dilated and blunted pulmonary arteries and evidence of With Generalized Weakness).
Clinical signs Endocrine testing involves measurement of total T4

and free-T4 (hyperthyroidism), blood and urine glu-
Dyspnea associated with myopathy or neuropathy is cose, fructosamine concentration (diabetes mellitus),
related to weakness of the intercostal and diaphragmatic or ACTH stimulation testing (hyperadrenocorticism)
muscle, causing diminished ventilation. if clinical signs are consistent.
Signs related to the underlying disease will be evident, Acetylcholine receptor antibodies assay is used for
for example: myasthenia gravis.
● Hyperthyroid myopathy is usually seen in older
cats. Signs include ravenous appetite, restlessness, Measurement of muscle enzymes (creatine phosphoki-
weight loss, poor haircoat, generalized muscle nase activity) and muscle biopsy are necessary for diag-
wasting and weakness. nosis of myositis.
● Hypokalemic myopathy occurs in older cats usu-
ally secondary to renal insufficiency, or in Burmese PNEUMONIA
cats less than 1 year of age. Ventroflexion of the
head, a stiff stilted gait, inability or reluctance to Classical signs
walk or jump are common signs. Sensitivity to
palpation of the larger muscle groups may be ● Cough.
evident. ● Inspiratory/expiratory dyspnea.
● Hypocalcemic myopathy results in episodic gen- ● Fever.
eralized weakness, tetany or tremors. It occurs ● Occasional nasal discharge.
most commonly after thyroidectomy, but occa-
sionally occurs with hypoparathyroidism, chronic Pathogenesis
renal failure, pancreatitis, eclampsia or phosphate-
containing enemas. Pneumonia may be primary or secondary and asso-
● Hyperadrenocorticism results in poorly controlled ciated with bacterial, mycoplasmal, Chlamydophila
diabetes mellitus, unkempt haircoat, pot-bellied felis, fungal or viral agents.
appearance and generalized muscle weakness. Primary bacterial pathogens include Bordetella
● Myasthenia gravis occurs typically in adult
bronchiseptica and Pasteurella multocida, which are
cats or Siamese < 1 year of age and presents common flora of the oropharynx, and can colonize the
as generalized muscle weakness and stiff stilted lower respiratory tree.
gait exacerbated with exercise. Severe dyspnea
may be evident if aspiration pneumonia is Secondary bacterial infection is possible with many
present. opportunist organisms including streptococci, Bordetella
● Polymyositis produces generalized pain on palpa- bronchiseptica, Pseudomonas spp., Nocardia spp. and
tion of muscle groups, and a stiff stilted gait. Actinomyces spp.
● Botulism toxicity results in flaccid paralysis of
Pneumonia may occur following lung damage from
skeletal or respiratory muscles. various sources, or associated with diseases that reduce
● Polyradiculoneuritis produces an ascending flac-
immunocompetence such as:
cid paralysis of sketetal and respiratory muscles. ● Aspiration as a result of esophageal dysmotility, or
● Tick paralysis from Demacentor spp. and Ixodes
during recovery from general anesthesia, etc.
spp. ticks, produces a rapidly progressive skeletal ● Metabolic disease including uremic pneumonitis,
and respiratory paralysis. hyperadrenocorticism and diabetes mellitus.
● Trauma (blunt, penetrating or surgical trauma).
● Immunosuppression from drugs, neoplasia, or
Diagnosis retroviral infection.
● Pre-existing infection.
Serum electrolytes (i.e., potassium and calcium) should
be measured to rule out hypokalemia and hypocal- Mycoplasma pneumonia is rare, but may be a sequel
cemia. of severe URT infection.
Chlamydiosis can result in pneumonitis in kittens. ● Hilar lymphadenopathy supports fungal or

mycobacterial pneumonia, although infiltrative
Protozoal (toxoplasmosis) and parasitic (capillariasis,
lymphosarcoma may mimic this.
aelurostrongylosis, Paragonimus kellicotti) pneumonia
may occur. Hematology may reveal neutrophilia with or without a
left shift and toxic neutrophils (Doehle bodies, etc.).
Primary fungal pneumonia is mainly restricted to
● Low-grade non-responsive anemia and monocyto-
Cryptococcus neoformans. Infection can occur as a
sis may support chronicity.
sequel to fungal rhinosinusitis, or as primary pneumonia.
Hypoxemia (PaO2 < 80 mmHg on room air or SPO2 <
Viral interstitial pneumonia with feline calici virus
90%) may be present, with trends monitored by arterial
has been reported.
blood gas or pulse oximetry.
Less common fungal pneumonias include blastomy- ● Note: the oxygen saturation curve drops steeply
cosis, histoplasmosis, aspergillosis and candidiasis. with SPO2 values <90%.
Samples for cytology and culture can be obtained
Clinical signs using percutaneous lung aspiration, transtracheal
wash, unguided bronchioalveloar lavage or broncho-
A deep productive cough may be heard, although
scopic lavage. Cultures for aerobic and anaerobic bac-
coughing is not as common as in dogs.
teria should be performed and a fungal culture is
Fetid breath halitosis. indicated if infection is possible within the geograph-
ical region. Results of cultures must be evaluated in
Fever is common, although a subnormal body tempera-
light of other data including the concentration of bac-
ture can occur if the cat is septic.
teria, cytological findings, etc.
Inspiratory and expiratory dyspnea may be evi- ● Bacterial pneumonia is characterized bysuppurative
dent, often with open-mouth breathing. inflammation involving degenerative neutrophils
with intracellular bacteria.
Adventitial breath sounds, including crackles,
● Fungal and mycobacterial diseases have pyo-
wheezes, snaps and pops may be audible. Breath
granulomatous inflammation, with characteristic
sounds may be absent over areas of lobar consolidation.
organisms seen on routine or special stains.
Lethargy and anorexia are typically present, and
Cryptococcal titers may aid in the diagnosis.
weight loss and ill thrift may be evident if the pneumo-
nia is more chronic.
Infectious pneumonia is uncommon in cats. A recent
Chronic small airway disease (feline asthma/ bronchi-
study of 39 cats with infectious pneumonia showed that
tis), pulmonary infiltrate with eosinophils (PIE) and
a substantial proportion had no clinical signs that were
lymphomatoid granulomatosis may share many similar
referable to the respiratory tract (36% of cats), they
historical, clinical and radiographic signs and need to be
lacked clinical signs of systemic illness (41%), and had
differentiated on clinical and histopathologic findings.
unremarkable findings on hematology (22%) and tho-
racic radiography (23%). Pulmonary neoplasia, either primary (squamous cell
carcinoma, bronchogenic carcinoma), or metastatic dis-
ease, is differentiated on histopathology.
Diagnosis
Thoracic radiography findings include focal or gen- Treatment
eralized alveolar densities with air bronchograms, or
focal areas of complete consolidation. Bacterial pneumonia requires antimicrobial therapy.
● A ventral distribution of lesions may signal aspira- ● The parenteral route is used in debilitated or septic
tion as the cause of pneumonia. patients, and oral therapy in outpatients.

● A miliary interstitial pattern is seen with blastomy- ● Antibiotic selection is best based upon specific cul-
cosis. ture and sensitivity testing.

● Initial empirical choices can be based upon Gram is worse in patients with pre-existing illness (neopla-
stain of the cytology sample. sia, multiple trauma, multiple organ failure), or
– Gram negative rods – amikacin, fluoro- patients on immunosuppressive therapy for immune-
quinolones, trimethoprim-sulfa, chloramphenicol. mediated disease or organ transplantation.
– Gram positive cocci – beta-lactams, trimetho-
Prognosis for cryptococcal pneumonia is generally
prim-sulfa, chloramphenicol.
fair to good provided the cat is not debilited on pres-
– Bordetella – amikacin, tetracycline, chloram-
entation, and therapy is continued sufficiently long
phenicol.
enough for antibody titers to fall to zero.
– Anaerobes – beta-lactams, second-generation
cephalosporins, clindamycin.
Fungal pneumonia requires antifungal therapy.
Prevention
● Itraconazole at 5–10 mg/kg PO daily is the drug
of choice, with 50–60% response rates quoted in Avoid the source of infectious agents, such as bird
cats. droppings and other risk factors, for example, aspira-
● Amphotericin B (0.25 mg/kg IV q 2 days), alone tion after anesthesia.
or in combination with itraconazole.
● If CNS signs are present with cryptococcosis, flu-
conazole (2.5–5.0 mg/kg PO daily) is the drug of
choice to cross the blood–brain barrier (see LARYNGEAL EDEMA
Cryptococcosis, page 27 in The Cat With Signs of
Chronic Nasal Disease). Classical signs
Viral pneumonia treatment is mostly supportive. ● Inspiratory dyspnea.
There is no clear evidence to suggest antiviral therapy ● Stertorous breathing.
is of benefit. Low-dose oral alpha interferon (30 IU
PO daily) may possibly be beneficial, although reports See main reference page 42 (The Cat With Stridor).
are anectdotal.
Supportive care is vital. Airway and systemic hydra-
tion are essential for mucociliary clearance. Clinical signs
● Intravenous crystalloids need to be used judiciously
Inspiratory dyspnea which may be associated with
if there is increased vascular permeability in the
severe respiratory distress.
lung.
● Nebulization with saline may be helpful. Stertor occurs, which is worsened with excitement or
● Physical therapy, such as positional changes, exercise.
coupage of the chest wall (percussion with a cupped
hand) and enforced mild exercise, all enhance the
clearance of debris from the lung.
Diagnosis
● Oxygen enrichment via nasal O catheter, oxygen
2
tent or cage may be essential in critical cases. Acute onset of inspiratory dyspnea.
● Bronchodilator therapy remains controversial in the
Laryngoscopic inspection under heavy sedation or
treatment of pneumonia.
reveals erythema and edema of the laryngeal mucosa.
Prognosis
Prognosis depends on the agent and the severity of the
infection. Differential diagnosis
Bacterial pneumonia has a fair to good prognosis if Laryngeal paralysis, laryngeal mass lesion or foreign
there are no other debilitating factors, but prognosis bodies.
GRASS AWNS, FOREIGN BODIES Diagnosis

Nasal and nasopharyngeal foreign bodies often result
Classical signs in little change on radiographs other than a unilateral
● Sneezing (nasal foreign bodies), coughing fluid density. Rhinoscopy is often both diagnostic and
(tracheobronchial foreign bodies). therapeutic, if the foreign body can be retrieved.
● Inspiratory/expiratory dyspnea, depending Tracheal foreign bodies may be seen radiographically.
on location. Rigid tracheoscopy allows for larger retrieval instru-
● Nasal discharge. ments to be utilized than with flexible endoscopy.
Bronchial foreign bodies may cause complete lobar
Pathogenesis atelectasis or abscessation radiographically. Right cau-
dal and accessory lobes are most often affected
Foreign bodies are usually inhaled or regurgitated with inhalation foreign bodies. Right middle lobe is
and rarely penetrate through the skin. Barbed grass affected commonly with aspiration of vomitus.
awns or seeds or blades of grass favor one-way migra-
tion (i.e., difficult to expel backwards). Differential diagnosis
Inhaled foreign bodies tend to lodge in the nasal cav- Other nasal diseases, such as infectious (especially fun-
ity in cats. gal), nasal cuterebriasis or neoplastic disease, tend to have
● As cats rarely mouth-breathe, inhaled tracheal for- a more insidious onset. Upper respiratory tract viral infec-
eign bodies occur much less commonly than in tion, especially calicivirus, causes acute paroxysms of
dogs. sneezing, which in the early stages could appear similar to
a nasal foreign body.
Penetrating foreign bodies can lodge in the nasal cavity,
such as pellets or a tooth broken from an opponent dur- Nasopharyngeal polyps tend to have a more insidious
ing a cat fight. onset.
Nasopharyngeal foreign bodies may lodge above the Tracheal or bronchial neoplasia have a more insidious
soft palate after vomiting. Food, hairballs and blades onset.
of grass are more common than grass seeds in this area.
Treatment
Tracheobronchial foreign bodies are often the result
of aspiration of regurgitated ingesta. Effective treatment involves removal of the foreign
body and most can be removed endoscopically. Nasal
foreign bodies may be endoscopically retrieved or
Clinical signs hydropulsed. Occasionally, rhinotomy is required,
especially for foreign bodies that have migrated into the
Nasal foreign bodies create intense sneezing, pawing frontal sinuses.
or rubbing the nose along the ground, and nasal dis-
charge (often unilateral) with stridorous (whistling) If a lung lobe is abscessed with a bronchial foreign
nasal breathing. body, lobectomy may be required.
Nasopharyngeal foreign bodies cause gagging, dys- Prognosis

phagia and reverse sneezing. Coughing may occur
Prognosis is excellent with removal of the foreign body.
secondary to post-nasal drip (aspiration of caudal nasal
discharge). Stertorous breathing (snoring) may occur.
Prevention
Tracheobronchial foreign bodies cause coughing and
Appropriate hairball prophylaxis with combing and
signs of fixed obstruction (i.e., both inspiratory and
oral lubricant/laxatives reduces the likelihood or vomit-
expiratory dyspnea).
ing and aspiration of vomitus or the hairball.
● The coughing is often harsh and productive, and
may be elicited with tracheal palpation. Avoidance of grass fields during seed time.
PULMONARY NEOPLASIA Diagnosis

Chest radiographs demonstrate a solid tissue mass(es)
Classical signs or nodular interstitial pattern.
● Sensitivity is limited to masses > 10 mm diameter,
● Non-productive cough, with or without
hemoptysis. and multiple views are important to maximize diag-
● Reduced activity. nosis. Hilar lymphadenopathy may be present.
● Tachypnea and dyspnea – subtle to Other imaging modalities, such as CT or MRI are use-
marked, especially if pleural effusion is ful if available.
evident.
● Fetid halitosis. Biopsy of mass(es) is required for definitive diagno-
● Mass lesion radiographically. sis, as well as for distinguishing the origin of tumor.
● Biopsy options include percutaneous needle aspira-
● Anorexia, weight loss, muscle wasting.
tion or core biopsy, bronchoscopy, or unguided
bronchioalveolar lavage, or transbronchial lung
Pathogenesis biopsy.
● Ultrasound is often a poor tool to guide
Pulmonary neoplasia may be primary or result from
secondary metastases from distant neoplasms. percutaneous biopsy needles, unless the entire
lung lobe has become consolidated, as the sonic
Primary tumors include bronchogenic carcinoma, beam is reflected by any aerated lung tissue.
pulmonary adenocarcinoma and squamous cell car- ● Triangulating the landmarks based on two orthogo-
cinomas. nal radiographic views is extremely effective for
Secondary metastatic tumors include a wide variety percutaneous biopsy.
● Transbronchial cytology (TTW or BAL) is often
of carcinomas (i.e., mammary adenocarcinomas) and
sarcomas (i.e., osteosarcoma), and local metastases disappointing, due to the interstitial nature of the
from primary lung tumors. lesion.
● Transbronchial lung biopsy is a promising tech-
Pleural malignancy may cause dyspnea, either by the nique for obtaining samples for histopathology, but
space-occupying nature of the mass, or from secondary is only available at some institutions.
pleural effusion.
Surgical biopsy may be performed via thoracotomy,
generally during lobectomy.
Clinical signs ● Local lymph nodes should be aspirated or biopsied
Reduced activity with reluctance to play or run may be for staging.
observed.
Thoracocentesis and cytology of pleural fluid is occa-
Inappetance or anorexia and weight loss are often sionally diagnostic if neoplastic cells have exfoliated.
present.
Fetid halitosis may be noticed on physical exam or by Differential diagnosis
the owner.
Infectious disease, especially fungal and parasitic gran-
A non-productive cough, with or without hemoptysis ulomas, foreign body reactions, inflammatory granulo-
is sometimes present. Dyspnea (inspiratory and expira- matous lesions, and lung lobe torsions may mimic
tory) and respiratory distress may be evident in the later neoplastic disease clinically and radiographically.
stages, or if pleural effusion develops.
Pleural effusion results in muffled heart and lung sounds Treatment
ventrally and worsening of dyspnea in lateral recumbency.
Surgical resection is the treatment of choice for soli-
Very rarely, lameness occurs from peripheral appendic- tary primary neoplasms. Cure or long-term remission is
ular bone lesions of hypertrophic osteopathy. possible with wide surgical margins. If non-resectible,
excision of nodules may palliate clinical signs tem- Treatment

porarily.
Corrective surgery for patent ductus arteriosis and
Chemotherapy and radiation have been attempted pulmonic stenosis (rare in cats) is available in special-
in generalized pulmonary neoplasms, with disap- ist centers.
pointing results. Metastases from distant tumors
carry a grave prognosis, although pulmonary lym- Most other problems require medical management
phoma may attain remission with chemotherapy. depending on the presenting signs (see page 140, The Cat
With Abnormal Heart Sounds and/or an Enlarged Heart).
General supportive care and nutrition are important.
LARYNGEAL PARALYSIS
Prognosis
Fair to excellent with surgically resectible primary Classical signs
pulmonary neoplasms without metastasis. ● Inspiratory dyspnea and increased airway
Grave with metastatic disease or malignant pleural noise.
effusions.
● Stertorous breathing (snoring).
● Stridor (high-pitched whistling =
obstructive).
CONGENITAL HEART DEFECTS ● Voice changes, absence of purring.
Classical signs See main reference page 43 (The Cat With Stridor).
● Reluctance to play or run.
● Anxious, uncomfortable breathing. Clinical signs
● Dyspnea – if present varies from mild to Inspiratory dyspnea.
severe.
● Abnormal heart sounds (murmurs, gallops, Stridor which is worse with excitement or exercise.
arrhythmias). Occasional stertorous breathing or snoring.
● Signs of pleural effusion – increased chest
excursions with little airflow. Voice changes such as an absent or whisper-like meow,
or harsh purring sounds.
Diagnosis
Clinical signs
Diagnosis is based on signs of laryngeal stridor, inspi-
Atrioventricular valve dysplasia, septal defects, aortic ratory dyspnea and visualization of the larynx.
and pulmonic stenosis (rare) and patent ductus arterio-
Laryngoscopic inspection under heavy sedation or
sus all lead to pressure and/or volume overload on the
heart, and potentially result in congestive heart failure.
reveals absent or paradoxical motion of the arytenoid
Heart murmurs at various locations (left apex for cartilages. Normally they should abduct on inspiration.
mitral valve dysplasia, right apex for ventricular septal If they close on inspiration, it is paradoxical motion.
defect), and intensities (continuous murmur of patent
Erythema and swelling (“kissing lesions”) of the ary-
ductus arteriosis) occur depending on the type of con-
tenoid mucosa may be evident as a result of repetitive
genital heart defect.
focal impact of the touching surfaces of the corniculate
The cat may be reluctant to play or run, and if pres- processes.
ent, dyspnea varies from mild to severe. Open-mouth
Low-dose ketamine (4–6 mg/kg IV), ketamine/
breathing or cyanosis may occur with severe defects.
Signs of pleural effusion include increased chest excur- (4–6 mg/kg IV) allows visual inspection without
sions with little airflow. diminishing laryngeal function.
Differential diagnosis Oronasal reflux, especially with fluids, occurs with

cleft palate.
Other causes of dynamic or fixed upper respiratory
tract obstruction are distinguished on laryngoscopic With stress, nasal obstruction may result in mouth
inspection (see Chapter 4, The Cat With Stridor). breathing.
Dynamic causes of upper respiratory tract obstruc-

tion are: Treatment
● Brachycephalic airway syndrome. This results in an
Treatment involves surgical correction of the defect, if
elongated soft palate causing partial laryngeal possible.
obstruction and entrapment of the epiglottis, and
lateral ventricle eversion causing ballooning of the
mucosa of the lateral ventricles into the lumen. ACUTE SYSTEMIC ANAPHYLAXIS
● Cervical tracheal collapse.
● Pyogranulomatous or lymphoplasmacytic laryngitis Classical signs
results in a roughened, proliferative mucosa of the
● Acute dyspnea
arytenoids and epiglottis.
● Hypotensive shock
Fixed causes of upper respiratory tract obstruction are: ● Collapse
● Oropharyngeal neoplasia (squamous cell carci- ● Pale mucous membrances
noma, oral melanoma, nasopharyngeal polyp).
● Tracheal neoplasia (intraluminal adenocarcinoma, See main reference on page 566 for details (The Cat
extraluminal masses). With Polycythemia).
● Tracheal foreign bodies.
Clinical Signs
CONGENITAL ANOMALIES OF THE UPPER ● Pulmonary signs such as severe acute dyspnea
RESPIRATORY TRACT predominate, because the lung is the “shock
organ” in cats.
Classical signs ● Signs of hypotensive shock, such as pallor and col-
● Dyspnea, usually fixed obstruction lapse, accompany the pulmonary signs.
(inspiratory and expiratory) due to stenotic ● The onset of clinical signs occurs in seconds to
nature of most defects. minutes after exposure to the inciting antigen.
● Inspiratory dyspnea and stertor occur with ● Occasionally, cutaneous swelling may be noted
the brachycephalic syndrome. around the face and paws.
See main reference on page 39 for details (The Cat Diagnosis

With Stridor).
● Diagnosis is made by a combination of appropri-
ate history and characteristic clinical signs.
Clinical signs ● No laboratory tests are currently available to
make a definitive diagnosis of acute systemic ana-
Stenotic nares, hypoplastic trachea, etc., potentially phylaxis.
create a non-dynamic, fixed obstruction leading to
inspiratory and expiratory dyspnea, although inspira-
tory dyspnea may be more prominent with stenotic CARDIAC TUMORS
nares and hypoplastic trachea, if there is a dynamic
component to the obstruction. Classical signs
Dynamic obstructions such as occur with elongated ● Dyspnea and trachypnea.
soft palate create inspiratory dyspnea with stertor.
Clinical signs Tracheobronchoscopy is valuable in both diagnosing

Cardiac tumors are extremely rare in cats.
Dyspnea may occur from obstruction of blood flow to PULMONARY FIBROSIS
or from the heart (i.e., aortic body chemodectomas), or
because the tumor acts as a space-occupying mass com- Classical signs
pressing the mainstem airways at the hilus.
● Dyspnea.
Malignant pleural or pericardial effusion may occur, ● Rare in cats.
creating dyspnea and weakness or lethargy.
Clinical signs
Diagnosis
Chronic progressive dyspnea associated with restrictive
Diagnosis is based or finding a mass lesion on the heart pulmonary disease and tachypnea.
base when imaged with radiography or ultrasonography.
Occasionally cats will cough, especially if a secondary
bacterial infection occurs.
TRACHEOBRONCHIAL COLLAPSE Very rare in cats, and may be associated with chronic
small airway disease (feline asthma/bronchitis com-
Classical signs plex) or chemotherapy.
● Harsh, honking cough. A recent paper cited an emerging syndrome of sponta-
● Stridor on inspiration if cervical segment neous feline idiopathic pulmonary fibrosis. In this
involved. study, chronic respiratory disease with pathology
● Very rare in cats. consistent with usual interstitial pneumonia (UIP)
spontaneously developed in domestic short- and long-
See main reference on page 44 for details (The Cat hair cats and Persians.
With Stridor). ● Duration of respiratory signs ranged from years
(6/22 cats) to acute death (3/22 cats). Cough
Clinical signs (12/16), dyspnea (16/19) and increased respiratory
Tracheobronchial collapse is very rare in cats and gen- rate (19/19 cats) were present. Crackles, wheezes,
erally occurs secondary to trauma or to compression and harsh or loud lung sounds were auscultated in
caused by an extraluminal mass. It has been reported some cats.
associated with proximal tracheal obstructions from a
trachael granuloma or polyp. Diagnosis
The cough is often harsh, non-productive and parox- Marked interstitial pattern is visible on radiographs.
ysmal, ending in a gagging episode which may appear
to be productive. Bronchioalveolar fluid may contain a predominance of
lymphocytes or non-lytic neutrophils, eosinophils and
Cervical trachea collapse produces inspiratory dyspnea, macrophages. Culture sample to rule out secondary
while intrathoracic tracheal or bronchial collapse will bacterial infection.
lead to mostly expiratory dyspnea. Stridor is occasion-
ally reported. Diffuse interstitial fibrosis is evident on histopathology
of a lung biopsy.
Diagnosis
Radiographs may show attenuation of the tracheal or Treatment
bronchial lumina. Fluoroscopy may be more sensitive Bronchdilators orally such as sustained release theo-
for dynamic collapse. phylline (TheoDur or Slo-bid Gyrocaps 25 mg/kg q
24 h in the evening) or inhaled via a face mask Because of the restricted expansion of the lungs during
(albuterol). inspiration, negative pressure is increased in the pleural
space, resulting in rapid reaccumulation of fluid.
Steroids at anti-inflammatory doses are usually the cor-
nerstone of therapy (prednisone 1 mg/kg q 12 h for
Clinical signs
7 days then 1 mg/kg q 24 h, then reducing to the mini-
mum effective dose over 2–4 months). Dyspnea occurs which is inspiratory and expiratory.
Antibiotics are indicated when signs worsen and do not Muffled lung and heart sounds are audible ventrally as
respond to steroids. If there are many neutrophils in the a result of the pleural effusion.
BAL fluid, a preliminary course of antibiotics may be
There is rapid return of hydrothorax, even after the
indicated before steroids are used, to see if there is any
pyothorax has been successfully treated.
improvement in signs. Be careful about combined use
of enrofloxacin and theophylline, as enrofloxacin has
Diagnosis
the potential to inhibit liver metabolism of theophylline
and increase plasma concentrations. Radiography may reveal distorted poorly expanded
rounded lung lobes.
FIBROSING PLEURITIS Diagnosis is frequently only made at surgery.
Classical signs Treatment

● Dyspnea. Stripping of the fibrotic pleura from the lungs followed
● Muffled heart and lung sounds ventrally. by glucocorticoid therapy has been attempted, but is
rarely successful.
Prognosis
Pathogenesis
Prognosis is generally poor.
Fibrosing pleuritis is a rare sequence of pyothorax and
other chronic pleural effusions, especially chyothorax.
Chronic pleuritis results in restrictive fibrosis of the
pleura, which prevents the lungs expanding.
RECOMMENDED READING
Mason RA. Dyspnea, tachypnea and panting. In: Tilley LP, Smith FWK (eds) The 5 minute veterinary consult, 2nd
edition. Baltimore, Lippincott Williams & Wilkins, 2000, pp 68–69.
Turnwald GH. Dyspnea and tachypnea. In: Ettinger SJ (ed) Textbook of Veterinary Internal Medicine, 4th edition.
Philadelphia, Saunders, 1995, pp 61–64.
Ware W. Dyspnea: diagnosis and management. In: August JR (ed) Consultations in feline internal medicine.
Williams K, Malarkey D, Cohn L, Patrick D, Dye J, Toews G. Identification of spontaneous feline idiopathic pul-
monary fibrosis: morphology and ultrastructural evidence for a type II pneumocyte defect. Chest 2004; 125(6):
2278–2288.
6. The cat with hydrothorax
Robert Allen Mason
KEY SIGNS
● Dyspnea worsened in lateral recumbency.
● Dull heart and lung sounds ventrally.
● Fluid aspirated from chest (chyle, blood, transudate, modified transudate,
exudates).
MECHANISM?
● Accumulation of fluid (blood, transudate, modified transudate, exudate, chylous) in the pleural
cavity.
● There is a delicate balance of the normal fluid dynamics between the slight transudation across
the parietal pleura and the slight absorption across the visceral pleura.
● Factors which facilitate pleural effusion include decreased oncotic or increased hydrostatic
pressure within blood vessels, increased vessel wall permeability, and lymphatic obstruction.
● Excessive fluid in pleural cavity (chlye, blood, transudate, modified transudate, exudate).
● Pleural effusion encroaches on the space generally occupied by the lungs, and creates
hydraulic pressure opposing expansion of the lungs.
WHERE?
● Pleural space is the cavity between the visceral and the parietal pleura. Generally, this space
contains a few milliliters of fluid to act as a lubricant.
WHAT?
● Chylothorax – secondary to congestive heart failure, mediastinal neoplasia, lymphangiectasia,
or trauma.
● Hemothorax – secondary to trauma, coagulopathy, or neoplasia.
Pyothorax – from penetrating chest wound, ruptured lung abscess, or systemic bacteremia.
● Transudation – secondary to hypoalbuminemia from hepatic failure, protein-losing enteropa-
thy, or protein-losing nephropathy. May also occur from increased hydrostatic pressure from
congestive heart failure or lymphaticovenous obstruction from a neoplastic or granulomatous
disease of the chest.
● Modified transudates result either from causes of chronic transudates or occur early in dis-
eases, which cause exudates such as vasculitis secondary to feline infectious peritonitis, ure-
mia, neoplasia or pancreatitis.
71

Diseases causing hydrothorax
DEGENERATIVE
● Congestive heart failure (cardiomyopathy)* (p 83)
Pleural effusion may result from right-sided or biventricular failure, most commonly associated
with cardiomyopathies. Cardiac tamponade from pericardial effusion may cause pleural effusion.
Abnormal heart sounds (gallops, murmurs, arrhythmias) are commonly noted. Cardiomegaly, pul-
monary venous congestion and pulmonary edema may be seen radiographically. Effusion fluid is
commonly a modified transudate or chylous effusion. Rarely, heartworm disease has been associ-
ated with pleural effusion of a clear transudate.
ANOMALY
● Chylothorax** (p 77)
Milky white, lipid-rich lymphatic fluid accumulates in the pleural space secondary to thoracic duct
hypertension. Idiopathic chylothorax is the most common form. Less commonly chylothorax is
associated with cardiomyopathy, or mediastinal neoplasia. Affected cats are often chronically ill
for several months prior to the onset of dyspneic signs of pleural space disease.
MECHANICAL
● Pleural/mediastinal masses (p 84)
Malignancies like thymoma or thymic lymphoma may cause obstruction of the lymphatic drainage
of the pleural cavity, leading to hydrothorax and dyspnea. Mass lesions may be observed radi-
ographically, especially after thoracocentesis. Dyspnea rarely may not improve significantly after
drainage. Transudate or exudate found on fluid analysis.
● Hemothorax (p 87)
Trauma or bleeding diatheses from congenital coagulopathies (hemophilia, Chediak–Higashi) or
acquired coagulopathies (rodenticide toxicity) may create hemothorax. Fluid is pink to frankly red
in color, but often defibrinated and does not clot. Evidence of blunt or penetrating chest trauma is
common. There may be other signs of coagulopathy (scleral hemorrhages, hematoma formation,
epistaxis, etc.).
METABOLIC
● Hypoproteinemia (p 88)
Protein-losing enteropathy, protein-losing nephropathy, and hepatic failure are common
causes of low serum protein, specifically hypoalbuminemia, which may result in decreased oncotic
pressure and transudation. This fluid is clear to lightly straw-colored. Signs include dyspnea,
weight loss, especially loss of muscle mass +/− icterus.
NEOPLASTIC
● Airway / Pulmonary neoplasia (p 87)
Tracheal adenocarcinomas (i.e., Siamese), primary pulmonary masses (pulmonary adenocarci-
noma) or secondary metastatic disease from distant neoplasms may create effusions. Fluid is often
modified transudate and is often grossly opaque. It is more common in middle-aged to older cats.
6 – THE CAT WITH HYDROTHORAX 73
INFECTIOUS
● Pneumonia (p 84)
Moist, productive cough, fever, halitosis may be seen. Parapneumonic pleural effusions are com-
monly sterile inflammatory exudates, often grossly serous or hemorrhagic rather than purulent.
They often resolve with treatment of the lung disease.
● Feline infectious peritonitis (FIP)* (p 81)
Vasculitis caused by the immune response to feline coronavirus causes exudation of a protein-rich fibri-
nous fluid into various body cavities including the pleura. Systemic illness is common.
● Pyothorax*** (p 75)
There is an accumulation of grossly obvious purulent exudate in the pleural cavity. Turbid, flocculent,
often fetid-smelling fluid with cells that are primarily degenerative neutrophils. Dyspnea, signs of
chronic disease (weight loss, ill-thrift), and fever are common signs.
● oncotic pressure.
INTRODUCTION ● systemic or pulmonary vascular pressure.
● lymphatic hydrostatic pressure, compliance or per-
meability.
MECHANISM? ● vascular permeability.
Pleural space is the cavity between the visceral pleura
Hydrothorax is the accumulation of fluid in the
(covering the lungs and the pericardium) and the pari-
pleural cavity, which may consist of blood, transudate,
etal pleura (covering the internal thoracic wall,
modified transudate, exudate or chylous fluid
diaphragm and mediastinum).
Various fluid types that may accumulate include:
Generally, this space contains a few milliliters of fluid
● Hemorrhage consists of frank blood, and may be
to act as a lubricant for motion of the lungs and the
caused by neoplasia, coagulation defects or trauma.
heart. This fluid is very close to the composition of
The hematocrit of the fluid is often much lower
serum.
than the peripheral blood, and it rarely clots after
Visceral and parietal pleurae have distinctly separate removal.
vascular supplies and lymphatics. The parietal pleural ● Transudates are low protein (< 15 g/L), low cellu-
lymphatics have stomata – gaps that exist to remove larity (< 1.0 × 109/L) fluids that leak out of the vas-
particulate matter from the pleural space. Absorption cular space secondary to lymphatic or venous
through these stomata may be facilitated by motion of occlusion from congestive heart failure, mediastinal
the chest wall during breathing. Obstruction of the mass obstruction or infiltration of the pleura.
stomata may decrease absorption of exudative ● Modified transudates or exudates are more cel-
effusions. lular (1.0–7.0 × 109/L and 5.0–20 × 109/L, respec-
tively), and higher protein (25–50 g/L and 30–80 g/L,
Normal fluid dynamics of the pleura balance between
respectively) fluids.
opposing hydrostatic and oncotic pressures across the
– Modified transudates are associated either with
pleurae. There is a delicate balance between the slight
diseases that cause chronic transudates, or
transudation across the parietal pleura and the slight
occur early in diseases that produce exudates.
absorption across the visceral pleura, that maintains a
Over time, chronic transudates produce pleural
steady ratio of production to drainage of fluid through
irritation that results in increased cell numbers
the pleural space.
and slightly increased protein in the fluid, which
Disease conditions that disrupt this balance can lead is then classified as a modified transudate.
to pleural effusion by changing; Modified transudates also occur early in diseases
that produce exudates from leaking blood ves- decreased oncotic pressure as a result of hypoal-
sels such as neoplasia, and vasculitis associated buminemia (protein-losing enteropathy, protein-
with feline infectious peritonitis, uremia, pancre- losing nephropathy or hepatic failure).
atitis or neoplasia. ● Chylothorax is usually idiopathic and associated
● Pyothorax is pus in the chest cavity from bacterial with lymphangiectasia, or may occur in association
infection. Protein is high (30–70 g/L) and nucleated with congestive heart failure, mediastinal neoplasia
cell counts are high (5–300 × 109/L). or thoracic duct rupture.
● Chylothorax is a lipid-rich tissue fluid from ● Pyothorax is most often associated with mixed
obstruction or trauma to the thoracic duct. Protein bacterial infections presumed from a penetrating
content ranges from 25–60 g/L and cell counts from wound or foreign body.
1.0–20 × 109/L. ● Thoracic exudates are most commonly associated
with feline infectious peritonitis, but may also occur
The fluid from these various forms of pleural effusion
with neoplasia, pancreatitis and uremia.
encroaches on the space generally occupied by the
● The most common forms of hydrothorax in the
lungs, and creates hydraulic pressure that opposes the
cat are pyothorax, neoplastic effusions, transuda-
expansion of the lungs. Fluid volumes greater than 50
tion from cardiac disease and chylothorax.
ml/kg result in dyspnea.
DIAGNOSIS
WHERE?
For cats with mild to moderate clinical signs, thoracic
Hydrothorax is the result of conditions that affect the
radiography may be diagnostic. Pleural fissure lines,
pleural space, especially conditions affecting the blood
separation of the lung borders from the thoracic wall,
vessels or lymphatics of the pleura.
loss of cardiac detail, blunting of the costophrenic
Blood vessel problems that contribute to hydrothorax angles (lateral and VD views), widening of the medi-
include: astinum (DV view) can all indicate the presence of fluid
● Increased hydrostatic pressure from congestive in the pleural space.
heart disease or vascular obstruction.
With severely affected cats in respiratory distress,
● Decreased oncotic pressure from hypoalbuminemia
radiography should be delayed until after thoracocen-
secondary to liver disease, kidney or gastrointesti-
tesis (cats with pleural effusions die in radiology!).
nal protein loss.
● Increased vascular permeability from inflammation An algorithm for the approach to the dyspneic cat fol-
(vasculitis). lows;
● Vascular rupture and hemorrhage (trauma, neoplasia). ● A – Airway – establish a patent airway.
● B – Breathing – be certain the patient is ventilating.
Lymphatic diseases that contribute to hydrothorax
● C – Centesis – if the dyspnea has not resolved with
include:
steps A and B, then evaluating for the presence of
● Obstruction from congestive heart disease, lym-
pleural space disease via thoracocentesis is not only
phangiectasia or neoplasia.
diagnostic, but therapeutic for both hydrothorax
● Rupture from trauma.
and pneumothorax. A negative tap would suggest
the presence of a mass lesion or primary parenchy-
WHAT? mal disease such as status asthmaticus.
The following conditions are most commonly associ- Thoracocentesis
ated with the different forms of hydrothorax in cats: ● In the acute, emergency setting, a butterfly set may
● Hemothorax usually results from trauma or coagu- be rapidly introduced to alleviate life-threatening
lopathy. accumulations.
● Transudation results from either increased hydro- ● In chronic or more stable cases, a polypropylene or
static pressure (mediastinal mass, lymphatic infil- Silastic IV catheter on an IV extension set with a
tration or obstruction, and cardiac disease) or from three-way stopcock attached to a 20–60 ml syringe
works very well. Local anesthetic blockade may or hydrostatic pressure (i.e., heart failure), or occur
may not be required, depending on the level of res- in acute inflammatory disease prior to exudation.
piratory distress. – Exudates vary from white to red, turbid to
● Technique opaque, are high protein (> 3.0 g/L), and highly
– Have the patient sitting, standing or in sternal cellular (TNCC > 7.0 × 109/L. They are associ-
recumbency. ated with inflammatory or neoplastic disease.
– Clip and aseptically prepare the 4th–7th inter- ● Thoracic radiography should be performed after
costal space – above and below the costochondral thoracocentesis to help to assess the success of
junction. pleural drainage and to facilitate imaging of
– Infiltrate around the 7th intercostals space just mediastinal masses, pulmonary lesions or cardiac
above the costochondral junction with local changes that may have contributed to the effusion.
anesthetic field block (optional if peracute and These changes may have been previously masked
in severe distress), using 2% lidocaine or 2% by the presence of the effusion.
mepivicaine. Block the skin, muscles and pari-
Other imaging may be required depending on the char-
etal pleura, as this is the most painful area.
acter of the effusion (i.e., cardiac ultrasound if transu-
– Use 25 gauge needles and INJECT SLOWLY!
date, lymphangiography if chylous effusion, etc.).
– Place the catheter at the 7th intercostal space
just above the costochondral junction. With a
syringe on the catheter, aspirate using minimal
negative pressure. DISEASES CAUSING HYDROTHORAX
– Direct the catheter ventrally for fluid removal. If
drainage is inadequate use a butterfly needle and PYOTHORAX***
aspirate the intercostal junction from the 4th–6th
intercostals or place a chest drain. Classical signs
● Fluid analysis should be performed to determine
the etiology of the hydrothorax. ● Dyspnea with exaggerated chest
– Cytologic, clinicopathologic, and bacteriologic excursions/poor airflow.
analysis will help determine the etiology. ● Muffled heart and/or lung sounds ventrally.
Common assessments include physical param- ● Orthopnea (positional dyspnea – reluctance
eters such as color, transparency, specific grav- to lay in lateral recumbency).
ity (SG), total protein (TP), and total nucleated ● Signs of chronic disease (weight loss, ill-
cell counts (TNCC) and some biochemical thrift), and fever are common.
parameters such as triglyceride, cholesterol, ● Grossly purulent exudate in the pleural cavity.
glucose and certain enzyme levels, such as lac- ● History of fight wounds several weeks
tate dehydrogenase (LDH). previous to presentation.
– Hemothorax is characterized by frank blood.
Erythrophagocytosis which is usually defibri-
nated may be evident cytologically, and gener- Pathogenesis
ally has a hematocrit lower than peripheral
Septic bacterial infection of the pleural cavity results in
blood.
purulent exudation.
– Transudates are clear and colorless with a spe-
cific gravity (SG) </= 1.013, total protein (TP) Multiple routes of infection, include:
< 2.5 g/L and low cellularity (total nucleated ● Hematogeneous with systemic sepsis spread via
cell count [TNCC] < 1.5 × 109/L). vasculature or lymphatics.
– Modified transudates are typically straw-colored ● Extension from an adjacent infected structure,
to pink-white. Total protein is between 2.5 and including parapneumonic spread from lung infec-
4.0 g/L, and TNCC between 1.0 and 7.0 × 109/L. tion or abscess, or from esophageal rupture, or
Modified transudates result from transudates mediastinitis.
modified from chronicity, prolonged increased
● Penetrating wound as a result of a fight, a foreign ● Thoracocentesis should be performed in all

body or thoracic surgery. acutely dyspneic animals, especially trauma
patients, prior to radiography. These patients are
Fibrinous exudation and cellular infiltration occurring
extremely fragile, and even the minimal restraint
in response to bacterial infection results in obstruction
involved in radiography may be excessive, and they
of the parietal pleural stomata, which further reduces
may die during the procedure!
drainage of the exudation.
● A negative tap for air or fluid suggests solid pleu-
Clinical signs of systemic illness result from the ral space disease (mass or herniated viscus), pri-
chronic sepsis. Eventually respiratory signs become mary pulmonary (i.e., contusion in the trauma
evident as fluid reaches critical volume (estimated in patient) or cardiac disease. If the tap is positive,
cats to be 50 ml/kg). remember that small animals may accommodate
up to 50 ml/kg free fluid in the chest prior to
becoming dyspneic.
Clinical signs ● Be certain to remove as much fluid as possible, do
not stop after you have a diagnostic sample.
Pyothorax is more common in intact males, and there
is a history of fight wounds several weeks prior to Cytology
presentation.
Cytology and Gram stain are important in identifica-
Heart and lung sounds are dull ventrally. Breathing tion of the pathogen, as culture is often negative.
sounds are harsh dorsally in standing or sternal
Pyothorax is characterized by a thick, fetid, septic sup-
recumbency. Chest wall percussion may be dull ven-
purative exudate. Cytology reveals a high protein fluid
trally.
(TP > 30 g/L), highly cellular (TNCC > 7.0 × 109/L)
Dyspnea is characterized by marked chest wall excur- with mostly degenerative neutrophils, often with intra-
sions with minimal airflow. Orthopnea, or positional cellular bacteria. Macrophages and reactive mesothelial
dyspnea is common. Dyspnea is worsened in lateral cells are common.
recumbency and cats often are reluctant to lie in lat- ● Bacterial infection is characterized by suppurative
eral recumbency. inflammation involving degenerative neutrophils
with intracellular bacteria.
Signs of chronic disease are often evident. The cat ● Fungal and mycobacterial diseases have pyogranu-
may appear sick, septic, thin and unkempt.
lomatous inflammation, with characteristic organ-
Fever or, in the latter stages, hypothermia may be isms seen on routine or special stains.
present.
Bacteriology
There may be caudal displacement of the liver due to
Bacterial culture for aerobic and anaerobic bacteria is
pleural fluid pressure on the diaphragm.
important, but negative cultures are not surprising, as
many bacteria have been killed or had their growth
inhibited by the lysozymes present in the exudate.
Diagnosis Gram staining is an excellent way to document the ini-
Typically there is a vague history of being unwell for tial categories of bacteria present, as well as following
weeks, with inappetance, weight loss and recent onset the response to therapy.
of dyspnea.
Thoracic radiographs show significant pleural effusion Hematology
with pleural fissure lines and loss of the cardiac silhou- Blood smear may reveal neutrophilia with or without
ette. Effusions are usually bilateral, although not a left shift and toxic neutrophils (Doehle bodies,
always. etc.).
Thoracocentesis may be both diagnostic and therapeu- A low-grade non-responsive anemia and monocytosis
tic in pleural space disease. may support chronicity.
Differential diagnosis ● Gram-positive rods – fluoroquinolones, chloram-

phenicol, clindamycin.
All causes of pleural effusion show similar signs of dys- ● Gram-positive cocci – beta-lactams, chloram-
pnea and dull chest sounds. Most other causes, however, phenicol.
do not show the same severe systemic signs, other than ● Note: aminoglycosides require oxygen-rich envi-
some forms of pleural or pulmonary neoplasia. ronments to be effective, and trimethoprim-sulfa
drugs may be inactivated in purulent debris. For
Treatment these reasons, these medications are not indicated
Thoracostomy (T) tube placement and chest drainage in pyothoraces.
is the cornerstone of therapy. Beta lactams such as ampicillin at 20–40 mg/kg IV ini-
● Tubes may be placed surgically or via a trocar.
tially q 4 hours for 48 hours, then PO q 6–8 hours are suf-
Placement along the ventral thoracic floor helps ficient for the majority of community-acquired infections.
maximize complete drainage.
● Continuous underwater sealed suction with 20 Clindamycin is effective against Bacteriodes fragilis,
cmH2O of vacuum appears to be superior to inter- found in approximately 15% of cases, and is dosed at
mittent drainage, but requires 24-hour direct super- 25 mg/cat PO q 12 hours.
vision. Disposable, self-contained collection units Recommendation for length of antibiotic therapy varies
are easily adaptable to cats. These are commercially from 4 to 12 weeks.
available one-piece plastic chambers that adapt to a
suction line on one end, and to the thoracostomy
tube on the other. The effusion is collected and vol- Prognosis
ume measured in the calibrated chamber. Prompt, aggressive and complete drainage of the
● Occasionally bilateral T-tubes are required for
abscess cavity in the pleural space is essential for suc-
complete drainage. Average duration of tube use is cessful therapy. The use of T-tube(s) with continuous
3–5 days with continuous suction. Intermittent suc- suction has increased the treatment success rate of this
tion generally requires longer duration of therapy. disease tremendously.
Tubes are usually removed once less than 2 ml/kg
of fluid is drained. Prognosis also varies with the presence or absence of
● Controversy exists as to the benefit of pleural underlying risk factors, such as pre-existing immuno-
lavage. There has been no convincing evidence suppressive disease with retroviral infection or sys-
showing any advantage to lavage, and the risk of temic neoplasia.
contamination is high. With aggressive therapy, lack of significant risk factors,
Systemic support with IV fluid hydration and antibi- and long-term therapy with appropriate antibiotics,
otic therapy is very important. Most patients are hypo- prognosis is very good to excellent.
volemic on presentation, and the initial fluid losses via
the T-tube can be tremendous. Fluid requirements must Prevention
include volume replacement, maintenance, and on-
going losses through the T-tube. Keeping the patient Neuter intact males. Prevent roaming and fighting.
well-hydrated helps to promote the “dialysis mem-
brane” effect of the pleura, effectively “washing” the CHYLOTHORAX**
pleural space and draining the excess fluid through the
T-tube. Serum potassium and phosphorus levels should Classical signs
be monitred and supplemented, when indicated.
● Muffled heart and/or lung sounds ventrally.
● Exaggerated chest excursions with poor
Antibiotics
airflow.
Antibiotic selection is best based upon specific culture and ● Orthopnea (positional dyspnea with
sensitivity testing. Initial empirical choices can be based reluctance to lie in lateral recumbency).
on the Gram stain of the cytology sample.
Pathogenesis controversy whether this finding represents a cause

and effect of lymphatic hypertension.
Chyle is the lymphatic fluid being transported from the ● Thoracic trauma is a less common cause of thoracic
abdominal organs to the prehepatic circulation. It conduct rupture, although this has been documented.
tains lipid-rich products such as chylomicrons, and ● Chronic chylothorax is irritating to the pleura and
grossly it is pink to milky white. Protein content may may cause fibrosing pleuritis and pericarditis.
vary, and measurement may be interfered with by the ● New evidence suggests this secondary fibrosing
presence of the lipids. Cells are primarily small lym- pericarditis may lead to increased right-sided pres-
phocytes, and the count (TNCC) is < 10 × 109/L. sures and decreased lymphaticovenous drainage,
The thoracic duct is the cranial continuation of the cys- resulting in diminished drainage of the thorax, and
terna chyli, the major lymphatic structure draining the persistence of the chylothorax.
abdominal organs. The thoracic duct passes through
the diaphragm at the aortic hilus and proceeds cra-
nially in the mediastinum dorsal to the thoracic aorta and Clinical signs
ventral to the azygous vein. It terminates cranially at the Chylothorax generally occurs in middle-aged cats,
lymphaticovenous junction at the thoracic inlet, either possibly more common in purebreds.
into left jugular, subclavian, or brachiocephalic veins.
Here the lymphatic fluid from the entire body, except the Vague signs of depression and lethargy, often for
right side of the face, the right pectoral limb, and the greater than 1 month, are common.
right thoracic wall, which drain into the right lymphatic Tachypnea, dyspnea and the ventilation pattern typical
duct, re-enters the venous circulation. for pleural space disease are present. This involves
The rate of lymph flow through the thoracic duct in cats increased chest wall excursion, often with the head and
has been estimated at 2 ml/kg/hour, increasing up to neck extended, but very little airflow present. Dyspnea
10-fold after a high-fat meal. Rapid accumulation of may be reported as acute in onset. Dyspnea is often
several hundreds of milliliters of fluid can occur with worsened in lateral recumbency and cats are reluctant
obstruction of or leakage from lymphatic drainage. to lie in lateral recumbency.
Chylous effusion in cats is most often idiopathic. Heart sounds are muffled but become more apparent
The most commonly known causes are associated after the chest tap and are generally normal.
with increased lymphatic hypertension from conges- Abnormal heart sounds such as murmurs, gallops or
tive heart failure or obstructive neoplasia (see sec- arrhythmias may be present if the chylous effusion is
tions under Cardiomyopathy or Mediastinal masses in associated with congestive heart disease, but are gener-
this chapter). ally absent in idiopathic chylous effusion.
Increased systemic venous pressure associated with Coughing may be present from pleural irritation.
dilated cardiomyopathy and rarely heartworm diseases
may result in lymphatic hypertension and, occasionally
chlyothorax. Diagnosis
Mediastinal neoplasia, especially lymphosarcoma and Clinically there are signs of pleural effusion and muf-
thymoma are most common neoplasias associated with fled heart sounds.
chylothorax.
Thoracocentesis should be performed prior to radiogra-
Occasionally thrombus formation associated with an phy in the severely dyspneic patients, both as an emer-
indwelling jugular catheter results in chylothorax. gency treatment and a diagnostic procedure.
Idiopathic chylous effusions are associated with tho- ● The typical effusion is grossly chylous with milky-
racic duct disease. white to pink fluid. Cell count is usually <1 × 19/L
● Thoracic duct lymphangiectasia, demonstrated via and is largely lymphocytes, unless the effusion is
contrast lymphangiography, is the most common chronic in which case large numbers of neutrophils
finding in primary chylothorax in cats. There is and macrophages may be present.
● Cholesterol and triglyceride levels of the serum and Chylous effusions may occur as part of congestive
the effusion may be measured and compared to heart failure. If cardiac abnormalities are detected, than
definitively diagnose true chylous effusion, but a complete cardiac diagnostic evaluation should be per-
these findings rarely change the prognosis or the formed (see Cardiomyopathy section in this chapter).
management. True chylothorax has higher triglyc-
eride and lower cholesterol levels than serum.
Treatment
● So-called pseudochylous effusions have the same
gross appearance but with higher cholesterol and Emergency thoracocentesis should be performed
lower triglyceride concentrations than serum. immediately in cats with severe respiratory distress.
Pseudochylous effusion has been discussed in the ● A 23 G butterfly infusion set on a 60 ml syringe is
veterinary literature for years, but there is little evi- introduced at the 5th–7th intercostal space (ICS) on
dence that this exists as a clinical entity in cats. the right, just above the costochondral junction.
Remove as much fluid as possible, or until breath-
Thoracic radiography should be performed after thora-
ing improves. This can usually be performed with-
cocentesis.
out sedation or local anesthetic block with the cat
● If cardiac or pulmonary vessel abnormalities are evi-
standing or in sternal recumbancy. Drainage at mul-
dent radiographically, this indicates the pleural effu-
tiple locations below the costochondral junction
sion may be secondary to congestive heart failure.
between the 4th and 6th intercostal space is some-
● Chronic chylothorax may result in fibrosing pleuri-
times more effective.
tis evidenced by rounded or collapsed lung lobes on
● Placement of a chest drain is recommended for all
radiography.
patients except those that are very debilitated.
● Contrast lymphangiography may be performed if no
● Fluid should be aspirated 1–2 times/day and the
underlying cardiac disease or neoplasia is detected.
tube removed once less than 1–2 ml/kg daily is
– A mesenteric lymphatic vessel is cannulated via
obtained.
celiotomy, and iodinated contrast media are
● Intermittent thoracocentesis may be required until
injected. Thoracic duct lymphangiectasia is the
definitive therapy has been effective.
most common finding with primary chylothorax
in cats. Radiographically, dilated, tortuous lym- Definitive therapy if congestive heart failure is diag-
phatics are found in the cranial mediastinum of nosed is based upon ultrasonographic characterization
affected cats. This procedure adds significant of the type and severity of the cardiomyopathy present
time under anesthesia, and may be technically (see page 128 The Cat With Abnormal Heart Sounds
difficult to perform without intraoperative radi- and/or an Enlarged Heart).
ography or fluoroscopy capabilities. There is
Removal of the jugular catheter and drainage of the
current debate whether this finding of lym-
chlye usually results in resolution of the chylothorax in
phangiectasia is the cause or an effect of tho-
those cases associated with an indwelling jugular
racic lymphatic hypertension.
catheter.
Echocardiography is the definitive modality for ruling
For idiopathic primary chylothorax, both medical and
out cardiomyopathy, pericardial effusion, or other
surgical management have been advocated.
causes of congestive heart failure.
Medical management
If the cat is only mildly dyspneic, ultrasound should be
● This is based around decreasing the lymphatic
performed before the pleural fluid is drained as the
flow through the thoracic duct. Restricting
fluid aids in the detection of a mediastinal mass.
dietary fats is the cornerstone of medical manage-
Severely dyspneic cats should have some fluid drained
ment. Parenteral intravenous feeding is used in
first, as the stress of ultrasound can be fatal.
humans, but is not a practical long-term solution in
cats. Low-fat-reducing diets, commercial or home-
made, help reduce chyle flow, but must be formu-
Other forms of pleural effusion may have similar clin- lated to meet the nutritional needs of the patient.
ical signs but the appearance of the fluid is different. MCT oil (medium chain triglycerides) is a way to
supply calories from fats that are absorbed directly and removed once the fluid production through
into the portal circulation and bypass the thoracic the tube falls below 1 ml/kg daily.
duct lymphatics. Whether this truly decreases tho- – There is current debate whether this procedure is
racic duct flow has come under question in the useful in idiopathic lymphangiectasia, or whether
dog, and information is still lacking in cats. MCT the lymphatic hypertension continues despite lig-
oil is generally reserved for extremely cachectic ation.
cats. It tastes terrible, and may worsen inap- – Pleuroperitoneal drainage, either with passive
petance. drains with diaphragmatic mesh implants, or
● Nutriceutical “fat binders” such as Chitin/ active sump drains between the pleural and peri-
Chitosan may be beneficial to decrease the fat- toneal cavities have been described, but there is
induced chlye flow. a lack of data on the outcomes of these proce-
● Rutin, another oral nutriceutical therapy, has dures in cats. Blockage of the drain is a problem.
shown mixed results in idiopathic chylothorax. – Some surgeons report success with pericardec-
● Rutin is a bioflavanoid and a derivative of vitamin tomy, as a means to decrease the underlying
C. It stimulates macrophage uptake of protein and lymphatic hypertension. Recent studies combin-
processing of inflammatory cells, thus improving ing pericardectomy with thoracic duct ligation
the absorption of the remaining fluid. Dose is 50 have resulted in 80% success in a group of ten
mg/kg tin, which can be mixed up with food. cats with chylothorax.
● Octreotide (Sandostatin, Novartis) a synthetic
somatostatin is being trialled in cats as a SQ injec-
tion tid, but its efficacy is currently unknown. Prognosis
● Medical management together with intermittent
The success of medical management has been docu-
thoracocentesis may be used during the treatment
mented at 20% or less. The author’s clinical experience
for the underlying disease (cardiac therapy, cancer
has been somewhat below that figure. Traumatic injuries
treatments, etc.).
to the thoracic duct may have a slightly better response
Surgical management. rate to medical management. Successful treatment of the
● Surgery should only be considered for patients who underlying disease process usually results in resolution
do not respond to medical management within 6–10 of the chylothorax for taurine-responsive dilated car-
days. Success following surgery is disappointingly diomyopathy and neoplasia. The poor success rate in
low. Surgery is best performed by a specialist with idiopathic chylothorax likely relates to persistence of the
experience in thoracic duct ligation. underlying pathophysiology.
– Ligation of the thoracic duct is the definitive
Prognosis for success of surgical ligation varies from
therapy for idiopathic chylothorax. Surgical
25–53%, and likely varies directly with the skill and
approaches and techniques are described in
experience of the surgeon. Continued effusion occurred
standard surgical texts. Some surgeons prefer
in 30% of cats after thoracic duct ligation in one study.
to give cream orally prior to surgery so that
Proponents of the primary lymphatic hypertension the-
the thoracic duct is filled with white chyle at
ory feel that surgical ligation does not change the under-
the time of surgery, for easier identification.
lying pathophysiology. New data regarding the success
Others prefer to perform a mesenteric lym-
rate of pericardectomy are very promising, with one
phatic dye study similar to what is described
report of an 80% remission rate in ten cats.
for lymphangiography, but using new methyl-
ene blue dye rather than radiographic contrast Chyle is a very irritating fluid to the pleura. Chylofibrosis
material. This dye is visible at the time of sur- and restrictive pleuritis may follow as a complication
gery to ease identification. even after successful surgical ligation. If the fibrosis is
– A postoperative contrast lymphangiogram may be severe, the lungs may fail to expand even after thoraco-
performed through the same mesenteric lymphatic centesis. Pleural stripping has been described, but is not
catheter to assess the success of the ligation. commonly performed in cats, so the success rate is
A thoracostomy tube is placed postoperatively unknown.
Prevention Clinical signs

Taurine supplementation of commercial cat foods in No real age, sex or breed predisposition. Kittens 6–12
North America has dramatically decreased the inci- months old and purebred queens up to 5 years of age
dence of dilated cardiomyopathy in cats. Other causes are over-represented. Another peak is reported in aged
of cardiomyopathies remain unclear at this time. cats. Cats from multi-cat environments are as greatest
risk.
FELINE INFECTIOUS PERITONITIS (FIP)* Anorexia, weight loss, depression, fever or
hypothermia (terminally), and dehydration may all
Classical signs occur, but none are specific to FIP.
● Muffled heart and/or lung sounds ventrally. The effusive form is more rapid and fulminant than the
● Exaggerated chest excursions with poor non-effusive form.
airflow.
Progressive accumulation of ascites and pleural effu-
● Orthopnea (positional dyspnea with
sion in an inappetant, lethargic and pyrexic cat is char-
reluctance to lie in lateral recumbency).
acteristic of effusive FIP. Dyspnea occurs in about 1/3 of
● Anorexia, weight loss, depression,
cats and results from the pleural restriction of the pleu-
dehydration and fever are common early
ral effusion as well as the compromised diaphragmatic
signs.
excursions secondary to the ascites.
See main reference on page 372, for details (The Typically the wet form progresses to death within 5–7
Pyrexic Cat). weeks of onset of clinical signs. This progression may
be shortened to a few days in young kittens.
Pathogenesis
Feline infectious peritonitis (FIP) is caused by a strain Diagnosis
of feline coronavirus called feline infectious peritonitis
Clinical signs of pleural and abdominal effusion with
virus (FIPV).
● This virus specifically infects the mononuclear
normal heart sounds in an inappetant, lethargic and
often pyrexic cat are highly suggestive of FIP.
phagocytic cells of the spleen, liver and lymph
nodes. Replication of the virus occurs primarily in Serology
these cells and creates a systemic viremic state ● Up to 10–40% of healthy cats have positive coro-
within 1 week of experimental exposure. navirus titers. A positive titer means exposure to a
● Virus and virus-infected circulating monocytes feline coronavirus, but not necessarily FIPV.
deposit in the endothelial lining of venules. ● High titers in the presence of typical signs of FIP in
Immune complex interaction to the viral antigen a cat from a one- or two-cat household may suggest
creates an intense vasculitis with complement- FIP, however, methodology is not standard between
mediated damage to the vessel walls. labs. Some healthy cats, especially pure-bred or
● The “holes” created in the vessels result in the exu- from multi-cat households, have very high titers.
dation of the fibrin-rich characteristic “FIP ● PCR (polymerase chain reaction) may be more
fluid”. accurate at detecting viral antigens. One study, how-
ever, showed 8/9 cats suspected with FIP (87.5%)
Three forms of FIP exist. The effusive or “wet” form
were positive, but 51/84 cats (61%) were positive in
is of most significance in creating pleural effusion. It is
non-suspects.
the damage caused by the humoral immune system,
● A 7B FIP ELISA test is available which detects
rather than viral cytotoxicity per se, that is the major
antibody to the 7B protein, which is specific to some
pathogenic mechanism in the formation of the effusion.
coronavirus strains causing FIP. Specificity and sen-
The large body cavities such as the chest and abdomen sitivity data have not been published. Anecdotal evi-
are most prone to fluid accumulation. dence suggests this is not sensitive for FIP.
Thoracocentesis or abdominocentesis and examina- effusive (humoral, beta cell mediated) and granuloma-
tion of the fluid are very valuable. tous (cell-mediated, T-cell response) forms of the dis-
ease, but generally have a very poor outcome in almost
The high protein (50–120 g/L) and fibrin content of
all cases. For a more thorough discussion, see page
the fluid makes it thick, viscous and straw-colored. Cell
458, The Cat With Abdominal Distention or
count is moderate (10 × 109/L), and consists predomi-
Abdominal Fluid.
nantly of non-degenerative neutrophils.
● For effusive FIP, several strategies have been advo-
Electrophoretic separation of the proteins within the cated, including:
fluid may be helpful. – Corticosteroids: prednisone 2–4 mg/kg/day PO.
● Fluid with gamma globulins > 32% has a high pos- – Cytotoxic drugs: cyclophosphamide 2.2
itive predictive value for FIP. mg/kg/day PO 4 days each week, or 50 mg/m2
● Fluids with protein comprised of > 48% albumin PO q 48 hours, or melphalan 2 mg/m2 PO q 48
had a very high negative predictive value for ruling h, or chlorambucil 1.5 mg/m2 PO q 24 hours.
out FIP. – Antiviral drugs: ribavirin 5 mg/kg IV q 24 h.
● Histopathology of liver, kidney or other abdom- Ribavirin is very toxic to cats, mainly myelosup-
inal tissue with inflammation is diagnostic. pressive. It has not been shown to substantially
improve the longevity, although a slight increase
in survival time (10 days) with fewer clinical
signs has been documented. Ribavirin can be
There are few other differential diagnoses for combined with interferon therapy. Low-dose
hydrothorax with a clear or straw-colored, highly pro- oral human interferon-alpha (Roferon) 30
teinaceous fluid. Other forms of pleural effusion with an IU/day PO has been advocated.
exudative fluid are usually turbid, such as pyothorax. – NB: in high risk, systemically ill cats, omitting
● Pyothorax may have systemic clinical signs and the cytotoxic and antiviral agents is recom-
effusion fluid that resembles FIP. FIP fluid has high mended.
protein content (50–120 g/L) with low to moderate
Ancillary treatment consists of using the serotonin
cellularity (10 × 109/L), and predominantly non-
antagonist cyproheptadine (1–2 mg PO q 12 hours) for
degenerative neutrophils, while pyothorax fluid has
appetite stimulation. Antibiotics have been used, espe-
moderately high protein levels (30–70 g/L), and
cially with neutropenia and fever, but with no data to
extremely high nucleated cell counts (5–300 ×
support efficacy. Amphotericin B has been shown to
109/L), which are mostly degenerative septic neu-
have in vitro antiviral effects against FIP, but its nephro-
trophils. Electrophoresis and bacterial culture of the
toxicity limits its use in cats.
fluid may help separate these entities. FIP fluid has
high gamma globulin and is sterile, where pyothorax
fluid has a balanced albumin/globulin ratio, and is a Prognosis
septic exudate, based on Gram stain or culture Long-term prognosis for effusive FIP is extremely
results. poor. Average survival from onset of clinical signs is
Pericardial effusion may present with ascites and 5–7 weeks, although some stronger “healthier” individ-
pleural effusion. uals may have a more insidious disease course, and
may survive for 6–8 months.
Treatment
Prevention
Emergency thoracocentesis should be performed in
Management strategies
cats with severe respiratory distress (see section on
● One study showed kittens raised in catteries with
Pleural effusions, this chapter).
all other cats or isolated from other cats except
Medical management queens had 30–50% positive titers for FIPV, and
● Management strategies for FIP take advantage of 1–2% death rate from clinical FIP. However, kit-
the different immunopathogenic mechanisms of the tens raised in a cattery, that were weaned and
separated from queens at 4–6 weeks of age had monary venous hypertension leads to pleural effu-
0% positive titer, 0% died of FIP. sion. This is suspected, but not proved, in cats.
● The recommendation from this study was to wean
Pleural fluid tends to be a modified transudate or chy-
early and separate kittens from the queen before
lous in nature with congestive heart failure.
the maternal antibodies are lost.
Cardiomyopathies such as hypertrophic, dilated or inter-
Vaccination
mediate forms are most often associated with pleural
● A heat-sensitive modified-live intranasal vac-
effusions. Dilated cardiomyopathy is more often associ-
cine was tested for efficacy. In this study, of 550
ated with pleural effusion than the other forms of car-
cats arriving at shelter, half were vaccinated and
diomyopathy, but it is now a rare disease following
2/254 developed clinical FIP, where 8/246 unvac-
taurine supplementation of commercial pet food.
cinated controls developed FIP. However, an
experimental study using a different challenge Rarely heartworm disease has been associated with
strain to the vaccine strain found no protection pleural effusion.
and antibody-dependent enhancement occurred
resulting in accelerated disease. Clinical signs
Dyspnea varies from mild and associated with
CONGESTIVE HEART FAILURE reduced activity levels and reluctance to play, to
(CARDIOMYOPATHY) acute, fulminant air-starvation with open-mouth breath-
ing and cyanosis.
Classical signs
Abnormal heart sounds (murmurs, gallops, arrhyth-
● Muffled heart and/or lung sounds ventrally. mias) may be present, or may be difficult to assess in
● Exaggerated chest excursions/poor airflow. the distressed patient.
● Orthopnea (positional dyspnea – reluctance
Signs of pleural effusion include increased chest
to lay in lateral recumbency).
excursions with little airflow (can be detected by lis-
● Dyspnea ranging from mild to acute and
tening close to muzzle during breathing).
severe with cyanosis.
● Abnormal heart sounds (murmurs, gallops, The cat may present with signs of aorto-iliac throm-
arrhythmias). boembolism, such as paresis of one or more limb, nail
bed cyanosis, cool anesthetic limb, firm cramping of
See main reference on page 128 for details (The Cat With the gastrocnemius muscle, vocalization and tachypinea
Abnormal Heart Sounds and/or an Enlarged Heart). or dyspnea.
Orthopnea (worsened dyspnea in lateral recumbancy)
or reluctance of the patient to lay in lateral recumbency
Pathogenesis
may be reported.
Mechanism of pleural effusion in cats with congestive
Muffled heart and lung sounds are audible ventrally,
heart failure is currently unknown, but there are two
with harsh breathing sounds dorsally in the standing or
leading theories:
sternal recumbency positions. Dull percussion of the
● Left-sided failure results in pulmonary venous and
chest wall is evident ventrally.
capillary hypertension, which leads to reflex pul-
monary vasoconstriction. The resultant pulmonary The liver may be displaced caudally due to fluid pres-
hypertension leads to right-sided heart failure and sure exerted on the diaphragm.
pleural effusion. Evidence against this theory is that
other signs attributed to right heart failure (right Diagnosis
heart enlargement, hepatic venous distention, etc.)
Typically there are clinical signs of pleural effusion
are rarely found in cats with congestive heart failure
together with abnormal heart sounds.
and pleural effusion.
● The visceral pleural veins in cats drain into the Thoracocentesis is indicated in the dyspneic patient
pulmonary veins (as seen in humans), and pul- with clinical signs of effusion.
● Thoracocentesis should be performed in all acutely tive in distinguishing cardiomyopathy from pericardial
dyspneic animals, prior to radiography. These effusion.
patients are extremely fragile, and even the minimal
restraint involved in radiography may be excessive,
Treatment
and they may die during the procedure.
● A transudate, modified transudate, or chylous Emergency thoracocentesis can be life saving in cats
effusion are the most common fluid types in heart with severe respiratory distress.
disease. ● A 23 G butterfly set on a 60 ml syringe is introduced
● Heart sounds are often more apparent after the at the 5th–7th intercostal space (ICS) on the right,
chest tap, and murmurs, gallops or dysrhythmias just above the costochondral junction. Remove as
may be heard. Be certain to remove as much fluid much fluid as possible, or until breathing improves.
as possible, do not stop after you have a diagnostic Thoracocentesis can usually be performed without
sample. sedation or local anesthetic block
● A negative tap for fluid suggests pulmonary edema
Oxygen therapy should be administered using an O2
rather than effusion from cardiac disease.
chamber, masks or tents.
Thoracic radiography
Furosemide (1–2 mg/kg IV or IM) should be admin-
● This is best performed in the acutely dyspneic patient
istered without stressing the patient.
after thoracocentesis and stabilization.
● Findings may include enlarged cardiac outline, pul- Use sedation if the cat is frantic (morphine 0.1 mg/kg
monary venous distention, and patchy alveolar infil- IM prn, or butorphanol 0.2–0.4 mg/kg IM q 4–6 h as
trates indicating pulmonary edema. needed).
Echocardiography Nitroglycerin 2% cream – 1/8 to 1/4 inch applied to
● This is the definitive modality for diagnosis of car- the skin of the medial pinna q 4–6 hours for 24 hours.
diomyopathy, as well as the primary tool for catego-
Take a “hands off” approach until stable, as the slight-
rization of the type and severity of disease. Various
est stress can cause lethal decompensation in these
forms of cardiomyopathy include hypertrophic
fragile cases.
(HCM), dilated (DCM), restrictive (RCM) and inter-
mediate (ICM). Therapeutic strategies and prognosis Definitive therapy is based upon ultrasonographic
rely heavily on the echocardiographic information. characterization of the type and severity of the car-
Thoracocentesis should be performed prior to echocar- diomyopathy present, but this is not performed until
diography in the severely dyspneic patient, otherwise the patient is stable.
death may occur during the procedure.
● Electrocardiography is important if an arrhythmia
is detected during physical exam or ultrasound Prognosis
exam. The prognosis is related to the clinical and echocar-
diographic severity. Severe left atrial enlargement pre-
Differential diagnosis disposes to aorto-iliac thromboembolism, which
worsens the prognosis.
Other forms of pleural effusion are not associated
with abnormal heart sounds (murmurs, gallops,
arrhythmias). Prevention
Pericardial effusion may create pleural effusion, an Taurine supplementation of commercial cat foods in
enlarged heart shadow on radiographs and possibly an North America has dramatically decreased the inci-
abnormal ECG pattern. Electrical alternans on ECG dence of dilated cardiomyopathy in cats. Causes for
tends to signal pericardial effusion, especially if the the other cardiomyopathies remain unclear at this
pleural effusion has been drained. Ultrasound is defini- time.
● Transesophageal ultrasonography is excellent for

PLEURAL/MEDIASTINAL MASSES
demonstrating mediastinal masses, but requires
specialized equipment and general anesthesia.
Classical signs
● Surgical or ultrasound-guided biopsy of the mass
● Muffled heart and lung sounds ventrally. may be required for a definitive diagnosis.
● Dyspnea characterized by excessive chest
Thoracocentesis and analysis of the fluid may be diagnos-
tic if the neoplasm has exfoliated into the fluid. This is,
however, a rare occurrence. Typically the fluid is a modi-
fied transudate, although occasionally it is an exudate.
See main reference on page 56 for details (The Dysp- Mediastinal lymphoma may have hypercalcemia as a
neic or Tachypneic Cat). paraneoplastic syndrome, but this is rare in the cat.
Tissue biopsy and histopathology are required for
Clinical signs definitive diagnosis.
Mediastinal masses are often thymomas, thymic
lymphoma or mediastinal lymphoma. Occasionally, Differential diagnosis
ectopic thyroid adenocarcinoma may create a space- Other causes of pleural effusion that typically cause a
occupying mass of the mediastinum. Pleural masses modified transudate are cardiac disease and other air-
include mesotheliomas, osteosarcoma or chondrosar- way neoplasias. Radiography and ultrasound can usu-
coma of the ribs or sternabrae. ally differentiate these.
Signs are related to the space-occupying nature of the
mass, or to obstruction of lymphatic drainage and sec- Treatment
ondary pleural effusion. Lymphoma of the thymus or mediastinal lymph nodes
Signs include increased dyspnea in lateral recum- is best handled with standard chemotherapy protocols
bency (i.e., orthopnea), tachypnea, minimal airflow for lymphoma (see page 676).
with increased chest excursions, muffled heart and Surgical excision is the treatment of choice for thy-
lung sounds or asymmetrical sounds if the heart is moma, and may be curative.
displaced laterally.
Mesothelioma is an infiltrative disease that cannot be
Extraluminal compression of the trachea can cause readily resected, and there are few reports in the litera-
dyspnea and cough. ture of effective chemotherapy. Local infusion of car-
Compression of the anterior thorax may reveal boplatin may be helpful with or without the addition of
decreased compliance. doxirubicin intravenously. Prognosis is grave.
PNEUMONIA
Diagnosis
Thoracic radiography may reveal the mass lesion or Classical signs
the secondary pleural effusion.
● Moist, productive cough, with adventitial
● Separation of the “cupolae” (anterior tips of the cra-
lung sounds.
nial lobes) on ventrodorsal projection, representing
● Fever.
widening of the anterior mediastinum, may be a
● Fetid halitosis.
sensitive indicator of a subtle mass lesion.
● Parapneumonic pleural effusion can create
Thoracic ultrasound can be extremely useful. dyspnea and decreased ventilation,
● Small mediastinal masses surrounded by aerated possibly with exaggerated chest
lung may not be visible from a paracostal approach, excursions/poor airflow.
and may require a thoracic inlet window.
continued
● On thoracocentesis there is a small volume of effu-

Classical signs—Cont’d
sion which is commonly a sterile inflammatory
● Muffled heart and/or lung sounds ventrally. exudate, and is often grossly serous or hemorrhagic
● Orthopnea (positional dyspnea with rather than purulent.
Cytology and culture samples from percutaneous lung
See main reference on page 62 for details (The aspiration, transtracheal wash or bronchoscopic lavage
Dyspneic or Tachypneic Cat). may be diagnostic. Fungal, aerobic and anaerobic bacter-
ial cultures are generally submitted.
Clinical signs Cryptococcal titers may aid in the diagnosis.
Infectious pneumonia is rare in cats.

A deep productive cough may be present, which gener-
ally is infrequent unless the pneumonia is secondary to Other causes of pleural effusion, such as pyothorax,
bronchitis (see page 104, The Coughing Cat). congestive heart failure, chylothorax, FIP and mediasti-
nal masses may mimic the parapneumonic effusion of
Inspiratory and expiratory dyspnea, often with some pneumonias. Typically, pneumonic patients are
open-mouth breathing is present when pneumonia is more severely dyspneic than would be attributed to the
severe and associated with a parapneumonia pleural subtle effusion, because of the associated compromise
effusion. of the lung parenchyma in pneumonia, which is not
Adventitial breath sounds, including crackles, usually found in other causes of effusion.
wheezes, snaps and pops are audible. Each of the infectious pneumonias can have overlap-
Heart sounds may be muffled and lung sounds poorly ping features.
audible ventrally, although the effusion volume is usu-
ally small.
Treatment
Systemic signs include lethargy, anorexia, weight loss,
Bacterial pneumonia
fever and ill thrift.
● Appropriate antimicrobial therapy is the mainstay
Halitosis may be noted. of therapy. The parenteral route is used if the patient
is debilitated or septic. The oral route can be used
Deep chest excursion and diminished oral airflow
with outpatients. Antibiotic selection is best based
occurs when parapneumonic pleural effusion is present.
upon specific culture and sensitivity testing.
Geographical location and other signs might suggest the ● Pending culture results, some therapeutic decisions
etiology of the pneumonia, including bacterial, fungal, may be based upon Gram stain results.
viral and Chlamydophila felis pneumonitis. – Gram-positive cocci – ampicillin, amoxicillin,
amoxicillin-clavulanic acid, trimethoprim-sulfa,
cephalosporins.
Diagnosis
– Gram-negative rods – chloramphenicol,
Thoracic radiography reveals alveolar densities (focal trimethoprim-sulfa, fluoroquinolones.
or generalized) and possible areas of complete consoli- – Bordetella – tetracycline, doxycyline, chloram-
dation. There is subtle radiographic evidence (e.g. pleu- phenicol, fluoroquinolones.
ral fissure lines) of a small-volume pleural effusion. – Suspected anaerobes – clindamycin, amoxi-
● Hilar lymphadenopathy supports fungal or cillin-clavulanic acid, metronidazole.
mycobacterial pneumonia.
Fungal pneumonia
On hematology neutrophilia is common, with or ● Systemic itraconazole given at 5–10 mg/kg PO
without a left shift or signs of toxicity. daily is the drug of choice. If there are CNS signs
● Low-grade, non-responsive anemia and monocyto- with cryptococcosis, use fluconazole (2.5–5.0 mg/kg
sis may support chronicity. PO daily) as it crosses the blood–brain barrier.
Viral pneumonia mostly involves supportive treat- Systemic signs such as anorexia and weight loss (can-
ment. cer cachexia) are often present.
Supportive care includes airway and systemic Dull chest sounds and dyspnea result from pleural
hydration, which are essential for mucociliary clear- effusion.
ance. Intravenous crystalloids should be used judi-
ciously. Nebulization with saline may be helpful.
Physical therapy including coupage, positional Diagnosis
drainage, position changes, etc., and oxygen enrich- Diagnosis is usually made by radiography followed by
ment are indicated. Bronchodilator therapy with beta biopsy via endoscopy, thorocolony or is ultrasound-
agonists such as terbutaline (0.625–1.25 mg PO q 12 guided.
hours) or methylxanthines such as sustained-release
theophylline (Theo-Dur 25 mg/kg PO q 24 hours) may Pleural effusion fluid is often a modified transudate
be helpful. and is often grossly opaque.
Thoracocentesis is rarely required for treatment, as the

parapneumonic pleural effusion generally resolves with Differential diagnosis
appropriate therapy for the pneumonia. Other causes of pleural effusion such as congestive
heart failure and mediastinal masses may produce a
AIRWAY/PULMONARY NEOPLASIA similar type of effusion but are differentiated on radi-
ography, ultrasound and biopsy.
Classical signs
● Muffled heart and/or lung sounds ventrally. Treatment
● Exaggerated chest excursions with poor
Surgical resection via partial or total lobectomy is
airflow.
the treatment of choice for solitary primary neoplasms.
Cure or long-term remission is possible with wide sur-
gical margins. If non-resectible, excision of nodules
● Non-productive cough, with or without
may palliate clinical signs temporarily.
hemoptysis.
● Mass lesion seen radiographically. Chemotherapy and radiation have been attempted in
● Anorexia, weight loss, muscle wasting. generalized pulmonary neoplasms, with disappointing
results. Metastases from distant tumors carry a grave
See main reference on page 66 for details (The prognosis, although pulmonary lymphoma may attain
Dyspneic or Tachypneic Cat). remission with chemotherapy.
Clinical signs
HEMOTHORAX
Tracheal adenocarcinomas (i.e., Siamese), primary pul-
monary masses (pulmonary adenocarcinoma) or sec- Classical signs
ondary metastatic disease from distant neoplasms may
create effusions. It is more common in middle-aged to ● Muffled heart and lung sounds ventrally.
older cats. ● Dyspnea characterized by excessive chest
A non-productive cough may be present, with or without ● Orthopnea.
hemoptysis. Dyspnea (inspiratory and expiratory) and ● Pallor, possibly other sites of bleeding
reluctance to lie in lateral recumbency, or respiratory dis- (epistaxis, hyphema, etc.).
tress is present if pleural effusion is of large volume.
Very rarely, lameness occurs from peripheral appendi- See main reference on page 493 for details (The Bleed-
cular bone lesions of hypertrophic osteopathy. ing Cat).
Clinical signs ● Send-out lab tests include prothrombin time (PT –

extrinsic system), partial tissue thromboplastin time
Hemorrhagic effusions generally result from either (PTT – intrinsic system), and PIVKA test for rodenti-
trauma or coagulopathy. History and physical exam find- cide toxicity. Factor analysis for deficiencies of factors
ings are vital in the separation of these causes. II, VII and X may be requested.
Signs related to pleural effusion and anemia include ● Common coagulopathies include rodenticide expo-
dyspnea, orthopnea (positional dyspnea), tachypnea, sure and genetic bleeding diatheses.
minimal airflow with increased chest excursions and
muffled heart and lung sounds ventrally. Differential diagnosis
Weakness, hemic heart murmur, watery thready Differential diagnoses include any cause of pleural effu-
femoral pulse, pale mucous membranes all support sion with bleeding into the pleural fluid, such as bleed-
possible blood loss. ing neoplasms, some chylothoraces (the fluid is less
bloody and more “tomato soup-like”), as well as iatro-
Trauma may have signs of external trauma such as
genic bleeding from previous thoracocenteses.
skin abrasions, rib fractures, penetrating thoracic
wounds, etc., present.
Treatment
Coagulopathies may involve other bleeding sites such as
abdominal effusion (hemoabdomen), epistaxis, hyphema Thoracostomy tube placement is generally contraindi-
and hematoma formation. Common coagulopathies cated, especially in coagulopathies as it may trigger
include rodenticide toxicity, factor VIIIC deficiency further bleeding.
(hemophilia A), and factor XII deficiency (although this Gentle handling and supportive care are indicated in
rarely causes clinical bleeding). trauma patients, as well as tending to other injuries.
Diagnosis Whole blood transfusion may be lifesaving in severe

thrombocytopenia or coagulopathy. Depending on the
Thoracic radiography reveals signs of pleural effu- breed (i.e., Persians) and the geographic location, cats
sion, indistinguishable from other causes. Alveolar with type B blood may be common. Cross-matching must
densities may be also present, indicating intrapul- be performed to avoid catastrophic transfusion reactions.
monary hemorrhage.
Results of coagulation tests may help with therapeutic
Thoracocentesis decisions.
● Analysis of the fluid reveals obvious bloody fluid, ● Vitamin K1 may be used for rodenticide toxicity.
often with a packed cell volume (PCV) lower than ● Fresh frozen plasma transfusions may be used for
peripheral blood, except in cases of severe peracute coagulation factor deficiency, etc.
frank hemorrhage where the PCV is similar to
peripheral blood. The blood is generally defibri-
nated with no platelets observed cytologically, but, HYPOPROTEINEMIA
in acute bleeding situations, frank clotting blood
with platelets may be present. Classical signs
Coagulation testing. ● Muffled heart and lung sounds ventrally.

● Coagulation tests help rule in and categorize types ● Dyspnea characterized by excessive chest
of coagulation disorders. excursions with poor airflow.
● In-clinic tests include activated clotting time (ACT, ● Orthopnea (positional dyspnea).
generally normal considered to be less than 65 sec- ● Muscle wasting, weight loss, ascites, limb
onds in the cat) to test the intrinsic cascade, blood edema.
smear for platelet numbers (should be 11–25 per
high-power field), and buccal mucosal bleeding See main reference on pages 358 and 760 for details
time (BMBT, normal considered to be 1–3 minutes) (The Thin, Inappetant Cat and The Cat With Signs of
for platelet function (i.e., Von Willebrand’s disease). Chronic Small Bowel Diarrhea).
Clinical signs Hypoalbuminemia (< 15 g/L) is a persistent finding.

● Protein-losing enteropathy (PLE) has panhypopro-
Protein-losing enteropathy, protein-losing nephropa- teinemia as the hallmark (hypoalbuminemia, globu-
thy and hepatic failure are common causes of low serum lin < 20 g/L) (see page 760, The Cat With Signs of
protein, specifically hypoalbuminemia, which may result Chronic Small Bowel Diarrhea).
in decreased oncotic pressure and transudation. ● Protein-losing nephropathy (PLN) is characterized
Signs are related to pleural effusion, ascites and muscle by proteinuria, urine protein:creatinine ratio > 2,
loss. hypoalbuminemia, possible hypertension and
hypercholesterolemia (nephrotic syndrome) (see
Orthopnea, tachypnea, minimal airflow with increased page 358, The Thin, Inappetent Cat).
chest excursions, muffled heart and lung sounds may be ● Hepatic failure may be characterized by low urea,
present if the pleural effusion volume is > 50 ml/kg. hypoalbuminemia, low to elevated cholesterol,
Weight loss with prominent muscle wasting is com- possible hypoglycemia, normal to low liver
mon. Distention of the abdomen from weakness of enzyme levels, elevated serum bilirubin levels
abdominal muscles, as well as presence of ascites may may be present (see page 421, The Yellow Cat or
be present. Hair coat is typically poor quality. Cat With Elevated Liver Enzymes).
Appetite may be ravenous in protein-losing enteropathy,

and diarrhea and weight loss are evident. Differential diagnosis
Rarely, signs of hepatic encephalopathy including Once hypoalbuminemia has been established and the
ptyalism, dementia, somnolence and pica occur with pleural effusion has been characterized as a pure tran-
liver failure. sudate, a general biochemistry panel will help to dis-
tinguish the major causes of hypoproteinemia.
Icterus may be present.
Treatment
Diagnosis Thoracostomy tube placement is generally not indicated.
Thoracic radiography demonstrates signs of pleural Treatment for the underlying disorders will be covered in
effusion, indistinguishable from other causes. the chapters for those conditions. If serum albumin can
● Thoracocentesis reveals a clear and colorless fluid, be increased above 15–20 g/L with treatment of the
which is a pure transudate with a specific gravity underlying disease, the hydrothorax and ascites will
(SG) < 1.013, low total protein (TP) < 2.5 g/L, and resolve providing there is not underlying hypertension or
low cellularity (TNCC < 1.5 × 109/L). vasculitis.
RECOMMENDED READING
Bauer T, Woodfield JA. Mediastinal, pleural, and extrapleural diseases. In: Ettinger SJ (ed) Textbook of Veterinary
Internal Medicine, 4th edition. Philadelphia, Saunders, 1995, pp 817–822.
Lehmkuhl LB, Smith FWK. Pleural effusion. In: Tilley LP, Smith FWK (eds) The 5 Minute Veterinary Consult, 2nd
edition. Baltimore, Lippincott, Williams & Wilkins, 2000, pp 1084–1085.
Padrid PA. Pulmonary diagnostics. In: August JR (ed) Consultations in Feline Internal Medicine 3. Philadelphia,
Saunders, 1997, pp 292–302.
7. The coughing cat
Robert Allen Mason and Jacquie Rand
KEY SIGNS
● Cough ranging from soft to harsh or honking.
● Gagging, which may appear as vomiting or regurgitation.
MECHANISM?
● Coughing is a reflex that produces rapid expulsion of air in response to mechanical or chemi-
cal irritation of the pharynx, larynx, trachea, bronchi and small airways, to free the airway of
foreign material.
WHERE?
● Coughing occurs in response to irritation of the upper respiratory tract (nasal cavity, pharynx,
larynx, trachea), lower respiratory tract (bronchial tree, small airways), lung parenchyma or the
pleural space.
WHAT?
● Coughing is usually a sign of small airway disease in cats. Unlike dogs, coughing is rarely
associated with congestive heart failure (CHF).

Diseases causing a coughing cat
DEGENERATIVE
● Cardiomyopathy (Dilated cardiomyopathy (DCM), hypertrophic (HCM), intermediate (ICM)
or restrictive (RCM)) (p 107)
Although dyspnea is common with congestive heart failure and pulmonary edema, coughing is an
uncommon presenting sign in the cat.
● Trachebronchial collapse (p 102)
Harsh “honking” cough caused by degeneration of the cartilage support of the large airway walls.
Rare in cats.
MECHANICAL
● Grass awns/foreign bodies (p 98)
Sudden onset of a harsh, productive cough and acute dyspnea from foreign objects that have been
inhaled, regurgitated or aspirated into the nasopharynx, trachea or bronchi.
90
7 – THE COUGHING CAT 91
● Inhalation of noxious agents (p 99)

Inhalation of gas, smoke, fumes, dust particles or hair can stimulate an aggressive cough reaction.
NEOPLASTIC
● Airway/pulmonary neoplasia (p 97)
Tracheal masses and primary or metastatic pulmonary masses in middle-aged to older cats may
cause coughing ranging from soft to harsh and productive. Weight loss and ill-thrift are also seen.
● Pleural/mediastinal masses (p 107)
These masses cause pleural effusion or extraluminal compression of the trachea resulting in dyspnea,
orthopnea, tachypnea and rarely cough. Heart and lung sounds are muffled from pleural effusion.
INFECTIOUS
Bacterial:
● Pneumonia (p 103)
Lethargy, inappetence, tachypnea, fever and halitosis are typical signs. Moist, productive cough and dysp-
nea may be present. Causes may include bacterial, fungal, viral, protozoal (toxoplasmosis) and chlamy-
dophila felis pneumonitis.
● Bordetella* (p 98)
Acute onset of pyrexia, sneezing and nasal discharge. Coughing may be spontaneous or only evi-
dent on tracheal pressure. Signs resolve in 1–2 weeks.
Parasitic:
● Parasitic pnemonia (p 106)
A variable degree of coughing occurs. Peripheral eosinophilia or parasitic larva/ova may be present
in the stool or lungwash. Lungworm (Aleurostrongylus abstrusus, Capillaria aerophilia), lung
flukes (Paragonumus kellicoti) and migrating nematodes (Toxacara cati) are potential causes.
● Heartworm disease* (p 104)
Coughing, dyspnea and vomiting may occur together. Acute respiratory failure and death may
occur from acute pulmonary inflammation and edema. Generally limited to cats from heartworm
endemic areas.
Immune:
● Feline asthma/bronchitis complex*** (p 92)
An inhalant allergic response leads to bronchitis and bronchospasm. Coughing is the most com-
mon clinical sign, along with expiratory dyspnea and wheezing.
● Pulmonary infiltrates with eosinophils (PIE)/Eosinophilic bronchopneumopathy* (p 96)
Coughing varies from mild to severe. Crackles or wheezes, or areas of diminished lung sounds are
heard on auscultation. Cats may have peripheral eosinophilia on CBC. Thoracic radiographs often
show an interstitial pattern, although patchy alveolar or nodular densities may occur.
● Laryngitis (p 101)
Laryngeal edema from allergic reactions and idiopathic laryngeal paralysis have been reported in
the cat. They may lead to aspiration of food, water or saliva and create significant harsh coughing.
Stridor, dysphonia and inspiratory dyspnea are reported.
Chronic coughing in cats is often caused by feline

INTRODUCTION asthma/bronchitis complex.
Unlike dogs, coughing is rarely associated with con-
MECHANISM? gestive heart failure (CHF).
Coughing is a reflex rapid expulsion of air in response
to mechanical or chemical irritation of the pharynx, lar-
DISEASES CAUSING COUGHING
ynx, trachea, bronchi and small airways, to free the air-
way of foreign material.
FELINE ASTHMA/BRONCHITIS
Afferent impulses from epithelial receptors reach the
COMPLEX***
cough center in the medulla via the vagus nerve. A com-
plex series of events transpires from this point, namely:
Classical signs
● Air is inspired to 2–3 times the tidal volume.
● There is closure of the epiglottis and vocal folds. ● Cough is a prominent sign.
● Contraction of the diaphragm, intercostal and exter- ● Expiratory dyspnea with wheezing.
nal abdominal muscles occurs against the closed ● Status asthmaticus – severe acute
glottis, which increases intrapleural pressure respiratory distress.
(Valsalva maneuver) and decreases the luminal ● Cyanosis, open-mouth breathing,
diameter of the small airways. wheezing.
● Sudden opening of the glottis occurs with rapid
expulsion of air from the small airway at speeds of
Pathogenesis
75–100 miles per hour.
● Explosive release carries the offending particulate Exposure of the respiratory epithelium to an
matter clear of the lower airways. inhaled antigen results in multiple inflammatory
responses that create airway obstruction, namely:
In acute conditions (aspiration, inhalation of noxious
● Edema.
fumes, etc.) this cough reflex is a protective mecha-
● Cellular infiltration into airway walls.
nism. In the chronic state, however, it becomes a
● Epithelial hypertrophy or metaplasia with erosion
debilitating problem. Chronic airway irritation
or ulceration.
decreases the threshold of the cough receptor, which
● Excessive mucus production.
brings about more coughing and more mucosal damage
● Decreased mucus clearance.
and irritation.
● Inflammatory exudation within the lumen.
● Hyperreactivity of the airway smooth muscle caus-
WHERE? ing bronchoconstriction fibrosis.
● Emphysema.
Cough receptors are found along the entire airway, but
are especially dense at the larynx and the carina. All Coughing results from enhanced airway sensitivity.
receptors are innervated by the parasympathetic system.
Wheezing is generated by air forced through narrowed
In cats, receptors have been found as far distally as the airways, caused by mucosal thickening (epithelial
alveoli. hypertrophy, infiltration and edema) and bronchocon-
striction.
WHAT? Crackles result from excessive airway mucus.
The most common cause of acute coughing in the cat is The systemic inflammatory reaction, increased work of
foreign body aspiration, often associated with hairballs breathing and airflow limitation all create systemic
trapped in the oropharynx. lethargy.
Aspiration of food or fluid can be more serious, creat- There are multiple inflammatory mediators involved
ing aspiration pneumonia. in the airways of cats:
● Serotonin Signs may be episodic (with asthma) or chronic (with

– Serotonin is released from feline mast cell gran- bronchitis).
ules during exposure to an allergen.
There may be a history of exposure to the offending
– Serotonin antagonists are useful in decreasing
allergen, including dusty litter, perfumes, carpet clean-
associated signs.
ers, smoke from fireplaces, cigarette smoke and insula-
– Mast cell stabilizing agents may play a role in
tion materials.
decreasing the severity and frequency of attacks.
● Histamine Cats may present severely air-starved, with cyanosis,
– It has been demonstrated that histamine does not open-mouth breathing, and a significant abdominal
play a role in feline asthma. expiratory push.
– Stimulation of the H3 receptors in the feline air-
way causes relaxation of the airway smooth
muscle, the exact opposite effect seen in
Diagnosis
humans.
– This work might suggest that antihistamines are Many cats with asthma may have eosinophilia on
contraindicated in feline asthma. hematology.
● Leukotrienes
On auscultation, typical lung sounds are wheezes and
– Cats have far fewer leukotriene (LT) receptors in
crackles, which may be worse on expiration.
the airways than do people, but enough are pres-
● Severely affected cats may have diminished air
ent to make a significant contribution to the
sounds from emphysema.
inflammatory cascade.
– Leukotrienes are released from eosinophils, Thoracic radiographs may be normal or abnormal.
and via the lipoxygenase cascade, are converted ● Asthma is characterized by hyperlucency, hyperinfla-
to various forms of leukotrienes, all with vari- tion and flattening of the diaphragm from air trap-
able inflammatory effects. ping.
– Because cats have poor glutathione pathways, ● Chronic bronchitis typically has a diffuse, promi-
the inflammatory leukotrienes LTC4 and LTD4 nent peribronchiolar pattern, with or without patchy
are not produced in significant amounts, but the alveolar infiltrates (especially the right middle lobe
pathway is directed toward LTB4 production. from atelectasis). Right heart enlargement may be
– LTB4 is a known chemotactic agent for present.
eosinophils. ● A lung wash for cytology and culture can be
– Recent evidence questions the role of obtained via transtracheal wash in the awake cat, or
leukotriene in asthmatic cats. using a catheter or bronchoscope to lavage the
– Mast cells have recently been incriminated in bronchi and alveoli in the anesthetized cat, which
having a more profound role is asthmatic patho- is the method preferred by most clinicians. Culture
genesis in humans than previously thought. for mycoplasma should be requested, because
Research is on-going in cats. mycoplasmal infection may cause chronic cough-
ing.
● Cytological examination typically reveals highly
Clinical signs
cellular samples with intact non-degenerative neu-
Signs can occur at any age, although the average is 2–8 trophils as the primary cells. Eosinophils are not a
years. reliable marker because of the increased prevalence
(up to 24%) in the airways of normal cats.
Typically there is a history of coughing for weeks or
Neutrophilic or mixed inflammatory cellular patterns
months. The cough may be mild to severe and inter-
are common.
mittent or continuous. It may be productive and stimu-
● There is on-going research looking for other bio-
lated with coupage of the chest wall.
chemical markers of asthma leukotriene levels,
Dyspnea may range from mild, to severe life-threaten- IgA, IgG and IgE titers, etc., but none is yet clini-
ing respiratory distress from bronchoconstriction. cally available as a test.
● Pulmonary function testing includes spirometry, ● Terbutaline 0.01 mg/kg SQ will usually result in
whole-body plethysmography and tidal breathing bronchodilation within 10–15 mins; for longer term
flow–volume loops (TBFVL). Increased airway therapy it can be administered orally (0.1 mg/kg PO
resistance with aerosol challenge, and decreased q 12 h (1/4 – 1/2 × 2.5 mg tablet) or inhaled
resistance with bronchodilator therapy are diagnos- (Brethine). In a crisis, it can be given IV (0.01
tic of asthma. This testing is rarely available outside mg/kg IV q 30 min for up to 4 h) until a response is
of teaching or research institutions. observed, or by inhalation.
● Asthma is differentiated from bronchitis on the basis ● Inhalant bronchodilators (beta2-adrenergic ago-
of a positive response to an inhaled bronchodilator nists such as terbutaline (Brethine), albuterol
with asthma. [also known as salbutamol] (Proventil, Ventolin)
may be used in a crisis situation (q 30 min repeated
for 2–4 h) with an effect seen in 5–10 min. This
Differential diagnosis route is more effective than IM, SC, or oral admin-
istration. They are administered using a spacer
Main differential for status asthmaticus is acute con-
chamber attached to the metered dose inhaler at one
gestive heart failure, usually due to cardiomyopathy,
end and a face mask at the other end. Aerokat®
although cats with heart failure rarely cough.
(www.aerokat.com) mask and spacer chamber is
Other respiratory diseases, such as upper airway made specifically for cats, or ones made for infants
obstruction (laryngeal paralysis), pulmonary disease such as the Pocket Chamber® combined with the
(pneumonia, neoplasia), and pleural space disease may smallest Panda Mask® (Ferraris Medical Inc) can
also cause chronic coughing. be used to deliver drug inhalant therapy. Empty toi-
let paper rolls or paper coffee cups have also been
used successfully as spacing chambers in cats. Two
Treatment “puffs” or metered doses of the bronchodilator is
used to fill the spacer chamber, and the mask is gen-
Status asthmaticus – oxygen supplementation is
tly placed over the cat’s mouth and nose while the
required during respiratory distress. An O2 chamber or
cat breathes 10–15 times (approx 30–45 secs).
tent is best tolerated by air-starved patients. Use
There are several anecdotal reports of success, lead-
injectible terbutaline (0.01 mg/kg SQ), and dexam-
ing to weaning off systemic drug dosages or
ethasone (0.25–0.5 mg/kg IV or IM), and in severe
decreasing severity and frequency of attacks.
cases, epinephrine (0.5 ml 1:10 000) SQ as a bron-
Albuterol is reported to be rapid acting, and may be
chodilator. Minimal handling and restraint of acutely
used in an emergency situation, or for chronic ther-
dyspneic patients is essential.
apy q 12 h as needed (prn). Salmeterol [Serevent]
Asthma has a slower onset and a 12 hour duration, and can
● As this is a bronchoconstrictive disorder, it be used for chronic therapy. Adverse effects of
responds more briskly to bronchodilators. beta2-adrenergic agonists are musculoskeletal
● Bronchodilators seem to have a synergistic effect twitchiness, excitability, insomnia, and anorexia,
when used with steroids, or when two classes of but are very rare in cats, suggesting these drugs
bronchodilator are combined. have a high safety margin in cats.
● Sustained release theophylline 25 mg/kg PO q 24 h
Bronchitis
or 10 mg/kg PO q 12 h. Consistent pharmacokine-
● As this is an inflammatory disease, anti-inflamma-
tics have only been demonstrated with a few prod-
tories, and perhaps leukotriene inhibitors and mast
ucts (Theo-Dur® (Key Pharmaceuticals), Slo-Bid
cell stabilizing agents are more indicated for long-
Gyrocaps® (Rhone-Poulene Rorer Labs), and
term therapy.
Theocap ER® and Theochron ER® (Inwood
Bronchodilators Laboratories or Forest Laboratories), and the first
Bronchodilators are an important part of therapy for two are unavailable in the US. Theochron ER®
asthmatic cats, and can be administered orally, tablets can only be broken along the scored line into
parentally or by inhalation. half, and Theocap ER® capsules can be opened
and divided into smaller doses by a compounding can be used to stabilize long-term patients. Use may
pharmacy. Beta2-adrenergic agonists are more allow for a decrease of steroid dosages (beneficial in
effective than the xanthine derivatives (theo- diabetic patients). It may decrease eosinophil
phylline) in producing bronchodilation. chemotaxis. This drug should be considered in cases
of severe eosinophilic inflammation, or cases refrac-
Glucocorticoids
tory to standard therapy. Liver damage has been
● Prednisone 1 mg/kg PO q 12 h for 5 days, then
infrequently reported in cats.
1 mg/kg PO q 24 h and slowly weaned to a mini-
● Montelukast (Singulaire®, 0.25–1.0 mg/kg SID)
mum effective dosage over 2 to 4 months. For sea-
is a leukotriene blocker that has been used in cats
sonal allergy, prednisone may be weaned entirely
for maintenance therapy but by itself is rarely
until the following year. Alternatively, the cat may
effective. Although the cat has insufficient
require chronic low dose therapy, 2.5–5.0 mg PO
leukotriene receptors for cysteinyl leukotrienes to
q 48 h. Some cats respond poorly to oral pred-
cause bronchoconstriction, anecdotal evidence
nisone, and may respond better to dexamethasone
suggests that montelukast may reduce bronchial
0.25 mg/kg PO q 12 h for 5 days, then wean slowly
inflammation and coughing. This effect may be
or switch to oral prednisone. Other cats require par-
mediated through blockage of leukotriene-medi-
enteral dosing with 20 mg methylprednisolone
ated attraction of inflammatory cells such as
acetate IM q 3-6 weeks. However, this potentially
eosinophils and neutrophils and their subsequent
has greater side effects, including inducing diabetes
release of inflammatory cytokines and other
mellitus, than alternate day prednisone therapy. In a
chemicals. Montelukast may allow for the dose of
crisis, methylprednisolone sodium succinate (100
steroids to be reduced or for cyroheptadine to
mg/cat IV) or dexamethasone (0.5–2 mg/kg IV or
replace the steroids.
IM) can be given.
● Inhaled steroids scuh as fluticasone (Flovent®)
Other agents
are beneficial in cats that tolerate face mask
● Mast cell stabilizers
inhalers. Topical therapy has less systemic side
– Cromolyn is an inhalant that stabilizes mast cell
effects, which may be important in diabetic cats and
degranulation. It may be helpful for long-term
cats predisposed to diabetes. In general, inhaled
control, and to diminish maintenance doses
steroids are preferred because of their reduced side-
of steroids. Use 1 metered dose (800 mcg)
effects, but they are more expensive. Fluticasone
q 12–24 h.
may take 5–10 days to work, so oral steroids should
– Amitryptiline is a systemic mast cell stabilizer.
be administered concurrently for 5–10 days,
There is no information on its use in cats for air-
depending on the severity of signs.
way disease, but it has been used for urine mark-
Oxygen supplementation is required during respira- ing and psychogenic dermatoses at 1.1–2.2
tory distress and an oxygen chamber or tent seems to be mg/kg PO q 12 h.
best tolerated by air-starved patients. Oxygen hoods ● Antitussives
made with an Elizabethan collar and cellophane have – Debate exists whether the cough of bronchitis
proven very useful in cats. should be suppressed, as it is a protective mech-
anism of the airway.
Minimal handling and restraint of acutely dyspneic
– Butorphanol (Torbutrol) can be dosed at
patients is essential.
0.05–0.6 mg/kg PO q 6–12 h, prn to control
Serotonin antagonists cough. “Pulse antitussive therapy” may be
● Cyproheptadine (Periactin®) − 2–4 mg/cat PO q helpful. This involves treating for 2–3 days to
12–24 h. This drug blocks serotonin, the major break the cycle of the harmful effects of the
inflammatory mediator from feline mast cells in cough, then stopping for 2–3 days to allow
airway disease. improved airway clearance. Administration must
be judged on a case-by-case basis.
Leukotriene receptor blockers
● Zafirlukast (Accolade®) 0.5–1.0 mg/kg PO q Therapeutic protocol recommended by Dr Phil
12–24 h. This drug is not useful in acute attacks, but Padrid:
● For mild signs (cough only): fluticasone 110 mcg q Recently, there appears to be epidemologic evidence of
12 h and albuterol prn decreased risk of asthma in male cats neutered before
● For moderate signs (cough and tires easily, 5.5 months of age.
and sleep disruption for client): prednisolone
1 mg/kg PO q 12 h for 5 days, and on an ongoing
PULMONARY INFILTRATES WITH
basis, fluticasone (Flovent®) 220 mcg q 12 h and
EOSINOPHILS (PIE) (EOSINOPHILIC
albuterol prn;
BRONCHOPNEUMOPATHY)*
● For marked signs (cough and dyspnea at rest with
diminished quality of life): prednisolone 1 mg/kg
Classical signs
PO q 12 h for 5 days, q 24 h for 5 days, q 48 h for
5 days, and on an ongoing basis, fluticasone 220 ● Coughing – mild to severe.
mcg q 12 h and albuterol prn; ● Crackles, wheezes or diminished lung
● For severe signs (dyspnea, open mouth breathing sounds.
+/– cyanosis) which are a life-threatening emer- ● Possible peripheral eosinophilia on CBC.
gency, it is important not stress the cat as this may
precipitate death. Administer oxygen via oxygen
cage or nasal canula, methylprednisolone sodium Pathogenesis
succinate (100 mg/cat IV) or dexamethasone
Interstitial or alveolar infiltration of pulmonary
(2 mg/kg IV) and terbutaline (0.01 mg/kg IV) q 30
parenchyma with eosinophils. The infiltrate may form
minutes for up to 4 h until a response is observed.
space-occupying eosinophilic granulomas measuring
Once stabilized, cats can be discharged with fluti-
up to 20 cm diameter. Varies from mild, self-limiting
casone 220 mcg q 12 h and albuterol q 6 h as
disease, to severe and life-threatening.
needed.
Antigenic source, such as migrating parasites (Toxocara
spp.) or heartworms may be found. Eosinophil-derived
Prognosis
cytokines (leukotrienes, major basic protein, etc.) can
Patients in status asthmaticus are extremely fragile, and damage the offending parasite or the host tissue, depending
may decompensate and die without rapid therapy on the circumstances or severity.
administered with minimal handling.
In most cases, the inciting allergen is not identified.
Chronic cases, or once status asthmaticus resolves,
have a fair to good prognosis with prolonged therapy.
Clinical signs
Cure is rare, but with long-term therapy, management is
frequently quite successful. Mild to severe coughing for weeks to months prior to
presentation is common.
Prevention Signs of systemic illness such as weight loss, anorexia
and depression, may be present.
Identification and removal of the offending antigen is
highly desirable, but often difficult. Adventitial lung sounds such as crackles or wheezes, or
areas of diminished lung sounds may be present on tho-
Clean the furnace or air-conditioning air ducts, shampoo
racic auscultation.
carpets (avoiding perfumed cleansers), remove scented
candles or potpourri, avoid using hair spray or aerosol Coughing may be elicited on tracheal palpation or
cleaners near the patient, switch to dust-free and coupage of the chest.
unscented cat litter, and quit smoking.
High-quality home air-filtration systems have been
Diagnosis
shown to help human asthmatics, and it is logical that
cats would also benefit. HEPA filters (class III and Peripheral eosinophilia is present on CBC in 50–75%
above) decrease inhaled particles significantly. of patients.
Thoracic radiography improvement noted, slowly taper the dosage over several
● Interstitial or alveolar patterns with air bron- months. Serial radiographs are useful for long-term mon-
chograms, ranging from mild to severe. itoring. Many cases require long-term therapy for
● Nodular interstitial densities may mimic neoplas- months to years, at the minimum effective dosage.
tic masses. Dilated and truncated pulmonary arter-
Cytotoxic drugs – if large mass lesions are present
ies indicate potential heartworm disease or
(eosinophilic granulomatosis), more aggressive
pulmonary hypertension. Hilar lymphadenopathy
immunosuppression may be required. Cyclophos-
may be present.
phamide (50 mg/m2 PO q 48 h) has been used in con-
Cytology junction with prednisone. Azathioprine should be
● Method of sample acquisition is dependent upon avoided in cats due to toxicity.
the predominant radiographic pattern.
● Peribronchiolar or alveolar infiltrates may produce
excellent samples via airway wash (transtracheal or Prognosis
bronchoscopic lavage). Eosinophilic inflammation can be very damaging to the
● Interstitial densities exfoliate poorly into the air- host tissues.
ways, and are better sampled via percutaneous
lung aspirates. If identification and elimination of the offending aller-
● Cytology reveals a heavy infiltration of non-neo- gen is possible, the prognosis is excellent. If no allergen
plastic eosinophils. Samples should be evaluated can be identified, the prognosis for cure is poor, but good
for the presence of antigens (parasites, fungal to excellent control may be achieved with long-term
agents). Some neoplasms may be chemotactic to therapy.
eosinophils. Eosinophilic granulomatosis carries a poor long-
Allied testing includes heartworm antigen or antibody term prognosis, although remission of weeks to
testing, fecal floatation and Baermann exams for para- months is possible.
site ova and larvae, fungal culture (Cryptococcus spp.)
from lung fluid, and fungal serology.
Prevention
Parasite prevention programs.
● Heartworm prophylaxis in endemic areas.
Pulmonary neoplasia may mimic the nodular infiltrates ● Routine anthelmintic treatments with pyrantel
radiographically. Cytology or lung biopsy is required pamoate or fenbendazole for nematodes such as
for differentiation. Toxocara cati and Aelurostrongylus spp.
● Limit exposure to intermediate hosts (i.e., crayfish
Congestive heart failure may also have alveolar infil-
for Paragonimus kellicotti).
trates, but usually other clinical signs (tachyarrhyth-
mias, murmurs, gallop rhythms) or radiographic signs Limit exposure to inhalant allergens. Clean the fur-
of heart disease such as cardiomegaly, pulmonary nace or air-conditioning air ducts, steam-clean carpets
venous congestion, pleural effusion are present. (avoiding perfumed cleansers), remove scented candles
or potpourri, avoid using hair spray or aerosol cleaners
near the patient, switch to dust-free and unscented cat
Treatment
litter (clumping litters may be especially dusty), and
Treatment of the underlying disease is preferable, reduce exposure to cigarette smoke (quit or smoke out-
where possible (i.e., parasiticide therapy with fenben- side), high-efficiency in-home air filtration systems may
dazole for lungworm, praziquantel for lung flukes, reduce antigenic load.
etc.). Changing to a dust free cat litter and eliminating
Avoid exposure to cats with respiratory tract infec-
passive smoke from the environment may help.
tions, as PIE patients may be more prone to serious
Glucocorticoids – prednisone 1–2 mg/kg PO q 12 h for respiratory infections, especially if receiving
5–7 days. Repeat thoracic radiographs, and if there is immunosuppressive therapy.
BORDETELLA* GRASS AWNS/FOREIGN BODIES
Classical signs Classical signs

● Pyrexia. ● Sneezing with nasal foreign bodies, and
● Sneezing and nasal discharge. coughing with pharyngeal and
● Mandibular lymphadenopathy. tracheobronchial foreign bodies.
● Coughing. ● Inspiratory/expiratory dyspnea, depending
● Dyspnea, cyanosis, pneumonia. on location.

With Acute Sneezing or Nasal Discharge). Pathogenesis
Foreign bodies may be inhaled directly into the rostral
nasal cavity or tracheobronchial tree, or may be regur-
Clinical signs gitated into the caudal nasopharynx. Common solid
foreign bodies include grass, seeds, hairballs, twigs and
Signs are most likely to occur in cats from multi-cat occasionally stones, while particulate foreign bodies
environments, especially rescue or shelter catteries include coal dust (UK) and metal dust from road grime
where calicivirus and herpesvirus are also a problem. (Australia).
Typically there is an acute onset of pyrexia, sneezing Occasionally, penetrating foreign bodies, such as pro-
and nasal discharge. jectiles (pellets) or a broken tooth from an opponent
Mandibular lymphadenopathy may be palpable. during a cat fight, can lodge in the nasal cavity or air-
way.
Coughing may be spontaneous, or only evident on tra-
cheal pressure; generally, coughing is not as pro- Tracheobronchial foreign bodies may be caused by
nounced as in dogs. aspiration of vomited or regurgitated ingesta.
Dyspnea, cyanosis, crackles and wheezes may be aus-

cultated over lung fields in some cats. Death from Clinical signs
pneumonia may occur, especially in young kittens less
Acute onset of sneezing and nasal discharge are com-
than 8 weeks old.
mon signs of nasal foreign bodies, although coughing
may be the predominant sign with post-nasal drainage
into the pharynx. These cats may be in sudden and
Treatment severe distress attempting to dislodge the foreign body.
Pawing at the face and mouth is commonly observed.
Oxytetracycline, doxycycline or enrofloxacin.
Coughing and signs of fixed obstruction – meaning
Montelukast (Singulaire, 0.25–1 mg/kg SID) is a
there is airflow limitation during both inspiratory and
leukotriene receptor blocker. Although the cat has
expiratory due to constant partial obstruction of the air-
insufficient leukotriene receptors for cysteinyl
way – may be seen with tracheobronchial foreign bod-
leukotrienes to cause bronchoconstriction, anecdotal
ies. The coughing is often harsh, and may be elicited
evidence suggests that montelukast may reduce sneez-
with tracheal palpation.
ing and nasal discharge associated with Bordetella.
This effect may be mediated through blockage of
Diagnosis
leukotriene-mediated attraction of inflammatory cells
such as eosinophils and neutrophils and their subse- Tracheal foreign bodies may be seen radiographically.
quent release of inflammatory cytokines and other Tracheobronchoscopy can be both diagnostic and ther-
chemicals. apeutic. Rigid tracheoscopy allows for larger retrieval
instruments to be utilized than with a flexible Fires may cause thermal damage to the upper airway.
endoscopy. Burning plastics release toxic fumes causing direct
chemical damage to lungs.
Bronchial foreign bodies may cause complete lobar
atelectasis or abscessation radiographically. The right Carbon monoxide exposure results in carboxyhemoglo-
caudal and accessory lobes are most often affected with bin formation, lowering the oxygen-carrying capacity
inhalation foreign bodies. The right middle lobe is of hemoglobin, and worsening the hypoxemia.
affected commonly with aspiration of vomitus.
Airways irritated by underlying disease such as bron-
chitis, may be hyperresponsive to cigarette smoke or
Differential diagnosis household fumes.
Nasopharyngeal polyps may cause similar signs of
nasal obstruction and sneezing, but tend to have a more
chronic course. Clinical signs
Tracheal or bronchial neoplasia may have similar Patients rescued from fires smell of smoke, have burned
signs, but again are more chronic in nature and can be hair or vibrissae, may be coughing, and are often
distinguished bronchoscopically. expectorating soot-tinged sputum.
Cherry-red mucus membranes indicate carboxyhe-
Treatment moglobinemia, and cyanosis indicates hypoxemia.
Removal of the foreign body, either surgically or endo- Stridor and inspiratory dyspnea suggest laryngeal
scopically, is often curative. Nasal foreign bodies may edema.
be endoscopically retrieved or hydropulsed, but occa-
sionally require surgical rhinotomy. Crackles indicate increased airway fluid.
Bronchial foreign bodies, especially with lung lobe Wheezes indicate diminished airway diameter via
abscesses, require lung lobectomy. bronchoconstriction, congestion, mucus accumulation,
and airway edema.
Prognosis
Excellent with removal of the foreign body. Diagnosis
Presumptive diagnosis is based upon evidence of recent
Prevention
exposure to noxious agent and acute onset of coughing.
Hairball prophylaxis.
Thoracic radiography.
Avoidance of grass fields during seed time. ● May vary from peribronchiolar to patchy interstitial
lung pattern, with possible lobar consolidation.
● Infiltrates are generalized, although the caudodorsal
INHALATION OF NOXIOUS AGENTS
fields may be more affected.
● These changes may lag several hours behind clinical
Classical signs
signs.
● Acute onset of severe coughing.
Pulse oximetry may indirectly assess oxygenation
● Evidence of inhalation of gas, smoke,
through SPO2 (hemoglobulin saturation).
fumes, dust particles or hair.
Blood gases.
● Arterial oxygen (PaO ) represents dissolved oxy-
Pathogenesis 2
gen content not bound to hemoglobin.
Poor ventilation, engine exhaust, smoke from fires or ● PaO < 60 mmHg indicates severe hypoxemia,
2
cigarettes, all can stimulate an aggressive cough reaction. ofetn associated with cyanosis.
● PaO2 may be misleading in CO toxicity due to Prevention

extreme carboxyhemoglobinemia and very low O2-
carrying capacity. Ensure proper ventilation for heaters and wood stoves,
● A profound mixed acidosis may be present. avoid exposure to aerosol chemicals, and reduce exposure
to cigarette smoke (quit smoking or smoke outdoors).
Measuring carboxyhemoglobin levels are needed to
diagnose carbon monoxide toxicity. Routine STAT
assays are available in human hospitals. AIRWAY/PULMONARY NEOPLASIA
Treatment Classical signs
Emergency treatment focuses on assessing three critical

● Dyspnea, other inspiratory and expiratory
areas – ABC – airway, breathing, circulation.
● Coughing, ranging from harsh and dry to
soft and productive.
A – airway
● If the upper airway is burned or edematous, establish-
ing a patent airway may require laryngeal suctioning, Pathogenesis
tracheal intubation, or transtracheal catheterization, Upper respiratory tract masses may produce a cough
or tracheostomy. from post-nasal drip.
B – breathing Pulmonary or airway masses cause coughing by stimu-
● Oxygen is the single most important drug to use. lation of cough receptors within the airway lumina, or
Carbon monoxide is displaced from the carboxyhe- from extraluminal compression and distortion of the
moglobin complex 8–10 times faster on 100% O2 than airway.
on room air. Continue 100% O2 until carboxyhemo-
globin < 10% on follow-up samples. Upper airway neoplasms include:
● Nasopharyngeal polyps, oropharyngeal squamous
● Bronchodilators – terbutaline (0.01 mg/kg SQ) can
be repeated every 4 hours. cell carcinoma, tracheal adenocarcinoma (Siamese),
nasal adenocarcinoma.
C – circulation
● Crystalloid administration supports the blood pres-
Pulmonary neoplasms include:
● Primary pulmonary neoplasia.
sure and cardiovascular status, promotes diuresis of
absorbed toxins, but must be used judiciously and – Bronchogenic carcinoma, pulmonary adeno-
monitored carefully for iatrogenic pulmonary carcinoma, and squamous cell carcinomas.
● Secondary metastases from distant neoplasms,
edema. Colloids (fresh frozen plasma, synthetic
starch products, synthetic blood substitutes) may be including a variety of carcinomas (i.e., mammary
beneficial. adenocarcinomas) and sarcomas (i.e., osteosar-
coma), as well as local metastases from primary
The prophylactic use of antibiotics is controversial. lung tumors.
Antibiotics reduce the normal flora, and may predis-
pose to a more serious nosocomial infection. If infec- Pleural malignancy may cause coughing.
tion is suspected, antibiotic selection should be based
on culture results of lung wash fluid. Clinical signs
Tracheal tumors create fixed obstruction, leading to
Prognosis inspiratory and expiratory dyspnea, and a harsh, dry
cough. Hemoptysis may be present.
The prognosis is directly related to the extent of the
injuries, both to the airways and non-respiratory dam- Bronchial tumors may be associated with a softer, pro-
age (i.e., skin burns, other organ damage, etc.). Signs ductive cough, fetid halitosis and hemoptysis.
may progressively worsen over the initial 24–48 Very rarely, lameness from hypertrophic osteopathy
hours. occurs.
Diagnosis Differential diagnosis

Radiographs. Inhaled and penetrating foreign bodies, benign or para-
● Cervical radiographs may show soft tissue masses sitic granulomas of the airways, and lung lobe torsions,
of the throat and trachea. abscesses and pulmonary infiltrates with eosinophils
● Thoracic radiographs showing solid tissue masses (PIE) may mimic neoplastic masses. Biopsy is often
or nodular interstitial pattern are highly supportive required to differentiate.
of neoplasia. Multiple orthogonal views (left and
right lateral projections, as well as both dorsoven- Treatment
tral and ventrodorsal views) are important to assess
Tracheal (adenocarcinoma) and some bronchial tumors
potential mass lesions. Hilar lymphadenopathy may
(bronchogenic carcinoma) may be surgically resectible.
be present.
Surgical resection is the treatment of choice for solitary
Other imaging modalities, such as CT or MRI may be
pulmonary neoplasms. Cure or long-term remission is
employed.
possible with wide surgical margins, generally meaning
Histological examination of the mass(es) is required for complete lung lobectomy. If non-resectible, excision of
definitive diagnosis, as well as for distinguishing the ori- nodules may palliate clinical signs.
gin of the tumor. Biopsy options include percutaneous
Chemotherapy and radiation have been disappointing in
fine-needle (20–22 gauge) aspiration, percutaneous core
generalized pulmonary neoplasms. Metastases from dis-
biopsy with 14–18 gauge TruCut®-style needle, bron-
tant tumors carry a grave prognosis, although pulmonary
choscopy for cytology via BAL or bronchial brushings, or
lymphoma may attain remission with chemotherapy.
transbronchial lung biopsy.
● Ultrasound is a poor tool to guide percutaneous General supportive care and nutrition are important.
biopsy needles, unless the entire lung lobe has
become consolidated, as the sonic beam is reflected
Prognosis
by any aerated lung tissue. Triangulating the land-
marks based on two right-angled radiographic views Prognosis is fair to excellent with surgically resectible
is extremely effective. However, pulmonary tumors primary pulmonary neoplasms that have not metasta-
in cats often have a thin rim of neoplastic tissue sur- sized at the time of surgery.
rounding a large necrotic mass, which makes it very
Prognosis is grave with metastatic disease or malignant
difficult to get diagnositic tissue using needle biospy
pleural effusions.
techniques.
● Transbronchial cytology (TTW or BAL) is often
disappointing, because of the interstitial nature of the Prevention
lesion, as neoplastic diseases rarely cross into the air-
None known.
way lumen. Transbronchial lung biopsy is a promis-
ing technique.
● Surgical biopsy during open thoracotomy is an LARYNGITIS
option, generally during lobectomy. Local lymph
nodes should be biopsied for staging of the tumor. Classical signs
There is evidence that any mass in the lung large
enough to biopsy requires thoracotomy and surgi- ● Dysphonia (voice changes) and stridor.
cal excision, because even benign inflammatory ● Harsh gagging cough.
diseases (i.e., eosinophilic granulomatosus) ● Inspiratory dyspnea.
respond poorly to medical management, and that
eventually, thoracotomy is required. Pathogenesis
Thoracocentesis and cytology of pleural fluid may be Laryngeal edema may occur secondary to laryngeal
diagnostic. trauma (bite wounds, endotracheal intubation, near-
strangulation from neck collars), excessive vocalization way obstruction such as tracheal collapse, are differen-
(senility, sexual behavior), or other laryngeal disease tiated with laryngotracheobronchoscopy.
(laryngeal paralysis).
Laryngeal trauma may directly inflame the larynx, or Treatment
may cause nerve damage, secondary laryngeal paraly-
Anti-inflammatories, especially glucocorticoids, are
sis and subsequent mucosal edema from abnormal ary-
used to diminish the local inflammation.
tenoid cartilage motion.
● Dexamethasone (0.1–0.25 mg/kg IV or IM), or
Aspiration of lavage solutions from dental prophy- prednisone (0.5–1.0 mg/kg PO q 12–24 h).
laxis or endodontics may be caustic to the laryngeal ● Little is known about the application of NSAIDs in
mucosa, creating significant edema. laryngeal edema.
Laryngeal edema may occur as part of a type I hyper- Antibiotics are only indicated if there is evidence of
sensitivity reaction to insect stings or vaccination. bacterial infection.
Inflammatory diseases like eosinophilic laryngeal granu- Antitussives may be indicated when the cough has
loma can cause edema (see The Cat With Stridor, page 45). become protracted and debilitating, and lower respira-
tory disease has been ruled out.
Coughing may occur from irritation of the laryngeal
● Butorphanol (0.2 mg/kg SQ q 6 h or 1 mg/cat PO
cough receptors, or from aspiration of food, water or
q 6–8 hours prn) may be effective.
saliva due to laryngeal paresis.
Prognosis
Clinical signs
Fair to excellent.
The cough is usually non-productive, but is typically
harsh and may stimulate a gag reflex and expectoration
of pharyngeal contents. Prevention
Inspiratory dyspnea and stridor, which is worse with Use of break-away neck collars on outdoor cats may
excitement or exercise, may be evident. significantly decrease strangulation injury to the larynx
and the laryngeal nerves.
Dysphonia or voice change, often a whisper-like or
hoarse sound, is frequently observed in cats. Avoidance of insect stings is helpful.
Neutering tom cats helps to prevent both fighting and
Diagnosis mating behaviors such as excessive vocalization.
Laryngoscopy requires deep sedation or anesthesia and
a rigid laryngoscope and blade, and often reveals ery- TRACHEOBRONCHIAL COLLAPSE
thema and edema of the laryngeal mucosa.
Samples of abnormal tissue may be taken for cytology Classical signs
and histology. Culture of the larynx is of questionable ● Harsh, honking cough.
value. ● Dynamic airflow limitation on inspiration if
If biopsies are taken, this may worsen edema. Post- cervical segment, and expiratory if
operative steroids may decrease iatrogenic edema. intrathoracic segment involved.
Occasionally, temporary tracheostomy may be required ● Very rare in cats.
after biopsy.
Clinical signs
The cough is often harsh, non-productive and paroxys-
Laryngeal mass lesion or foreign bodies are differenti- mal, ending in a gagging episode which may appear to
ated visually and by biopsy. Other causes of upper air- be productive.
Cervical trachea collapse produces inspiratory dyspnea, Clinical signs

while intrathoracic tracheal or bronchial collapse will
lead to mostly expiratory dyspnea. Deep productive cough, may be soft and ineffective.
Generally occurs secondary to trauma or to compres- Inspiratory and expiratory dyspnea, often with open-
sion caused by an extraluminal mass. mouth breathing.
Adventitial breath sounds, including crackles, wheezes,
Diagnosis snaps and pops.
Radiographs may show attenuation of the tracheal or History of signs consistent with bacterial, fungal, viral,
bronchial lumina. Fluoroscopy may be more sensitive mycoplasmal and Chlamydophila felis pneumonitis.
for dynamic collapse.
Constitutional signs include lethargy, anorexia, weight
Tracheobronchoscopy is valuable in both diagnosing loss, fever and ill thrift.

Tracheitis from feline rhinotracheitis virus is generally Thoracic radiography shows alveolar densities (focal
associated with other upper respiratory tract signs. or generalized) and possible areas of complete consoli-
Laryngeal paralysis or edema, tracheal foreign body dation. Hilar lymphadenopathy supports fungal or
and tracheobronchial neoplasm can be differentiated mycobacterial pneumonia.
endoscopically. Hematology often shows neutrophilia with or without a
Small airway disease (feline asthma/bronchitis com- left shift or signs of toxicity. Low-grade, non-respon-
plex) can worsen upper airway collapse, but generally sive anemia and monocytosis may support chronicity.
diagnosis is based on radiographic peribronchiolar pat- Cytology and culture of lung samples may be
tern and airway inflammation on lung wash cytology. obtained via percutaneous lung aspiration, transtracheal
wash, or bronchoscopic lavage. Fungal, aerobic and
Treatment anaerobic bacterial cultures are generally submitted.
Medical treatment is indicated if the collapsing seg- Serology may aid in the diagnosis of cryptococcal
ment is short and minimally attenuated, and consists pneumonia.
primarily of antitussive therapy (butorphanol 1 mg/cat
PO q 6–12 h prn).
Surgical therapy may be indicated with severe collapse Differential diagnosis
due to trauma. This generally requires referral to a spe- Chronic small airway disease (feline asthma/bronchi-
cialist with experience in airway surgery. tis), PIE and lymphomatoid granulomatosis, and pul-
Weight loss and avoidance of neck collars can be very monary neoplasia, either primary or metastatic disease,
beneficial in affected cats. may mimic pneumonia.
Small airway disease tends to have peribronchiolar
PNEUMONIA infiltrates compared to the alveolar pattern of pneu-
monia. Also, although asthmatic cats may be
Classical signs severely dyspneic, systemic signs of fever, or neu-
● Moist, productive cough. trophilic leukocytosis are rare.
● Fever or hypothermia may be present. PIE, granulomas or neoplasms tend to have a nodu-
● Fetid halitosis. lar or interstitial density on radiographs, but biopsy
● Adventitial lung sounds are common. results are required to distinguish these diseases.
See main reference on page 64 for details (The Each of the infectious pneumonias can have overlap-
Dyspneic or Tachypneic Cat). ping features.
Treatment Pathogenesis
Bacterial pneumonia – antimicrobial therapy, par- Dirofilaira immitis larvae (L3) infect the cat follow-
enteral if debilitated or septic, and oral if cat is an out- ing a bite from an infected mosquito.
patient. Antibiotic selection best based upon specific
Larvae molt and migrate to the pulmonary arteries,
culture and sensitivity testing.
arriving as immature heartworms (L5) approxi-
Fungal pneumonia – systemic itraconazole at 5–10 mately 100 days or more after initial infection.
mg/kg PO daily is the drug of choice. If there are CNS
Cats typically have fewer adult worms than dogs.
signs with cryptococcosis, fluconazole (2.5–5.0 mg/kg
Less than six adults is usual and often only one or two
PO daily) crosses the blood–brain barrier.
worms are present. Adult worms live shorter lifespans
Viral pneumonia – mostly supportive. in cats compared to dogs, typically 18 months to 3
years.
Supportive care is essential. Adequate airway and sys-
temic hydration are essential for mucociliary clearance. The prevalence of heartworm infection in cats is approx-
Intravenous crystalloids are important for systemic imately 5–10% of the infection rate in dogs in the same
hydration, but should be used judiciously to avoide location, although the ratio may be higher in some areas.
over-hydration. Nebulization with saline may be help- A recent report from Florida showed 5% of necropsied
ful. Physical therapy, oxygen enrichment and bron- cats were positive for the parasite, and 17% of tested cats
chodilator therapy may be helpful. were seropositive. In a similar study in Georgia, D. immi-
tis were found in four of 184 cats (2.1%).
Prognosis Indoor cats are as likely to be infected as outdoor cats.
Prognosis depends on the etiological agent and the In some studies, male cats had a higher incidence of
severity of the infection. infection and had a higher worm burden.
Bacterial pneumonia has a fair to good prognosis, but Cats infected with heartworm may be asymptomatic,
the prognosis is worse in patients with pre-existing ill- have chronic coughing, acute respiratory distress or
nesses or patients on immunosuppressive therapy. die suddenly.
The prognosis for aspiration pneumonia depends on Clinical signs are most likely to occur at the time of
the degree of tissue damage. arrival of the immature heartworms in the lungs or with
death of adult worms.
Cryptococcal pneumonia generally has a fair to good
prognosis, although it is poor if CNS signs are present. Initial arrival of the immature worms results in a
marked inflammatory response, and signs similar to the
feline asthma/bronchitis complex may occur. With mat-
uration to the adult worm, signs may improve or
Prevention resolve.
Avoid the source of infectious agents (i.e., aspergillus Death of adult heartworms may produce acute severe
from bird droppings) and risk factors (i.e., aspiration). pulmonary inflammation with edema, and an acute res-
piratory distress syndrome characterized by general-
ized respiratory failure.
FELINE HEARTWORM DISEASE
Clinical signs
Classical signs
Harsh and productive coughing is the most common
● Cough. sign.
● Acute-onset dyspnea.
● Vomiting together with respiratory signs. Dyspnea may be acute and life threatening. Acute
dyspnea is associated with pulmonary thromboem-
bolism, or acute pulmonary inflammation and edema ● Lung changes vary from patchy pulmonary infil-
associated with worm death. Acute respiratory distress trates to severe alveolar densities suggestive of
syndrome (ARDS) and generalized respiratory failure lung lobe atelectasis or consolidating pneumonia.
are not uncommon. Occasionally pleural effusion is present.
Acute death is reported in approximately 30–45% of Cardiac ultrasound may show hollow linear densi-
cats presenting with clinical signs of heartworm disease. ties (worms) in the right chambers and pulmonary
artery, as well as pulmonary arterial dilation.
Vomiting is often reported and when it occurs together
● Cardiac ultrasound has similir sensitivity to anti-
with respiratory signs, it is suggestive of chronic feline
gen tests. False negatives occur because worms
heartworm disease.
may reside in the extremities of the pulmonary
A gallop rhythm is sometimes audible. arteries where they cannot be detected with the
ultrasound. Occasionally, false-positive results
Neurological signs such as blindness and vestibular
may occur from linear densities detected where
signs may be associated with aberrant migration of L4
the main pulmonary artery branches.
larvae to the brain.
A report describes two cases of cutaneous nodular
lesions associated with D. immitis adult parasites in Differential diagnosis
domestic short-haired cats living in an endemic area
in northern Italy. Other causes of chronic coughing or acute respiratory
distress should be considered as differentials.
● Lungworm and lung flukes are diagnosed with
fecal Baermann exams.
Diagnosis ● Feline asthma is not associated with vomiting, and
Mild non-regenerative anemia, peripheral basophilia, basophilia is uncommon.

eosinophilia and hyperglobulinemia are sometimes ● Cardiomyopathy is diagnosed with echocardiog-
evident. raphy.
● Hydrothorax is diagnosed radiographically and
Heartworm testing. classified based on examination of the fluid.
● Antigen tests (ELISA test) are highly specific, but ● Other forms of pneumonia, (bacterial, viral,
only moderately sensitive. False negatives occur fungal, inflammatory), and neoplastic disease
with low numbers (< 5) worms, and as most cats may appear similar, and are differentiated by lack
have only one or two worms, the test is positive in of evidence of feline heartworm on serology,
less than 50% of infected cats. radiology and ultrasound. Radiography, serology
● Antibody tests are more sensitive, but less specific and cytological or histological examination of tis-
for active infection than antigen testing, as they sue may provide a definitive diagnosis.
may remain positive for 18 months after infection
has resolved.
● A higher sensitivity and specificity is obtained if
Treatment
both the antigen and antibody tests are performed
and the results considered together. Asymptomatic cats do not require treatment and
● Microfilarial tests are unreliable in the cat spontaneous resolution of infection may occur as
because the concentration of microfilaria is very worms live only about 1.5–2 years in cats.
low and microfilaremia is transient, lasting only
Symptomatic cats.
1–2 months.
● Stabilize with oxygen therapy, prednisone (1–2
Thoracic radiographs may show dilated and blunted mg/kg PO q 12–24 h for 10–14 days, then slowly
pulmonary arteries, which are most prominent in the wean down), bronchodilator therapy (Theophylline,
caudal pulmonary arteries, particularly the right side. The TheoDur® 25 mg/kg PO q 24 h) and if needed
dilation may not be evident beyond the cardiac shadow. antiemetics.
● Adulticide therapy is not recommended as Dyspnea and exercise intolerance, evidenced as

there is a high risk (25–30%) of mortality, lethargy, physical inactivity, reluctance to play or weak-
mostly from pulmonary thromboembolism within ness, may occur.
the first 5 days. The death rate following treat-
Weight loss, poor coat and ill-thrift may be evident.
ment is at least as high as the death rate in
untreated cats. Vomiting sometimes occurs with feline heartworm dis-
● Manual removal of worms by a specialist is ease.
associated with a lower mortality rate than killing
the worms with parasiticides. This technique is
only recommended in symptomatic cats with Diagnosis
worms visible in the right heart and main pul-
Feline heartworm disease – peripheral basophilia,
monary arteries on ultrasound. Shock-like signs
positive heartworm antibody testing, dilated and
and death may occur if the worms are damaged
blunted pulmonary arteries and patchy pulmonary infil-
during extraction.
trates on radiographs, and evidence of heartworms on
ultrasound (see page 105 for details).
Prevention
Lungworm infection with Capillaria aerophilia is
The currently available drugs licensed for prevention diagnosed by finding eggs in the stools or lung wash,
of heartworm in cats are ivermectin (24 μg/kg once and with Aelurostrongylus abstrussus by finding lar-
monthly) and selamectin (Revolution®, Pfizer Animal vae in the lung wash or fecal Baermann.
Health, 6 mg/kg once every 30 days). Milbemycine
Lung flukes (Paragonimus kellicotti) produce opercu-
oxime (Interceptor®, Novartis Animal Health, 500
lated eggs in the stool.
μg/kg once monthly) is effective but not licensed for
use in cats. Toxoplasmosis rarely produces clinical disease in cats.
Mixed fluffy interstitial and alveolar patterns are typi-
Imidacloprid and moxidectin (Feline Advantage
cally evident on radiographs. Tachyzoites may occa-
Heart®, Bayer Health Care) topical solution as monthly
sionally be recovered on lung wash.
treatment for prevention of heartworm infection in cats.
As indoor cats are as likely to be infected as outdoor
cats, restricting the cat to indoors is not effective pre- Differential diagnosis
vention.
Other forms of pneumonia, namely bacterial, viral, fun-
gal, inflammatory and neoplasia need to be considered
PARASITIC PNEUMONIA if no larvae or ova are found in the stool or lung wash.
Classical signs
● Variable cough. Treatment
● +/- Eosinophilia.
Feline heartworm disease, see page 105 for main reference.
● +/- Larva/ova in stool.
Lungworm – Capillaria aerophilia and Aelurost-
rongylus abstrussus – fenbendazole (50 mg/kg PO q
Clinical signs 24 h for 3 days) or ivermectin (400 μg/kg PO, SQ).
Etiological agents include heartworm disease, lung- Lung flukes – Paragonimus kellicotti, fenbendazole
worm (Capillaria aerophilia or Aelurostrongylus (50 mg/kg PO q 24 h for 3 days), or praziquantel (25
obstrussus), lung flukes (Paragonimus kellicotti), mg/kg PO q 8 h for 2 days).
migrating nematodes and toxoplasmosis.
Toxoplasmosis – clindamycin (12.5 mg/kg PO q 12 h),
Coughing may be present, and is typically harsh and potentiated sulfa (trimethoprim or ormetoprim), or
productive. azithromycin (7–15 mg/kg PO q 12 h).
Migrating nematodes – Toxocara spp., pyrantel

PLEURAL/MEDIASTINAL MASSES
pamoate (20 mg/kg PO, repeat 7–10 days).
Classical signs
● Dyspnea, orthopnea, tachypnea or rarely,
CARDIOMYOPATHY
coughing.
(DILATED CARDIOMYOPATHY (DCM),
● Muffled heart and lung sounds from
HYPERTROPHIC (HCM), INTERMEDIATE
pleural effusion.
(ICM) OR RESTRICTIVE (RCM))
Classical signs See main reference on page 85 for details (The Cat
With Hydrothorax).
● Dyspnea.
● Gallop rhythm, murmur or arrhythmia.
● Coughing is an uncommon presenting sign Clinical signs
in the cat.
Mediastinal lymphoma, thymomas, and mesothe-
See main reference on page 54 for details (The lioma cause pleural effusion or extraluminal compres-
Dyspneic of Tachypneic Cat). sion to the trachea.
Extraluminal compression of the trachea can cause
dyspnea and coughing.
Clinical signs
Other signs that may be present include orthopnea
Coughing is very uncommon in cats, even in (recumbent dyspnea), tachypnea, minimal airflow with
advanced congestive failure. increased chest excursions, or muffled heart and lung
Dyspnea is common with CHF and pulmonary edema, sounds from a mass or effusion.
and signs vary from mild exercise intolerance (lethargy,
weakness, reluctance to move or play) to severe, open-
mouth breathing with cyanosis. Treatment
Abnormal heart sounds (murmurs, gallops, arrhyth- Lymphoma is best handled with standard chemotherapy
mias) are often present. protocols. See page 676 for details.
Surgical excision is the treatment of choice for thy-
Treatment moma, and may be curative.
Oxygen therapy (O2 chamber or tents work well), Mesothelioma is an infiltrative disease that cannot be
furosemide (1–2 mg/kg IV or IM), sedation if frantic readily resected. Although there are few reports in the
(morphine 0.1 mg/kg IM prn, or butorphanol 0.2–0.4 literature of effective chemotherapy, local infusion of
mg/kg IM q 4–6 h prn), and emergency thoracocentesis if carboplatin may be helpful. Prognosis is grave with
hydrothorax is present. See page 84 for treatment details. or without doxirubicin intravenously.
RECOMMENDED READING
Atkins CE, DeFrancesco TC, Coats JR, Sidley JA, Keene BW. Heartworm disease in cats: 50 cases (1985–1997).
JAVMA 2000; 217(3): 355–358.
Court EA, Litster A, Menrath V, Gunew M. Forty five cases of feline heartworm disease. Australian Veterinary
Practitioner 2000; 30(1): 11.
Dye JA, McKiernan BC, Rozanski EA, et al. Bronchopulmonary disease in the cat: historical, physical, radiographic,
clinicopathologic, and pulmonary functional evaluation of 24 affected and 15 healthy cats. J Vet Int Med 1996;
10: 385–400.
Ettinger SJ. Coughing. In: Ettinger SJ (ed) Textbook of Veterinary Internal Medicine, 5th edition. Philadelphia,
Saunders, 2000, pages 162–166.
Ettinger SJ. Dirofilariasis in dogs and cats. In: Ettinger SJ (ed) Textbook of Veterinary Internal Medicine, 5th edi-
tion. Philadelphia, Saunders, 2000, pages 937–963.
Noone KE. Asthma, bronchitis – cats. In: Tilley LP, Smith FWK (eds) The 5 Minute Veterinary Consult, 2nd edition.
Baltimore, Lippincott Williams & Wilkins, 2000, pages 464–465.
Padrid PA. Feline asthma. In: Bonagura J (ed) Current Veterinary Therapy XIII. Philadelphia, Saunders, 1999,
pages 805–810.
Padrid PA. Feline asthma – diagnosis and treatment. Vet Clin Nth Am: SA pract 2000; 30(6): 1279–1293.
8. The cyanotic cat
Grainne Muire McCarthy
KEY SIGNS
Bluish discoloration of the skin and/or mucous membranes.
MECHANISM?
● Cyanosis is bluish discoloration of the skin and/or mucous membranes due to reduced oxygen
saturation of hemoglobin in the blood causing hypoxia. Hypoxia producing cyanosis results either
from central (cardiac or respiratory) or peripheral causes.
WHERE?
● Central hypoxia results from cardiac or respiratory disease, including disease of the upper
or lower respiratory tract, pleural cavity, thoracic wall or diaphragm.
● Peripheral hypoxia may be generalized and associated with generalized vasoconstriction, or is
localized and the result of arterial or venous obstruction.
● Occasionally abnormal hemoglobin with decreased oxygen carrying capacity is the cause of
the cyanosis.
WHAT?
● The commonest causes of cyanosis are central causes and include bronchial and pulmonary
disease, pleural effusions, cardiac disease, mediastinal neoplasia, diaphragmatic hernia and poi-
soning with acetaminophen.
Peripheral cyanosis is usually the result of arterial thromboembolism.

Diseases causing a cyanotic cat
CENTRAL HYPOXIA
WHERE? – CARDIAC HYPOXIA
ANOMALY
● Congential heart anomaly (p 113)
Tetralogy of Fallot, reversed shunting (R–L), patent ductus arteriosus, tricuspid valve atresia,
Eisenmenger’s syndrome, endocardial cushion defect, and transposition of the great arteries can all
cause cyanosis. Cats with congenital cyanotic heart conditions are usually stunted and cyanotic, and
frequently present with a history of lethargy and syncope. Abnormal heart sounds may be audible.
continued
109
continued
NEOPLASTIC
●Heart base tumors (p 113)
Muffled heart and lung sounds, pleural effusion and ascites.
INFECTIOUS (PARASITIC)
● Dirofilariasis** (p 112)
Most cats are asymptomatic, others may have non-specific signs of cough, lethargy, anorexia.
Sudden death may occur.
IDIOPATHIC
●Cardiomyopathy*** (p 112)
Dyspnea and tachypnea and cats with arterial thromboembolism may present with posterior paresis.
WHERE? – RESPIRATORY HYPOXIA
ANOMALY
●Diaphragmatic hernia (p 115)
Usually occurs following trauma, but may be congenital. Clinical signs of dyspnea and tachypnea
may be present early in life or may not occur for years. Vomiting, regurgitation or inappetence
may also occur.
MECHANICAL
●Airway obstruction (p 117)
Acute onset of inspiratory dyspnea and cough occur with foreign bodies lodged in airways.
Coughing and wheezing occur when the obstruction is due to bronchoconstriction.
● Pleural effusion/pneumothorax*** (p 114)
Multiple causes of pleural effusion, both cardiac and non-cardiac, result in dyspnea and tachypnea.
Inappetence, weight loss and pyrexia may occur depending on the cause.
● Pulmonary thromboembolism associated with heartworm disease (p 116)
Sudden onset of coughing, dyspnea, pulmonary crackles on ausculation and occasionally hemopt-
ysis. Vomiting may also occur.
NEOPLASTIC
● Cranial mediastinal lymphosarcoma** (p 115)
Dyspnea, tachypnea, regurgitation and reduced compressibility of the cranial thorax may be evi-
dent. Inappetence and weight loss may also occur.
INFLAMMATION (INFECTIOUS)
●Bacterial/viral/fungal/parastitic/protozoal/mycoplasmal
Pneumonia; depression, fever, tachypnea, cough and dyspnea. The cat may also show signs of
upper respiratory tract disease.
INFECTIOUS (IMMUNE)
● Feline bronchopulmonary disease/feline bronchitis complex/feline asthma** (p 114)
Typically, there is wheezing and coughing which may progress to severe dyspnea, open-mouthed
breathing and cyanosis.
8 – THE CYANOTIC CAT 111
TRAUMA
● Diaphragmatic hernia* (p 115)
Dyspnea and tachypnea may occur acutely or months or years following blunt trauma. Vomiting,
regurgitation, inappetence and weight loss may also occur.
● Central nervous system damage to the respiratory center (p 118)
Persistent or episodic weakness, Cheyne–Stokes respiration and cyanosis.
TOXIC
● Drug overdosage (p 117)
Excessive administration of barbiturates, narcotics, opiates, tranquilizers or anesthetic agents may
lead to decreased respiratory effort, loss of consciousness and cyanosis. During anesthesia,
reduced bleeding at surgical sites and indicators of a deep plane of anesthesia are present.
PERIPHERAL HYPOXIA
WHERE? – GENERALIZED
MECHANICAL
● Vasoconstriction* (p 118)
Peripheral hypoxia occurs due to vasoconstriction as a consequence of hypovolemic, cardiogenic
or septic shock or due to hypothermia. Clinical signs, physical findings and history point to one of
these causes. There may be evidence of shock, trauma, dehydration, pyrexia, blood loss or reduced
urinary output. Signs of cardiac failure include dyspnea, cardiac murmur, gallop rhythm, slow cap-
illary refill time, pale/cyanotic mucous membranes and pulse deficits. Frequent or severe vomiting,
diarrhea or diuresis may indicate fluid loss.
LOCALIZED
MECHANICAL
● Arterial thromboembolism** (p 120)
Ninety percent lodge at the distal aortic bifurcation causing bilateral hindlimb pain and paresis, weak
or absent femoral pulses, cold, cyanotic footpads and lack of spontaneous movement of the muscles of
the hindlimbs. Other areas embolized less commonly are the thoracic aorta, renal, mesenteric, coro-
nary, cerebral and branchial arteries which cause acute, severe and variable clinical signs.
● Venous obstruction (p 121)
Clinical signs relate to the area drained by the obstructed vein, mainly edema and vasodilatation
distal to the site of obstruction. Cranial vena caval obstruction results in edema of the neck, ventral
head, cranial thorax and forelimbs.
ABNORMAL HEMOGLOBIN WITH DECREASED OXYGEN-CARRYING CAPACITY
WHERE? – HEMOGLOBIN IN RED BLOOD CELLS
WHAT?
TOXICITY
● Paracetamol/acetaminophen toxicity (p 121)
Acute onset and rapid progression of salivation, vomiting and depression. Cyanosis develops
within 4–12 hours of ingestion. Subcutaneous edema of the face may be evident, which may be
accompanied by lacrimation and puritis. Hematuria, hemolysis and Heinz bodies occur associated
with methemoglobin formation.
INTRODUCTION CARDIAC HYPOXIA
MECHANISM? CARDIOMYOPATHY***
Cyanosis is bluish discoloration of the skin and/or
Classical signs
mucous membranes due to reduced oxygen saturation
of hemoglobin in the blood causing hypoxia. Cyanosis ● Dyspnea and tachypnea.
most commonly results from decreased oxygen satura- ● Lethargy.
tion of normal hemoglobin. Only rarely it results from ● Anorexia/vomiting.
abnormal hemoglobin with decreased oxygen-carrying ● Posterior paresis.
capacity. Hypoxia producing cyanosis results either from ● Abnormal heart sounds.
central (cardiac or respiratory) or peripheral causes.
WHERE?
Clinical signs
Hypoxia (i.e. decreased oxygen saturation of normal
hemoglobin). Dyspnea and tachypnea, or in severe cases open-
mouthed breathing, occur because of pleural effusion
Central hypoxia results from congenital cardiac and/or pulmonary edema.
anomalies such as tetralogy of Fallot and pulmonary
arterial hypertension secondary to a large PDA, VSD, Lethargy, anorexia and occasional vomiting may be
ASD or truncus arteriosus, respiratory diseases present.
including tracheal and laryngeal neoplasia (rare), pleu- Occasionally, acute onset of posterior paresis occurs with
ral effusions, pulmonary edema, pneumonia, thoracic painful hardening of the quadriceps and gastrocnemius
wall lesions and rupture of the diaphragm. groups of muscles, cyanosis of the nail beds and cold
Peripheral hypoxia is either generalized as a result of extremities associated with aortic thromboembolism.
generalized vasoconstriction due to hypothermia, heart
failure or shock or localized as a result of arterial or Diagnosis
venous obstruction. Acute arterial obstruction may
Thoracic radiography may show cardiac enlargement,
result from thromboembolism or thrombosis occurring
pleural effusion and pulmonary edema.
with cardiomyopathy, bacterial endocarditis, hyperco-
agulable conditions and cold agglutinin disease. Echocardiography may show left ventricular hypertro-
Venous obstruction occurs as a result of throm- phy and left atrial enlargement in hypertrophic car-
bophlebitis and restrictive devices such as a rubber diomyopathy or left atrial and ventricular dilation with
band around the limb. reduced contractility in dilated cardiomyopathy.
Abnormal hemoglobin with decreased oxygen-
carrying capacity. DIROFILARIASIS**
Classical signs
WHAT? ● Most cats are asymptomatic.
In the cat, the commonest causes of cyanosis include ● Cough, lethargy, anorexia, vomiting,
bronchial and pulmonary disease, pleural effusions, dyspnea and syncope.
cardiac disease, mediastinal neoplasia, diaphragmatic ● Acute dyspnea and sudden death.
hernias and poisoning with acetaminophen. Peripheral
cyanosis is usually the result of arterial thromboem- See main reference on page 104 for details (The
bolism. Coughing Cat).
Clinical signs great vessels and an obstruction to pulmonary

blood flow.
Many cats are asymptomatic.
This leads to right-to-left shunting and results in mix-
Sudden death occurs in 30–40% of cats with clinical ing of unsaturated and saturated blood which is then
signs from dirofilaria. ejected into the systemic circulation.
Most cats are presented with non-specific signs such as Tetralogy of Fallot, reversed shunting (R–L), patent duc-
lethargy, anorexia, vomiting, coughing, dyspnea and tus arteriosus, tricuspid valve atresia, Eisenmenger’s syn-
syncope. drome, endocardial cushion defect and transposition of
Acute dyspnea may result from acute thromboembolism. the great arteries can all cause cyanosis.
Right-sided heart failure is rare. Clinical signs

Cyanosis in a young cat or kitten frequently is sug-
Diagnosis gestive of a congenital heart anomaly.
Thoracic radiography may show prominent blunted They may present with lethargy, exercise intolerance,
or tortuous caudal lobar arteries and right heart enlarge- syncope and tachypnea.
ment.
Signs of congestive heart failure or abnormal heart
Laboratory tests reveal eosinophilia and a non- sounds may be present.
regenerative anemia in 33% of cases. Adult antigen
tests detect only about 25% of infected cats because Diagnosis
of low worm numbers. Tests for circulating anti-
body to heartworm are more sensitive, but there are Dorsoventral thoracic radiographs may show
problems with false positives and negatives. enlargement of the right atrium at the 8–11 o’clock
Antibodies may persist for up to 18 months after position, right ventricular enlargement at the 5–9
worms have died, so a positive test does not neces- o’clock position or post-stenotic dilation of the pul-
sarily indicate current infection. monary artery at the 1–2 o’clock position.
Echocardiography may reveal worms in the pul- Lateral thoracic radiographs may show rounding of the
monary artery, right heart or vena cava. cranial border of the heart with increased sternal contact
and elevation of the trachea in the cranial thorax. On both
Non-selective angiography may show linear filling views the pulmonary vessels may be underperfused.
defects associated with the presence of worms.
Echocardiography is useful for visualizing the abnor-
mal cardiac and vascular shunts. Doppler studies will
CONGENITAL HEART ANOMALY help to identify the presence and direction of shunts.
Classical signs Hematological examination may indicate a poly-

cythemia with a PCV often in excess of 75%.
● Stunting.
● Cyanosis.
● Signs of congestive heart failure. HEART BASE TUMORS
● Abnormal heart sounds.
Classical signs
● Muffled heart sounds.
● Right heart failure.
● Pale mucous membranes.
Pathogenesis
● Weak arterial pulses.
Congenital cardiac anomalies causing cyanosis
result from defects in the partitions of the heart or See main reference on page 137 for details.
Clinical signs If due to a cranial mediastinal mass it may result in a

non-compressible cranial thorax.
Heart base tumors are rare in cats.
Heart sounds are often muffled associated with a peri- Diagnosis
cardial/pleural effusion.
Thoracic radiograph may show the presence of fluid,
Weakness, dyspnea and tachypnea are often present. air or a mediastinal or other space-occupying mass.
Ascites is commonly present due to cardiac tamponade. Thoracocentesis may yield fluid which can be classi-
Edema of the head, neck and forelegs occurs if the fied as transudate, exudate, chylous or hemorrhagic
tumor presses on the cranial vena cava. effusion.
Weight loss may be present. Thoracocentesis may yield air indicative of a pneu-
mothorax.
Diagnosis FELINE BRONCHOPULMONARY

Thoracic radiography may show a rounded cardiac DISEASE/FELINE BRONCHITIS
silhouette and pleural effusion. COMPLEX/FELINE ASTHMA**
Pericardiocentesis, cytological analysis and contrast Classical signs
pericardiography may help diagnose a heart base tumor.
● Cough.
Echocardiography may enable visualization of the ● Wheeze.
tumor and enable ultrasound-guided fine-needle aspi- ● Severe dyspnea, open-mouthed breathing
rate biopsy of the tumor for histologic analysis. and cyanosis.
See main reference on page 92 for details (The

RESPIRATORY HYPOXIA Coughing Cat).
PLEURAL EFFUSION/PNEUMOTHORAX***
Clinical signs
Classical signs Coughing of variable severity is frequently seen as a
● Dyspnea. result of bronchoconstriction.
● Tachypnea. Dyspnea and tachypnea will appear if there is severe
bronchconstriction or marked cellular infiltration into
See main reference on page 54 for details (The the lung parenchyma.
Dyspneic or Tachypneic Cat).
Dyspnea may be inspiratory or there may be end-
expiratory grunting due to difficulty in expelling air
Clinical signs from the cat’s hyperinflated lungs.
Progressively worsening dyspnea frequently occurs Acute exacerbations may cause severe dyspnea, orthop-
with thoracic fluid accumulation. nea, open-mouth breathing and cyanosis, which may be
life-threatening.
Acute dyspnea may occur with traumatic pneumo-
thorax and tension pneumothorax.
Diagnosis
Muffled lung sounds occur due to the presence of tho-
racic fluid. The clinical findings are very supportive of a diagno-
sis as there are few other clearly recognized causes of
Lung sounds may be inaudible with a pneumothorax. coughing and dyspnea in the cat.
Wheezing and crackling with moist gurgling sounds See main reference on page 56 for details (The
can be heard on auscultation. Dyspneic or Tachypneic Cat) and page 676 for details
of treatment.
Thoracic radiographs may show a bronchial or a
mixed bronchial/interstitial or alveolar pulmonary pat-
tern throughout the entire lung field.
Clinical signs
In the acute phase there may be hyperinflation of the
Dyspnea and tachypnea are often associated with a
lungs and flattening of the diaphragm. Occasionally
pleural effusion.
collapse of the right middle lung lobe may be seen.
Regurgitation may occur due to compression of the
Bronchoalveolar lavage fluid usually shows an inflam-
esophagus by the mass.
matory response which is usually eosinophilic but may
be neutrophilic in nature. Cyanosis may result from compression of the medi-
astinal vessels.
Differential diagnosis Reduced compressibility of the cranial mediastinal
Lungworm and lung fluke infestation are diagnosed thorax may be evident because of a space-occupying
with fecal Baermann exams. mass.
Heartworm disease is often associated with vomiting,

and sometimes basophilia. On radiographs, dilated and Diagnosis
blunted pulmonary arteries, which are most promi-
nent in the caudal pulmonary arteries, particularly the Thoracic radiography shows a space-occu-
right side, may be seen. Lung changes vary from pying lesion causing widening of the cranial
patchy pulmonary infiltrates to severe alveolar den- mediastinum. A pleural effusion is frequently present.
sities, and sometimes are difficult to differentiate from Cytologic evaluation of pleural fluid is useful as it
those of feline bronchopulmonary disease/ asthma. often contains lymphoblastic cells.
Fine-needle aspiration of the mass under ultrasound
Treatment
guidance will yield a sample for histopathologic exam-
Acute respiratory distress requires a rapid-acting ination.
corticosteroid such as methylprednisolone sodium
Test cat for FeLV as approximately 60% of cats with
succinate given intravenously at a dose of 30–50
mediastinal lymphosarcoma are FeLV-positive in
mg/kg, oxygen and terbutaline at a dose of 0.01
USA. This may be lower in countries where FeLV is
mg/kg IM or SQ q 4 h.
rare.
Long-term management involves eliminating potential
Test for FIV as this virus is also associated with
allergens and intermittent anti-inflammatory and bron-
increased rates of lymphosarcoma.
chodilator therapy.
CRANIAL MEDIASTINAL
LYMPHOSARCOMA** DIAPHRAGMATIC HERNIA (CONGENITAL
ANOMALY OR TRAUMATIC)*
Classical signs
Classical signs
● Dyspnea.
● ● Dyspnea.
Tachypnea.
● ● Tachypnea.
Regurgitation.
● Pleural effusion.
● Non-compressible cranial thorax. See main reference on page 58 for details (The
Dyspneic or Tachypneic Cat).
Clinical signs Clinical signs

Acute tachypnea/dyspnea may develop after a blunt Acute dyspnea is associated with pulmonary throm-
traumatic event. There may be signs of shock and boembolism or acute pulmonary inflammation and
other injuries related to an event such as a road traffic edema associated with worm death. Acute respira-
accident. tory distress syndrome (ARDS) and generalized res-
piratory failure is not uncommon.
Acute exacerbations of chronic diaphragmatic hernia
may occur following the development of a pleural Cats usually have an acute onset of severe dyspnea,
effusion or dilation of a herniated stomach. tachypnea and cyanosis, and may mouth breathe.
In chronic cases, signs may be restricted to exercise Dyspnea may be worsened in lateral recumbency
intolerance, or signs of gastrointestinal upset may (orthopnea) and the cat is reluctant to lie in this posi-
occur, weeks or months after the trauma. tion.
Entrapment of viscera following traumatic diaphrag- There may be splitting of the second heart sound,
matic hernia may lead to pleural effusion. Even resulting in a gallop rhythm, due to acute pulmonary
partial herniation of liver may result in significant arterial hypertension.
effusion.
Congenital peritoneo-pericardial hernias also occur
causing similar clinical signs. Diagnosis
Thoracic radiographs may show evidence of parenchy-
mal lung disease, right-sided cardiomegaly, or
enlargement of the caudal lobar arteries or may be
Diagnosis normal.
Clinical findings of muffled lung sounds, displace-
Ultrasound examination may reveal heartworm as
ment of cardiac apex, gut sounds audible in thorax
hollow linear densities in the main pulmonary
and reduced volume of abdominal contents are
artery or right artrium, as well as pulmonary arterial
suggestive.
dilation.
Thoracic radiography may show loss of diaphrag-
Definitive diagnosis of the thromboembolism requires
matic line, abdominal contents in the thorax or pleural
angiography or pulmonary scintigraphy.
effusion.
Blood chemistries may indicate the presence of a
Thoracic ultrasound can identify the presence of
hypercoagulable condition.
abnormal contents in the thorax and loss of continuity
of the diaphragmatic line. Heartworm tests may be positive.
PULMONARY THROMBOEMBOLISM PNEUMONIA

ASSOCIATED WITH HEARTWORM
DISEASE Classical signs
● Fever.
Classical signs ● Tachypnea.
● Severe dyspnea. ● Cough.
● Tachypnea. ● Dyspnea.
● Cyanosis. ● Inappetance.
See main reference on page 104 for details (The See main reference on page 62 for details (The
Coughing Cat). Dyspneic or Tachypneic Cat).
Clinical signs See main reference on page 65 for detail. (The Dyspneic
or Tachypneic Cat (Foreign bodies)) and page 92 (The
Cats are usually inappetent, dull, febrile and lethar- Coughing Cat (Feline asthma/bronchitis complex)).
gic and may have a productive cough or fetid halitosis
with bacterial pneumonia. Clinical signs
Tachypnea and dyspnea may be evident, and open- Acute-onset inspiratory dyspnea and stridor occur
mouth breathing may occur with stress. shortly after inhalation of a foreign body. Tracheal
Aspiration pneumonia after oral dosing with liquid foreign bodies are more common in cats than dogs.
paraffin or mineral oil, or associated with megaesopha- Coughing is likely with bronchial foreign bodies and
gus may also result in coughing. the right middle lobe most likely to be involved.
Viral pneumonia with feline calicivirus causes a non- Tracheobronchial compression caused by space-
productive cough. occupying lesions (most often lymphoma or thy-
moma) usually lead to coughing and dyspnea.
Diagnosis Airway obstruction caused by bronchoconstriction
Crackles and wheezes may be heard on pulmonary associated with feline asthma or bronchitis complex
auscultation especially in the ventral lung fields. leads to severe dyspnea, wheezing and coughing.
Thoracic radiographs show a patchy interstitial or Diagnosis

alveolar pattern, and possibly lung lobe consolida-
tion in the cranioventral lung fields. There may be Thoracic radiography may reveal foreign bodies, tumors
evidence of megaesophagus present. or other structures compressing or obstructing the airways.
Tracheal and bronchoalveolar lavage cytology may Bronchoscopy may reveal structures compressing the
reveal a neutrophilic inflammatory response with many airway or a foreign body or other material in the airways.
degenerate neutrophils. Alternately, the presence of
eosinophils may indicate an allergic, parasitic or neo- DRUG OVERDOSAGE
plastic etiology.
Microbial culture of cytospun lavage fluid deposit Classical signs
may reveal a primary pathogen (bacterial, fungal, para- ● Decreased respiratory effort.
sitic or myoplasma). ● Absence of voluntary respiration.
● Loss of consciousness.
Bronchoscopy may show inflammatory exudate in the
● Cyanosis.
airways.
● Reduced bleeding from surgical site.
Routine hematologic examination may reveal a left
shift in bacterial pneumonia.
Clinical signs
Check FeLV and FIV status in cats with chronic
pneumonia as they may be immunosuppressed. Respiratory depression or even failure can result from
excessive administration of barbiturates, narcotics,
opiates, tranquillizers or anesthetic agents.
AIRWAY OBSTRUCTION
This leads to loss of consciousness and cyanosis due
Classical signs to hypoxemia.
● Inspiratory dyspnea. If it occurs during a surgical procedure, there may be

● Cough. reduced bleeding from the surgical site and the color
● Stridor. of the blood darkens. Loss of blink reflex indicates
● Cyanosis. a deep plane of anesthesia and is associated with
increased respiratory depression.
Diagnosis Pathogenesis
Diagnosis is based on clinical signs together with Peripheral hypoxia occurs due to vasoconstriction as
anesthetic records indicating drug overdose, or a a consequence of hypovolemic, cardiogenic or septic
history of access to sedative, narcotic or anesthetic shock or due to hypothermia. This leads to inade-
drugs. quate capillary perfusion and oxygen delivery to
peripheral tissues becomes impaired, which may lead
to generalized peripheral cyanosis.
CENTRAL NERVOUS SYSTEM DAMAGE Hypovolemia occurs when blood volume is diminished
TO THE RESPIRATORY CENTER by whole blood loss or by extracellular fluid losses.
Compensatory mechanisms include splenic and venous
Classical signs constriction to translocate blood from the venous
● Persistent or episodic weakness. capacitance vessels to the central arterial circulation;
● Cheyne–Stokes respiration. arteriolar constriction to maintain diastolic blood pres-
● Cyanosis. sure and increasing heart rate to increase cardiac out-
put. When severe, hypovolemic shock ensues resulting
in generalized peripheral hypoxia.
Clinical signs Cardiogenic shock occurs with any condition that

interferes with forward outflow from the heart to
Central respiratory depression as a result of CNS such an extent that adequate tissue perfusion is not
infection, increased intracranial pressure or head achieved. Examples include acute or chronic heart fail-
injury leads to slow, gasping respirations (Cheyne– ure, cardiomyopathy, intracardiac thrombosis, pericar-
Stokes respiration). dial tamponade, heartworm disease and severe
The cat may be unconscious and cyanotic. arrhythmias.
Other evidence of trauma, or neurologic deficits may be When an animal’s blood has become infected by bac-
present. teria, viruses, rickettsia, fungi or protozoa it is con-
sidered septic. Some of these organisms produce
toxins which are directly vasoactive or release vasoac-
tive substances. When the infection is affecting the ani-
Diagnosis mal to the extent that tissue perfusion is compromised,
Neurological examination demonstrates neurologic septic shock has ensued.
deficits consistent with a medullary lesion together Hypothermia results when heat loss exceeds heat pro-
with a typical respiratory pattern. duction. Decreasing body temperature decreases the
partial pressure of oxygen, increases solubility and
shifts the oxygen–hemoglobin dissociation curve to the
PERIPHERAL HYPOXIA – left. These changes impede oxygen unloading at the tis-
GENERALIZED sue level. Thermoregulatory vasoconstriction further
decreases oxygen delivery.
VASOCONSTRICTION*
Clinical signs
Classical signs
Generalized cyanosis together with signs of severe
● Generalized cyanosis. hypovolemia, severe cardiac disease, hypothermia
● Signs of hypovolemic, cardiogenic, or septic or sepsis, which suggest vasoconstriction is leading to
shock or hypothermia. inadequate capillary perfusion and impaired oxygen
delivery to peripheral tissues.
Signs of cardiac failure include dyspnoea, cardiac mur- therapy includes cage rest where necessary, weight reduc-
mur, gallop rhythm, slow capillary refill time, pale/cyan- tion, avoidance of pregnancy and general reduction in car-
otic mucous membranes and pulse deficits. diac workload. See page 130 (The Cat With Abnormal
Heart Sounds and/or an Enlarged Heart) for treatment.
Evidence of shock, trauma, pyrexia, blood loss or
reduced urinary output may indicate cause of periph- For shock, treatment depends on the cause. For
eral vasoconstriction. hypovolemia administer intravenous fluids, and if indi-
cated, a blood transfusion and control any continuing
History of frequent or severe vomiting, diarrhea or
blood loss. For septic shock, fluid therapy and intra-
diuresis are suggestive of marked fluid loss leading to
venous broad-spectrum antibiotic therapy is indicated.
hypovolemia.
For anaphylactic shock, in addition to fluid therapy,
Fluid accumulations in the thoracic or abdominal cavi- epinephrine is of proven efficacy. Careful monitoring
ties or in intracellular spaces suggest cardiac disease, of acid–base balance, urine output, heart rate, pulse
sepsis, bleeding or severe hypoalbuminemia is the cause quality, capillary refill time, mucous membrane color
of the vasoconstriction and cyanosis. and mental state are important. The reader is advised
to consult a specialist source for an in-depth review of
Acute weakness, bradycardia and cyanosis, with or
shock therapy.
without a history of polyuria/polydipsia or GIT signs,
in a young to middle-aged dog is suggestive of hypo- Rewarming is required for hypothermia. When the
adrenocorticism (Addisons disease). body temperature is less than 32 degrees Centigrade
(90 degrees Fahrenheit) active central rewarming is
required. This includes the use of warmed (to 35
Diagnosis degrees Centigrade/95 degrees Fahrenheit) IV fluids,
Diagnosis is based on clinical signs and physical flushing stomach, rectum and open body cavity with
findings which suggest that hypovolemia, severe car- warmed isotonic fluids, and providing warmed,
diac disease, sepsis or hypothermia are causing humidified air. If body temperature is between 32 and
marked vasoconstriction and generalized peripheral 36 degrees Centigrade (90 and 96 degrees Fahrenheit)
cyanosis. active surface rewarming can be carried out using hot
water bottles, heat pads, radiant heaters and hair dryers.
Cardiovascular examination, including echocardiogra- At body temperatures above 36 degrees Centigrade (96
phy are important in assessing cardiac function. degrees Fahrenheit) passive rewarming by covering the
Complete blood profile may indicate sepsis or hypov- cat with blankets is sufficient.
olemia.
Thoracic and abdominal radiographs may show car- Prognosis
diomegaly, fluid accumulations, evidence of hypov-
olemia, evidence of trauma or masses such as With hypovolemia recovery rates can be high, provid-
abscesses. ing adequate correction of fluid deficits can be
achieved.
Cardiogenic shock is usually associated with advanced
Treatment heart disease and so recovery rates are less.
For cardiogenic shock, treatment is directed at restoring
Mortality rates in septic shock are high.
organ perfusion to provide adequate tissue oxygenation,
i.e. supporting arterial blood pressure, forward cardiac The systemic consequences of mild to moderate
output and vascular volume. Diuresis, vasodilation, cal- hypothermia are minimal but those of severe pro-
cium channel- or beta-blocking drugs, anti-arrhythmics, longed hypothermia are serious and fraught with many
oxygen and thoracocentesis may be required in hyper- complications including cardiac arrhythmias, elec-
trophic cardiomyopathy. Continuous monitoring of car- trolyte disturbances, coagulopathies, blood glucose
diac, pulmonary and renal status is essential. Supportive upset and cold diuresis.
Typically there is an acute onset of posterior pare-

PERIPHERAL HYPOXIA – LOCALIZED sis/paralysis.
Weakness or absence of one or both femoral pulses is
ARTERIAL THROMBOEMBOLISM** evident.
Classical signs There is early severe pain in hindlimb muscles which

are swollen and turgid. The pain subsides as sensory
● Acute onset of posterior paresis/paralysis.
nervous input is lost over several hours.
● Cyanosis of footpads and cold extremities.
● Marked pain and swollen, turgid hind limb Pallor and cyanosis of footpads and coldness of
muscles. extremities are evident.
● Weak or absent femoral pulses.
Later over days to weeks, depending of the degree of
arterial obstruction, neurological deficits begin to
See main reference on page 915 for details (The Weak
resolve.
and Ataxic or Paralyzed Cat).
Other organs may be affected depending on deposi-
Pathogenesis tion of emboli.
Arterial thromboembolism is a relatively common

and serious sequela to feline cardiomyopathy.
Diagnosis
Thrombi form in the left atrium due to a combina-
tion of factors including sluggish blood flow, Diagnosis is based primarily on clinical findings.
endothelial damage and increased blood coagulabil-
Lack of blood flow to hindlimbs can be confirmed using
ity. The blood flow through the atria of cats with car-
a Doppler arterial blood pressure monitor.
diomyopathy is normal to slow. Slow blood flow
enables red cells and other blood factors to clump Echocardiography is valuable to identify cardiomy-
together and platelet aggregability in cats with car- opathy.
diomyopathy is reported to be increased.
Biochemical profiles may help to identify other organ
Once a thrombus is formed it may remain in the atrium involvement.
and cause no symptoms. It may become an embolus
and travel to the distal aorta and extend down the
external iliac arteries forming a “saddle thromboem- Differential diagnosis
bolus” obstructing blood flow to the hindlimbs. Ninety
percent of cats with arterial thromboembolism are thus Other causes of posterior paresis/paralysis such as
affected. road traffic accidents and trauma should be consid-
ered.
It is thought that the embolus releases serotonin and
thromboxane A2, which are powerful vasoconstric-
tors. This results in very poor collateral blood flow Treatment
beyond the embolus, leading to tissue hypoxia and
muscular ischemia. Treatment is mostly palliative, such as cage rest and
consider the administration of drugs such as aspirin,
Other emboli may obstruct the femoral, brachial, heparin or arteriolar dilators. Heparin is given to pre-
renal, mesenteric, coronary or cerebral arteries caus- vent new thrombus formation at an initial dose of 220
ing a wide variety of clinical signs. U/kg IV followed by a maintenance dose of 70–200
U/kg SC every 6 hours. The dose should be tailored to
Clinical signs increase the activated thromboplastin time to at least
1.5 times baseline.
Many cats are in heart failure and therefore are
tachypneic and dyspneic, and may have a heart mur- Surgical intervention to remove the embolus and bal-
mur or a gallop rhythm. loon embolectomy may lead to reperfusion syndrome
and most cats will be in heart failure, so are poor anes- If all veins draining an area are obstructed, edema,
thetic risks. cyanosis and necrosis may occur.
Thrombolytic therapy using tissue plasminogen Cranial vena caval obstruction results in edema of the
activator reduces time to reperfusion and ambu- neck, ventral head, cranial thorax and forelimbs.
lation, however 50% of treated cats died during clin-
ical trials. Diagnosis
Pain treatment in the early stages of the disease using Diagnosis is based on historical and clinical findings.
oxymorphone (0.05–0.15 mg/kg IM or IV every 6
hours) and butorphanol (0.02–0.4 mg/kg every 4 hours
Treatment
IM or SC) is essential.
Thrombosis is usually self-limiting once catheters are
Acetylpromazine (0.05–0.1 mg/kg IV) may be useful
removed. Broad-spectrum antibiotic cover may be nec-
as an anxiolytic.
essary for septic lesions.
Treatment of the heart failure must also be undertaken.
Surgical management is by drainage of abscesses and
hematomas, and debulking of tumors where indicated.
VENOUS OBSTRUCTION Treat the underlying cause of lymphadenopathy using
antibiotics, chemotherapy or surgical excision where
Classical signs appropriate.
● Localized cyanosis and edema referable to
site of obstruction. Prognosis
● Edema of neck, ventral head, cranial thorax
and forelimbs (vena cava obstruction). Prognosis depends on the primary disease process.
Pathogenesis
ABNORMAL HEMOGLOBIN WITH
Localized peripheral hypoxia resulting from venous DECREASED OXYGEN-CARRYING
obstruction is usually the result of thrombosis, phlebitis CAPACITY
or venous obstruction from external compression.
● Thrombosis is typically caused by blunt trauma
and perforating injury, such as venepuncture or pro- ACETAMINOPHEN (USA)/PARACETAMOL
longed venous catheterization. (EUROPE, AUSTRALIA) TOXICITY
● Phlebitis may result from tissue inflammation
extending to the veins, or originate from a venous Classical signs
intimal lesion. ● Salivation, vomiting and depression and
● Venous obstruction may be caused by compression cyanosis.
by abscesses, hematomas, tumors or enlarged ● Subcutaneous edema of face and
lymph nodes. extremities.
● Lacrimation and facial pruritis.
Clinical signs ● Hematuria and hemolysis.
Clinical signs depend on the anatomic location and

the extent of the obstructive process, the collateral ves-
sel reserve and the capacity of the draining lymphatics. Pathogenesis
Large lesions may result in edema and cyanosis in the Feline hemoglobin is particularly susceptible to oxida-
area, which is usually short-lived because of large col- tive damage, and therefore to the formation of methe-
lateral circulation. moglobin and Heinz bodies in erythrocytes.
Most species biotransform acetaminophen by hepatic Finding the pills in stomach contents is confirmatory.
conjugation with glucuronic acid and excrete it in the
Frequent laboratory findings include; methemo-
urine.
globinemia, depletion of erythrocyte-reduced glu-
However, cats have limited ability to conjugate drugs tathione, Heinz bodies and a decreased packed cell
as glucuronides and so they excrete the majority of volume.
acetaminophen as a sulfate conjugate.
Elevated hepatic enzyme levels and total and direct
This pathway is saturated at relatively low drug con- bilirubin levels are evidence of hepatic necrosis.
centrations leading to early oxidative toxicity in the cat.
Hepatocellular injury associated with acute acetamin- Differential diagnosis
ophen toxicity in other species is not seen in cats
Other causes of methemoglobinemia include, benzo-
because cats develop oxidative toxicity at much lower
caine (used as a laryngeal local anesthetic spray to
doses than those required for hepatotoxicity in other
facilitate intubation), DL methionine (used as a uri-
species.
nary acidifier), phenacetin (used as an analgesic in
Accumulation of oxidative metabolites produces humans) and phenazopyridine (used as a urinary anal-
methemoglobin, which reduces oxygenation of blood. gesic drug).
Methemoglobinemia leads to the denaturing of hemo- Methylene blue, a drug previously used to treat cats
globin and Heinz bodies are formed from the precip- with methemoglobinemia may actually cause Heinz
itation of this denatured haemoglobin within the red body formation and hemolytic anemia.
blood cells.
Familial methemoglobin reductase deficiency has
Heinz bodies lead to increased osmotic fragility of red been reported in a family of domestic shorthair cats and
blood cells causing hemolysis and anaemia. is thought to have an autosomal recessive form of
inheritance.
The feline toxic dose of acetaminophen is 50–100
mg/kg, and the average size of a regular tablet is 325
mg (USA) or 250 mg (Europe). Treatment
Induce emesis and administer activated charcoal if the
cat is treated within the first 4 hours post-ingestion.
Clinical signs N-acetylcysteine will provide the cysteine moiety
required for the increased synthesis of gluthathione
Salivation, vomiting and depression progress rapidly
and may increase the concentration of free serum sul-
and cyanosis develops within 4–12 hours of ingestion.
fate. A dose of 140 mg/kg IV should be followed by 70
Hematuria and hemolysis appear when blood levels mg/kg IV every 6 hours for a total of seven treatments.
of methemoglobin reach 20%.
Ascorbic acid provides a reserve system for the non-
Subcutaneous edema of face and extremities may enzymatic reduction of methemoglobin back to
happen and be accompanied by lacrimation and pru- hemoglobin and can be given at a dose of 30 mg/kg IV
ritis. four times a day.
Death may occur. Blood transfusion may provide a lifesaving fraction of
functional hemoglobin until the methemoglobin can
Jaundice is seen 2–7 days post-exposure if the cat sur-
be reduced.
vives.
Cimetidine, which works differently to acetylcysteine
and ascorbic acid in the metabolism of acetaminophen,
Diagnosis
has been used in an attempt to reduce hepatotoxicity.
Diagnosis is based on the history of exposure and clin- The suggested dose rate is 15 mg/kg IV every 8 hours
ical signs. or 100 mg/kg orally every 8 hours.
Prognosis ophen ingested is the other important consideration.

The sooner the animal is treated the better the out-
The time between ingestion and initiation of therapy come. Most cats treated within the first 24 hours
is of primary importance and the dosage of acetamin- will survive.
RECOMMENDED READING
Aronson LR, Drobatz K. Acetaminophen toxicosis in 17 cats. J Vet Emerg Crit Care 1996: 6: 65–69.
Dunn J. Cyanosis. In: Textbook of Small Animal Medicine. W.B. Saunders, London, 1999, pp 118–122.
Ettinger S, Feldman E. Cyanosis. In: Textbook of Veterinary Internal Medicine, Volume 1, Sixth Edition, 2005, W.B.
Saunders, London, pp 219–222.
Osweiler GD. In: Toxicology. The National Veterinary Medical Series. Williams and Wilkins, Philadelphia, 1996.
PART 3
Cat with signs of heart disease
9. The cat with abnormal heart sounds

and/or an enlarged heart
Luis A H Braz-Ruivo and Kathy A Arrington
KEY SIGNS
● Heart murmur.
● Gallop rhythm.
● Muffled, displaced or absent heart sounds.
MECHANISM?
● Murmurs are abnormal heart sounds caused by turbulent blood flow due to valvular stenosis or
insufficiency.
● Innocent or functional murmurs may be present in the absence of morphologic heart disease.
● Gallop rhythms are caused by extra heart sounds and are due to abnormalities in myocardial
relaxation.
● Displaced, absent, or muffled heart sounds are caused by intrathoracic masses, effusions or
structural changes.
● Cardiac enlargement is the result of alterations of blood flow causing volume overload,
myocardial hypertrophy or due to primary myopathic processes.
WHERE?
● Heart.
● Mediastinum.
124
9 – THE CAT WITH ABNORMAL HEART SOUNDS AND/OR AN ENLARGED HEART 125
● Diaphragm.
● Thoracic skeleton.
WHAT?
● Most cats with heart murmurs are not symptomatic for heart disease.
● The most common form of acquired heart disease in cats is hypertrophic cardiomyopathy.
● Some cats with cardiac enlargement have normal physical exam findings.

Diseases causing abnormal heart sounds and/or an enlarged heart
DEGENERATIVE
● Valvular endocardiosis (p 155)
A murmur localized to the left sternal apex is heard. It is a rare disease of old cats. Some cats may
present with congestive heart failure.
ANOMALY
● Ventricular septal defect* (p 140)
A congenital systolic murmur is heard which is loudest over the right sternal border. Most cats are
asymptomatic.
● Patent ductus arteriosus (p 142)
A congenital continuous murmur loudest over the left cranial thorax is heard. A palpable thrill is
usually present. It is more common in Siamese and Persian cats.
● Tetralogy of Fallot (p 149)
A systolic murmur is heard over the left cranial thorax (pulmonic area). A split second heart sound
may also be found. Cyanosis is usually present.
● Atrial septal defect (p 144)
A breed predilection in Persian cats is reported. A systolic murmur over the left cranial thorax is
heard.
● Mitral valve dysplasia/stenosis (p 145)
This is the most commonly encountered congenital valvular malformation and is associated with a
systolic and/or diastolic murmur over the left cardiac apex.
● Aortic stenosis (p 146)
Aortic stenosis is associated with a systolic murmur over the left aortic area. There is an increased
incidence in Siamese cats.
● Pulmonic stenosis (p 148)
Pulmonic stenosis is associated with a systolic murmur over the pulmonic area and is usually seen
with other defects.
● Tricuspid dysplasia
Tricuspid dysplasia is associated with a low-frequency systolic murmur over the right thorax.
continued
126 PART 3 CAT WITH SIGNS OF HEART DISEASE
continued
● Peritoneal–pericardial diaphragmatic hernia (p 153)

A murmur may or may not be heard. The cardiac silhouette is extremely enlarged on thoracic radi-
ographs. Many cats are asymptomatic, but some cats present for gastrointestinal signs or respira-
tory distress.
METABOLIC
● Hypertensive heart disease*** (p 133)
A systolic murmur, tachycardia and/or gallop rhythm may be heard. Hypertension in cats is most
commonly secondary to chronic renal failure or hyperthyroidism. Essential or idiopathic hyperten-
sion is less common.
● Hyperthyroid heart disease*** (p 131)
A systolic murmur, tachycardia and/or gallop rhythm may be heard. Hyperthyroid heart disease is
associated with other clinical signs of hyperthyroidism including weight loss, restlessness, palpa-
ble thyroid nodule, low frequency of gastrointestinal signs and is seen in older cats.
● High cardiac output state* (p 138)
A murmur, gallop rhythm or tachycardia may be heard on auscultation. It can be caused by ane-
mia secondary to other disease states or hyperthyroidism. The heart size may be variable
depending on the disease or the chronicity of the anemia.
NEOPLASTIC
● Neoplasia** (p 137)
Displaced or muffled heart sounds can be caused by neoplasia from a mass or effusion. Lymphoma
is the most common neoplasia seen in cats and occasionally infiltrates the myocardium.
INFECTIOUS
● Infectious
Infectious diseases can rarely cause secondary cardiomyopathies in cats. Most cats die unexpect-
edly and/or are systemically ill. Etiologies suspected are viral (feline infectious peritonitis), sec-
ondary bacterial or parasitic (toxoplasmosis). Bacterial (pyothorax, myocarditis, pericarditis) and
viral (myocarditis, pericarditis) infections can cause displaced or muffled heart sounds and/or
arrhythmias (p 157).
● Heartworm disease* (p 139)
Dirofilaria immitis (heartworm disease) in cats is less common than in dogs. Cardiac signs are
variable and may include signs of right heart failure, gallop rhythm or murmurs. Coughing, vomit-
ing or sudden death may also occur. Heartworm disease in cats is more common in male cats, out-
door cats, and occurrence depends on geographical location.
IDIOPATHIC
● Hypertrophic cardiomyopathy*** (p 128)
A systolic murmur varying in location, arrhythmia and/or gallop rhythm may be heard. It is the
most common form of heart disease in cats and occurs usually in male and middle-aged cats. It
can also be seen in young (less than 1 year of age) cats and older cats. It may be genetically trans-
mitted in some pure-breed cats. The heart may or may not be enlarged on radiographs.
● Restrictive and unclassified cardiomyopathies** (p 135)

A systolic heart murmur, gallop rhythm and/or arrhythmia may be heard. Abnormal heart sounds
are not always heard on auscultation. The heart is usually enlarged.
● Dilated cardiomyopathy (p 151)
A systolic murmur, gallop rhythm and/or arrhythmia may be heard. The heart shows generalized
enlargement. Dilated cardiomyopathy can occur in cats eating taurine-deficient diets.
● Chylous effusion* (p 139)
Displaced or muffled heart sounds may be heard. Etiologies are trauma, infection, cardiomyopathy,
neoplasia and idiopathic. In most cases, the cause is idiopathic.
TRAUMATIC
● Diaphragmatic hernia (p 154)
Displaced and/or muffled heart sounds may be heard. Dyspnea may or may not occur.
(neoplasia) and/or effusions (cardiomyopathy, neoplasia

INTRODUCTION or infection) or rarely structural changes (hernias or pec-
tus excavatum).
MECHANISM? Cardiac enlargement most commonly results from
Abnormal heart sounds are defined as follows: cardiomyopathy secondary to hypertrophy.
Systolic murmurs are common and are caused by tur-

bulent blood flow secondary to a valvular stenosis or WHERE?
insufficiency. Systolic murmurs are the most common
Abnormal heart sounds and/or cardiac enlargement
and account for >95% of murmurs.
result from problems in any of the following sites:
Diastolic and continuous murmurs are rare.
Heart, mediastinum, diaphragm, thoracic skeleton, lungs.
Continuous murmurs occur during diastole and sys-
tole and most commonly occur from a patent ductus
WHAT?
arteriosus.
The most common cause of cardiac disease is hyper-
In thin cats, murmurs may be caused by mechanical
trophic cardiomyopathy. It is usually acquired and
compression of the chest during auscultation.
idiopathic.
Gallop rhythms are extra heart sounds due to abnor-
Congenital heart disease is rare and a murmur is usu-
malities in relaxation. The gallop rhythm is classified as
ally heard at a young age.
either S4 or S3 but it is difficult to distinguish between
these in cats. The most common congenital defect in cats is ventral
septal defect followed by mitral valve dysplasia.
Arrhythmias are disturbances in rate and rhythm and
are noted by an irregular rhythm. Most cats with heart murmurs are asymptomatic.
Tachycardia is defined as a heart rate greater than 220 Abnormal heart sounds in asymptomatic cats
bpm. always warrants a cardiovascular work-up.
Loud heart sounds are usually normal in thin cats and Cats with abnormal heart sounds may or may not
during tachycardia. have cardiac enlargement.
Displaced heart sounds and muffled heart sounds are Lack of cardiac enlargement on radiographs in cats with
most commonly caused by masses within the thorax abnormal heart sounds does not exclude heart disease.
Diagnosis is based on history, physical examination, trodorsal view or dorsoventral view, the maximum
radiography, electrocardiography and echocardiography. width of the normal heart occupies up to 50% of the
width of the chest cavity at the same level.
Normal echocardiographic values for the interven-
tricular septum and left ventricular posterior wall
in diastole are up to 5 mm in thickness. The dimension DISEASES CAUSING ABNORMAL
between 5–6 mm represents questionable hypertrophy. HEART SOUNDS AND/OR AN
ENLARGED HEART
Normal echocardiographic values of the left atrium are
up to 13 mm or a left atrium to aorta ratio less than 1.5.
HYPERTROPHIC CARDIOMYOPATHY***
Normal left ventricular dimension in diastole is up
to 17 mm. Increased dimensions are consistent with Classical signs
left ventricular eccentric hypertrophy (dilation).
● Heart murmur (in some cases it may not be
Fractional shortening (percent change between the present).
left ventricular diastolic and systolic dimensions) ● Gallop rhythm.
ranges from 35–55%. ● Arrhythmia.
The above values can be obtained from the two- ● Dyspnea.
dimensional image or the M mode. ● Collapse.
● Lameness, paralysis or paresis from
Cardiomegaly on radiographs is an indicator of heart systemic thromboembolism.
disease although a normal-size heart does not rule
out heart disease. Cardiac enlargement on radiographs
Pathogenesis
can be determined by conventional methods or the ver-
tebral heart scale. Hypertrophic cardiomyopathy is defined as the pres-
ence of left ventricular hypertrophy in the absence of
The vertebral heart scale (VHS) compares cardiac
systemic disease causing secondary hypertrophy.
dimensions to the length of the thoracic vertebrae,
Hypertrophy may be generalized or focal.
which is an indicator of body size.
Focal hypertrophy may be recognized in the interven-
The VHS method is as follows: The long axis and short
tricular septum, left ventricular free wall or papillary
axis dimensions of the heart are transposed onto the
muscles.
vertebral column and recorded as the corresponding
number of vertebrae as measured caudally from the cra- Any combination of hypertrophic changes is possible.
nial edge of T4. These values are added to obtain the
Hypertrophic cardiomyopathy (HCM) is recognized to
vertebral heart size (VHS).
be genetically determined in selected families of cats:
The depth of the thorax is measured from the dorso- Persian, Maine Coon, American Shorthair and possibly
caudal border of the seventh sternebra to the closest in Ragdolls. Transmission is suspected to be autoso-
edge of the vertebral column. mal dominant.
Normal cats’ VHS are: mean VHS in lateral radi- The cause for hypertrophy is probably related to
ographs, 7.5 v (upper limit 8.0 v), mean cardiac short genetic alteration of the β-myosin heavy chain.
axis in lateral radiographs, 3.2 v (upper limit 3.5; mean
An association with increased levels of growth hor-
cardiac short axis in VD or DV radiographs, 3.4 v
mone concentration has also been found.
(upper limit 4 v); The cardiac long axis in the lateral
view approximates the length of three sternebrae, Echocardiographically there are two distinct varieties,
measured from S2 to S4. a non-obstructive form and an obstructive form.
Conventional methods of evaluating heart size in cats The non-obstructive form results primarily in dias-
are on the lateral view with the normal heart width tolic dysfunction due to delayed or decreased myocar-
approximately 2–2.5 intercostal spaces. On the ven- dial relaxation.
The obstructive form is caused by anterior motion of Most cats with aortic saddle thrombosis present for
the mitral valve during systole, which obstructs the acute onset of hindlimb paralysis, hypothermia, pain,
left ventricular outflow tract. This results in decreased absent femoral pulses, cool extremities and cyanosis of
cardiac output at faster heart rates, in addition to the nail bed. In some cases a history of episodic lame-
abnormal diastolic function. ness is given.
The outflow obstruction may contribute to the presence
of ventricular concentric hypertrophy. Diagnosis
Histologically there is myocardial fiber disarray Clinically, cats with hypertrophic cardiomyopathy
and diffuse myocardial fibrosis. HCM is usually lim- present with a history of a heart murmur, arrhythmia,
ited to the left ventricle but in some cases, concur- collapse or respiratory distress. Radiographic and elec-
rent right ventricular hypertrophy is present. trocardiographic findings may support the diagnosis,
but echocardiography is required for a definitive diag-
The development of left ventricular hypertrophy is
nosis.
associated with altered intracellular calcium regulatory
mechanisms. This results in the development of relax-
ation abnormalities during diastole.
The cardiac image varies from normal to obvious left
The chronic diastolic dysfunction ultimately results in ventricular and atrial enlargement.
left atrial dilatation, elevation of left atrial pressures
and finally congestive heart failure. Enlargement of the pulmonary veins may be seen, rep-
resenting venous congestion.
Clinical signs Areas of focal alveolar densities representing pul-

monary edema may be found. In some cases, pleural
Hypertrophic cardiomyopathy most commonly occurs effusion may be present.
in middle-aged male cats.
A heart murmur is usually present, but in some cases Electrocardiographic findings
may not be present. When present, the murmur is sys- Tachycardia (HR > 220 bpm), left anterior fascicular
tolic and varies in location and intensity. block (evidenced as left axis deviation with a mean
electrical axis (MEA) from 0 to –60 degrees, a QRS
A gallop rhythm is commonly heard. It is identified
in lead I and aVL with a QR pattern, and large
when more than two heart sounds are present on auscul-
S waves in leads II, III, aVF), tall R waves on lead II
tation. The extra sound is classified as S3 or S4.
(>0.9 mV), and notched QRS in any lead may be seen.
The fast heart rate in cats makes it often impossible to
Ventricular arrhythmias are more common than
distinguish between a S3 and S4 sound.
supraventricular arrhythmias.
Arrhythmias are occasionally heard as premature
Atrial fibrillation is rare but if present is always asso-
heart beats with pulse deficits. Ventricular arrhythmias
ciated with extreme dilatation of the left and/or right
are most common.
atria.
Dyspnea is seen in symptomatic cases together with
an increased respiratory rate (greater than 30 Echocardiographic findings
breaths/min) at rest or with open-mouth breathing in Left ventricular hypertrophy (diastolic dimension of
extreme cases. the interventricular septum and/or LV posterior wall
greater than 6 mm), which may be global or focal (see
Collapse may result from impaired cardiac output
Pathogenesis), and left atrial enlargement (dimension
associated with either ventricular tachycardia or the
greater than 13 mm) can be seen.
obstructive form of hypertrophic cardiomyopathy.
● Elongated mitral valve leaflets with systolic ante-
Sudden onset of lameness, paralysis or paresis may rior motion (anterior displacement into the left ven-
occur and is usually the result of systemic thromboem- tricular outflow of the anterior mitral valve leaflet)
bolism. causing secondary left ventricular outflow obstruc-
tion as determined by Doppler study (velocity of Treatment of the asymptomatic cat.

blood flow >2.0 m/s) is seen in the obstructive ● Hypertrophic non-obstructive cardiomyopathy
form. (HCM) – Wall dimensions larger than 6 mm and
normal Doppler LV outflow study (LVOTmax less
than 1.8 m/s).
– Normal left atrial size – no therapy.
Congenital heart disease – Increased left atrial size (>13 mm or LA/Ao >
● A murmur is usually present from birth. Most con- 1.5).
genital murmurs do not change in loudness with – Beta-blocker
alterations of the heart rate. Congenital murmurs Atenolol 12.5 mg/cat PO q 12–24 h.
are usually relatively loud. OR
– Calcium channel blockers:
Dilated cardiomyopathy.
Diltiazem 7.5–15 mg PO q 8 h OR
● Murmurs are usually very soft, and in many cases may
Diltiazem slow release − 60 mg PO daily.
not be present. A gallop rhythm is usually present.
● Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy. (HOCM) with presence of systolic anterior motion
● It is difficult to differentiate from hypertrophic car- of the mitral valve and LV outflow obstruction
diomyopathy on auscultation; many cases have a (LVOTmax <3.5 m/s).
gallop rhythm. – Normal left atrial size – no therapy.
– Increased left atrial size – beta-blocker as
Intra-thoracic masses.
above.
● A murmur may not be present unless there is com-
● Hypertrophic obstructive cardiomyopathy (pres-
pression of the heart by the mass or concurrent unre-
ence of systolic anterior motion of the mitral valve
lated heart disease. Most commonly, dyspnea and
and LV outflow obstruction -LVOTmax >3.5 m/s).
lethargy are seen.
– Normal or increased left atrial size – beta-
Feline asthma or chronic bronchitis. blocker as above.
● Unless cardiac disease is also present, most cats do
Treatment of the symptomatic cat with congestive heart
not have a murmur. Cough and increased respiratory
failure (acute management).
rate are common. Symptoms in the cat with feline
Criteria to start therapy:
asthma may be episodic and seasonal.
● Respiratory distress (open-mouth breathing or very
Chylous effusion. abnormal respiratory pattern).
● A murmur may not be present. In most cases, car- ● Pulmonary congestion (moderate to severe) on
diac disease is not present. The most common clin- radiographs and/or pleural effusion.
ical signs are dyspnea, increased respiratory rate ● Hypothermia.
and lethargy. – Oxygen.
– Diuretics
Neurological disease causing collapse or hindlimb
– Furosemide 1–2 mg/kg IV or IM q 6–12 h until
paralysis
respiration rate and pattern are normalized.
Cardiac signs are usually absent, however a full cardiac – Furosemide constant rate infusion (if normal
work-up may be warranted to rule out the presence of renal values at presentation) 0.5–1 mg/kg/hr
silent heart disease. Neurological disease usually is not until congestion is resolved but not for longer
associated with alterations of peripheral systemic per- than 24 hours.
fusion. – Nitroglycerin ointment (2%) 1/4 of an inch
(6 mm) q 8 h until resolution of the congestion.
– Angiotensin-converting enzyme inhibitor.
Treatment
– Enalapril 0.25–0.5 mg/kg q 24 h OR
The treatment recommended depends on the severity of – Benazepril 0.25–0.5 mg/kg q 24 h.
signs and the presence of left ventricular outflow tract – Thoracocentesis if there is evidence of moderate
(LVOT) obstruction. to severe pleural effusion on radiographs.
– Aspirate from the right thorax to avoid punctur- [Meq/L]) should receive solutions with 20 mmol/L
ing the enlarged auricles. [Meq/L] added.
– Hypertrophic non-obstructive cardiomyopathy –
In cases of hypokalemia refer to standard guidelines of
use calcium channel blocker OR beta-blockers
therapy. Do not exceed rates of potassium 0.5 mmol/L
as above.
(Meq)/kg/h.
– Hypertrophic obstructive cardiomyopathy – use
beta-blockers as above. Chronic diuretic administration is not required in
some cases. Multiple diuretic therapy can be used for
Symptomatic cat with congestive heart failure (chronic
refractory cases but monitor renal function and hydra-
management).
tion carefully.
Criteria to start therapy:
● Maintenance therapy after initial therapy to control Renal function and electrolytes should be monitored
signs of acute onset of congestive heart failure. in all cats on diuretics and angiotensin-converting
● Any patient found to have early evidence of con- enzyme inhibitor therapy.
gestive heart failure (usually on radiographs) but
Some cats develop anorexia or poor appetite while
without symptoms, that will require acute interven-
taking Diltiazem slow-release preparations.
tion if untreated.
Hypertrophic non-obstructive cardiomyopathy – use Prognosis
calcium channel blocker or beta-blocker as above. Hypertrophic cardiomyopathy and hypertrophic
Hypertrophic obstructive cardiomyopathy – use beta- obstructive cardiomyopathy ultimately result in con-
blocker as above. gestive heart failure and/or aortic saddle thromboem-
bolism. Sudden death occurs in some cases, usually in
Diuretics: younger cats less than 3 years old.
● Furosemide 1–2 mg/kg IV or IM q 6–12 h until res-
piration rate and pattern are normalized. Median survival time for cats without congestive heart
● Furosemide constant rate infusion (if normal renal failure is 732 days (over 33% alive after 5 years).
values at presentation) 0.5–1 mg/kg/hr and conges- Median survival for cats with congestive heart failure is
tion is resolved but not for longer than 24 hours. 92 days.
● Hydrochlorothiazide 1–2 mg/kg PO q 12 h
OR/AND Median survival time for cats with thromboembolism is
● Spironolactone 2–4 mg/kg PO q 12 h. 61 days.
Heart rate less than 200 beats per minute at initial pres-
Angiotensin-converting enzyme inhibitor:
● Enalapril 0.25–0.5 mg/kg q 24 h OR
entation is associated with longer survival (1830 days vs
● Benazepril 0.25–0.5 mg/kg q 24 h.
152 days).
Diuretics should be used cautiously in cats. Overzealous

HYPERTHYROID HEART DISEASE***
therapy for 1–2 days may rapidly result in severe fluid and
electrolyte imbalances and metabolic alkalosis.
Classical signs
Judicious concurrent administration of low-sodium ● Weight loss.
solutions (NaCl concentration ≤ 0.45%) with potassium ● Polyphagia.
supplementation may be required in some cases that are ● Heart murmur.
clinically dehydrated after diuretic therapy. ● Tachycardia.
The volume of fluid administered varies with the
degree of dehydration present, but in severe cases rates See main reference page 304 (The Cat With Weight
up to twice maintenance can be infused. While infusing Loss and a Good Appetite).
fluids in a cardiac patient, special attention to respira-
tory function is recommended. Clinical signs
Potassium supplementation should be based on serum Cats are usually older than 8 years of age (mean age is
levels. Patients with normal potassium (3.5–5.5 mmol/L 13 years old) with no breed or sex predilection.
Typically there is progressive weight loss with a good Electrocardiographic findings

appetite. Sinus tachycardia (Heart rate > 220 bpm) is common.
A heart murmur is heard in some cases, and a gallop Increased R wave amplitude (>0.9 mV), supraventricu-
rhythm may be noticed. lar premature beats and ventricular arrhythmias are
commonly found.
Tachycardia is persistent even at rest. Many cats
have heart rates above 240 bpm. Echocardiographic findings
Arrhythmias are present in more advanced cases. Heart chambers may be of normal size but in many
cases, some degree of ventricular concentric hyper-
A hyperkinetic peripheral pulse, usually the femoral trophy is present. Interventricular septum and LV free
pulse, is very easy to palpate. wall measurements in diastole are greater than 6 mm.
Loud heart sounds and a strong precordial impulse are The “typical” hyperthyroid heart shows mild to moder-
typically present, which is the result of increased ate increase in wall thickness (see above), upper range
sympathetic tone and decreased fat deposits over of normal ventricular chamber size (LV diastolic
the chest. dimension 16–17 mm) and increased contractility
Increased respiratory rate or panting is particularly (fractional shortening higher than 55%) reflecting
seen in cats in a crisis (thyroid storm). This may be hyperdynamic cardiac function.
mistaken for respiratory distress when it is only hyper- Variable degrees of left atrial dilation are present.
ventilation.
In some cases (usually advanced cases), a dilated
Respiratory distress may occur secondary to heart form of cardiomyopathy may be seen. It is difficult
failure when pulmonary edema and/or pleural effusion to differentiate from restrictive or dilated cardiomy-
are present. opathy.
Cats are often difficult to handle and owners report a
change in behavior (irritability and restlessness). Systemic blood pressure
Polyuria, polydipsia and vomiting are seen in approxi- Hypertension is commonly found. Systolic arterial
mately 50% of the cases. blood pressure, measured by Doppler technique, con-
Palpable thyroid nodules are common. sistently above 180 mmHg is diagnostic.
Diagnosis Treatment
An increased serum total thyroxine (T4) is usually Antithyroid drugs (Methimazole, Carbimazole),
diagnostic. The upper range of normal is 51 nmol/L radioactive iodine and thyroidectomy are treatment
(4.0 μg/dl). choices for hyperthyroidism (for further details refer to
page 305).
A single random serum T4 level is usually diagnostic.
Tachycardia and hypertension should be treated with
If a random serum T4 level does not confirm the disease beta-blocking drugs. This class of drugs controls the
in a highly suspected case, repeat serum T4 or free T4 in cardiovascular effects of hyperthyroidism and improves
1–2 weeks or perform a T3 suppression test. clinical signs.
Radiographic findings Beta-blockers do not decrease serum thyroid hor-

mones. Beta-blockade therapy is discontinued upon
Heart size varies from normal to severe dilation of all
normalization of serum thyroid hormones and resolu-
chambers.
tion of cardiovascular signs.
Pleural effusion and/or pulmonary edema may be pres- ● Propranolol 0.5–1.0 mg/kg PO q 8 h OR
ent in severe cases. ● Atenolol 12.5 mg/cat PO q 12 h.
If congestive heart failure is present refer to the sec- ● The vascular beds most sensitive to chronic
tion on hypertrophic cardiomyopathy for therapeutic hypertension are the ocular, renal, cerebrovascular
options (page 128). and cardiac vessels.
HYPERTENSIVE HEART DISEASE*** Clinical signs
Classical signs Signs directly related to the systemic hypertension are

not common.
● Heart murmur.
● Gallop rhythm. Ocular changes (retinal hemorrhages, hyphema,
● Tachycardia. arterial tortuosity and retinal detachments) are the
● Blindness due to retinal hemorrhage or most common clinical signs seen in hypertensive cats.
● Most cats initially present for blindness secondary
detachment.
● Hyphema. to retinal detachment and hemorrhages.
● Retinal examinations should be done in all cats
diagnosed with systemic hypertension.
Pathogenesis ● Retinal examination is a good way to evaluate the organ
Hypertension is defined as systemic arterial pressure damage resulting from systemic hypertension.
higher than 180/100 mmHg (systolic/ diastolic). Weight loss, polyuria and polydipsia seen in hyper-
Hypertension is most commonly secondary to an tensive cats are secondary to the underlying disease
underlying etiology. (CRF or hyperthyroidism) and are not directly referable
● The two most common causes in cats are hyper- to the hypertension.
thyroidism and chronic renal failure (CRF). Seizures and syncope are rare neurological abnormal-
● The mechanism for development of hypertension
ities seen in hyertensive cats.
in hyperthyroidism is the increased number and ● They are the results of cerebrovascular accidents
sensitivity of adrenergic receptors coupled with from the hypertension.
an increase in cardiac output.
● The mechanism for development of hypertension in
CRF is renal hypertension with retention of salt and Diagnosis
activation of the renin-angiotensin aldosterone system.
Retinal vascular changes with evidence of retinal
● The hypertension of hyperthyroidism is
hemorrhage and detached retinas are commonly seen
reversible upon control of the thyroid state while
in hypertensive cats on ocular examination.
the hypertension secondary to CRF requires con-
● Indirect and direct ophthalmoscopy should be done
tinued therapy and monitoring.
on all hypertensive cats.
● There is no correlation between the degree of
● Cats are often presented blind with dilated non-
renal disease and the severity of hypertension.
responsive pupils. Aged cats with a sudden
● Essential hypertension is an exclusion diagnosis
onset of blindness should be evaluated for hyper-
when diagnostic tests failed to identify a specific
tension.
cause.
● Common findings are retinal hemorrhages,
Chronic untreated hypertension has several long- hyphema, retinal edema and partial or complete
term adverse effects. retinal detachments.
The increase in systemic vascular resistance results in Elevated systemic arterial pressure (higher than 180
increased afterload and development of left mmHg systolic pressure) is seen.
ventricular hypertrophy.
Hyperthyroidism or chronic renal disease are com-
Chronic elevation of arterial pressure results in mon underlying etiologies.
dysregulation of endothelial homeostasis leading ● Hyperthyroidism is diagnosed with an increased
to hypertensive vasculopathy. total thyroxine greater than 51 mmol/L (4 μg/dl) and
consistent clinical signs (weight loss, ravenous ● Cats with cardiomyopathy usually do not have
appetite, palpable thyroid nodules, polyuria, poly- weight loss but may show dyspnea secondary to
dipsia). congestive heart failure.
● Chronic renal disease is diagnosed with an increased
Cats with coagulopathy, optic neuritis, systemic
urea of greater than 11.6 mmol/L (32.5 mg/dl),
infectious disease and neoplasia may have similar
increased creatinine greater than 163 μmol/L (1.84
ocular signs (retinal hemorrhages, hyphema and
mg/dl) with a decreased urine specific gravity less
detached retinas) as hypertensive cats.
than 1.035.
Documentation of hypertension is needed to help dif-
ferentiate these diseases from hypertensive cats.
Radiographic findings Cerebrovascular accidents in cats with hypertension are
Heart size varies from normal to marked generalized rare.
cardiomegaly. Cats with cerebrovascular accidents are usually sec-
Enlarged aortic arch is seen in chronic cases. ondary to an underlying neurological disease.
Undulation of the caudal aorta is suggestive of hyper-

tension. Treatment
Beta-blockers – refer to page 306 on hyperthyroidism.
Electrocardiographic findings
Amlodipine is the drug of choice if the etiology is
Tachycardia with a heart rate greater than 220 bpm is CRF or unknown. The dose is 0.625 mg (cat < 5 kg)
usually present with hyperthyroidism. to 1.25 mg (cat ≥ 5 kg) orally once a day for hyper-
Electrocardiogram is usually normal but evidence of tension caused by diseases other than hyperthy-
left ventricular hypertrophy (R wave > 9 mm on lead II) roidism.
may be seen. ACE inhibitors (Enalapril or Benazepril) can be used
as adjuvant therapy.
Echocardiographic findings
● ACE inhibitors can be used carefully in cases with
Mild to moderate left ventricular hypertrophy may concurrent chronic renal failure. Close follow-up of
be seen. Left atrial size is usually normal. renal function is mandatory.
Transmitral inflow velocity Doppler profile may show ● If serum creatinine is higher than 265 μmol/L (3.0
evidence of impaired relaxation (small E and tall A mg/dl) at baseline, ACE inhibitors should not be used.
wave). ● Start at 0.25–0.5 mg/kg once a day for Benazepril
OR Enalapril.
Enlarged aortic arch equal or greater than 11 mm is ● Obtain baseline renal values and recheck at 5 and
seen in chronic cases. 10 days after starting medications.
For findings in hyperthyroidism see page 132 In refractory cases, multiple drug therapy may be required
(Hyperthyroid heart disease). (amlodipine, beta-blockers, diuretics, ACE inhibitors).
Low-salt diets may be used in refractory cases.
The goal of therapy is to decrease systolic blood pres-
Cats with either hypertension or cardiomyopathy com- sure to 140–160 mmHg.
monly have murmurs. ● Drugs should be titrated to effect.
● However, cats with hypertension most commonly
present with ocular signs.
● Most hypertensive cats have polyuria, polydipsia or
Prognosis
weight loss consistent with chronic renal disease or Hypertension caused by hyperthyroidism is usually
hyperthyroidism. reversible with normalization of the serum thyroid levels.
Hypertension caused by other diseases requires Abnormal chamber compliance results in inadequate
long-term life-long management. ventricular filling. The non-compliant ventricle rapidly
reaches end-diastolic filling pressure typically during
the first half of the diastolic phase.
RESTRICTIVE AND UNCLASSIFIED
Chronic diastolic dysfunction leads to the progressive
CARDIOMYOPATHIES**
development of increased left atrial size and second-
ary increase in left atrial pressures resulting in pul-
Classical signs
monary venous congestion, pulmonary edema and in
● Heart murmur (in some cases may not be advanced cases pulmonary artery hypertension.
present).
Chronic pulmonary artery hypertension will result in
● Gallop rhythm.
right-sided congestive heart failure.
● Arrhythmia.
● Dyspnea. Classification of these forms of cardiomyopathies is
● Hypothermia. poorly defined.
● Collapse.
Clinically it is difficult to distinguish between restric-
tive and unclassified forms of cardiomyopathy.
systemic thromboembolism.
Clinical signs
Pathogenesis There is no age or sex predilection.
Endocardial, subendocardial and myocardial fibro- Burmese cats seem to have a higher incidence of
sis are the primary pathologic characteristics of restrictive cardiomyopathy.
restrictive cardiomyopathy. Myocardial fibrosis is also
Heart murmur is often present but in some cases may
present in intermediate/unclassified cardiomyopathy.
not be present. When present, a systolic murmur
Geometrically the left ventricle may be normal or mis-
varies in location and intensity with variations in heart
shapen.
rate.
Histopathologically, myocardial infarction is reported
Gallop rhythm is commonly heard. It is identified when
to be a feature of intermediate/ unclassified car-
more than two heart sounds are present on auscultation.
diomyopathy, but it can also be seen in cases with
restrictive cardiomyopathy. Arrhythmias are frequently heard as premature heart
beats with pulse deficits. Ventricular arrhythmias are
Adhesions of papillary muscle and chordae tendinae
most common.
may interfere with normal ventricular blood flow during
systole, causing mid-ventricular obstruction. Mono- Dyspnea is seen in symptomatic cats with an increased
nuclear infiltration of the myocardium suggests an respiratory rate (greater than 30 breaths/min) at rest or
inflammatory process, resulting in endomyocarditis. with open-mouth breathing in extreme cases.
Left atrial (echocardiographic dimension > 13 mm), In symptomatic cats, hypothermia is common.
biatrial and right ventricular enlargement (maximal
Collapse may result from impaired cardiac output (ven-
internal diameter > 7 mm) are often found. Intracardiac
tricular tachycardia).
thrombi are frequently observed. Infiltrative myocar-
dial disease may be present. Lameness, paralysis or paresis is usually the result of
systemic thromboembolism. Aortic saddle thrombosis
Hemodynamically this disease is characterized by
resulting in hindlimb paralysis may be seen. In some
pure diastolic dysfunction due to abnormally low
cases, embolism may only cause lameness.
compliance of the ventricular chambers. Systolic
function is usually preserved or just slightly Most cats with aortic saddle thrombosis present for
decreased. acute onset of hindlimb paralysis, pain, absent femoral
pulses, cool extremities and cyanosis of the nail bed. In ity (E wave > 1.1 m/s) and normal or decreased atrial
some cases a history of episodic lameness is given. flow component.
Thrombi (homogeneous mass) in the left atrium and/or
Diagnosis ventricle may be found.
Usually a history of heart murmur, arrhythmia, col-
lapse or respiratory distress is present. Some cats
Differential diagnoses
may not have an audible murmur but a gallop rhythm is Congenital heart disease.
commonly heard. ● A murmur is usually present from birth. Most con-
genital murmurs do not change in loudness with
Diagnosis is based on supportive radiographic, electro-
alterations of the heart rate. Congenital murmurs
cardiographic and especially echocardiographic findings.
are usually relatively loud.
Radiographic findings Dilated cardiomyopathy.
Severe left atrial or biatrial enlargement. ● Murmurs are usually very soft, and in many cases may
Enlarged pulmonary veins can be seen. not be present. A gallop rhythm is usually present.
Pulmonary edema with or without pleural effusion Hypertrophic cardiomyopathy.

● It is difficult to differentiate on auscultation from
may be present.
restrictive or intermediate/unclassified cardiomy-
Electrocardiographic findings opathy. A gallop rhythm may be more common in
Ventricular arrhythmias are more common than with restrictive or intermediate/unclassified cardiomy-
other types of feline myocardial disease. opathies.
Atrial fibrillation is more common than with HCM; Intrathoracic masses.

and if present is usually associated with extreme ● A murmur may not be present unless there is com-
dilatation of the left and/or right atria. pression of the heart by the mass or concurrent
unrelated heart disease. Most commonly, dyspnea
Tachycardia (heart rate above 220), ventricular conduc- and lethargy are seen.
tion disturbances (notched QRS), tall R waves on lead
II (>0.9 mV) may be seen. Feline asthma or chronic bronchitis.
● Unless cardiac disease is also present, most cats do
Echocardiographic findings not have a murmur. Cough and increased respira-
Severe left atrial or biatrial enlargement is com- tory rate are common. Symptoms may be seasonal.
monly found. Left atrial to aortic ratio is usually >2.0.
Chylous effusion.
Left ventricular size may be normal to mildly dilated (LV ● A murmur may not be present. In most cases, car-
end-diastolic dimension up to or above 16 mm). diac disease is not present. The most common
clinical sign is dyspnea, increased respiratory rate
Systolic function is normal or mildly decreased (nor-
and lethargy.
mal FS is between 35–55%)
Right ventricular dilatation may be seen (RV end- Neurological disease causing collapse or hindlimb
diastolic dimension > 7 mm) paralysis.
● Cardiac signs are usually absent, however a full car-
Hyperechoic endocardium and/or myocardium are diac work-up may be warranted to rule out the pres-
frequently observed. ence of silent heart disease. Neurological disease
Focal areas of myocardial hypertrophy bordering usually is not associated with alterations of periph-
areas of myocardial thinning are seen which probably eral systemic perfusion.
represent myocardial infarction.
Treatment
The mitral inflow profile is recorded at the tips of the
mitral valve from the four-chamber left parasternal Asymptomatic cat.
view. It commonly shows increased early inflow veloc- ● Angiotensin-converting enzyme inhibitors
– Enalapril 0.5 mg/kg PO q 24 h OR ● Anti-thrombotic therapy:

– Benazepril 0.5 mg/kg PO q 24 h. – Heparin and Warfarin therapy are controver-
sial and should be utilized under the guidance of
Symptomatic cat with congestive heart failure (acute
an experienced clinician.
management). Criteria to start therapy:
– Low-molecular-weight heparins have been
● Respiratory distress (open-mouth breathing or very
recently suggested. This class of heparins does
abnormal respiratory pattern).
not require continued monitoring of coagulation
● Pulmonary congestion (moderate to severe) on radi-
parameters.
ographs and/or pleural effusion.
– Enoxaparin (Lovenox ®) 1 mg/kg SQ q 24 h.
● Hypothermia.
– Aspirin 80 mg PO q 48–72 h is recommended by
● Oxygen.
some clinicians but its efficacy has not been estab-
● Diuretics.*
lished. A lower dose (5 mg/cat PO q 24 h) has
– Furosemide 1–2 mg/kg IV or IM q 8–12 h until
also been recommended, because of concerns of
respiratory rate and pattern are normalized.
that prostacyclin production is inhibited at the
– Furosemide constant rate infusion (if normal renal
higher dose.
values at presentation) 0.5–1 mg/kg/hr until con-
Thrombolytic therapy is contraindicated if an intracar-
gestion is resolved but not for longer than 24 hours.
diac thrombus is present, and controversial in aortic
● Venodilator.
saddle thrombus (see page 916, The Weak and Ataxic
– Nitroglycerin ointment (2%) 1/4 of an inch
or Paralyzed Cat).
(6 mm) q 8 h.
● Thoracocentesis (right thorax to avoid puncturing
of the enlarged auricles) if there is evidence of mod- Prognosis
erate to severe pleural effusion on radiographs.
● Angiotensin-converting enzyme inhibitor. Almost all cats after development of congestive heart
– Enalapril 0.25–0.5 mg/kg PO q 24 h OR failure have a poor prognosis.
– Benazepril 0.25–0.5 mg/kg PO q 24 h. It is unknown if early therapy of asymptomatic cats
Symptomatic cat with congestive heart failure (chronic results in delay of onset of clinical signs.
management). Criteria to start therapy:
● Maintenance therapy after initial therapy to control NEOPLASIA**
signs of acute congestive heart failure.
● Any patient found to have early evidence of con- Classical signs
gestive heart failure (usually on radiographs) but
● Anorexia.
without symptoms, that will require acute inter-
● Weight loss.
vention if untreated.
● Diuretics*
– Furosemide 0.5–1.0 mg/kg PO q 12–24 h OR
Clinical signs
– Hydrochlorothiazide 1–2 mg/kg PO q 12 h
OR/AND Cats commonly present with anorexia and secondary
– Spironolactone 2–4 mg/kg PO q 12 h. weight loss.
● Angiotensin-converting enzyme inhibitor
A cranial mediastinal mass may cause a non-compli-
– Enalapril 0.25–0.5 mg/kg PO q 24 h OR
ant chest wall during compressive palpation.
– Benazepril 0.25–0.5 mg/kg PO q 24 h.
● Arrhythmia control The presence of intrathoracic or pericardial masses may
– Sotalol 15–30 mg/cat PO q 8 h OR cause effusions which will result in muffled heart
– Propranolol 0.5–1.0 mg/kg PO q 8 h OR sounds or displaced lung and/or heart sounds.
– Atenolol 12.5 mg/cat PO q 12–24 h OR
If a mass compresses the heart, a new murmur can result.
– Diltiazem 15 mg/cat PO q 8 h.
● Associated intracardiac thrombus or systemic Some cats with pericardial effusion secondary to neo-
thromboembolism. plasia present for the evaluation of ascites.
Diagnosis For hyperthyroid heart disease refer to page 131.
Clinical signs
Soft tissue density seen within the cranial mediastinum.
A systolic blowing murmur louder at the heart base is
Elevated trachea. usually present.
Pleural effusion. A gallop rhythm may be present.
Electrocardiographic findings Sinus tachycardia is usually present, with heart rates
Normal. above 220 bpm.
Displaced and/or muffled heart sounds are heard sec-
Echocardiographic findings ondary to intrathoracic masses displacing the heart. In
Normal cardiac function unless concurrent heart dis- some cases, this finding may be due to the presence of
ease is present. pleural effusion.
A cardiac mass may be seen (rare). Other systemic signs:
● Pale mucus membranes, prolonged capillary refill
Ultrasound of the cranial mediastinum may reveal a
mass. time, petechiae, anorexia, ravenous appetite, weight
loss and palpable thyroid glands bilaterally.
Pleural effusion may be seen.
Diagnosis
HIGH CARDIAC OUTPUT HEART DISEASE* Anemia is present if the hematocrit is less than 0.24
L/L (PCV = 24%).
Classical signs Secondary cardiac changes are not usually present
● Heart murmur. unless a chronic anemia with a hematocrit less than
● Gallop rhythm. 0.15 L/L (PCV ≤ 15%) is present.
● Tachycardia. Hyperthyroidism is considered present if total thyrox-
ine is increased and there are consistent clinical signs.
Pathogenesis Refer to page 304 (The Cat With Weight Loss and a Good
Appetite).
High cardiac output heart disease in cats is secondary to
hyperthyroidism or chronic anemia. Radiographic findings
High cardiac output heart disease is uncommon. Heart size ranges from normal to severe enlargement.
Etiologies of chronic anemia are infectious (feline Pulmonary edema may be present in rare cases.
leukemia virus, feline immunodeficiency virus), neo- Electrocardiographic findings
plastic (lymphoma, thymoma), and metabolic diseases
Tachycardia (>220 bpm) and increased R wave ampli-
(chronic renal failure). Refer to page 526, (The Anemic
tude in lead II (>0.9 mV).
Cat) for a more detailed description of anemia.
In chronic anemia, increased cardiac output results Echocardiographic findings
from decreased blood viscosity and systemic arteriolar In anemia, a normal to moderate increase in left ventric-
tone augmenting stroke volume. ular dimension (LVIDd > 18 mm) with hyperkinetic (FS
> 55%) cardiac function is found. Left atrial size is usu-
Anemia causes high cardiac output, which increases
ally normal to mildly increased.
cardiac work and results in congestive heart failure
when a co-existing cardiac disease or a hyperkinetic In rare cases, findings similar to dilated cardiomyopa-
state is present. thy are present.
In chronic anemia, the heart rate may be normal or only Refer to page 132 for echocardiographic findings in
mildly increased. hyperthyroidism.
Differential diagnosis Cats with symptoms may show open-mouth breathing

and/or cyanosis after mild to moderate exercise.
Cardiomyopathy.
Hyperthyroidism. Diagnosis
Treatment Thoracocentesis findings

Aspiration of the chest fluid commonly yields a milky
Treatment should be directed towards the underlying
white fluid (can be slightly pink). This fluid may feel
disease.
greasy.
Refer to page 305 (The Cat With Weight Loss and a Determination of fluid triglyceride level with a paired
Good Appetite) for hyperthyroidism and page 526 (The serum triglyceride sample (obtained at the same time)
Anemic Cat) for anemia. always reveals a higher triglyceride level in the chest
If congestive heart failure is present, with concurrent fluid.
myocardial failure refer to section on dilated cardiomy- Cytological evaluation usually reveals a homogeneous
opathy, page 151. population of mature lymphocytes and neutrophils.
If congestive heart failure is present without myocar- Bacterial culture is negative.
dial failure refer to section on hypertrophic cardiomy-
opathy, page 128. Radiographic findings
Marked pleural effusion.
Prognosis
Elevated trachea.
Varies depending on disease process.
Obscured cardiac silhouette.
CHYLOUS EFFUSION* Collapsed lung lobes.
Classical signs
Normal.
● Dyspnea/tachypnea.
Abnormalities may be seen if there is concurrent heart
● Anorexia.
disease.
● Lethargy.
See main reference page 77 (The Cat With Hydrothorax). Many cats have a normal echocardiogram.
Clinical signs In some cases, chylous effusion may be secondary to
severe heart disease of any etiology.
Chylous effusion in cats is often of unknown cause.
The most common causes are right heart failure from
cardiomyopathy or heartworm or mediastinal neoplasia HEARTWORM DISEASE*
associated with lymphoma or thymoma. Chylothorax
may occur secondary to a thrombus associated with an Classical signs
indwelling jugular catheter.
● Respiratory distress.
Dyspnea and tachypnea are common presenting clini- ● Coughing.
cal signs. Commonly an abdominal respiratory compo- ● Vomiting.
nent is seen. ● Sudden death.
The presence of chest fluid results in muffled
heart sounds and absent lung sounds in the ventral Clinical signs
thorax.
Many cats are asymptomatic.
Cats develop poor appetite when a large amount of
fluid is present (> ~150 ml). Sudden death is seen in some cases.
Vomiting, lethargy, anorexia and syncope are seen in Blood examination and serologic findings
symptomatic cases. Microfilaremia is rare in cats and transient (possibly
Respiratory signs such as cough or dyspnea are common. about 1 month). If present, the number of microfilaria
is small.
Respiratory signs may be quite similar to feline
chronic bronchitis or asthma. Serologic testing should include both an antibody and
antigen test.
Some cats can present for evaluation of pneumotho-
rax/chylothorax. A positive antibody test is consistent with exposure
with or without current infestation. It is a useful screen-
Occasionally aberrant larval migration results in neuro- ing test and cats with a positive test should be followed
logical signs such as seizures, collapse, blindness and up with antigen test.
vestibular signs.
A positive antigen test may be consistent with cur-
See main reference page 104 (The Coughing Cat). rent infestation. The sensitivity of the current antigen
tests is considerably less than the antibody test.
Diagnosis
Combining results from serum Ab and Ag tests
Radiographic findings achieves higher sensitivities than using serum Ab and
Ag test results alone.
Enlarged and tortuous caudal pulmonary arteries
are visible on both projections of the chest, but espe- Negative serologic findings do not absolutely rule out
cially the DV/VD views. heartworm infestation. If clinical signs are compatible,
repeat Ab and Ag testing by a different method, evalu-
Diffuse pulmonary infiltrates characterized by a
ate chest radiographs and consider echocardio-
mixed interstitial and peribronchial pattern.
graphic examination.
The ECG is generally not useful in diagnosis of feline Treatment
heartworm disease.
Adulticide treatment is not usually recommended in
Sinus tachycardia (HR > 220 bpm) cats because of severe side effects. Infestation is
Right heart enlargement in advanced cases. The MEA small (1–2 worms) and their lifespan is short (average
is usually beyond +180 degrees clockwise. 2 years).
Surgical removal of the worms through a jugular
Echocardiographic findings approach can be attempted in severe cases.
Main pulmonary artery may be normal or enlarged.
Medical treatment is mainly symptomatic.
Linear parallel densities may present in the main pul-
monary artery or the main branches.
VENTRICULAR SEPTAL DEFECT*
Dilatation of the right ventricle is seen in advanced
cases; RV internal dimension in diastole > 6 mm. Classical signs
Echocardiography has high specificity for the diagno- ● Systolic murmur loudest over the right
sis of feline heartworm disease, but sensitivity is highly sternal border.
dependent on the experience of the ultrasonographer.
Cardiac catheterization findings

Pathogenesis
Non-selective angiography may show:
● Linear filling defects within the pulmonary arterial tree. The shunting of blood depends on the size of the defect
● Dilated and tortuous pulmonary arteries. and the relative resistance of the systemic and pul-
● Dilated right ventricle. monary circulations.
● Normally, shunting occurs from the left to Diagnosis

the right, unless right heart pressures rise above
systemic pressures causing reversal of shunting of Congenital systolic ejection murmur is heard over
blood flow. the right sternal border in a young cat.
In most cases, the defect is present in the perimembra- VSD is the most common cause of a congenital mur-
nous area of the interventricular septum, immediately mur in the cat.
below the aortic valve annulus.
● The right ventricular location of the defect is Radiographic findings
commonly situated below the septal leaflet of the Pulmonary over-circulation demonstrated by a promi-
tricuspid valve, but can also be located in other nent and enlarged vasculature of the lungs.
areas of the perimembranous septum.
● Primary muscular defects of the septum are rare. Left atrium and ventricular dilation with variable degrees
of right ventricular enlargement can be seen.
With small defects, the amount of blood being
shunted is small and unlikely to create volume over-
load of the pulmonary circulation and the left heart. Echocardiographic findings
● However, with large defects different degrees of Most defects are not visualized except for large ones.
volume overload can be expected, depending on the Demonstration of shunting and direction of blood flow
shunt fraction. across the interventricular septum is possible using
● In some cases chronic volume overload may lead to
Doppler technique.
the development of left-sided congestive heart fail-
ure. Left atrial and ventricular dilation may be present.
● In rare instances, chronic volume overload of the
High-velocity flow across the pulmonic valve may be
pulmonary circulation may result in increased pul- found (relative stenosis due to high volume if large
monary vascular resistance with significant elevation shunting fraction is present). Usually maximal blood
of right ventricular systolic pressures that may flow velocity obtained with continuous flow Doppler is
result in reversal of the direction of shunting higher than 1.8 m/s.
(Eisenmenger’s syndrome).
● Large defects can result in abnormal morphology In severe cases, right ventricular dilation is observed.
of the aortic valve annulus leading to aortic valve If shunting from right to left, an injection of saline from
prolapse and variable degrees of aortic insuffi- a peripheral systemic vein will demonstrate “bubbles”
ciency. traveling from the right ventricle to the left ventricle
and/or aorta.
Clinical signs In large defects, aortic insufficiency is commonly found.
No sex or breed predilection is reported and it is seen

usually in cats less than 1 year old.
Cardiac catheterization
Systolic murmur is heard over the right sternal border
Left ventricular injection with angiographic contrast
(the louder the murmur the smaller the VSD).
shows shunting of blood from the left ventricle to right
In many cases, a thrill is felt over the right sternal border. ventricle.
Most cases are asymptomatic. If direction of shunting is right to left, a right ventric-
ular injection of contrast shows shunting to the left
Tachypnea and/or dyspnea may be a clinical complaint.
ventricle.
The femoral pulses are normal.
Increase in oxygen saturation equal to or above 5%
Bounding pulses occur in cases with significant aortic from the right atrium to the right ventricle is diagnostic
insufficiency (usually with large VSDs). for a left to right ventricular septal defect.
Differential diagnosis Pathogenesis

Cardiomyopathy is uncommon in young cats. Cardiom- The ductus arteriosus should normally close within the
yopathy murmurs are usually not as loud. Cardio- first 72 hours of life. Failure of the ductus arteriosus
myopathy murmurs may sound different with serial to close will maintain a patent ductus and allow for
auscultations. shunting between the aorta and pulmonary artery and is
called a patent ductus arteriosus (PDA).
In pulmonic or aortic stenosis, the murmur is usually
louder on the left cranial thorax and its character is The most common direction of shunting is left to right
harsher than a VSD murmur. (aorta to pulmonary artery).
In tricuspid valve dysplasia, the murmur is usually The amount of blood being shunted is proportional to
lower frequency and a thrill is uncommon. the size of the ductus.
In tetralogy of Fallot, peripheral cyanosis may be pres- Volume overload of the pulmonary circulation and
ent; the murmur is similar to the murmur of pulmonic the left heart may be present and ultimately lead to the
stenosis. development of congestive heart failure.
Chronic overload of the left atrium and ventricle results
Treatment in progressive dilatation of these chambers, and
increased left ventricular filling pressures.
Treatment is not required in most cases.
Ventricular dilatation causes changes in geometry of the
Pulmonary arterial banding should be considered in left ventricle and results in functional mitral regurgitation.
cases where severe volume overload of the left heart is
evident. Typically, systolic arterial pressures are increased
due to the increased stroke volume and diastolic pres-
If signs of congestive heart failure are present refer to sures are lower than normal explaining the bounding
hypertrophic cardiomyopathy section for treatment pulse.
detail (page 130).
In some cases, it is believed that chronic volume overload
of the pulmonary circulation results in vascular changes,
Prognosis which increase pulmonary vascular resistance.
The prognosis is good in most cases, unless congestive If pulmonary vascular resistance is elevated above sys-
heart failure is present at the time of presentation. temic vascular resistance, the direction of shunting of
Most cats have a normal lifespan. blood is right to left (pulmonary artery to aorta) resulting
in lower arterial oxygen content and an increase in red
blood cell numbers (polycythemia).
Systemic hypoxemia results in signs of dyspnea, panting
PATENT DUCTUS ARTERIOSUS and decreased energy, which may be followed by collapse.
Classical signs Right to left shunting is uncommon.

● Continuous murmur is heard loudest over
the left cranial thorax. Clinical signs
● Palpable thrill, which may be present
bilaterally. No breed or sex predilection is seen. Cats at presenta-
● Bounding arterial pulses. tion are usually less than 1 year of age.
● Strong precordial impulse. No symptoms are present in 1/3 of the cases at initial
● Signs of left-sided heart failure may be presentation.
present (respiratory distress, tachypnea,
crackles). Cats are usually presented for abnormal respiration
(29%), lethargy (24%) and stunted growth (14%).
A continuous murmur is located over the heart base in 71% A small amount of aortic insufficiency may be seen.
of the cases. The other 29% have systolic murmurs only.
Bounding arterial pulses are commonly found.
Diagnosis
Right to left shunt.
A strong precordial impulse is commonly found and
● These cases are rare.
results from the cardiomegaly.
● There is a history of a loud murmur that resolved or
Arrhythmias can be found in severe cases. is only diastolic now.
● A loud second heart sound, which may be split,
Faint diastolic murmur or no murmur is present in right
may be heard.
to left PDAs.
● Lethargy, dyspnea and/or collapse are common.
Polycythemia with PCV exceeding 65% may be found
in right to left PDA. Radiographic findings
Generalized cardiomegaly with a large main pulmonary
Concurrent cardiac defects are found in 29% of the
artery is seen.
cases.
Pulmonary over-circulation is not seen with a right to
Diagnosis left shunt.
Left to right shunt:
● Congenital continuous murmur is heard with
bounding arterial pulses. Right heart enlargement pattern (right axis deviation) is
seen.
Left atrial and ventricular enlargement can be seen.
Right ventricular hypertrophy is seen (RVIDd > 6 mm
Large pulmonary vessels suggesting over-circulation and RVFWd > 3 mm).
can be seen.
Left heart enlargement (LVIDd > 18mm) may also be
Enlarged main pulmonary artery and aortic arch can be present.
seen.
Doppler flow across PDA from right to left or bi-direc-
Pulmonary edema may be present in complicated cases. tional flow can be seen.
Electrocardiography Differential diagnosis

Left ventricular hypertrophy (R wave in lead II > 0.9 Aorticopulmonary window can only be differentiated
mV) is common. by echocardiographic study; continuous blood flow
Left atrial enlargement (P wave > 40 ms) can be seen. with shunting between the aorta and MPA is seen at the
level of the aortic root.
Tachycardia can be seen.
Truncus arteriosus can be differentiated by echocar-
Arrhythmias are uncommon. diography; a common large outlet for the left and right
ventricles is seen.
Pulmonary arteriovenous fistula will produce similar
Left heart enlargement (LVIDd > 18 mm), hyperkinetic
hemodynamic abnormalities as a left to right PDA but
left ventricular function (FS > 55%), enlarged main pul-
the flow within the main pulmonary artery is normal.
monary artery (MPA > 10 mm) and aortic arch are seen.
Doppler shows persistent flow of blood within the Treatment
main pulmonary artery through all phases of the car-
Surgery is curative for left to right PDA. The success
diac cycle.
rate of surgery is 85% when performed by an experi-
Mitral regurgitation may be present. enced surgeon.
● Surgery should be accomplished as soon as the tion, the shunt fraction increases and if significant, vol-
patient is a good anesthetic risk. ume overload of the right and left heart is present.
● If heart failure is present, a period of stabilization
Mitral regurgitation may occur secondary to left heart
prior to surgery is required.
volume overload or congenital abnormalities of the for-
● See treatment for HCM (page 130) for therapy of
mation of the valve.
heart failure.
● Surgery is contraindicated in right to left shunts. Kittens with severe disease develop left-sided conges-
Treatment is mainly palliative. tive heart failure by 6 weeks of age.
● If clinical signs of lethargy, tachypnea and/or col-
lapse are present and if the packed cell volume Clinical signs
is above 60–65% periodic phlebotomy is indicated.
Signs depend on the degree of shunt fraction.
Phlebotomy decreases blood viscosity and improves
peripheral perfusion. The presence of clinical signs Most cats are asymptomatic.
alone is an indication for phlebotomy.
At the left heart base, a soft systolic ejection murmur is
● If there are signs of right-side heart failure, diuret-
heard. It is often also heard on the right side of the chest.
ics will be necessary.
● Rest is recommended. Signs of increased respiratory rate, dyspnea or col-
lapse may be seen while playing.
Stunted growth is seen in severe cases.
Prognosis
Some cases present with ascites, suggesting right-side
Left to right PDA.
heart failure.
● Prognosis is good for long-term survival after sur-
gical correction.
Diagnosis
● Even in animals presented in heart failure, success-
ful correction of the PDA results in resolution of Congenital murmur is found over the left heart base.
signs. A normal life expectancy is seen in most of The murmur is systolic and usually soft.
these cases.
● Right to left PDA. Radiographic findings
– Prognosis is poor for long-term survival, how- Pulmonary over-circulation demonstrated by a promi-
ever many cats can still live for several years nent and enlarged vasculature of the lungs.
with minimal symptoms.
Areas of focal alveolar densities representing pul-
monary edema may be found.
ATRIAL SEPTAL DEFECT Generalized cardiomegaly.
Classical signs Electrocardiographic findings
● Soft systolic murmur is heard over the left Sinus tachycardia (HR > 220 bpm) if heart failure is
heart base and may radiate to the apex. present
● Dyspnea. Evidence of left ventricular hypertrophy with a tall
● Collapse. R wave in lead II (> 0.9 mV)
In cases where the defect may interrupt or deviate the
Pathogenesis His bundle, notching and prolongation of the QRS may
be seen.
Left to right shunting occurs through the atrial septal
defect. Echocardiographic findings
In the absence of significant mitral regurgitation, the Echocardiographic evidence of an atrial septal defect is
shunt fraction is small and animals may not have any seen as echo drop out at the regions of the interatrial
symptoms. With increased amounts of mitral regurgita- septum.
It is important to note that due to the thickness of If the patient is in congestive heart failure, refer to
the septum in a normal heart, many times there is hypertrophic cardiomyopathy section (page 130) for
the illusion of an echo drop out. Multiple views must treatment details.
be obtained to reach a diagnosis.
Doppler confirmation of left-to-right shunting is doc- Prognosis
umented across the atrial septal defect.
Prognosis is good in most cases, but it depends on the
Doppler study may show variable degrees of mitral degree of shunt fraction, which is dependent on the degree
regurgitation. of mitral regurgitation present.
Relative pulmonic stenosis (blood flow velocity > 2.0 Many cats have a normal lifespan.
m/s) secondary to increased volume of blood may be
seen with significant shunt fractions.
In severe cases, biatrial and bi-ventricular enlargement MITRAL VALVE DYSPLASIA/STENOSIS
can be seen.
Classical signs
Cardiac catheterization
● Systolic and/or diastolic murmur is heard
A catheter can be passed across the interatrial sep- over the left apex.
tum into the left atria and ventricle. ● Dyspnea.
An increase greater than 5% in oxygen saturation at the ● Thromboembolic disease
level of the right atrium when compared with blood
from the caudal vena cava is indicative of an atrial sep- Pathogenesis
tal defect with left-to-right shunting.
Congenital mitral valve malformation will result in poor
Angiographic contrast study from the left atria will coaptation of its leaflets and secondary regurgitation.
show shunting of blood into the right heart with opaci-
fication of the right atria and ventricle. In some cases, the mitral valve is thick and misshapen
with restricted motility during diastole, causing impaired
Differential diagnosis blood flow from the left atrium to the left ventricle.
Cardiomyopathy is uncommon in young cats. In some cases, more than two leaflets may be present.
Cardiomyopathy murmurs are usually not as loud. Most commonly, the anterior leaflet may be subdivided
Cardiomyopathy murmurs may sound different with and it is called a cleft mitral valve.
serial auscultations.
Ventricular septal defects usually have a louder murmur
Clinical signs
on the right sternal border and the character is harsher. A heart murmur is heard loudest over the left heart apex
and is present from a young age.
Mitral valve dysplasia occurs with a murmur louder at
the apex, in some cases a diastolic murmur may be pres- Dyspnea or respiratory distress occur if congestive
ent if there is significant mitral stenosis. heart failure is present.
Pulmonic or aortic stenosis present with louder and Signs of increased respiratory rate, dyspnea or col-
harsher murmurs than atrial septal defects. lapse may be seen while playing.
Lameness, paralysis or paresis may result from sys-
Treatment
temic thromboembolism.
Many cases are asymptomatic and there is no need for
Atrial arrhythmias may be present if there is severe left
therapy.
atrial enlargement. Atrial premature contractions,
Definitive therapy requires surgical repair, which is paroxysmal atrial tachycardia or atrial fibrillation can
very difficult to accomplish in veterinary medicine. be seen.
Diagnosis In cases with severe mitral regurgitation, secondary

left ventricular enlargement (LV end-diastolic
Radiographic findings dimension >17 mm) is usually seen.
Marked left atrium enlargement is seen, as demon-
strated by elevation of the carina and bulging of the Severe mitral regurgitation and stenosis do not nec-
caudal atrial wall on the lateral view. A valentine- essarily have to co-exist in the same patient.
shaped heart may be seen on the V/D view.
Pulmonary venous congestion defined by a larger pul-
Cardiomyopathy is uncommon in young cats. Cardio-
monary vein than the accompanying artery, with or
myopathy murmurs are usually not as loud. Cardiomy-
without pulmonary edema may be present.
opathy murmurs may sound different with serial
Left ventricular enlargement is seen with the cardiac sil- auscultations.
houette larger than two intercostal spaces on the lateral view,
Pulmonic or aortic stenosis is present with louder and
secondary to severe mitral valve regurgitation.
harsher murmurs than mitral valve dysplasia/ stenosis.
Electrocardiographic findings Atrial septal defects usually have soft murmur present
Left ventricular hypertrophy demonstrated by a tall R at the left heart base.
wave in lead II (> 0.9 mV).
Differential diagnosis solely based on physical exam
Sinus tachycardia (HR > 220 bpm) if heart failure is may be difficult.
present.
Treatment
Some cases may have atrial premature contractions
or paroxysmal atrial tachycardia. If atrial fibrillation is Many cases are asymptomatic and there is no need for
present, there is invariably severe left atrial enlargement. therapy.
If the patient is in congestive heart failure, refer to the
Echocardiographic findings hypertrophic cardiomyopathy section (page 130) for
A thick and misshapen mitral valve is seen which may treatment details.
have poor motility during diastole.
Prognosis
Systolic anterior motion of the mitral valve may be
seen (anterior displacement into the left ventricular out- Prognosis is good in most cases. Cats with marked
flow of the anterior mitral valve leaflet causing outflow mitral regurgitation may only develop symptoms of
obstruction). congestive heart failure between 5–10 years of age.
Variable degrees of mitral regurgitation are found on Patients with severe regurgitation may present in con-
Doppler study. gestive heart failure within the first year of life.
Determination of the mitral valve inflow velocity pro- Prognosis is worse with the presence of co-existent
file is essential to determine the presence and degree of thromboembolic disease.
mitral stenosis.
● The early diastolic wave (E wave) of mitral inflow
AORTIC STENOSIS
shows delayed deceleration of blood flow in mid-
diastole, and there is fusion with the atrial diastolic
Classical signs
wave (A wave). This results in an M-shaped mitral
inflow profile or in severe cases a rectangular shape. ● Systolic murmur is heard over the left heart
base or over the cranial aspect of the sternum.
Secondary left atrial enlargement occurs with the left
atrial to aortic ratio usually > 2.0. Left atrial enlarge-
Pathogenesis
ment is either secondary to restriction of filling of the
left ventricle by a stenotic valve or because of severe With congenital valvular malformation of the aortic
regurgitation. valve, there is thickening of the valve leaflets and
poor motility during systole, resulting in fixed A subvalvular or supravalvular fibrous ridge may be
obstruction of outflow of blood. In some cases, identified.
supravalvular or subvalvular stenosis may be found.
In some cases, left atrial enlargement may be present.
Secondary left ventricular hypertrophy may develop.
Doppler study of the left ventricular outflow reveals
The degree of hypertrophy is directly dependent on the
increased velocity of blood flow (> 2.0 m/s).
severity of the stenosis. Valvular gradients above 100
mmHg are classified as severe.
Clinical signs Cardiac catheterization findings
A systolic murmur is heard over the left heart base or over Cardiac catheterization is not routinely done, since the
the cranial aspect of the sternum. introduction of echocardiography.
Most cats are asymptomatic. Most common symptoms Injection of contrast in the left ventricle will show:
● Left ventricular hypertrophy.
in severe cases are exercise intolerance and syncope.
● Narrow left ventricular outflow.
If severe, in the first 1–2 years of life, cats may die sud- ● Filling defect at the aortic valve level (due to a
denly or develop congestive heart failure. thickened valve).
● Post-stenotic dilatation of the aortic arch.
Diagnosis ● Subvalvular or supravalvular filling defects may be
seen.
There is widening of the cranial mediastinum as a result
of post-stenotic dilation of the aortic arch. This is evi- Differential diagnosis
dent on both views (dorsoventral view and lateral view).
Hypertrophic obstructive cardiomyopathy (HOCM) dif-
Left ventricular enlargement with elongation of the fers from aortic stenosis in the location and pathophysi-
left heart occurs secondary to hypertrophy. ology of the stenosis. With HOCM the stenosis is
If congestive heart failure is present, pulmonary venous dynamic (changes with heart rate) while in aortic steno-
distention (pulmonary vein larger than accompanying sis the obstruction to blood flow is fixed.
pulmonary artery) and evidence of pulmonary edema
may be seen (focal areas of marked interstitial or alve-
olar densities). Treatment
In mild and moderate cases (Doppler-derived pres-
sure gradient less than 100 mmHg and asymptomatic),
The electrocardiogram may be normal or have evidence
there is no benefit from medical therapy.
of left ventricular hypertrophy with a tall R wave in
lead II (> 0.9 mV). In cases complicated with ventricular arrhythmias
and/or left ventricular concentric hypertrophy,
Left axis deviation and/or left fascicular anterior block
beta-blockers may reduce the likelihood of sudden
may be present.
death and/or collapse. Refer to section in hypertrophic
Ventricular arrhythmias may be present, but are not cardiomyopathy (page 130).
common.
If congestive heart failure is present, refer to hyper-
Echocardiographic findings trophic cardiomyopathy section (page 130).
Left ventricular hypertrophy is seen (diastolic Caution with the use of angiotensin-converting
dimension of the interventricular septum and/or LV enzyme inhibitors, which may increase the pressure
posterior wall greater than 6 mm). gradient across the stenosis.
If valvular stenosis is present, the valve appears thick No surgical therapy is currently being offered for treat-
and has restricted opening. ment of this disease.
Prognosis The murmur is best heard at the left heart base. It is an

ejection systolic murmur, which varies in intensity dur-
Prognosis is dependent on severity of the stenosis and ing systole because of the crescendo and decrescendo
the presence of congestive heart failure with or without character.
collapse.
Characterization of the ejection murmur may be diffi-
Some cats may have a normal lifespan. cult in a cat because of the fast heart rate.
Severely affected cats die within the first 1–2 years of life.
Cats with aortic stenosis are at an increased risk of Diagnosis
developing bacterial valvular endocarditis.
Normal cardiac size or right ventricular enlargement is
PULMONIC STENOSIS found.
Classical signs Dilated main pulmonary artery (post-stenotic dilata-

tion) is seen as a bulge in the left cranio-lateral part of
● Systolic murmur is heard over the left heart the cardiac silhouette in the ventro-dorsal view or
base over the pulmonic area. dorso-ventral view.
Under-perfused pulmonary circulation is seen as
Pathogenesis hypovascular lung fields characterized by hyperinflated
With congenital valvular malformation of the pulmonic lungs and a decreased peripheral pulmonary vasculature.
valve, there is thickening of the valve leaflets and
poor motility during systole, resulting in fixed
obstruction of outflow of blood. In some cases, Tachycardia is frequently seen with a heart rate greater
supravalvular or subvalvular stenosis may be found. than 220 bpm.
The increased resistance to blood flow across the pul- Right axis deviation is seen between −60 and −180
monary valve stenosis results in elevation of right ven- degrees in the frontal plane.
tricular systolic pressure. Secondary right ventricular Deep S waves are seen on leads II, aVF and III.
hypertrophy and dilation may develop, along with
arrhythmias. Echocardiographic findings
Dilation and hypertrophy of the right ventricle may Pulmonary valve stenosis is present. Pulmonary
result in secondary tricuspid insufficiency. artery hypoplasia and a dysplastic pulmonic valve
may be evident.
Signs of right-sided congestive heart failure may develop.
Doppler study across the pulmonary valve will deter-
Pulmonic stenosis is often seen with other cardiac mine the degree of stenosis. Velocities of blood flow
defects such as tetralogy of Fallot, septal defects and obtained by continuous wave Doppler above 2.0 m/s are
tricuspid dysplasia. diagnostic of stenosis.
It is a rare congenital defect in cats.
Cardiac catheterization findings
Clinical signs Selective angiography of the right ventricle will show:
● Right ventricular hypertrophy.
Many cats are asymptomatic and present for evalua-
● Pulmonary valve stenosis and post-stenotic dilata-
tion of a heart murmur.
tion of the main pulmonary artery.
The age of presentation varies from the first few
months of life until middle age.
Cats with symptoms may show dyspnea or open-mouth
breathing after mild to moderate exercise. Tetralogy of Fallot.
● The murmur of pulmonic stenosis may be similar to Pathogenesis

the murmur heard in tetralogy of Fallot.
● Cyanosis or brick-red mucus membranes are not Tetralogy of Fallot implies four separate anatomic
seen with pulmonic stenosis. abnormalities:
● Large ventricular septal defect (VSD).
Cardiomyopathies. ● Pulmonic valvular stenosis.
● The murmur is usually not as loud and may vary in ● Overriding aorta (dextroposition of the aorta)
intensity. results from the cranial displacement of the aorta
relative to the interventricular septum. This leads to
the abnormal alignment of the aorta and the left
Treatment ventricular outflow tract. A portion of the aorta is
Use furosemide if congestive heart failure is present positioned over the right ventricular outflow tract.
and treat arrhythmias (see page 160 The Cat With
Tachycardia, Bradycardia or an Irregular Rhythm). These abnormalities have a common morphogenetic
Surgical options are available but rarely performed. cause and result from anterior deviation of the inter-
● Blalock–Taussig shunt can be recommended (artifi-
ventricular septum during development.
cial shunt from the left subclavian artery to the pul- It is a rare congenital disease in the cat and is inherited
monary artery). This increases blood flow through as a simple autosomal recessive trait.
the pulmonary circulation.
● Other modified techniques have been described.
The increased resistance to blood flow across the pul-
Consult with an experienced surgeon. monary valve stenosis results in elevation of right ventric-
ular systolic pressures above left ventricular systolic
Catheter balloon valvuloplasty can be very success- pressures. These hemodynamic alterations cause the shunt-
ful in reducing the gradient across the stenotic valve. ing of blood through the large ventricular septal defect.
The catheter is positioned through the valve and the
The cranial displacement of the aortic root allows for
balloon inflated to dilate the stenosis.
direct ejection of blood from the right ventricle into the
aorta.
Prognosis
The degree of shunting is relative to the amount of pul-
Most cats reach middle age and some even have a monary stenosis and dextroposition of the aorta. In
normal lifespan. some patients, minimal shunting occurs at rest, and
symptoms are only present during exercise.
Long-term prognosis depends on the severity of
obstruction to blood flow. Chronic hypoxia results in polycythemia (PCV >
65%).
TETRALOGY OF FALLOT
Clinical signs
Classical signs Many cats are asymptomatic at rest and present for
evaluation of a heart murmur.
● Systolic murmur over the cranial ventral
thorax. The age of presentation varies from the first few
● Cyanosis or brick-red mucus membranes months of life until middle age.
may be present.
Cats with symptoms may show open-mouth breathing
● Signs of increased respiratory rate (with
and/or cyanosis after mild to moderate exercise. In
open-mouth breathing), dyspnea or collapse
some cats, syncope is seen.
may be seen while playing.
● Many cats are asymptomatic on The mucus membranes may be pink or cyanotic
presentation. depending on the degree of the polycythemia and
shunting.
The murmur is usually due to the pulmonic stenosis and Cardiac catheterization findings
best heard at the left heart base. It is an ejecti on systolic
murmur, which varies in intensity during systole because Selective angiography of the right ventricle will show:
of the crescendo and decrescendo character.
● Large VSD.
Characterization of the ejection murmur may be diffi- ● Pulmonary valve stenosis and post-stenotic dilata-
cult in a cat because of the fast heart rate. tion of the main pulmonary artery.
● Overriding aorta.
Diagnosis Cardiac catheterization demonstrates equalization of

right ventricular and left ventricular pressures.
Normal cardiac size or right ventricular enlargement is Pulmonary artery pressures are normal.
found.
Dilated main pulmonary artery (post-stenotic dilata- Differential diagnosis
tion) is seen as a bulge in the left cranio-lateral part of Pulmonary stenosis.
the cardiac silhouette in the ventro-dorsal view or ● Cyanosis or brick-red mucus membranes are not
dorso-ventral view. seen with pulmonic stenosis.
● The murmur of pulmonic stenosis may be similar to
Under-perfused pulmonary circulation is seen as
hypovascular lung fields characterized by hyperinflated the murmur heard in tetralogy of Fallot.
lungs and a decreased peripheral pulmonary vascula- Right to left PDA.
ture. ● In many cases, no murmur is heard although cyanosis
and exercise intolerance are usually present.
Electrocardiographic findings ● Cyanosis of the right-to-left PDA is usually periph-
Tachycardia is frequently seen with a heart rate greater eral and localized to the caudal portion of the body.
than 220 bpm.
Cardiomyopathies.
Right axis deviation is seen between −60 and −180 ● Cyanosis is only present in cases of severe pul-
degrees in the frontal plane. monary edema.
● The murmur is usually not as loud and may vary in
Deep S waves are seen on leads II, aVF and III.
intensity.
A large perimembranous ventral septal defect is seen Treatment
below an overriding aorta.
Medical therapy consists of periodic phlebotomy to
Pulmonary valve stenosis is present. Most cases have control clinical signs.
pulmonary artery hypoplasia and a dysplastic pulmonic ● Blood of volume removed = [BW (kg) × 0.08] × 1000
valve. ml/kg × Actual Hct.–Desired Hct./ – Actual Hct.
● Repeat PCV in 2 hours. The goal is to decrease PCV
Doppler study of the flow across the VSD will deter-
to ~60%. CAUTION–removing too much red cell
mine the direction of shunting of blood. Most fre-
mass may render the patient symptomatic at rest.
quently, there is right to left shunting.
Avoid heavy playing and keep confined within the
Doppler study across the pulmonary valve will deter-
household.
mine the degree of stenosis. Velocities of blood flow
obtained by continuous wave Doppler above 2.0 m/s Use beta-blockers if the heart rate is greater than 200
are diagnostic of stenosis. Usually the degree of steno- bpm at rest.
sis is severe (Vmax > 5.0 m/s). ● Propranolol – 0.5–1 mg/kg q 8 h OR
● Atenolol 6.25–12.5 mg/cat q 12 h.
Saline contrast studies may be helpful in identifying the
direction of shunting. Surgical options are available but rarely performed.
● Blalock–Taussig shunt can be recommended (artifi- In cats fed commercially available feline diets, DCM is
cial shunt from the left subclavian artery to the pul- a rare form of cardiomyopathy.
monary artery). This increases blood flow through
All cardiac chambers are dilated. Atrophy of papil-
the pulmonary circulation.
lary muscles is present.
● Other modified techniques have been described.
Consult with an experienced surgeon. Myocardial sections on post-mortem show patchy
white areas. Microscopically there is myocyte atrophy
Prognosis with interstitial fibrosis.
Most cats can reach middle age and some even have The hemodynamic hallmark is severe systolic dys-
a normal lifespan. function.
Long-term prognosis depends on the severity of blood
flow. Clinical signs
There is no age or sex predilection.
DILATED CARDIOMYOPATHY Usually cats with dilated cardiomyopathy have a his-
tory of being fed a non-commercial diet, or dog food.
Classical signs
A heart murmur is often present, but in some cases may
● Heart murmur (in some cases may not be
not be. When present, a systolic murmur varies in loca-
present).
tion and intensity with variations in heart rate.
● Gallop rhythm.
● Arrhythmia. Gallop rhythm is commonly heard. It is identified when
● Dyspnea. more than two heart sounds are present on auscultation.
● Hypothermia.
Arrhythmias can be heard as premature heart beats with
● Collapse.
pulse deficits.
systemic thromboembolism. Dyspnea is seen in symptomatic cats with an increased
respiratory rate (greater than 30 breaths/ min) at rest or
with open-mouth breathing in extreme cases. Pleural effu-
Pathogenesis sion may be present and result in muffled heart sounds.
This disease in most cats is due to a deficiency in tau-
In symptomatic cats, hypothermia is common.
rine concentration. Taurine supplementation in com-
mercially available diets has reduced significantly its Collapse may result from impaired cardiac output (ven-
incidence. tricular tachycardia)
Any cat fed a non-commercial diet should have tau- Lameness, paralysis or paresis are usually the result of
rine supplementation. Cats fed home-made vegetarian systemic thromboembolism.
diets are at high risk of taurine deficiency. However,
Most cats with aortic saddle thrombosis present for
not all cats experimentally fed a taurine-deficient diet
acute onset of hindlimb paralysis, pain, absent femoral
have developed dilated cardiomyopathy.
pulses, cool extremities and cyanosis of the nail bed. In
Dilated cardiomyopathy (DCM) is not always the some cases a history of episodic lameness is given.
result of taurine deficiency. Currently most of the
Ascites is found in a small minority of cases.
cases are idiopathic.
Retinal degeneration changes consistent with taurine
Diagnosis
deficiency are present in 33% of cats.
Other potential causes for DCM include a late expres- Radiographic findings
sion of chronic myocarditis, genetic abnormalities, and Severe generalized cardiomegaly and enlarged pul-
in some cats, the cause is unknown. monary veins are seen. Pulmonary edema with or without
pleural effusion may be present. Pleural effusion is Treatment of the symptomatic cat with congestive
more common in dilated cardiomyopathy than in other heart failure (acute management).
forms of cardiomyopathy. The fluid may be a transu- Criteria to start therapy:
date, modified transudate or chylous. ● Respiratory distress (open-mouth breathing or very
abnormal respiratory pattern).
Electrocardiographic findings ● Pulmonary congestion (moderate to severe) on radi-
Ventricular arrhythmias are present in about 50% of ographs and/or pleural effusion.
cases. ● Hypothermia.
● Oxygen.
Tachycardia, ventricular conduction disturbances ● Diuretics.
(notched QRS), or tall R waves on lead II (> 0.9 mV) – Furosemide 1–2 mg/kg IV or IM q 8–12 h until
are commonly found. respiratory rate and pattern are normalized.
Atrial fibrillation is more common than in HCM and – Furosemide constant rate infusion (if normal renal
is usually associated with extreme dilatation of the left values at presentation) 0.5–1 mg/kg/hr until con-
and/or right atria. gestion is resolved but not for longer than 24 hours.
● Venodilator.
Echocardiographic findings – Nitroglycerin ointment (2%) 1/4 of an inch (6

mm) q 8 h.
The echocardiographic findings reveal severe biventric-
● Inotropic support.
ular dilatation with severe biatrial enlargement. The
– Dobutamine continuous rate infusion, IV 1–3
left atrial to aortic ratio is usually >2.0.
μg/kg/min (watch for vomiting or seizures). OR
Left ventricular systolic function is markedly dimin- – Pimobendan 0.25 mg/kg PO q 12 h (only if able
ished (fractional shortening is less then 20–25% in most to pill without causing distress)
cases). Normal FS is between 35–55%. ● Thoracocentesis (right thorax to avoid puncturing
of the enlarged auricles) if there is evidence of moder-
Left ventricular internal dimensions in diastole is
ate to severe pleural effusion on radiographs.
usually larger than 20 mm. Intracardiac thrombi may
● Angiotensin-converting enzyme inhibitor (see
be found. Normal LV end-diastolic dimension is up to
above).
17 mm.
● Taurine supplement (see above).
In taurine-deficient cats, improvement in chamber ● Thermoregulatory support (heating blanket).
size and contractility is seen 6–8 weeks after starting – Fluid therapy should be done cautiously until
supplementation. stable cardiac function is established.
Laboratory findings Symptomatic cat with congestive heart failure (chronic

Plasma taurine levels (heparinized sample) are less than management).
30 nmol/ml in most cats. Plasma levels of 40–60 Criteria to start therapy:
nmol/ml may be consistent with taurine deficiency. ● Maintenance therapy after initial treatment for
acute congestive heart failure.
Cats with congestive heart failure may show azotemia ● Any patient found to have early evidence of con-
due to decreased renal perfusion. gestive heart failure (usually on radiographs) but
without symptoms, that will require acute interven-
tion if untreated.
Treatment
– Diuretics
Treatment of the asymptomatic cat: – Furosemide 0.5–1.0 mg/kg PO q 12–24 h OR
● Angiotensin-converting enzyme inhibitors – Hydrochlorothiazide 1–2 mg/kg PO q 12 h
– Enalapril 0.25–0.5 mg/kg PO q 24 h OR OR/AND
– Benazepril 0.25–0.5 mg/kg PO q 24 h. – Spironolactone 2–4 mg/kg PO q 12 h.
● Nutraceuticals ● Angiotensin-converting enzyme inhibitor (see above)
– Taurine PO 250–500 mg q 12 h. ● Taurine supplement (see above)
Inotropic Support Prevention

● Digoxin 0.016 mg/cat PO q 24–48 h (monitor for
anorexia and gastrointestinal signs). OR Cats should be maintained on a diet designed for the
– For monitoring, obtain a serum sample 8 hours feline patient, which has adequate amounts of taurine.
after giving digoxin dose. Do not store the serum
in plastic tubes, since digoxin binds to plastic. PERITONEAL–PERICARDIAL
Therapeutic serum concentrations range from DIAPHRAGMATIC HERNIA (PPDH)
1.3–3.2 nmol/L (1.0–2.5 ng/ml). The authors pre-
fer not to exceed levels higher than 1.9 nmol/L Classical signs
(1.5 ng/ml). The side effects usually are GI signs
● Vomiting.
and anorexia.
● Diarrhea.
● Pimobendan 0.25 mg/kg PO q 12 h.
● Weight loss.
● Arrhythmia control.
● Dyspnea.
– Improvement is usually seen with supportive
treatment.
– Caution should be exercised if beta-blockers or Pathogenesis
calcium channel blockers are used, due to the
Persistent communication occurs between the peri-
negative inotropic effects of these drugs.
cardial and peritoneal cavities because of abnormal
– For ventricular or supraventricular arrhythmias:
fusion of the septum transversum with the pleuroperi-
– Procainamide SR 10–20 mg/kg PO q 8 h.
toneal folds during development.
– Associated intracardiac thrombus or systemic
thromboembolism. The hernia is of variable size.
● Anti-thrombotic therapy: The most likely organs to be herniated are the liver and
– Heparin and Warfarin therapy are controver- gallbladder, small intestine, spleen, stomach.
sial and should be utilized under the guidance of
an experienced clinician. Clinical signs
– Low-molecular-weight heparins have been
recently suggested. This class of heparins does Signs are mostly related to the gastrointestinal system
not require continued monitoring of coagulation and include vomiting, diarrhea and weight loss.
parameters. Most cases are asymptomatic and it is an incidental
– Enoxaparin (Lovenox ®) 1 mg/kg SQ q 24 h. finding. An increased incidence in Persian cats is sus-
– Aspirin 80 mg PO q 48–72 h is recommended by pected.
some clinicians but its efficacy has not been estab-
lished. A lower dose (5 mg/cat PO q 24 h) has Physical exam is often normal. In some cases, the heart
also been recommended, because of concerns that sounds may be muffled.
prostacyclin production is inhibited at the higher In symptomatic patients, respiratory signs can be pres-
dose. ent, particularly under stressful conditions.
Thrombolytic therapy is contraindicated if an intracar-
diac thrombus is present, and controversial in aortic
saddle thrombus. Diagnosis
Prognosis Extreme enlargement of the “cardiac” silhouette.
Prognosis is good if the etiology is taurine deficiency. Dorsal displacement of the trachea.
Most cases currently seen are not due to taurine defi- Silhouetting of the caudal border of the heart with the
ciency and the prognosis is poor. diaphragm.
Heterogeneous densities of the “cardiac” silhouette Surgical correction should be reserved for
due to varied contents of the pericardial cavity. cases with symptoms attributed to this condition.
● Post-operative care may be complicated in some
Abdominal radiographs may show an absent or smaller
cases. Consult with an experienced surgeon.
than normal liver.
Electrocardiographic findings Prognosis

Some patients have a normal ECG. Asymptomatic patients have a good prognosis in general.
The expected QRS complexes in a cat with a severely Surgically corrected patients have an excellent prognosis.
enlarged heart diagnosed by radiography are not pres-
ent in patients with peritoneopericardial diaphrag-
matic hernia. DIAPHRAGMATIC HERNIA
The mean electrical axis may be shifted (depending on Classical signs

the abnormal deviation of the heart by the viscera).
● Dyspnea/tachypnea.
See main reference page 57 (The Dyspneic or
The cardiac exam is commonly normal.
Tachypneic Cat).
In cases where primary cardiac disease is present, it is
difficult to obtain a true evaluation of the heart due to Clinical signs
compression by nearby organs.
Trauma associated with a motor vehicle accident or a
Abnormal blood flow patterns may be caused fall from several stories is the most common cause,
by compression forces of the viscera against the heart. although it can occasionally occur as a congenital
The liver and other organs can be visualized in direct problem.
contact with the heart. Tachypnea and dyspnea are often evident, and may
begin at the time of trauma or a few hours later. In some
Cardiac catheterization findings cats, the respiratory signs improve after a few days and
Non-selective angiography demonstrates that the peri- are most evident only after physical activity.
cardial sac is filled with other organs. Typically there is a vague history of gastrointestinal
signs including vomiting, inappetance and weight loss,
Differential diagnosis usually beginning some time after a motor vehicle acci-
dent or fall.
Pericardial effusion is usually associated with clinical
signs of cardiac or infectious disease. Radiographically Physical examination may be normal. Often the heart
the cardiac silhouette lacks heterogeneous densities. sounds are muffled on one or both sides of the chest.
There may be an impression of an “empty” abdomen
Dilated cardiomyopathy is usually associated with
on abdominal palpation because of organ displacement.
signs indicative of heart disease. Radiographically the
heart never develops the degree of enlargement seen
with PPDH. Diagnosis
In a diaphragmatic hernia the heart, size is normal Radiographic findings

and displaced. There is loss of distinct diaphragmatic Abdominal viscera are identified within the thorax.
borders. A history of trauma is common. Stomach and small intestine can be easily identified as
gas-filled or fluid-filled structures.
Treatment
Displacement of abdominal and thoracic structures is
If the patient is asymptomatic and the diagnosis is inci- found due to shifting of the organs through the
dental, then surgery is not necessary. diaphragmatic surface.
Partial or complete loss of the thoracic–diaphrag- Left ventricular enlargement.

matic surface outline is seen.
Dorsal displacement of the trachea.
In some cases, pleural effusion is detected.
Pulmonary edema.
Electrocardiographic findings Dilatation of the pulmonary veins relative to the pul-
Mean electrical axis may be shifted due to the altered monary arteries.
position of the heart in the chest.
Pleural effusion may be present (rare).
A typical mean electrical axis shift cannot be expected,
due to the variable position of the heart in each indi- Electrocardiographic findings
vidual case. Sinus tachycardia if heart failure is present.
Echocardiographic findings Left ventricular enlargement (R wave > 0.9 mV on

A normal echocardiogram is found, unless concurrent lead II).
heart disease is present. Left anterior fascicular block (LAFB) may signify left
The abdominal viscera may displace the heart making ventricular enlargement. In LAFB the QRS duration
it difficult to obtain standard imaging planes. is normal, there is marked left axis deviation (between
−60 and −90 degrees), small Q wave and tall R wave in
Abdominal organs are visualized within the chest leads I and aVL, deep S waves in lead II, III and aVF.
cavity.
Arrhythmias are uncommon.
VALVULAR ENDOCARDIOSIS
Classical signs Thick and prolapsing mitral valve.
● Systolic murmur. Marked mitral regurgitation.

● Marked left atrial enlargement
● Gallop.
● Variable degrees of left ventricular enlargement occur
● Dyspnea or tachypnea if symptomatic.
depending on the degree of valvular insufficiency.
● Hyperkinetic left ventricle (contraction is exuber-
Pathogenesis
ant, stronger than normal) with a fractional shorten-
This is a rare disorder in cats. ing often greater than 55%.
Degeneration of the collagen matrix of the valve
occurs resulting in laxity of the chord apparatus and Differential diagnosis
prolapse of the valve.
Any type of cardiomyopathy.
There is thickening of the valve leaflets. ● Cardiomyopathy cases have in general normal
valvular morphology.
Clinical signs ● In cardiomyopathy patients, the degree of valvular
Systolic murmur located over the apex of the heart. insufficiency is usually less than with endocardiosis.
Gallop rhythm may be present.

Treatment
Tachypnea or dyspnea may be present in cases with
concurrent congestive heart failure. If not in congestive heart failure:
● Treatment is not required and probably will not
Diagnosis change the outcome.
● If severe left atrial enlargement is present (left atrial
Radiographic findings to aortic ratio >2), consider beta-blocker therapy
Marked left atrial enlargement. (refer to HCM section for doses, page 130).
If in congestive heart failure (respiratory distress with Prognosis

open-mouth breathing or very abnormal respiratory pat-
tern, pulmonary congestion on radiographs with or with- The prognosis is variable and depends on the severity
out pleural effusion and hypothermia) refer to section on of the mitral regurgitation and degree of cardiac
HCM for therapy (page 130). enlargement present.
If congestive heart failure is present, life expectancy is
around 1–2 years.
RECOMMENDED READING
Ettinger SJ, Feldman EC. Textbook of Veterinary Internal Medicine. Philadelphia, PA, WB Saunders Co., 2005.
Fox PR. Textbook of Canine and Feline Cardiology: Principles of Clinical Practice. Philadelphia, WB Saunders,
1999.
Kittleson MD, Kienle RD. Small Animal Cardiovascular Medicine. St. Louis, MO, Mosby, 1998.
Tilley LP. Essentials of Canine and Feline Electrocardiography, 3rd edition. Interpretation and Treatment. Malvern,
PA, Lea and Febiger, 1992.
Tilley LP, Smith FWK (eds) The Five Minute Veterinary Consult, 3rd Edition. Baltimore, Lippincott, Williams &
Wilkins, 2004.
10. The cat with tachycardia, bradycardia
or an irregular rhythm
Luis A H Braz-Ruivo, Kathy A Arrington and Fiona
Campbell
KEY SIGNS
● Tachycardia.
● Bradycardia.
● Irregular heart sounds or pulse.
MECHANISM?
● Arrhythmias are caused by two basic abnormalities: disorders of impulse formation and disor-
ders of impulse conduction.
● Alterations of impulse formation are usually the result of diseased myocardial cells.
● Alterations of electrical impulse conduction occur secondary to primary diseases of the con-
duction system.
WHERE?
● Arrhythmias can occur wherever there is excitable cardiac tissue in the heart.
WHAT?
● Most cats with a cardiac arrhythmia are asymptomatic.
● The most common arrhythmia is ventricular premature contractions (VPCs).

Diseases causing tachycardia, bradycardia or an irregular rhythm
TACHYARRHYTHMIAS
ANOMALY
● Ventricular pre-excitation
This is a rare cardiac arrhythmia resulting from the presence of a congenital bundle of muscle across the
atrioventricular annulus – allowing bypass of the electrical impulse to the ventricles.
It can occur at any age; in many cases, it is an incidental finding. The most common symptom is
syncope or lethargy during the periods of supraventricular tachycardia.
continued
157
continued
METABOLIC
● Tachyarrhythmias (sinus tachycardia, supraventricular/atrial tachycardia, ventric-
ular premature beats and ventricular tachycardia)*** (p 160)
Tachyarrhythmias can result from hyperthyroidism, acidosis and uremia or be drug-induced.
Cats tolerate tachycardia better than other species. Syncope, lethargy and weakness are the most
common signs in addition to the sign of the underlying disease.
● Ventricular arrhythmias (ventricular premature beats, ventricular tachycardia)***
(p 164)
Ventricular arrhythmias may result from hyperthyroidism, acidosis, uremia or be drug-induced. In
addition to the signs related to the underlying disease, cats may present with lethargy, weakness,
anorexia and syncope.
● Atrial arrhythmias (supraventricular/atrial tachycardia, atrial fibrillation) (p 161)
Atrial arrhythmias may be seen in hyperthyroidism. In addition to the signs related to the underly-
ing disease, cats may present with lethargy, weakness and syncope.
NEOPLASTIC
● Ventricular arrhythmias (ventricular premature beats, ventricular tachycardia) (p 164)
Ventricular arrhythmias may be seen in primary or metastatic cardiac disease. Most patients do not
show clinical signs from the arrhythmia. Most of the clinical signs are related to the underlying
disease.
INFECTIOUS
Ventricular arrhythmias may be seen with bacterial infections (endocarditis, myocarditis) and viral
infections (myopericarditis). Fever, lethargy, anorexia and a new heart murmur are the most com-
mon clinical signs.
IDIOPATHIC
● Ventricular arrhythmias (ventricular premature beats, ventricular tachycardia)***
(p 164)
Ventricular arrhythmias are most commonly seen in cases of feline cardiomyopathies. The major-
ity of the cases do not have symptoms related to the arrhythmia. Periods of ventricular tachycardia
(rates above 300 bpm) may cause lethargy or syncope.
● Atrial fibrillation* (p 162)
Atrial fibrillation can be seen in end-stage cardiomyopathies when severe left atrial enlargement
is present. Clinical signs include worsening of heart failure, weakness or syncope. Signs related
to systemic thromboembolism (paresis/paralysis of hindlimbs) may be present.
● Supraventricular arrhythmias (supraventricular/atrial tachycardia, atrial fibrilla-
tion)** (p 161)
Atrial tachycardias, atrial premature beats and other forms of supraventricular tachycardias can
occur in cats with cardiomyopathies. The majority of the cases do not have symptoms related to
the arrhythmia. Periods of supraventricular tachycardia (rates above 300 bpm) may cause lethargy
or syncope.
10 – THE CAT WITH TACHYCARDIA, BRADYCARDIA OR AN IRREGULAR RHYTHM 159
TRAUMATIC
Ventricular arrhythmias can be seen in cases following severe trauma to the chest. These are usu-
ally secondary to traumatic myocarditis. The majority of the cases do not have symptoms related
to the arrhythmia. Periods of tachycardia (rates above 300 bpm) may cause lethargy or syncope
BRADYARRHYTHMIAS
DEGENERATIVE
● Atrioventricular block (p 169)
Several degrees of atrioventricular block are due to His bundle degeneration, vacuolization and fibrosis.
Bradyarrhythmias cause clinical signs of lethargy, weakness and syncope. Depending on the
degree of the bradyarrhythmia, many cats may not show clinical signs and usually are an inciden-
tal finding.
METABOLIC
● Sinus bradycardia (p 168)
Sinus bradycardia can result from hyperkalemia, hypokalemia, hypoglycemia, acidosis and
hypothermia or be drug-induced. In addition to the signs related to the underlying disease, cats
may present with lethargy, weakness, anorexia and syncope. Heart rate is <120 beats/min.
● Atrial standstill (p 168)
Atrial standstill can result from hyperkalemia primarily associated with urethral obstruction or
from long-standing cardiac disease, most commonly dilated cardiomyopathy. In addition to the
signs related to the underlying disease, cats may present with lethargy, weakness, anorexia and
syncope.
TOXIC
● AV block** (p 169)
AV block can be drug-induced with digitalis, beta-blockers and calcium-channel blockers. In addi-
tion to the signs related to the underlying disease, cats may present with lethargy, weakness,
anorexia and syncope.
INTRODUCTION Alterations of electrical impulse formation occur sec-

ondary to instability of the resting membrane potential
and are usually the result of diseased myocardial cells.
MECHANISMS? ● If the electrical impulse forms earlier than expected, a
The normal electrical impulse is generated in the SA premature beat is generated. If the electrical impulse
node and spreads through the atria via the Bachmann forms later than expected, a pause in the cardiac
bundles, continues down through the AV node, His bun- rhythm is seen.
dle, bundle branches and Purkinje fibers and finally
Alterations of electrical impulse conduction occur sec-
reaches the ventricles.
ondary to primary diseases of the conduction system.
Arrhythmias are caused by two basic abnormalities, These either result in block of conduction of the electri-
disorders of impulse formation and disorders of cal wave, or alterations that facilitate the perpetuation
impulse conduction. of the electrical wave in a circuit (re-entry).
Abnormal conduction of the electrical impulse can be Class II anti-arrhythmics are beta-blockers. This group
either blocked, choose an alternative pattern of conduc- antagonizes the action of cathecolamines and is most
tion (aberrantly conducted) or re-enter previously excited useful when increased sympathetic tone is present. Most
tissue (re-entry). common examples include propranolol (non-selective)
and atenolol (beta-1 selective). They are contraindicated
An arrhythmia should always be suspected whenever an
for cats with symptomatic respiratory disease.
irregularity in cardiac rhythm or arterial pulse is
detected. Class III anti-arrhythmics block the potassium chan-
nels. This group hyperpolarizes the cells making it
more difficult to reach threshold, and they prolong the
WHERE? refractory period. The most common used drug is
Arrhythmias can occur wherever there is excitable sotalol. Sotalol, besides class III properties, also has
cardiac tissue in the heart. class II properties.
Arrhythmias that originate in the atria, interatrial Class IV anti-arrhythmics block the calcium channels.
septum, or above the AV node are termed supraven- These drugs inhibit transmembrane calcium transport
tricular. and the most pronounced effects are at the sinoatrial and
atrioventricular nodes. The most common example is
Arrhythmias that originate in the ventricles or anywhere diltiazem.
below the bifurcation of the His bundle are termed ven-
tricular.
DISEASES CAUSING TACHYCARDIA

WHAT? OR AN IRREGULAR RHYTHM
The most common arrhythmia is ventricular premature
contractions (VPCs).
SINUS TACHYCARDIA***
Cats with cardiac arrhythmias are generally suspected
of having myocardial disease, even if radiographic and Classical signs
echocardiographic findings are within normal limits.
● Heart rate greater than 220 beats per
Cardiomyopathies are the most common form of car- minute.
diac disease associated with arrhythmias. ● Strong precordial impulse.
● Loud S1 heart sound.
The diagnosis of atrial fibrillation in a cat is almost
invariably associated with the presence of severe left
atrial enlargement.
Pathogenesis
Most cats with a cardiac arrhythmia are asymptomatic.
This arrhythmia originates from the sinoatrial node, the
Ventricular arrhythmias in young cats with severe left normal pacemaker of the heart.
ventricular hypertrophy may be associated with a high
It results from increased sympathetic tone. The
risk of sudden death.
causes of increased sympathetic tone include stress,
fever, pain, metabolic disease (hyperthyroidism),
TREATMENT hypovolemia, thromboembolic disease, shock and
anemia.
Most cats do not require specific therapy with anti-
arrhythmics unless they are symptomatic.
Class I anti-arrhythmics block the sodium channels and Clinical signs
result in decreased excitability of the diseased cells. The
most common examples are procainamide and lidocaine In the majority of patients, clinical signs are related to
(high risk of toxicity). the underlying disease.
Clinical signs related to a fast heart rate (> 280 bpm) If associated with low systemic blood pressure and the
include restlessness, tachypnea, open-mouth breath- cause is not hypovolemia, shock or blood loss, and sys-
ing, poor pulse quality and delayed capillary refill tolic myocardial function is preserved, consider heart
time. rate control with:
● Propranolol at 0.5–1 mg/kg PO q 8–12 hours.
● Atenolol at 6.25–12.5 mg/cat PO q 12 hours.
Diagnosis ● Sotalol at 10–20 mg/cat PO q 12 hours.
The diagnosis is based on physical examination and an ● Diltiazem at 7.5–15 mg/cat PO q 8 hours.
electrocardiogram (Figure 10.1).

The heart rate is above 220 bpm. Prognosis
The cardiac rhythm is regular. The prognosis depends on the underlying etiology.
There is a P wave for every QRS complex with a con- Most cases have a favorable outcome.
stant P-R interval.
The morphology of the P wave is normal. SUPRAVENTRICULAR/ATRIAL
TACHYCARDIA**
The QRS complex morphology is normal.
The changes in the heart rate occur gradually (i.e. Classical signs
gradual acceleration or deceleration of the heart rate). ● Fast and regular heart rate above 220 bpm.
● Strong precordial impulse.
● Loud S1 heart sound.
● Weakness/collapse.
Supraventricular tachycardias including atrial tachy-
cardia, AV nodal re-entrant tachycardia, atrial flutter
with 2:1 conduction need to be differentiated from sinus Pathogenesis
tachycardia. Supraventricular tachycardia may look The arrhythmia originates from anywhere above and
identical to sinus tachycardia on the ECG. Excessive including the atrioventricular node.
heart rate (greater than 250 bpm) is more likely to be
supraventricular tachycardia. Supraventricular tachycar- Supraventricular/atrial tachycardias most commonly
dia may have abnormal P wave morphology or lack P result from primary myocardial disease.
waves compared to sinus tachycardia where P waves are These arrhythmias are most commonly seen in associa-
normal. tion with hypertrophic or restrictive cardiomyopathies.

Before initiating treatment, determine the underlying In the majority of patients, clinical signs are related to
etiology, and treat appropriately. the underlying disease such as cardiomyopathy rather
RHYTHM STRIP: II
QRS
50 mm/sec;I cm/mV P T
Figure 10.1. Sinus tachycardia at 225 bpm.

than the tachycardia, and include a heart mumur, dysp- Treatment

nea, weakness, collapse and lameness, paralysis or pare-
sis from systemic thromboembolism. If the patient is symptomatic (hypotension, cardiogenic
shock, collapse) for the arrhythmia, then treatment is
Clinical signs related to a fast heart rate (> 280 bpm) required. The following drugs can be used in succes-
include restlessness, tachypnea, open-mouth breathing, sion and are written in order of preference if the previ-
poor pulse quality and delayed capillary refill time. ous drug is not effective.
● Diltiazem at 0.1–0.3 mg/kg IV slow bolus over
3–5 minutes. The dose can be repeated in 5–10
Diagnosis minutes if sustained SVT. After IV bolus an intra-
The diagnosis is based on physical examination and an venous constant rate infusion can be started at
electrocardiogram. 5–20 μg/kg/min. Diltiazem is compatible with any
type of IV fluids.
The heart rate is above 220 bpm. ● Esmolol at 250–500 μg/kg IV bolus given slowly
The cardiac rhythm is regular. over 1 minute. The bolus can be followed with
a constant rate infusion at 50–200 μg/kg/min.
The QRS complex morphology is normal. Esmolol is compatible with 5% dextrose.
● Propranolol at 20 μg/kg IV slow bolus over
There is a P wave for every QRS complex, but the P
wave morphology may or may not be different from 5 minutes. Propranolol can be given up to a total
normal sinus beats. dose of 100 μg/kg in repeated boluses.
P waves may be “buried” in the S–T segment. If the patient is not symptomatic for the arrhythmia:
● Atenolol at 6.25–12.5 mg/cat PO every 12 hours.
The arrhythmia may be sustained or occur in parox- ● Diltiazem at 7.5–15 mg/cat PO every 8 hours.
ysms. ● Propranolol at 2.5–5 mg/cat PO every 8–12 hours.
● Sotalol at 10–20 mg/cat PO every 12 hours.
The changes in the heart rate are abrupt. The
arrhythmia may terminate spontaneously with a
sudden decrease in heart rate.
The QRS complex may be slightly aberrant in the Prognosis
beginning of the paroxysm of tachycardia. The prognosis depends on the underlying etiology.
The QRS complex may alter its configuration (electri- In general, the presence of this arrhythmia suggests
cal alternans) in the first few seconds of the run of advanced underlying cardiac disease.
tachycardia.
In cases where the etiology is due to the existence of a
by-pass tract, the cat may have a good prognosis, pro-
Differential diagnosis viding there is good control of the tachycardia.
Sinus tachycardia may look identical to supraventricu-
lar tachycardia sinus on the ECG. Excessive heart rate
(greater than 250 bpm) is more likely to be supraventric- ATRIAL FIBRILLATION*
ular tachycardia. Supraventricular tachycardia may have
abnormal P wave morphology or lack P waves compared Classical signs
to sinus tachycardia where P waves are normal.
● Fast and irregularly irregular variable heart
Motion or electrical artifact can usually be resolved rate.
by improved ECG recording technique: repositioning ● Strong precordial impulse.
the electrodes, moistening the skin with alcohol, posi- ● Loud and variable S1 heart sound.
tioning the cat on a non-metal table isolated from other ● Weakness/collapse (rare).
electrical devices.
Pathogenesis which appear similar to P waves, but these can be

distinguished from true P waves because they do not
This arrhythmia results from rapid disorganized atrial occur in every lead. With atrial flutter, P waves can be
activity “bombarding” the AV node. identified in all leads with a regular P–P interval.
The heart rate may be normal or increased. Frequent paroxysmal supraventricular tachycar-
Its presence is usually associated with severe left atrial dia: Usually paroxysmal supraventricular tachycardia
enlargement. is sustained for several beats. These beats have a regu-
lar R–R interval compared to atrial fibrillation where
the R–R interval is always irregular.
Clinical signs
In the majority of patients, clinical signs are related to Treatment
the underlying cardiac disease. The goal is to obtain a heart rate below 180 beats per
Clinical signs related to a fast heart rate (> 280 bpm) minute in the exam room. The heart rate should be
include restlessness, tachypnea, open-mouth breathing, determined by ECG rhythm strip. Several recheck
poor pulse quality and delayed capillary refill time. visits, usually weekly, may be needed for adjustment
of medication to reach the target heart rate.
The onset of atrial fibrillation may be marked by decom-
pensation of the heart disease with pulmonary conges- For cats with underlying dilated cardiomyopathy:
tion. ● Digoxin at 1/4 of 0.125 mg tablet/cat PO every
24–48 hours. Cats should be monitored carefully for
signs of toxicity, and medication stopped if anorexia
or vomiting develop.
Diagnosis
The heart rate may be normal or increased (Figure 10.2). For cats with preserved myocardial systolic function:
● Atenolol at 12.5 mg/cat PO every 12 hours.
There are no visible P waves in any lead. ● Diltiazem at 7.5–15 mg/cat PO every 8 hours.
● Propranolol at 2.5–5 mg/cat PO every 8–12 hours.
Small fluctuations on the baseline (f waves) may be
seen and are not related to the QRS complex.
The ventricular rate is irregularly irregular, and the
Prognosis
QRS complex has a normal configuration.
In general, this arrhythmia is associated with end-stage
cardiac disease and with severe left atrial enlarge-
Differential diagnosis ment. It may predispose to the development of throm-
boembolic disease.
Atrial flutter with variable conduction: With atrial
fibrillation the baseline may have some deflections The prognosis for long-term survival is poor.
RHYTHM STRIP: II
50 mm/sec; I cm/mV f f
Figure 10.2. Atrial fibrillation. Note fibrillatory “f” waves.

VENTRICULAR TACHYCARDIA*** Diagnosis

The heat rate is above 220 bpm (Figure 10.3).
Classical signs
There is no association between P waves and the QRS
● Fast and regular heart rate above 220 beats complex (P waves may be seen anywhere in the cardiac
per minute. cycle).
● Strong precordial impulse.
● Loud S1 heart sound. The QRS morphology is aberrant.
● Weakness/collapse (rare). This arrhythmia is usually regular, but some degree of
variability of the cardiac rhythm may be present.
This arrhythmia may be sustained or occur in parox-
Pathogenesis ysms.
The arrhythmia originates from the ventricles. Changes in heart rate are abrupt.
Ventricular tachycardias most commonly result from Differential diagnosis

primary cardiac disease.
Supraventricular tachycardia (supraventricular tachy-
Most often, it is the result of myocardial fibrosis asso- cardia with aberrant ventricular conduction, or atrial
ciated with a cardiomyopathy. flutter without variable conduction but with aberrant
Sustained ventricular tachycardia may be caused by ventricular conduction) may appear similar to ventricular
myocardial infarction. tachycardia on the ECG. Supraventricular tachycardia
may have P waves preceding the QRS complex.
Other causes of ventricular tachycardia include meta-
bolic acidosis and drug-induced (digitalis). Motion or electrical artifact can usually be resolved
by improved ECG recording technique: repositioning
the electrodes, moistening the skin with alcohol, posi-
tioning the cat on a non-metal table isolated from other
Clinical signs electrical devices.
In the majority of patients, clinical signs are related to

the underlying disease. Treatment
Some patients do not show clinical signs from the If the patient is symptomatic (hypotension, cardio-
tachycardia. genic shock, collapse), or sustained heart rate greater
than 220 bpm, then immediate therapy is recom-
Clinical signs related to a fast heart rate (> 280 bpm) mended.
include restlessness, tachypnea, open-mouth breath-
ing, poor pulse quality and delayed capillary refill Correct any metabolic, electrolyte or acid–base abnor-
time. malities.
Lead II 25 mm/s 1cm/mV

V V V V V V V V V
F F
Figure 10.3. Ventricular tachycardia. “V” marks VPCs. Fusion beats are marked “F”.
● The authors use procainamide at 5–10 mg/kg slow

SUPRAVENTRICULAR PREMATURE BEATS
IV bolus. This bolus can be repeated once if neces-
(SVPBS)***
sary.
● Esmolol at 250–500 μg/kg IV bolus given slowly
Classical signs
over 1 minute. The bolus can be followed with a con-
stant rate infusion at 50–200 μg/kg/min. Esmolol is ● Pulse deficits.
compatible with 5% dextrose. ● Interruptions of rhythm regularity.
● Propranolol at 20 μg/kg slow IV bolus. Repeat
boluses can be given up to a total maximum dose of
100 μg/kg. Pathogenesis
DO NOT USE LIDOCAINE IN CATS. Severe neu- Premature beats result from two mechanisms, alter-
rotoxicity can occur. ations in impulse formation and alterations in impulse
If patient is not symptomatic for the arrhythmia: conduction.
● Atenolol 6.25–12.5 mg/cat PO every 12 hours.
Alterations of impulse formation depend on the
● Propranolol at 2.5–5 mg/kg PO every 8 hours.
intrinsic automaticity of diseased cardiac cells.
● Sotalol 10–20 mg/cat PO every 12 hours. ● Diseased myocardial cells outside the specialized con-
● Procainamide 10–20 mg/kg PO every 8–12 hours.
duction system can acquire automaticity because of
changes in the resting membrane potential.
Prognosis Alterations of impulse conduction result from re-

entry and by-pass tracts.
Most cats with sustained ventricular tachycardia have ● Re-entry, is a self-sustaining electrical circuit that
severe myocardial damage and are at high risk of sud- repeatedly depolarizes surrounding tissue.
den death. ● By-pass tracts alter the normal pathway of conduc-
The prognosis is fair. tion by providing an alternative pathway around

the AV node.
PREMATURE BEATS
Clinical signs
The following are definitions of electrocardiographic
findings necessary to understand the distinguishing fea- Most patients show no evidence of clinical signs.
tures between supraventricular and ventricular prema-
In some cases panting, restlessness and anxiety may be
ture beats:
seen.
● A fusion beat occurs when the ventricles are
activated by two different wave fronts, resulting
in abnormal/aberrant appearance of the QRS Diagnosis
complex.
The heart rate is normal and the cardiac rhythm is irregu-
● An interpolated beat is when a ventricular beat
lar because of the premature beats (Figure 10.4).
occurs between two normal beats without disturb-
ing the cardiac rhythm. The ectopic P wave is premature, the configuration may
● The re-setting or non-resetting of the sinoatrial be different from normal sinus beats.
node refers to the influence of the premature beat
The morphology of the QRS complex is similar to a
on the basic sinus rhythm.
normal sinus beat.
● If the rhythm is disturbed by the premature beat
then the rhythm is reset. Resetting of the basic The QRS complex is usually narrow, but in very pre-
rhythm is also referred to as non-compensatory mature beats it may be wider (longer duration) than
pause. normal.
RHYTHM STRIP: II
50 mm/sec; I cm/mV
APC
Figure 10.4. Atrial premature contraction (APC).
There is association between P waves and the QRS not likely to severely compromise the patient’s
complex. outcome.
Supraventricular premature beats cause re-setting of If the arrhythmia is frequent and is a result of severe
the sinoatrial node. left atrial enlargement, these beats may reflect atrial
electrical instability and precede the development of
Supraventricular tachycardia is always regular.
atrial fibrillation.
VENTRICULAR PREMATURE BEATS
Marked respiratory sinus arrhythmia is rare in cats
(VPBS)***
but may mimic the presence of premature beats. Sinus
arrhythmia is rare in cats and only occurs at slow
Classical signs
heart rates. Increasing the heart rate above 180 bpm
by excitement or atropine (0.04 mg/kg parenterally) ● Pulse deficits.
will abolish sinus arrhythmia. ● Interruptions of rhythm regularity.
Motion or electrical artifact may mimic premature
beats. Premature beats can be distinguished from motion Pathogenesis
artifact because they occur simultaneously in all leads.
Premature beats result from two mechanisms, alter-
Ventricular premature beats without a wide QRS ations in impulse formation and alterations in impulse
complex may be erroneously classified as supraventric- conduction.
ular premature beats. Supraventricular premature beats
will usually reset the sinus rate. Alterations of impulse formation depend on the
intrinsic automaticity of diseased cardiac cells.
● Diseased myocardial cells outside the specialized
Treatment conduction system can acquire automaticity
Isolated premature beats do not require therapy unless because of changes in the resting membrane poten-
they present with other more severe arrhythmias. tial.
If there is suggestion of hemodynamic compromise Alterations of impulse conduction result from re-
therapy may be considered: entry and by-pass tracts.
● Re-entry, is a self-sustaining electrical circuit that
● Diltiazem at 7.5–15 mg/cat PO every 8 hours. repeatedly depolarizes surrounding tissue.
● By-pass tracts alter the normal pathway of con-
● Propranolol at 0.5–1 mg/kg PO every 8–12 hours.
● Sotalol at 10–20 mg/cat PO every 12 hours. duction by providing an alternative pathway
around the AV node.
Prognosis
Clinical signs
The prognosis depends on the underlying cardiac
disease, but in general, this class of arrhythmias is Most patients show no evidence of clinical signs.
In some cases with frequent VPBS panting, restlessness fied as ventricular premature beats. Supraven-tricular
and anxiety may be seen. premature beats will usually reset the sinus rate.
Diagnosis Treatment
The heart rate is normal and the cardiac rhythm is irregu- Isolated premature beats do not require therapy
lar because of the premature beats (Figure 10.5). unless present with other more severe arrhythmias.
The morphology of the QRS complex is abnormal/ If there is a large number of ventricular premature beats
aberrant when compared with the normal sinus beat. where the premature QRS falls within the preceding
T wave (R on T phenomenon), therapy should be con-
The QRS complex is wider than normal and has a sidered.
bizarre appearance.
If there is suggestion of hemodynamic compromise
VPBs may occur as a fusion beat. therapy may be considered:
VPBs may occur as an interpolated beat.
● Propranolol at 0.5–1 mg/kg PO every 8–12 hours.
There is no association between the P waves and the ● Procainamide at 10–20 mg/kg PO every 8–12
QRS complex. hours.
VPBs do not re-set the sinoatrial node.
Prognosis
The prognosis depends on the underlying disease.
Marked respiratory sinus arrhythmia is rare in
cats but may mimic the presence of premature beats. In most cases isolated premature beats are not life
Sinus arrhythmia is rare in cats and only occurs at threatening.
slow heart rates. Increasing the heart rate above 180 When R on T phenomenon is present, patients may be
bpm by excitement or atropine (0.04 mg/kg parenter- predisposed to the development of ventricular tachy-
ally) will abolish sinus arrhythmia. cardia and/or sudden death.
Motion or electrical artifact may mimic premature If VPBs are due to primary heart disease, this likely
beats. Premature beats can be distinguished from motion reflects an advanced stage and may be associated with
artifact because they occur simultaneously in all leads. a less-favorable prognosis.
Supraventricular premature beats with aber- If due to causes other than primary heart disease, the
rant ventricular conduction may be erroneously classi- prognosis is dependent on the underlying disease.
RHYTHM STRIP: II
50 mm/sec; I cm/mV VPC VPC VPC VPC
05-40Hz
Figure 10.5. Ventricular premature contractions.
Recording several leads, especially chest leads, will

DISEASES CAUSING BRADYCARDIA facilitate identification of P waves.
SINUS BRADYCARDIA* Treatment
Classical signs Treat the underlying disease.
● Heart rate less than 120 beats per minute. The response to atropine administration should be
● Pulse is regular. determined to assess normal sinus node function.
● Weakness.
● Collapse. Prognosis
The prognosis depends on the underlying disease.
Pathogenesis
ATRIAL STANDSTILL*
This arrhythmia originates from the sino-atrial node,
the normal pacemaker of the heart. It is usually indica- Classical signs
tive of severe underlying cardiac disease or second-
● Weakness.
ary to extracardiac disease.
● Collapse.
Extracardiac causes most commonly associated with ● Lethargy.
this arrhythmia are:
● Respiratory disease.
● Intracranial disease. Pathogenesis
● Electrolyte disturbances (hyper or hypokalemia).
The arrhythmia can result from atrial cardiomyopathy.
● Metabolic disturbances (acidosis, hypoglycemia).
● Hypothermia and hypoxia. The arrhythmia can occur in long-standing cardiac
● Overdose of beta-blockers or calcium channel disease, more commonly seen in the dilated form.
blockers, anesthetic agent or digitalis. The arrhythmia can result from hyperkalemia,
primarily because of feline urethral obstruction
Clinical signs syndrome.
If the heart rate is less than 100 beats per minute, weak- A serum potassium greater than 8.5 mEq/L (mmol/L)
ness, collapse and lethargy may be seen. results in disappearance of P waves and results in atrial
standstill.
In the majority of patients, clinical signs are related to
the underlying disease.
Clinical signs
Diagnosis
Signs may be related to the underlying disease.
The heart rate is lower then 120 bpm.
Weakness, lethargy and collapse are most commonly
There is a P wave for every QRS complex. seen.
The QRS complex morphology is normal.
The atropine response test is normal (give 0.04 mg/kg IV Diagnosis
while recording rhythm strip, if no response in 2 minutes The heart rate is slower than 120 bpm (Figure 10.6).
repeat dose).
There are no P waves in any lead.
Differential diagnosis The ventricular rhythm is regular.
Sinus bradycardia may be diagnosed as a junctional escape The QRS complex morphology may be normal or
rhythm in cases where P waves are isoelectric. increased in duration and bizarre in morphology.
LEADII at 50 mm/sec 1 cm/m//v
Figure 10.6. Atrial standstill with right bundle branch block. Note lack of P waves.
P waves should not be present in any lead. Pathogenesis

In hyperkalemia T waves are tall and peaked. The arrhythmia results from intermittent block of the
atrial electrical wave through the AV node. There are
two different types:
Mobitz type I
Sinus bradycardia with isoelectric P waves can mimic ● This type of second-degree AV block is usually the
atrial standstill. result of enhanced parasympathetic tone and is not
Recording several leads, especially chest leads, will associated with conduction system disease.
● The block is usually located above the His bundle
facilitate identification of P waves.
bifurcation.
● It is found in some patients with cardiomyopathy
and in some cases may be drug induced (digitalis,
Treatment
beta-blockers, calcium channel blockers).
Treat the underlying disease. If patient is sympto-
Mobitz type II
matic for the slow heart rate, a pacemaker is indicated.
● This type of second-degree AV block is the result of
Pacemaker lead should be implanted on the epi- primary conduction system disease, either due to
cardium. degeneration of the His bundle, infiltrative cardiac
disease or cardiomyopathy.
● The site of block is located at or below the His
Prognosis
bundle.
Normal atrial activity will not be restored unless the
cause is hyperkalemia. Clinical signs
After a successful pacemaker implantation, the progno- Mobitz type I
sis is fair because the underlying atrial myopathy is ● This type of AV block is usually not associated with
likely to progress to congestive heart failure or throm- clinical signs.
boembolic disease.
Mobitz type II
● Most cases are asymptomatic, when symptoms are
present the most common are:
SECOND DEGREE ATRIO-VENTRICULAR
– Weakness.
BLOCK**
– Lethargy.
– Collapse.
Classical signs
● Weakness.
Diagnosis
● Lethargy.
● Collapse. Second degree AV block Mobitz type I (Figure 10.7).
● The basic rhythm is a sinus rhythm.
RHYTHM STRIP: II
50 mm/sec; I cm/mV P P P (blocked)
Figure 10.7. Second-degree AV block Mobitz type 1. Note progressive lengthening of the P–R interval.
● The heart rate may be normal or lower than normal. ● The response to atropine should be determined. With
● There is progressive prolongation of the P–R normal AV nodal function, blocked P waves should
interval. disappear and the rhythm becomes regular.
● The P–R interval prolongation is seen at progres-
Second-degree AV block Mobitz type II:
sively decreasing increments.
● The treatment depends on the severity of the block.
● There is progressive shortening of the R–R interval.
● If the ventricular rate is adequate and the patient
● One or more of the P waves are blocked.
does not have symptoms that are explained by the
● The P–R interval of the beat immediately after a
cardiac rhythm, then treat the underlying disease.
blocked P wave is shorter than the beat immedi-
● If the patient is symptomatic for the bradyarrhythmia:
ately before the blocked beat.
– Medical therapy can be tried:
Second-degree AV block Mobitz type II. – Theophylline 20 mg/kg PO every 24 h.
● The basic rhythm is a sinus rhythm. – Propantheline bromide 7.5 mg/cat PO every
● The P–R interval and the R–R interval are 8–12 h.
constant. – Terbutaline 0.625 mg/cat PO every 8–12 h.
● There is unexpected failure of a P wave to conduct – Responses to medical therapy are variable and
to the ventricle. usually temporary, and a pacemaker is usu-
● The ventricular rate is slower than the atrial rate. ally indicated.
● The degree of block, i.e. the relative number of
P waves and QRS complex is variable.
Prognosis
● The QRS complex morphology may be abnormal.
Second-degree AV block Mobitz type I:
● The prognosis is good.
Second degree AV block Mobitz type II:
When the atrial and ventricular rates are multiples of ● If the patient is asymptomatic and there is no pro-
each other and variable in rate, third-degree AV block gression of the severity of the AV block, then the
may mimic second-degree AV block Mobitz type II. prognosis is favorable.
Usually the QRS complexes are wide and bizarre with ● This form of AV block may progress to third-
third-degree AV block, but look normal with second- degree AV block.
degree AV block. ● Restoration of normal AV conduction is not expected.
Artifact mimicking a blocked P wave. Premature beats

can be distinguished from motion artifact because they THIRD-DEGREE AV BLOCK
occur simultaneously in all leads.
Classical signs
● Weakness.
Treatment
● Lethargy.
Second-degree AV block Mobitz type I: ● Collapse.
● Usually does not require therapy.
Pathogenesis The QRS complex morphology is more commonly

abnormal and is wide and bizarre.
This arrhythmia results from complete block of the
atrial electrical wave through the AV node.
The site of block is at or below the bundle of His.
Advanced second-degree AV block may mimic inter-
The most common etiologies are: mittent third-degree AV block.
● Cardiomyopathy.
● Degeneration, fibrosis or infiltration of the conduc-
tion system.
Treatment
Clinical signs Many cats are asymptomatic with this arrhythmia;
therefore treatment is not indicated for these patients.
In some cases, no clinical signs are present.
If symptoms of collapse or weakness are present med-
If there are clinical signs these are due to a combination ical therapy can be tried:
of the underlying disease and the degree of bradycardia. ● Theophylline 20 mg/kg PO every 24 h.
Usually the heart rate is below 100 beats per minute ● Propantheline bromide 7.5 mg/cat PO every 8–12 h.
and the signs are: ● Terbutaline 0.625 mg/cat PO every 8–12 h.

● Weakness.
Responses to medical therapy are variable and usually
● Lethargy.
temporary and a pacemaker is indicated.
● Collapse.
Diagnosis Prognosis
In third-degree AV block there is complete dissocia- The prognosis is poor for restoration of normal AV con-
tion between the atrial rhythm and the ventricular duction.
rhythm (Figure 10.8).
Successful pacemaker implant is associated with a
The P–P interval and R–R interval are usually con- good prognosis if severe morphologic cardiac disease is
stant. not present.
The atrial rate is higher than the ventricular rate. ● Epicardial leads are recommended. The authors
do not recommend the use of transvenous pace-
The P wave configuration is normal. maker leads in cats. Transvenous pacemaker leads
The QRS complex morphology is normal if the escape are commonly associated with post-operative com-
focus responsible for ventricular activation is located plications, resulting in severe pleural effusion due
above the bifurcation of the His bundle. to thrombosis of the cranial vena cava.
P P P P P P P
* * * *
Figure 10.8. Third-degree AV block. Note the lack of relationship between P waves and QRS complexes
marked with asterisk.
RECOMMENDED READING
Ettinger, J and Feldman, C. Textbook of Veterinary Internal Medicine. Philadelphia, PA W.B. Saunders., 2004.
Fox P, Sisson D, Moise NS. Textbook of Canine and Feline Cardiology: Principles and Clinical Practice.
Philadelphia, PA, WB Saunders Co., 1999.
Kittleson MD, Kienle RD. Small Animal Cardiovascular Medicine. St Louis, MO, Mosby, 1998.
Tilley LP. Essentials of Canine and Feline Electrocardiograph: Interpretation and Treatment. Philadelphia, PA, Lea
& Febiger, 1992.
Tilley LP. ECG for the Small Animal Practitioner. Jackson, WY, Teton NewMedia, 1999.
PART 4
Cat with urinary tract signs
11. The cat straining to urinate

Lucio John Filippich
KEY SIGNS
● Straining to urinate.
● Excessive time spent in the litter box.
● Urination in inappropriate places.
MECHANISM?
● Straining in cats during micturition is due to increased urethral outflow resistance and/or
lower urinary tract inflammation or pain.
● Hematuria associated with difficult or painful urination indicates lower urinary tract bleeding.
● Cats straining to urinate may also spend excessive time in the litter box or have inappropriate
urination which needs to be differentiated from constipation, and behavioral causes of inappropriate
urination.
WHERE?
● Lower urinary tract (urinary bladder, urethra and prostate gland).
WHAT?
● Although several lower urinary tract diseases can cause cats to strain, most are idiopathic, fol-
lowed by urolithiasis and bacterial cystitis/urethritis.
173
174 PART 4 CAT WITH URINARY TRACT SIGNS

Diseases causing straining to urinate
MECHANICAL
● Hypercontractile bladder* (p 190)
Occurs when detrusor muscle contractions are triggered at low volumes and pressure, resulting in
urinary bladder storage dysfunction. It may be due to reduced bladder capacity, excessive sensory
input or neurologic disorders. Clinical signs include incontinence and pollakiuria associated with a
relatively empty urinary bladder.
●Urethral stricture (p 191)
Dysuria associated with urine dribbling and an over-distended urinary bladder.
METABOLIC
● Urolithiasis** (p 184)
Mainly seen in middle-aged cats showing persistent or recurring cystitis and hematuria. The for-
mation of small uroliths can lead to urethral obstruction, especially in male cats. Most frequent
uroliths are calcium oxalate and struvite.
NEOPLASTIC
● Neoplasia* (p 191)
Tumors of the lower urinary tract are rare, often malignant and mainly seen in cats over 8 years of
age. Dysuria and intermittent or persistent hematuria may occur depending on the type and loca-
tion of the neoplasm.
INFLAMMATORY
● Infectious cystitis/urethritis* (p 187)
Infectious agents, usually bacterial, may cause inflammation of the urinary tract. Most bacterial
infections are secondary to other causes of lower urinary tract disease or the use of indwelling uri-
nary catheters. Clinical signs include dysuria, pollakiuria with or without hematuria. The urinary
bladder is usually empty.
IDIOPATHIC
● Obstructed lower urinary tract disease (LUTD)** (p 179)
Urethral plugs are formed causing mechanical urethral obstruction that can lead to bladder disten-
tion, post-renal renal failure and death. Occurs mainly in male cats under 5 years of age. Acute
onset of dysuria, pollakiuria and stranguria. Abdominal palpation reveals a non-expressible, firm,
often painful, over-distended urinary bladder. Signs of uremia include depression, vomiting, dehy-
dration, hypothermia, bradycardia and general muscle weakness.
● Non-obstructed lower urinary tract disease (LUTD)/feline idiopathic
cystitis*** (p 176)
Hemorrhagic cystitis of unknown etiology mainly seen in cats 2–6 years of age. History of recur-
ring bouts of dysuria, pollakiuria and hematuria. Abdominal palpation reveals a small contracted,
painful urinary bladder. The urine usually contains frank blood and the duration of the hematuria
varies.
11 – THE CAT STRAINING TO URINATE 175
TRAUMA
● Urethral trauma* (p 189)
May result from pelvic fractures, surgery and catheterization especially when associated with ure-
thral obstruction. Urethral rupture may result in subcutaneous accumulation of urine in the perineal
region leading to swelling, discoloration and necrosis of the skin.
TOXIC
● Cyclophosphamide toxicity (p 191)
The use of cyclophosphamide as a therapeutic agent can lead to hematuria and dysuria.
Stretch receptors in the detrusor muscle are gradually

INTRODUCTION stretched during bladder fill. Afferent pelvic nerve
fibers (parasympathetic) detect changes in the
MECHANISM? amount of stretch during filling and when the thresh-
old of bladder capacity is reached, they discharge
Straining in cats during micturition is due to
impulses to the sacral spinal cord.
increased urethral outflow resistance and/or lower ● These impulses are relayed through the spinoretic-
urinary tract inflammation or pain.
ular pathways to the pons (pontine mesencephalic
Straining cat exhibits clinical signs such as dysuria reticular activating system) in the brain stem where
(difficult or painful urination), stranguria (slow and a detrusor response is integrated.
painful urination with a narrow or dribbling urine ● Efferent motor impulses descend the spinal cord via
stream), pollakiuria (abnormally frequent urination) the reticulospinal pathway to the sacral parasympa-
with or without hematuria. thetic nucleus, and then on to the detrusor muscle
via the pelvic nerve.
Hematuria associated with dysuria indicates lower uri-
nary tract bleeding.
Each muscle fiber in the detrusor muscle does not
Owners may complain of inappropriate urination or receive direct innervation; rather “pacemaker” fibers
excessive time spent in the litter box, so these need to scattered through the detrusor are depolarized with sub-
be differentiated from behavioral causes of inappropri- sequent spread of excitation to adjoining muscle fibers
ate urination and constipation. through “tight junctions”. Tight junctions are areas of
fusion of the outer components of the cell membrane.
Urinary bladder innervation is primarily autonomic.
The storage phase is controlled by sympathetic The resulting wave of excitation causes contraction of
innervation. the detrusor, which pulls the neck of the bladder
● During the filling phase, sympathetic autonomic open like a funnel and squeezes out the urine.
activity (hypogastric nerve) dominates and
Simultaneously with detrusor muscle contraction,
causes the body of the bladder to relax (β-adren-
inhibitory interneurons are activated in the sacral
ergic stimulation) and the internal sphincter to
spinal cord, which synapse on pudendal motor neu-
contract (α-adrenergic stimulation).
rons. The pudendal neurons are inhibited, resulting
● There is also an α-receptor-mediated inhibition of
in relaxation of the external urethral sphincter.
parasympathetic ganglion transmission.
Once the bladder is empty, pelvic nerve activity ceases
Pudendal nerves (somatic innervation) stimulate con-
and the hypogastric and pudendal nerves are no longer
traction of the external urethal sphincter (and anal
inhibited. Detrusor muscle relaxation and urethral
sphincter).
sphincters contraction returns and the filling phase
Bladder emptying is under parasympathetic control. begins again.
A thin mucus layer of glycosaminoglycans (GAGs) Pathogenesis

which help prevent transepithelial movement of urinary
substances covers the urinary bladder mucosa. Defects in Non-obstructed idiopathic LUTD, also known as
surface GAGs may allow urinary substances (protons, idiopathic or interstitial cystitis, commonly presents
potassium ions or hyperosmolar fluid) to penetrate the as hemorrhagic cystitis. It is the most common cause
bladder mucosa initiating sensory nerve stimulation, mast of signs of lower urinary tract disease in cats, and
cell activation and/or induce an immune-mediated or neu- accounts for 60–70% of cases.
rogenic inflammatory response. The syndrome is self-limiting, but recurring.
Excitation of sensory afferent neurons (c-fibers) and Although the etiology is unknown, uropathogens, and
release of neuropeptides and/or activation of mast cells inflammation triggered by neurogenic mechanisms or
in proximity to neuropeptide-containing sensory neurons urinary constituents have been postulated.
may lead to inflammation, pain and tissue injury.
Stress may play a precipitating role in some cases.
Mast cell activation results in secretion of biologically Cats were significantly more likely to be male, over-
active substances (histamine) that may be responsible weight and pedigree. Several stress factors were
for the inflammation, pain and smooth muscle contrac- found to be involved including living with another cat
tion seen in bladder disease. with which there was conflict.
Signs and pathophysiology appear analogous to inter-
WHERE? stitial cystitis in human beings.
Lower urinary tract (urinary bladder, urethra and Feline idiopathic or interstitial cystitis has been asso-
prostate gland). ciated with local abnormalities in the bladder, and
abnormalities in the endocrine system, the central nerv-
ous system, and the efferent and afferent neurons.
WHAT?
Bladder abnormalities include decreased urine glu-
Incidence is about 0.5–0.8% of hospital admissions.
cosaminoglycan (GAG) excretion, submucosal petechial
Although several lower urinary tract diseases can cause
hemorrhage (glomerulations) visible when the bladder
cats to strain, most are idiopathic, followed by
is distended with water at low or high pressure,
urolithiasis and bacterial cystitis/urethritis.
increased mast cells in the bladder wall, and increased
bladder permeability.
DISEASES CAUSING SIGNS OF Increased concentrations of the neurotransmitter P and

STRAINING its receptor are present in the bladder wall which may
increase the inflammatory response.
NON-OBSTRUCTED IDIOPATHIC LUTD Increased sympathetic outflow from the brain is pres-
(IDIOPATHIC CYSTITIS, INTERSTITIAL ent, and this may result in increased inflammatory
CYSTITIS)*** response in the bladder and increased permeability.
● Stress and pain increase the sympathetic outflow
Classical signs from the brain, and stress appears to precipitate

signs in susceptible cats.
● Frequently seen trying to urinate (pollakiuria).
● Spends more time in litter box. Cats with interstitial cystitis have reduced cortisol
● Strains with little or no urine passed concentrations after stimulation with ACTH, and
(stranguria/dysuria). have smaller adrenal glands with smaller zona fascicu-
● Blood tinged urine ± blood clots (hematuria). lata and reticularis than healthy cats. These findings
● Cat may cry out during urination. suggest cats with interstitial cystitis have primary adre-
● Cat may urinate in inappropriate places. nal insufficiency. Reduced adrenal cortical reserve
may result in increased sympathetic nervous system
output. Replacement therapy is not effective and not ● Urinalysis is more suggestive of a bleeding disorder
indicated. (hematuria; >5 RBC/hpf, <5 WBC/hpf) than an
inflammatory disease (pyuria > 5 WBC/hpf).
Cats with interstitial cystitis are more likely to have
– Erythrocytes in urine may be at various stages of
gastrointestinal signs and behavior abnormalities,
degeneration, suggesting chronic bleeding.
suggesting multiple organ abnormalities. Recent data
– Pyuria (>5 WBC/hpf) is not a feature of this
suggest interstitial cystitis represents a neuroendocrine
disease.
disorder rather than a primary bladder disorder.
● Urine is bacteriologically sterile.
● Crystalluria is usually absent, and when pres-
ent, the crystals (struvite) are of normal size and
Clinical signs number.
More common in female cats in some countries, for
Radiography or ultrasonography.
example Australia, although equal sex distribution is ● Survey abdominal radiographs are usually
reported in other countries (USA).
normal.
Mainly occurs in cats 2–6 years of age. ● Contrast radiographs may reveal bladder wall
thickening and mucosal irregularities.
Typical history is of recurring bouts of hematuria ● Ultrasonographic finding may be normal or
lasting a few hours to several days associated with
reveal hyperechoic material presumed to be crys-
frequent urination and straining. The cat urinating in
talline in nature, blood clots and mural irregulari-
inappropriate places is also often reported.
ties or thickenings.
Abdominal palpation reveals a small contracted uri- ● Imaging can be used to exclude urolithiasis and
nary bladder, which is often painful on palpation. neoplasia.
The urine usually contains frank blood and the dura- Cystoscopic examination may show increased mucosal
tion of the hematuria may vary from a few hours to vascularity, superficial urothelial desquamation and
many days. Blood clots may be seen occasionally in the submucosal hemorrhage.
voided urine.
Bladder wall biopsy via cystoscopy is increasingly
being used in practice and may show epithelial hyper-
plasia, mucosal necrosis, muscular degeneration,
Diagnosis edema, fibrosis, and perivascular accumulation of lym-
Diagnosis of non-obstructed idiopathic LUTD or idio- phocytes and hemorrhage.
pathic cystitis is one of exclusion. It is based on the
presence of signs of lower urinary tract disease, and
exclusion of other causes of signs using urine culture,
and imaging techniques such as plain radiographs, con- Cystitis/urethritis typically occurs in middle-aged or
trast radiography and ultrasonography. older cats and is characterized by pyuria and bacteriuria.
History and physical examination can exclude urethral Urolithiasis occurs in middle-aged or older cats, and
obstruction. External abdominal palpation reveals a imaging reveals a urolith.
small, often firm, urinary bladder that may go into
Hypercontractile bladder is usually not associated
spasm on palpation. In contrast, with urethral obstruc-
with hematuria, despite signs of straining and pollak-
tion, the bladder is large on palpation.
iuria.
Urinalysis.
Neoplasia occurs in older cats and ultrasound or con-
● A voided sample is sufficient to confirm hematuria
trast radiography reveals a mass.
but a cystocentesis sample is required for urinalysis
and culture. If the bladder is empty at presentation, Behavioral causes of inappropriate urination are
the cat will need to be admitted and bladder fill mon- generally not associated with hematuria, dysuria
itored (see page 188, Infectious Cystitis). and stranguria.
LUTD, and the benefit of these diets may be from the

TREATMENT
reduction in urine SG.
Goals of therapy are to relieve the discomfort and
Canned food has been shown to reduce the incidence
pain associated with cystitis and to reduce the fre-
of feline lower urinary tract disease compared to dry
quency of recurrence.
food, probably because of the lower urine SG pro-
Signs are self-limiting despite therapy. Remission duced. Constancy of diet may help as dietary change
usually occurs within 7 days. can precipitate signs.
Several treatments, such as antimicrobials, glucocor- Aim for a low urine specific gravity (eg. 1.020), by
ticoids, progestagens (megestrol acetate), intravesic- adding water or a meat-flavored liquid to the food.
ular administration of DMSO (10–20 ml of 10% Urine should look like water and have no odor. If feed-
solution instilled in bladder for 10 minutes under ing dry food, add 1 cup of water to 1 cup of dry food
general anesthesia), anticholinergic agents, diuretics and allow it to soak for at least 5 minutes.
(furosemide), elimination diets, pentosan polysulfate
Amitryptyline (2.5–5 mg/cat orally at night) may be
and the surgical placement of a copper ring in to the
useful in some cats to reduce signs of irritative voiding
bladder have been advocated, but their efficacy is
but not hematuria. It is a tricyclic antidepressant which
questionable.
prevents mast cell degranulation and has anti-inflam-
Antispasmodic drugs can provide symptomatic relief matory, analgesic, anticholinergic and alpha adrenergic
from straining. Flavoxate (50 mg BID), propantheline blocking effects. A significant reduction in the frequency
bromide (7.5 mg/cat sid PO), or phenoxybenzamine of recurrence may occur with prolonged use, without
(2.5–10 mg PO q 8–12 h). improvement in urinalysis or cystoscopy findings.
Adverse reactions reported in cats include sedation,
Pain relief via opiates (including a fentyl patch, butor-
weight gain, unkempt haircoat, urine retention, throm-
phanol elixir) are indicated for cats that are frequently
bocytopenia and neutropenia.
straining to urinate.
Reduction of stress and environmental change may
Anti-inflammatory drugs such as piroxicam (0.3 mg/kg
help to prevent recurrence. In susceptible cats,
PO sid) may decrease straining and pollakiuria.
episodes can be triggered by environmental change
Megestrol acetate 5 mg sid PO for 5 days has been (e.g. changes in food, house, animals or people in the
reported by one author (Norsworthy) to be the most house).
effective drug for relieving dysuria. ● Use of the synthetic feline facial pheromone
(Feliway, Ceva Animal Health), which reduces anx-
Hydrodistension of the urinary bladder (80 cm of
iety in cats may be beneficial in some situations. In
water for 10–15 minutes) may give relief of signs in
cats with interstitial cystitis, there was a trend to
some cats and prevent reoccurence.
show fewer days with clinical signs of cystitis in
Cosequin (pentosan polysulfate (Elmiron) 8 mg/kg PO cats where the environment was treated with the
q 12 h) is a glycosaminoglycan (GAG) which is used pheromone.
in humans with interstitial cystitis to promote urothelial
Ensure that there are sufficient litter boxes and they are
GAG formation. It can be mixed in the food and given
cleaned frequently.
indefinitely to reduce recurrence. However, GAG
replacers have not been proven to be more effective If signs do not resolve within 7 days, the cat should be
than placebo in cats with interstitial cystitis. re-evaluated for other diseases causing these signs.
Feed exclusively a specially formulated non-calcino-
genic diet that is used to minimize struvite crystal
Prognosis
formation and maintain a low urine pH (<6.5) and
specific gravity (<1.030). Such diets have been shown Prognosis for recurrence is guarded because the etiol-
to be effective. However, struvite crystalluria does not ogy is unknown and treatment is largely supportive in
appear to be a significant factor in non-obstructed nature.
Recurrence of signs within 6–12 months occurs in a ● Acid–base status of the urine is important in crystal
high percentage of cats. formation, with alkaline urine favoring struvite for-
mation and acid urine favoring oxalate formation.
● The role of viruses is controversial.
OBSTRUCTED IDIOPATHIC LUTD**
Occasionally urethral obstruction is from a urolith,
Classical signs rather than a plug. Calcium oxalate urate and cystine
uroliths are more common causes of urethal obstruction
● Straining with little or no urine passed
than struvite uroliths. The mechanism for urolith for-
(stranguria/dysuria).
mation is different from plug formation, and is covered
● Frequently seen trying to urinate
on page 184 in Urolithiasis.
(pollakiuria).
● Cat may cry out during urination. Urethral obstruction can result in post-renal renal
failure (obstructive nephropathy).
● The severity of the renal failure depends on the
Pathogenesis
degree and duration of the obstruction.
Historically, diets or components of diets, such as mag- ● Post-renal renal failure can be biochemically
nesium and phosphate, have been implicated in the detected by 24 hours after complete obstruction,
pathogenesis of some forms of idiopathic LUTD in cats. and by 48 hours clinical and metabolic changes can
become life threatening.
Although the etiology is unknown, urethral plugs are
● Post-renal renal failure is invariably reversible with
formed causing mechanical urethral obstruction that
appropriate treatment.
can lead to bladder distention, post-renal renal failure
and death. Bladder over-distention may result in ischemia,
● It occurs mainly in male cats possibly because their edema, hemorrhage and loss of epithelium. The ure-
urethra is longer, narrower and less distensible. thra, proximal to the obstruction, will have similar
● The urethral plugs are composed of colloidal injuries with desquamation of epithelium, edema and
matrix into which are embedded crystals, usually infiltration of neutrophils around blood vessels, lamina
struvite crystals (magnesium ammonium phos- propria and muscle layers.
phate).
Post-obstructive diuresis may occur following relief
– The ratio of matrix to crystalline material varies
of the obstruction and last for several days.
with some urethral plugs (about 5%) lacking
● The diuresis is possibly due to the clearance of
crystalline material and are known as non-
accumulated metabolites and a temporary loss of
crystalline matrix plugs.
concentrating ability by the renal tubules.
– Other crystals that occur less commonly
● Dehydration and possibly hypokalemia can occur
include ammonium acid urate, and calcium
during this polyuric phase.
phosphate and calcium oxalate.
– Some urethral plugs may also contain erythro-
cytes.
Clinical signs
– The exact chemical composition and origin
of the matrix are unknown although Tamm- Almost always seen in male cats under 5 years of age.
Horsfall protein of renal origin has been impli-
History of excessive licking around the perineal area
cated.
and the penis is often seen extruded from the prepuce.
● The factors(s) involved in the formation of urethral
plugs are unknown and may be different for the dif- Acute onset of dysuria.
ferent plugs.
The cat may cry out during urination.
● Since minerals other than struvite may be found
in some urethral plugs, suggesting matrix per se Close inspection of the penis may show a whitish,
may play an important primary role in the forma- chalky material blocking the urethral orifice and the
tion of some plugs. tip of the penis traumatized due to excessive licking.
Abdominal palpation reveals a non-expressible, firm, – Widened QRS interval.

often painful, over-distended bladder. Cats obstructed – Spiked T wave.
for over 48 hours may show little or no signs of pain
Blood tests.
on abdominal palpation and in such cases, the bladder
● Changes in blood values (urea, creatinine, potas-
may rupture if handled other than with extreme care
sium, phosphorus, pH) depend on the severity of
and gentleness.
the renal failure.
Cats with partial obstruction may be able to maintain a ● Serum values are usually normal in cats with lower
small bladder size and not develop renal failure. Such urinary tract disease unless there is outflow obstruc-
cats show stranguria (painful urination with a narrower tion or rupture.
urine stream). – Post-renal azotemia (increased urea, creati-
nine), hyperphosphatemia, hyperkalemia
Signs of uremia indicate complete obstruction for at
become evident by 24 hours. Hypocalcemia is
least 48 hours.
variable. Mild hyperglycemia may be present.
● Depression, anorexia, vomiting, dehydration and
● The absence of clinical signs of hyperkalemia
hypothermia.
(bradycardia) does not eliminate the possibility of
● Hyperkalemia can cause bradycardia, ventricu-
severe hyperkalemia.
lar arrhythmia and general muscle weakness.
● Metabolic acidosis may exacerbate the effects of
hyperkalemia on the myocardium. Differential diagnosis
● Shock.
Urolithiasis occurs more often in middle-aged or older
Diagnosis cats.
History and physical examination. Functional urethral obstruction is often associated

● Acute onset of dysuria in a male cat. with other neurologic signs (see The incontinent cat).
● A distended, firm and often painful urinary blad- Urethral trauma usually has a history and hindquarter
der on abdominal palpation. lesions which are suggestive.
● Whitish, chalky material seen blocking the urethral
orifice or around the prepucal/perineal area. Stricture is usually preceded by a history of catheteri-
zation or trauma.
Urinalysis.
● Varying degrees of hematuria depending on the Neoplasia.
duration of the obstruction.
● Pyuria is variable.
TREATMENT
● Crystalluria is often seen and on many occasions
large crystals are found in the urine. The signifi- Depends on the severity of the clinical signs at presen-
cance of these large crystals is unclear. tation.
● Urinary pH and specific gravity values, at presenta-
If the cat is not showing clinical signs of renal failure or
tion, are variable, but pH is usually acidic and spe-
has not been obstructed for more than 24–36 hours,
cific gravity generally approaches 1.020 with
relieving the urethral obstruction and giving a bal-
prolonged obstruction.
anced electrolyte solution, subcutaneously or intra-
● Glucosuria is variable.
venously at 70 ml/kg is usually sufficient.
Radiography. Urethral plugs are often not visible on
If the cat is showing signs of renal failure, or has been
plain radiographs.
obstructed for more than 36–48 hours, correcting
Electrocardiography. the fluid and electrolyte imbalance takes priority
● Hyperkalemia (>6.0 mmol (mEq)/L). ECG changes over restoring urethral patency.
are often evident when K > 7 mmol(mEq)/L. ● Cats in post-renal renal failure must first be stabi-
– Bradycardia. lized before diagnostic tests, other than blood and
– Absence of a P wave. urine sampling, are undertaken.
● Consider cystocentesis for temporary relief of – Exteriorize the penis from the prepuce and
bladder distention. extend it caudally so as to straighten the natural
● Give dextrose saline solution IV (0.9% NaCl with curvature of the cat’s penis. Clean with warm
5% dextrose – add 100 ml of 50% dextrose per liter water.
of fluids) to rehydrate the patient over 4–6 hours – As aseptically as possible, fill a 3.5 French,
and reduce hyperkalemia, metabolic acidosis and open-ended urinary catheter (olive tip ure-
azotemia. thral catheters, Jorgensen Laboratories) with
● Cats in renal failure are frequently hypothermic and lubricating gel (xylocaine jelly at room tem-
should be warmed to normal body temperature. perature) and gently pass the catheter into the
urethra, until it comes in contact with the
Remove the obstruction. obstructing material, which is usually at the
● Immobilization. level of the bulbo-urethral gland where the
● Sedation during catheterization will help mini- urethra narrows and becomes the penile portion.
mize further urethral trauma and urethral or – Instill 0.25 ml of lubricating gel through the
bladder rupture. catheter into the urethra and remove the catheter.
● Urethral trauma from catheterization can lead to After 3 minutes, the jelly usually has lubricated
inflammation with edema of the periurethral tissue and broken up the obstructing mass, allowing it
and subsequent functional urethral obstruction. to be spontaneously extruded like toothpaste by
● Inappropriate force or the cat struggling during the high urethral pressure cranial to the obstruc-
catheterization may result in urethral or bladder tion. If the material re-obstructs, repeat the
rupture. procedure several times using 0.15 ml of gel,
● The degree of sedation required will depend on the until urine appears. This technique ensures that
cat’s clinical condition and temperament. all the obstructing material in the urethra has
● An opiate (pethidine (meperidine)) 1 mg/kg SC; been removed and little if any has been pushed
butorphanol (0.05–0.4 mg/kg IV, SC; buprenor- into the bladder. If spontaneous resolution of the
phine 0.005–0.01 mg/kg IV, SC) and acepromazine obstruction does not occur, apply gentle pres-
(0.02–0.05 mg/kg IV, SC) or an opiate and sure to the bladder. Great care should be exer-
diazepam (0.25 mg/kg SC, IV) can be used. cised when applying pressure to the urinary
● Premedicate with atropine sulfate (0.03 mg/kg) bladder, as it can lead to bladder rupture.
subcutaneously or intravenously combined in the – Retropulsion with a saline flush is commonly
same syringe as the opiate. Intravenous ultra used in practice, but is more likely to lead to re-
short-acting barbiturates (sodium thiamylal or obstruction, because obstruding material is
thiopentone (thiopental)), propofol, alfaxalone and pushed into the bladder.
inhalant anesthetics (isoflurane) can be used. – If local anesthetic agents are combined in the
Depressed cats can be masked down with isoflurane lubricating gel to anesthetize the urethral mucosa,
and oxygen. Beware of intubating the cat before it they should be used sparingly to avoid local
has reached a suitable plane of anesthesia, as intu- and systemic toxic effects that are more likely to
bation may cause reflex bradycardia or cardiac occur in the presence of damaged urothelium.
arrest. Spray the larynx with lignocaine (lidocaine) – Recatheterize with a long, soft, flexible Teflon
prior to attempting intubation. urinary catheter (3.5–4 French), secured in
● Succinylcholine is contra-indicated as it increases place with sutures, to empty the bladder com-
serum potassium levels. pletely.
● Catheterization of the bladder in cats with severe – Once the bladder has been catheterized, urine is
renal failure may be possible by using physical allowed to drip freely. Avoid removing urine by
restraint only. negative pressure (syringe) or by applying
● Catheterization. external pressure on the urinary bladder as this
– The method employed and the instrumentation can unnecessarily traumatize the bladder mucosa.
used to remove the obstruction must ensure that – If the urine is visibly clear: Instill 5–10 ml of
no further urethral or bladder trauma occurs. sodium acetate/acetic acid buffer solution
(Wallpoles buffer solution) into the bladder to – A closed urine drainage system is often imprac-
dissolve any struvite crystals. If the catheteri- tical in the cat. However, it should be used if
zation was achieved with minimal trauma, an indwelling catheters are to be left in for more
indwelling catheter is not required. than 3–4 days. A closed drainage system
– If hematuria is present: Wallpoles buffer involves connecting the urinary catheter, via
solution should not be used. extension tubing, to a sterile, empty fluid bag
– Instill 100 mg of ampicillin in 20 ml of normal below the cat.
saline into the bladder. Give parenteral antimi- – Indwelling catheters should be used for as short
crobials that are not nephrotoxic, such as amox- a time as possible to minimize catheter-induced
icillin/clavulanate, enrofloxacin. Leave the iatrogenic disease.
urinary catheter in situ for as shorter a time as – Beginning the cat on phenoxybenzamine
possible. Indwelling catheters can induce further (2.5–10 mg PO q 8–2 h) may help to reduce re-
damage to the urothelium by disrupting its gly- obstruction or dysinergia once the catheter is
cosaminoglycan coating and thus promote removed.
microbial adherence and urinary tract infection. – An Elizabethan collar and/or hobbles on the hind
Remove the indwelling catheter once hema- legs using self adhesive tape or elastoplast may
turia is no longer visible. be necessary to prevent the cat interfering with
● An indwelling catheter is required if: the urinary catheter.
– Obstructing material was expelled into the uri- – Most cats will not interfere with a properly
nary bladder. placed or correctly selected indwelling urinary
– Severe urethral trauma occurred associated with catheter. Interference usually indicates poor
removal of the plug. Significant trauma occurs if catheter placement or catheter-induced irritation.
excessive force or repeated catheterization – The use of antimicrobial therapy to prevent sec-
attempts are necessary to unblock the urethra. ondary urinary tract infection is controversial.
– A large amount of potentially obstructing debris – To avoid developing resistant organisms, it is
is present in the bladder, which may be deter- recommended that a broad-spectrum antimicro-
mined during bladder empting, by palpation of bial, such as amoxicillin be used only once
the empty bladder, or by radiography/ultra- infection occurs.
sonography. – Evidence that an infection is occurring includes
– Urine stream after relief of the obstruction is the appearance of hematuria or increasing hema-
narrower than normal. turia, bacturiuria and pyuria.
– The urinary bladder does not contract normally – Removal of the catheter at the first signs of uri-
after emptying, indicating atony. nary infection may obviate the need for antimi-
– Re-obstruction occurs, especially within 24 crobial therapy.
hours. – Follow-up urine culture and susceptibility tests
– Measurement of urine flow rate is required dur- are essential to determine treatment success.
ing intensive care of critically ill cats. – Once the catheter is removed, the cat should be
– In these situations, the advantages of maintain- keep in hospital for a further 24 hours to ensure
ing urethral patency and decompression of a that it can urinate freely.
chronically distended, devitalized bladder out- ● If the obstruction cannot be relieved:
weighs the disadvantages of ascending bacterial – General anesthesia in an unanesthetized patient
infection and ongoing damage to the urethral may help to relieve urethral spasm, and the
mucosa. intraluminal pressure present in the urinary blad-
– Silicone elastomer catheters (Wysong urethral der and urethra may facilitate the removal of the
catheter) are preferred as they are soft, pliable, obstructing material.
less irritant to the urethral mucosa and curl – The use of acid buffer solutions to dissolve the
up inside the bladder without kinking as the obstructing material is ineffective and time
bladder empties, thus avoiding bladder wall wasting, especially if the cat is in post-renal
irritation. renal failure.
– Decompress the bladder by cystocentesis ● Hypokalemia may occur with prolonged diuresis or
using a 23 G × 32 mm (1.25 in) needle attached the use of potassium-free fluids. Potassium sup-
to an extension tube, a 2-way valve and 50 ml plementation can be given in intravenous fluids
syringe. Removal of approximately 30 ml of (0.5 mmol/kg/h) or orally (2–6 mmol/cat/day) until
urine from the bladder may trigger sponta- the cat starts eating.
neous micturition. The bladder should not be ● The gluconate form of potassium is preferred
manually palpated for the next 24 hours. orally.
– Consider cystotomy with placement of an ● Once the cat voluntarily eats and drinks, the fluid
indwelling catheter (Foley catheter, 8 French; rate is decreased over 24 hours while hydration sta-
Stamey suprapubic catheter, 10 French) in the tus is monitored.
urinary bladder, and percutaneous prepubic uri-
Prevention.
nary drainage or a perineal urethrostomy.
● Feed exclusively a specially formulated non-cal-
– Perineal urethrostomy is only recommended
cinogenic diet to minimize struvite crystal forma-
as a last resort because it does not prevent
tion and maintain a low urine pH (<6.5) and low
reoccurrence of non-obstructed disease and it
specific gravity (<1.030, ideally 1.020). Meat- or
can predispose to ascending urinary tract
fish-flavored liquid or water can be added to
infection, urine scald dermatitis and urethral
increase water intake.
stricture.
– Canned food produces a lower urine specific
– Perineal urethrostomy is recommended if fre-
gravity than dry food, and decreases the fre-
quent urethral obstruction occurs despite ade-
quency of recurrence in cats. If feeding dry food,
quate medical management or urethral
add 1 cup of water per 1 cup of diet and allow to
lesions exist that cause recurrent or persistent
soak at least 5 minutes before feeding.
obstruction.
Prednisolone (2.5 mg/cat orally every 12 hours for 3–5 Prognosis

days) may reduce urethral inflammation but may pre- The prognosis depends on the duration of the obstruc-
dispose to urinary tract infection. tion, on the ease of obtaining and maintaining urethral
Functional urethral obstruction due to urethral irrita- patency, and correction of renal failure.
tion and inflammation resulting in urethral spasm can Prognosis is grave if:
occur following mechanical obstruction. This is diffi- ● The duration of the obstruction is more than 60
cult to differentiate from mechanical urethral obstruc- hours.
tion, however, failure to encounter obstructing material ● The packed cell volume of centrifuged bloody
or a grating sensation during recatheterization, suggests urine is greater than 2%.
function urethral obstruction. ● Urinary specific gravity is below 1.020.
Phenoxybenzamine (5 mg/cat orally daily for 3–5 days) The recurrence rate is 35–50%, mainly within 6
may help reduce urethral outflow resistance. months after hospitalization. Recurrence appears to be
Bladder atony may occur due to overdistention and can higher in cats under 4 years of age.
be corrected (see The Incontinent Cat). Studies on the efficacy of specially formulated diets in
naturally occurring idiopathic LUTD are limited but the
Postobstructive diuresis.
results are encouraging. Such diets have been formu-
● Following relief of the obstruction, a marked
lated to reduce magnesium and phosphate intake and
diuresis may occur and last for 2–10 days.
promote a dilute, acid urine. However, the pH of these
● Intravenous fluid therapy is required to maintain
diets may predispose to oxalte uroliths in susceptible
hydration and electrolyte balance. Initially a dex-
cats.
trose saline solution is used to hydrate the patient
over 4–6 hours, followed by a balanced electrolyte The prognosis following urethrostomy is good in that
solution (lactated Ringers solution) to maintain recurrence of urethral obstruction is unlikely, but
hydration and correct electrolyte imbalance. recurring episodes of non-obstructed cystitis may
occur. Post-surgically, urethral strictures and/or incon- Hypercalcemia (primary hyperparathyroidism,

tinence have been reported, but are uncommon follow- pseudohyperparathyroidism, idiopathic, hypercalcemia
ing uncomplicated surgery. Urethrostomy may and vitamin D intoxication) results in hypercalciuria,
predispose to ascending urinary tract infection. which has been associated with calcium oxalate
urolith formation. However, most cats with calcium
oxalate uroliths have normal serum mineral levels.
UROLITHIASIS**
Congenital portovascular anomalies and renal tubu-
Classical signs lar reabsorptive defects have been associated with
purine (urate) uroliths. Urate uroliths consist of either
● Blood-tinged urine (hematuria).
ammonium biurate (which occur with porto/vascular
● Frequently seen trying to urinate
anomalies), uric acid or sodium acid urates (occur with
(pollakiuria).
tubular defects). Predisposed cats fed a high purine diet
● Spends more time in litter box.
(e.g. liver) and producing concentrated, acidic urine are
● Straining to urinate (dysuria).
at a greater risk of producing purine uroliths.
● Cat may urinate in inappropriate places.
Cystinuria due to proximal renal tubular dysfunction
can predispose to cystine urolith formation.
Pathogenesis
Uroliths, especially those in the bladder, can cause
Urolithiasis in cats is uncommon and represents
lower urinary tract disease.
less than 5% of cats presented with hematuria and
dysuria. The formation of small uroliths can lead to urethral
obstruction, especially in male cats.
Urolithiasis is the formation of stones called uroliths
(calculi) in the urinary tract.
Clinical signs
Uroliths are made up of crystalloid with very little
organic matrix, and although a particular chemical Mainly seen in middle-aged adult cats.
type usually predominates, the chemical composition
There appears to be no sex or breed predisposition.
of the urolith can be mixed.
● The main chemical composition of uroliths Most cystoliths are asymptomatic.
reported in cats, include magnesium ammonium
Persistent or recurring cystitis may occur and present
phosphate (struvite; 42%), calcium oxalate
as increased frequency of urination, straining to urinate
(46%), purine (uric acid and urates; 6%), calcium
or increased time spent in the litter box or urinating in
phosphate (<1%) and cystine (<1%).
inappropriate places.
● Each chemical type should be considered a separate
disease process. Hematuria varies from microscopic hematuria
● The incidence of struvite uroliths appears to be (>5 RBC/hpf) to gross hematuria.
decreasing while calcium oxalate uroliths are
Urethral obstruction may occur occasionally, more
increasing. This is thought to be due to the
commonly with calcium oxalate, urate or cystine
increased use of acidifying diets in cats.
uroliths than with struvite uroliths.
Urolithiasis is not a single disease entity, but rather the
end result of one or more physiological and/or patho-
Diagnosis
logical processors, interrelated with some predispos-
ing factor(s), such as urine pH and concentration, Physical examination. Cystic uroliths are usually dif-
excessive excretion of endogenous crystalloid-form- ficult to palpate (<10%) because most are flattened
ing substances (uric acid, amino acid cystine), exces- disc-shape and few in number.
sive mineral intake and genetic factors.
Urinalysis.
Unlike the dog, struvite uroliths in cats are usually not ● Most uroliths and crystals in a urine sample are cal-
associated with urinary tract infection. cium oxalate or struvite, although heavy crystal-
luria with amorphous urates and phosphates is thra. To minimize back leakage, digital pressure
occasionally seen. around the catheter and urethra can be applied or
● Urine sediment containing struvite crystals balloon-tipped catheters (4 or 5 French) can be
(three- to six-sided colorless prisms) suggests that used to occlude the urethra. Radiographs are
the urolith is struvite in composition. taken during the infusion of the last portion of
● Urine sediment containing calcium oxalate dihy- the bolus dose.
drate (colorless envelopes with dipyramidal or
Ultrasonography.
octahedral form) or monohydrate crystals (small
● Abdominal ultrasonography can be used to identify
spindles or dumbbells) suggests that the urolith is
radiodense and radiolucent cystic uroliths, as
calcium oxalate in composition.
well as soft tissue masses.
● Ammonium biurate crystals (yellow-brown
spherulites; thorn apples) are common in cats with Blood tests (biochemistry).
portosystemic vascular anomalies, however urate ● Elevated serum urea and creatinine levels suggest
uroliths are uncommon. Rarely urate uroliths also renal involvement.
occur due to tubular disease (cat has no signs of ● Elevated liver enzymes and/or low urea levels sug-
liver disease and normal pre- and post-prandial bile gest liver dysfunction. Typically cats with ammo-
acids). Urate crystals associated with tubular dis- nium biurate uroliths associated with portosystemic
ease appear different from biurates, and are com- shunts have reduced serum urea levels, increased
posed of uric acid or sodium acid urate. serum uric acid and bile acid levels and hyperam-
● However, crystal type in urine and urolith com- monemia.
position can be different. ● Hypercalcemia may suggest a calcium-containing
● Uroliths found in alkaline urine are likely to be stru- urolith.
vite or calcium phosphate (amorphous or long thin
Urolith analysis.
prisms).
● Urolith analysis provides valuable information that
● Urinary tract infections are usually absent (<2%).
can be used in therapy to prevent the recurrence of
● Hypercalciuria may occur with calcium containing
urolithiasis.
uroliths.
● Crystallographic, X-ray diffraction and infrared
Radiography. spectroscopy techniques are preferable to qualitative
● Plain abdominal radiographs may detect radiodense chemical analysis (Oxford Stone Analysis Kit).
uroliths in the kidneys, bladder or urethra. A proper quantitative analysis gives all the min-
– Radiodense uroliths contain calcium salts, eral components of the urolith by percentage and
such as calcium oxalate. by location (surface, middle and center).
– Struvite uroliths may contain calcium and Prevention therapy is based on the mineral com-
become slightly radiodense. position of the center of the urolith as precipitation
● Double-contrast cystography can be used to of the central mineral initiates urolith formation.
detect radiolucent uroliths. The technique
involves instilling, via a urinary catheter, 1–2 ml Differential diagnosis
of water-soluble iodinated contrast material (pos-
itive contrast) into the urinary bladder, followed Infectious cystitis/urethritis is differentiated on the
by a slow infusion of carbon dioxide or nitrous presence of bacteriuria and a positive culture.
oxide gas (negative contrast), sufficient to distend Idiopathic LUTD tends to occur in young adult cats.
the bladder (approximately 30 ml). Fatal air
embolism can occur in cats with hematuria when
air is used.
Treatment
● Retrograde contrast urethrography. The tech- Uroliths can be removed by medical dissolution or sur-
nique involves infusing, as a bolus, 5 ml of posi- gical resection. The type and location of the urolith, the
tive contrast material through an open-ended severity of the clinical signs, the anesthetic risk, con-
urinary catheter positioned in the distal ure- current diseases, the sex and age of the cat, and the
owner’s wishes will all influence which procedure is pH should stay below 6.5 long term. Cats passing
most appropriate. alkaline urine should be recultured.
● Surgical removal.
Struvite urolithiasis.
– Cystotomy is performed via a ventral midline
● An acidifying, low-magnesium, low-phosphorus
abdominal approach. An avascular area near the
and low-calcium diet is recommended.
apex of the bladder is selected, stay sutures (3-0
● Alternatively, urine acidifiers (ammonium chlo-
silk) placed on either side of the intended inci-
ride or DL methionine) to effect (approximately
sion line and the bladder is emptied by cysto-
1000 mg/cat/day) can be given orally at mealtime
centesis. A 2-cm incision is made into the
to ameliorate the postprandial alkaline tide. Acute
bladder wall and the uroliths removed. Before
toxicity with high doses cat occur, especially in
closure of the bladder, a urinary catheter
kittens.
attached to a saline-filled syringe is used to flush
● Chronic metabolic acidemia due to long-term acid-
out any uroliths in the bladder neck and urethra.
ification can have adverse effects.
● Medical dissolution.
– Only nephroliths and cystoliths can be med- Calcium oxalate urolithiasis.
ically dissolved. Medical dissolution of uroliths ● A non-acidifying regular diet is recommended.
in the ureters or urethra should not be ● Diets used to prevent struvite urolithiasis should not
attempted. be used.
– Calcium oxalate uroliths can not be medically ● If the diet does not maintain the urine pH above
dissolved. 7.5, potassium citrate (50–75 mg/kg orally 12
– Struvite uroliths can be medically dissolved. hourly) therapy may be used. Monitor total CO2 to
– Mineral composition of the urolith should be ensure alkalosis does not occur. Keep TCO2 about
determined before dissolution therapy is 20 mmol(mEq)/L.
attempted. However, this is often not possible, ● Vitamin B6 (2 mg/kg orally every 24–48 hours)
and crystals in the urine sediment are used as a may be useful.
guide. ● The cause of hypercalcemia, if present, should be
– Dissolution diets are designed to produce an determined and treated.
acidic, low-mineral, dilute urine environment in ● Thiazide diuretics (chlorthiazide, 10 mg/kg orally
which cystic struvite uroliths dissolve over a 12 hourly) with potassium supplementation have
period of 4–8 weeks. Nephroliths usually take been used in normocalcemic dogs with oxalate
longer to dissolve. uroliths.
– The dissolution diet should be fed for at least
Urate urolithiasis.
2–4 weeks after uroliths are no longer visible
● Avoid acidifying diets and diets high in purine pre-
radiographically or on ultrasound.
cursors (e.g. liver).
– Failure to dissolve the uroliths may be due to
poor owner compliance, the presence of urinary Cystine urolithiasis.
tract infection or the mineral composition of the ● Acidifying diets should not be fed.
urolith is not struvite.
Prognosis
Prevention
Recurrence rates of 19% and 37% have been reported.
Long-term prevention strategies to prevent or minimize
reoccurrence should be based on mineral composition Prognosis is guarded because in some cases recur-
of the urolith. rences occur despite the implementation of adequate
preventative measures.
If infection is present, this must be treated and the urine
(culture, urinalysis especially pH) monitored long term Unless preventative measures are implemented,
to ensure that the infection has been eliminated. Urine urolithiasis will reoccur.
● Damage to the bladder mucosal defense barrier due

INFECTIOUS CYSTITIS/URETHRITIS*
to trauma (catheterization, surgery, uroliths) or
neoplasia.
Classical signs
● Changes in urine composition (alkaline pH, glu-
● Frequently seen trying to urinate cosuria).
(pollakiuria). ● Chronic renal failure.
● Straining with little urine passed (dysuria).
Infectious agents include:
● Blood-tinged urine (hematuria).
● Bacterial cystitis/urethritis (cystourethritis).
● Cat may urinate in inappropriate places.
– Rare in cats and most are aerobic infections.
– Common organisms cultured include Escherichia
coli, Staphlococcus intermedius, Streptococcus
Pathogenesis
spp., Proteus, Pasteurella, Klebsiella, Pseudo-
Inflammation of the feline urinary tract is rarely caused monas and Enterobacter. Occasionally Myco-
by an infectious agent. plasma and Ureaplasma are reported and these
organisms do not grow on routine culture
About 5–10% of cats with lower urinary tract disease
media.
have urinary tract infections, which may be primary
– Mycoplasma cultures should be considered if
or secondary.
pyuria is present but no aerobic bacterial
The prevalence of urinary tract infections increases growth occurs.
with age, being uncommon in young adult cats to mid- – Recurrent ascending urinary tract infections
dle age of either sex. occur in immunosuppressed cats (FeLV, FIV,
● Urinary tract infection accounts for less than 2% of diabetes mellitus), and are common in cats with
cases of lower urinary tract disease in cats from urethral incompetence, which occurs most fre-
1–10 years of age. quently following perineal urethrostomy.
● Of cats older than 10 years of age with signs of ● Viral
lower urinary tract disease, 46% had a positive – A herpesvirus has been isolated from cats with
urine culture and a further 17% had a positive cul- sterile lower urinary tract inflammation but its
ture associated with urolithiasis. Two thirds of cats significance is unclear.
with a positive culture not associated with urolithi- ● Fungal
asis had chronic renal failure. – Infections are rare and due to Candida albicans
● Of cats with chronic renal failure, 30% had one or Aspergillus fumigatus.
or more positive urine cultures over a period of 4–8 – Mainly reported in cats on long-term antibiotic
months which were all E. coli. therapy with impaired host defenses (perineal
urethrostomy and urine stasis).
Most bacterial infections in cats are secondary to other
● Parasitic
causes of lower urinary tract disease, perineal urethros-
– Rarely reported but include Capillaria feliscati
tomy, the use of indwelling urinary catheters or chronic
and Encephalitozoon cuniculi.
renal failure.
– Capillaria feliscati has been reported in
Predisposing causes of urinary tract infection Australia and USA. It is a trichurid nematode
include: that usually attaches superficially to the bladder
● Anatomical abnormalities (ectopic ureter, patent mucosa and so most cats are asymptomatic.
urachus, perineal urethrostomy). However, on rare occasions it may produce
● Urethral incompetence (usually associated with recurrent bouts of hematuria and dysuria.
perineal urethrostomy).
● Loss of mechanical washout of the bladder and ure-
Clinical signs
thra due to bladder atony, urolithiasis, painful
hindquarters and debility. Dysuria, pollakiuria with or without hematuria.
Cats with chronic renal failure may or may not have Bacteriology.
clinical signs, and pyuria and bacteriuria may not be ● Quantitative bacterial cultures ≥ 103/ml of urine
obvious on examination of the urinary sediment. obtained by cystocentesis indicate urinary tract
infection.
Cats with urinary tract infection are rarely systemically
● Aerobic cultures and antimicrobial susceptibility
affected.
testing are indicated in cats with pyuria (>5
● Clinical signs of fever, lethargy, dehydration,
WBC/hpf) or elevated urine pH (>6.5) whether
anorexia, vomiting, polydipsia, polyuria, weight
or not bacteriuria is seen.
loss, anaemia are consistent with renal involve-
● Fungal cultures are indicated if blastospores (yeast)
ment and indicate ascending pyelonephritis.
or hyphae are seen in the urine.
Capillaria infestation is usually reported in cats over 8
Blood tests.
months of age and produces minimal clinical signs, but
● Leucocytosis and elevated serum urea and creati-
recurring bouts of hematuria and dysuria have been
nine levels indicate renal involvement in lower uri-
observed.
nary tract disease.
Encephalitozoon infestation may lead to renal failure.
Radiology.
● Plain and contrast radiography may help to identify
Diagnosis
some predisposing causes of urinary tract infec-
Urinalysis. tions, as well as, determine the chronicity of the
● If the urinary bladder is empty, cats can be given infection (thickened bladder wall, bladder fill
normal saline (70 ml/kg) subcutaneously, and blad- capacity).
der fill monitored. Alternatively, frusemide (1
mg/kg) intravenously can be used. Animals with Differential diagnosis
acute lower urinary tract infection are usually pollak-
iuric, so several attempts to collect urine may be nec- Non-obstructed idiopathic LUTD. Some cats diag-
essary throughout the day. nosed as having bacterial cystitis/urethritis often repre-
● Hematuria (>5 RBC/hpf), pyuria (>5 WBC/hpf) sent with a recurrence of lower urinary tract disease
and proteinuria (>3.5 g (35mg)/kg/day) or increased with sterile urine during or after appropriate antimicro-
protein/creatinine ratio >1.0 (N.B protein and creati- bial therapy. These cats have non-obstructed idiopathic
nine values must be converted to mg/dl and μmol/L, LUTD with secondary bacterial infection and can only
respectively to calculate the ratio) indicate inflam- be identified by reoccurrence of signs associated with
mation of the urinary tract. If bacteria are also seen sterile urine.
or cultured, then the inflammatory process is due to
or complicated by bacteria. If bacteria are not seen Treatment
under light microscopy, it does not mean that an
The principal objectives in the treatment of urinary
infection is not present as they, especially cocci, are
tract infection are to eliminate the infectious agent, cor-
not always readily visualized.
rect the predisposing cause, if possible, and prevent the
● White blood cell casts or granular casts indicate
recurrence of infection.
renal tubular involvement as in pyelonephritis.
White blood cell casts appear as tubular struc- Eliminate the infectious agent.
tures composed of white cells and Tamm–Horsfall ● For bacterial infections.
mucoprotein. These may degenerate and form – Antimicrobial drugs, selected on the bases of
granular casts, which are indistinguishable from bacterial sensitivity, should be used at appropri-
degenerated renal tubular epithelial casts. ate doses for 14 days for acute urinary tract
● Blastospores (yeast) or hyphae (Aspergillus spp.) in infection and for 28 days for chronic or recur-
urine indicate fungal infection. rent urinary tract infection.
● Capillaria ova (bipolar) or Encepalitozoon spores – Antimicrobial drugs often effective include
can be seen in the urine. Heavy infestations of sulfa-trimethoprim, enrofloxacin and amoxi-
C. feliscati may be associated with proteinuria. cillin with clavulinic acid.
– Nephrotoxic antimicrobials (aminoglycosides) Prevent the recurrence of infection.

should be avoided and when used, they should ● Bacterial.
not be given for more than 7–10 days without – If urinary tract infection recurs, determine if it
carefully monitoring renal function, especially is due to a relapse or reinfection. Reoccurrence
urinalysis for evidence of casts. of infection with the same organism (relapse)
– Response to therapy should be based on urinal- usually indicates that the original treatment
ysis and bacterial culture, rather than on clini- did not eliminate the infection. Recurrence of
cal response to treatment, as most cats will show infection with a different organism (reinfection)
a marked clinical improvement, despite unsuc- suggests that the original treatment was effec-
cessful eradication of the urinary tract infection. tive but predisposing factors have allowed a new
– Repeat urinalysis without culture should be infection to occur.
done 7 days after commencement of therapy to – Urinary acidifiers can be used for long-term
ensure that bacteriuria is no longer present. therapy to provide a less-favorable environment
– A urine sample for urinalysis should be examined (pH < 6.5) in the urinary tract.
on the last day of antimicrobial therapy for evi- – Encourage the patient to urinate more fre-
dence of pyuria (>5 WBC/hpf). Urinalysis and quently by providing clean litter trays or ready
bacterial culture should be repeated 7 days access to outdoors, thus utilizing mechanical
after antimicrobial therapy has ceased and washout.
again at monthly intervals until two consecutive – If urinary tract infection persists because pre-
urine samples are negative. disposing causes cannot be corrected, ampi-
– Treatment for urinary tract infections associated cillin, amoxicillin, sulfa-trimethoprim and
with indwelling catheters may be delayed, if signs methenamine can be used for long-term ther-
are absent, until the urinary catheter is removed, apy. Give half the daily dose late in the evening.
to avoid developing antimicrobial resistance.
● For viral infections.
Prognosis
– Use lysine (250 mg/cat orally every 12 hours) or
interferon alpha (30 U/cat orally daily). Prognosis depends on the causative agent, the use of
● For fungal infections. appropriate drug therapy and the identification and cor-
– Ketoconazole and itraconazole have been sug- rection of predisposing causes.
gested but their efficacy in the cat with urinary
tract infection has not been determined.
● For parasitic infestations. URETHRAL TRAUMA*
– For Capillaria use fenbendazole (25 mg/kg orally
every 12 hours for 3–10 days). Alternatively, Classical signs
methyridine 200 mg/kg orally once has been
● History of trauma, especially following
used.
motor vehicle accidents, falling from high
– No known effective treatment has been reported
places and after forceful or excessive
for Encephalitozoon in cats, but albendazole and
urethral catheterization.
the antibiotic fumagillin have been shown to
● Dysuria.
have efficacy in humans and mice.
● Perineal swelling.
Correct predisposing cause, if possible.
● Anatomical abnormalities, such as ectopic ureter(s)
Pathogenesis
should be surgically corrected.
● Urethral incompetence and loss of mechanical Urethral trauma may result from motor vehicle acci-
washout should be corrected, if possible. dents or abdominal trauma, especially those that result in
● The continued use of indwelling catheters associ- pelvic fractures, perineal surgery via scalpel blade or
ated with secondary urinary tract infections should excessive handling of the urethra, and catheterization,
be reassessed. especially when associated with urethral obstruction.
Urethral rupture may result in subcutaneous accumu- Clinical signs

lation of urine in the perineal region leading to
swelling, discoloration and necrosis of the skin. Small amounts of urine are frequently voided while the
urinary bladder is still small.
Clinical signs Dribbling urine (incontinence) associated with a small

bladder.
Dysuria.
Pollakiuria.
Stranguria.
Palpation of the bladder often initiates the act of
Perineal swelling. urination.
Red discoloration of the perineal skin.
Abdominal pain. *Diagnosis
Signs of post-renal renal failure. Diagnosis is based on clinical signs, especially that the
cat frequently urinates or dribbles urine when the
Diagnosis bladder is quite small.
History of trauma or catheterization. Urodynamic procedures, such as cystometrography,

demonstrate reduced threshold volumes and pressure,
Clinical signs of swelling, discoloration or necrosis in which indicate reduced bladder compliance or
the perineal region. detrussor hypercontractility.
Positive-contrast urethrography will demonstrate Urinalysis may reveal pyuria or neoplasia.
extravasation of contrast into the periurethral soft tis-
sue. If the rupture is at the proximal end of the urethra, Radiography may help to determine the underlining
contrast agent may enter the abdomen. cause, for example neoplasia and cystitis (thickened
bladder wall).
FeLV test.
HYPERCONTRACTILE BLADDER*
Classical signs Differential diagnosis

● Small urinary bladder. Infectious cystitis/urethritis – hematuria, pyuria and
● Dribbling urine. bacteriuria are usually present.
● Pollakiuria.
Non-obstructed LUTD – hematuria is usually present.
Pathogenesis
Treatment
Hypercontractility of the urinary bladder occurs when
detrusor muscle contractions are triggered at low Management of storage dysfunction of the urinary
volumes and pressure, resulting in dysfunction of uri- bladder may include elimination of urinary tract
nary bladder storage. inflammation, correction of neurologic disorders or
pharmacologic manipulation to reduce detrusor muscle
It may be due to reduced bladder capacity (hypoplas-
excitability.
tic bladder, neoplasia), excessive sensory input
● Always treat urinary tract infections first before
(inflammation) or neurologic disorders (upper motor
attempting pharmacologic manipulation.
neuron lesions).
● Parasympathetic inhibitors (anticholinergic
Bladder hypercontractibility (idiopathic detrusor insta- agents), such as propantheline (5–7.5 mg /cat
bility), not associated with any known cause, has been orally every 72 hours or more frequently as
reported in one cat with FeLV that responded to anti- required) and oxybutynin (0.5–1.25 mg/cat orally
cholinergic therapy. every 8–12 hours) may be used.
● Tricyclic antidepressants, such as imipramine ● One cat with transitional cell carcinoma also had
(2.5–5 mg/cat orally every 12 hours) may improve hypereosinophilia.
urinary bladder compliance.
Abdominal palpation of a soft tissue mass in the blad-
Clip the hair and clean around the perineal/abdomi- der neck.
nal area to minimize urine scolding.
Ultrasonography or contrast radiography shows a
soft tissue, space-occupying mass. Generally, a water-
soluble iodinated contrast agent (5–10 ml/kg or enough
NEOPLASIA* to moderately distend the bladder) is used.
Biopsy via exploratory laparotomy or cystoscopy pro-
Classical signs
vides a definitive diagnosis.
● Hematuria.
● Distended bladder.
Treatment
● Dysuria.
Surgical resection is rarely feasible due to the high
percentage of tumors that are malignant, the frequently
late presentation and location of the tumor.
Pathogenesis
Tumors of the urinary bladder are rare and those of the
ureters and urethra even rarer.
URETHRAL STRICTURE
Most are malignant epithelial tumors such as transi-
tional cell carcinomas, squamous cell carcinomas Classical signs
and adenocarcinomas.
● Dribbling urine.
Benign tumors occur very infrequently. ● Distended bladder.
● Dysuria.
● Stranguria.
Clinical signs
Usually occurs in cats over 8 years of age. See main reference on page 199 for details (The
Incontinent Cat).
Dysuria and intermittent or persistent hematuria
may occur depending on the type and location of the
neoplasm. Clinical signs
Soft tissue mass may be palpable in the bladder neck. Incontinence associated with a distended bladder (over-
flow incontinence) and dysuria.
Secondary infection may occur.
History of unresponsiveness to treatment for
Diagnosis
cystitis.
Radiography. Retrograde urethrography.
Diagnosis Urodynamic procedures. Urethral pressure profilom-
etry may be used to identify focal urethral obstructions.
Urinalysis.
● Hematuria (RBC > 5 phf).
● Pyuria and bacteriuria occur due to secondary uri- CYCLOPHOSPHAMIDE TOXICITY
nary tract infection.
● Sediment may show abnormal transitional cells. Classical signs
Blood tests (hematology and biochemistry). ● Hematuria.
● Normal unless urinary tract obstruction has occurred.
Clinical signs Diagnosis

Hemorrhagic cystitis may occur during cyclophos- History of access to toxic material.
phamide therapy (< 5% of cases) in cats due to the
Urinalysis reveals a sterile hematuria (RBC >5 hpf).
action of acrolein on the mucosa resulting in mucosal
edema, necrosis and ulceration.
RECOMMENDED READING
Barsanti JA, Finco DR, Brown SA. Diseases of the lower urinary tract. In: Sherding RG (ed) The Cat: Diseases and
Clinical Management, 2nd edn, Churchill Liverstone, Melbourne, 1994, pp 1769–1823.
Cameron ME, Casey RA, Bradshaw JW, Waran NK, Gunn-Moore DA. A study of environmental and behavioural
factors that may be associated with feline idiopathic cystitis. J Small Anim Pract 2004; 45(3): 144–147.
Kalkstein TS, Kruger JM, Osbourne CA. Feline idiopathic lower urinary tract disease. Parts I to IV. Compendium 21,
1999: 15, 148, 387, 497.
Norsworthy GD. Feline Urologic Syndrome; Urolithiasis The Feline Patient: Essentials of Diagnosis and Treatment,
Williams and Wilkins, Baltimore 1998.
Osborne CA, Finco DR. Canine and Feline Nephrology and Urology. Williams and Wilkins, Baltimore, 1995.
Westropp JL, Buffington CA. Feline idiopathic cystitis: current understanding of pathophysiology and management.
Vet Clin North Am Small Anim Pract 2004; 34(4):1043–1055.
Westropp JL, Welk KA, Buffington CA. Small adrenal glands in cats with feline interstitial cystitis. J Urol 2003;
170(6 Pt 1): 2494–2497.
12. The incontinent cat
Lucio John Filippich
KEY SIGNS
● Urinary incontinence.
● Urine soiling around the perineal area.
● Perineal dermatitis.
MECHANISM?
● The incontinent cat has lost voluntary control over urination and intermittently or continuously
dribbles urine. Maintenance of urinary continence in the cat depends on normal lower urinary
tract anatomy and function and an intact nervous system. Urinary incontinence results from
abnormalities of either the filling or emptying processes.
● During the filling phase (sympathetic stimulation), the body of the bladder acts as a reservoir
with flaccid walls that generate little pressure, while the outlet of the bladder is a high-resist-
ance duct preventing the passage of urine.
● During the emptying phase (parasympathetic stimulation), the roles are reversed and the body
of the bladder becomes a pump that expels urine under high pressure while the outlet of the
bladder reflexly opens and becomes a low-resistance duct.
● The two phases are functionally independent and depend on the cerebral cortex for co-ordina-
tion and voluntary control.
WHERE?
● Lower urinary tract (lower ureter, urinary bladder, urethra).
WHAT?
● Urinary incontinence in cats is uncommon. In juvenile cats, it is more likely due to a congeni-
tal abnormality (ectopic ureter); in the adult cat it is more likely neurologic in origin.
Secondary urinary tract infections are common.
193

Diseases causing an incontinent cat
ANOMALY
● Ectopic ureter(s)* (p 198)
A congenital or acquired anomaly where one or both ureters fail to terminate normally into the uri-
nary bladder. Mainly seen in young cats showing continuous or intermittent dribbling of urine with
wetness and dermatitis around the perineal area. The urinary bladder, if palpable, is not distended.
● Patent urachus (p 201)
Kittens show urine leakage from the umbilicus because the urachus between the urinary bladder and
the umbilicus remains functionally patent after birth.
● Spinal dysraphism (p 201)
Young cats, especially Manx cats. Overflow incontinence occurs because of malformation of the
sacral spinal cord segments and disruption of nerve pathways responsible for micturition.
Commonly seen with other hindquarter abnormalities.
● Colorocystic fistula (p 202)
The fistula between the urinary bladder and colon predisposes to urinary incontinence and urinary
tract infection.
● Ectopic uterine horns (p 202)
Ectopic uterine horns terminate in the urinary bladder and result in persistent urinary incontinence
and cystitis.
● Exstrophy (p 203)
Urine dribbling from defects in the ventral abdominal wall, urinary bladder and external genitalia.
MECHANICAL
● Hypocontractile bladder (detrusor atony)*** (p 195)
Results from detrusor dysfunction or occurs secondary to increased urethral outflow resistance.
Overflow incontinence occurs and the bladder may or may not be easily expressed. Often associ-
ated with hindquarter abnormalities.
● Urethral incompetence* (p 200)
Intermittent leakage occurs without a distended badder, often while the cat is sleeping or relaxed.
Results from trauma, dysraphism, urethral hypoplasia and possibly feline leukemia virus infection
and desexing. More common in aged cats.
● Urethral stricture* (p 199)
May present as overflow incontinence and dysuria in a young cat (congenital), but more common
secondary to trauma, inflammation or iatrogenic following traumatic catheterization of a blocked cat.
IDIOPATHIC
● Dysautonomia (p 203)
Overflow incontinence is associated with gastrointestinal and ocular signs due to an autonomic
polyganglionopathy. Sudden onset of anorexia and depression occurs together with dilated unre-
sponsive pupils, bradycardia, dry mucous membranes and GIT signs.
12 – THE INCONTINENT CAT 195
Incontinence, pollakiuria or nocturia associated

INTRODUCTION with an empty bladder reflect storage disorders
(reduced bladder capacity, hyperactivity of the detrusor
MECHANISM? muscle, urethral incompetence).
The incontinent cat intermittently or continuously In contrast, urine retention with overflow, or incom-
dribbles urine because it has lost voluntary control plete voiding and a distended bladder indicate emp-
over urination. tying disorders (detrusor atony, urethral obstruction).
Cats that urinate at inappropriate times or in inappro- Following spontaneous bladder emptying there
priate places need to be differentiated from incontinent should be less than 0.5 ml of urine remaining in a
cats through history taking and clinical examination. normal cat.
Maintenance of urinary continence in the cat depends

on normal lower urinary tract anatomy and an WHERE?
intact sympathetic, parasympathetic and somatic Lower urinary tract (lower ureter, urinary bladder, urethra).
nervous system.
● Anatomical abnormalities can bypass (ectopic
ureter) or negate (urethral hypoplasia) neuromuscu- WHAT?
lar control mechanisms. Urinary incontinence in cats is uncommon. In juvenile
Continence during the filling stage is maintained via cats, it is more likely due to a congenital abnormality
the following mechanisms: sympathetic stimulation (ectopic ureter): in the adult cat it is more likely neu-
(hypogastric nerve) during the filling phase causes rologic in origin. Secondary urinary tract infections are
the body of the bladder (detrusor muscle) to relax common.
(β-receptors) and the bladder neck and urethral smooth
muscles to contract (α-receptors). DISEASES CAUSING SIGNS OF
● Additional urethral resistance is supplied by the ure- URINARY INCONTINENCE
thral striated muscle, which reflexively contracts
and is under voluntary control (pudendal nerve).
HYPOCONTRACTILE BLADDER***
The emptying phase occurs as follows: Parasympathetic (DETRUSOR ATONIC/HYPOTONIC
stretch receptors in the detrusor muscle detect blad- BLADDER)
der fill, and when the threshold of bladder capacity is
reached, they discharge impulses via the sacral spinal Classical signs
cord to the pons in the brain stem, where a detrusor
response is integrated.
● Distended urinary bladder.
Efferent motor impulses descend the spinal cord to the ● ± Hindquarter ataxia or paresis.
detrusor muscle via the pelvic nerve causing detrusor ● ± Tail paralysis.
muscle contraction.
● Simultaneously, inhibitory interneurons are acti-
vated in the sacral spinal cord, which synapse on Pathogenesis
pudendal motor neurons, resulting in a relaxation
of the external urethral sphincter. Hypocontractile bladder can occur due to detrusor dys-
function or secondary to prolonged bladder distention.
Once the bladder is empty, parasympathetic activity
ceases and the sympathetic and pudendal nerves are no Detrusor dysfunction.
● Lesions cranial to the sacral spinal cord may
longer inhibited.
disrupt sensory and motor pathways to the urinary
Detrusor muscle relaxation and urethral sphincter con- bladder. This results is an upper motor neuron
traction returns and the filling phase begins again. bladder:
– Detrusor function is lost resulting in a flaccid Feline dysautonomia may result in urinary inconti-
bladder. nence. There is an inability to contract the bladder and
– Urethral sphincter tone is maintained. the bladder is easy to express manually. Urinary incon-
– Loss of inhibition may lead to increased puden- tinence is one of the less common signs. Typically there
dal nerve activity and thus, increased urethral is a sudden onset of depression and anorexia over 24–48 h,
outflow resistance. and a variety of signs reflecting autonomic dysfunction,
– Over time, intrinsic spinal reflexes may re-estab- such as pupillary dilation with loss of PLR, dry eyes and
lish detrusor activity but voiding is usually invol- nose, regurgitation, prolapsed 3rd eyelids, bradycardia
untary and incomplete. and constipation or fecal incontinence.
● Lesions involving the sacral spinal cord seg-
ments, cauda equina (sacrum) or peripheral nerves
supplying the bladder and urethra result in a lower Clinical signs
motor neuron bladder.
A hypocontractile bladder presents as urinary inconti-
– Loss of most sensory and all motor input to the
nence associated with a distended urinary bladder
detrusor muscle.
and inability to completely void urine.
– Loss of urethral sphincter tone.
– The urinary bladder is areflexic and easily The cat may or may not voluntarily attempt to urinate.
expressed.
The bladder may or may not be easily expressed
– Overflow incontinence occurs when the bladder
manually.
is distended or when intravesicular pressures
exceed urethral pressure. With suprasacral (cranial to sacrum) spinal cord
lesions, the bladder is initially distended, firm and
Prolonged bladder distention.
difficult to express.
● Prolonged bladder distention leads to loss of tight
● Over time there is emergence of the sacral reflex,
muscular junctions in the bladder wall resulting in
and some bladder contractile function may return,
detrusor atony. Prolonged bladder distention results
resulting in frequent, uninhibited, incomplete void-
from reduced bladder emptying which may be from
ing of small volumes of urine.
a number of causes:
● If outflow resistance is high at this time, detrusor-
– Mechanical (urethroliths, urethral plugs, stric-
urethral dyssynergia occurs resulting in dysuria (dif-
tures, bladder neck or urethral masses, inflam-
ficult or painful urination) and interrupted urination.
mation).
● Other clinical signs associated with suprasacral
– Functional (neurologic injury, urethral muscle
spinal cord lesions may include proprioceptive
spasm). When bladder fill pressures exceed ure-
deficits, paraparesis or tetraparesis and hyperreflexia.
thral resistance, overflow of urine occurs.
– Associated with hindquarter disorders (pain) or With sacral spinal cord and peripheral nerve lesions,
forced recumbency. the urinary bladder is usually distended but flaccid, and
outflow resistance is generally low, so the urinary
Neurologic injury, resulting in urethral hyperactiv-
bladder is easily expressed.
ity/dyssynergia, has been rarely documented in cats. It
● The cat may attempt to urinate, but fail to produce
can occur with sacral spinal cord and cauda equina
an adequate stream of urine.
injuries, resulting in the urethral musculature failing to
● Clinical signs may also include hindlimb paresis or
relax during detrusor contraction, thus maintaining a
paralysis, reduced anal tone and perineal reflexes,
high outflow resistance.
fecal incontinence and tail paralysis.
Urethral muscle spasm may occur following urethral
Incontinence associated with increased urethral out-
or pelvic surgery or secondary to urethral inflamma-
flow resistance is initially characterized by bladder dis-
tory disease.
tention and difficulty in manually expressing urine,
Functional urethral obstruction and detrusor atony are a large residual urine volume following voiding, dysuria
common sequels to mechanical urethral obstruction. and an attenuated urine stream (paradoxic incontinence).
If the cat initiates voiding but the urine stream is rapidly ● If detrusor activity is initiated and the cat begins to
interrupted, consider detruso–urethral dyssynergia. urinate, observe if the urine stream is abruptly inter-
rupted and voiding is incomplete (functional ure-
Fecal incontinence and/or constipation may also be
thral obstruction).
present.
● If detrusor activity is not initiated and the bladder is
easily expressed, bladder atony is present.
Diagnosis
Ultrasonography is often useful in bladder diseases
History may help to characterize the problem, differ- (neoplasia, urolithiasis) but does not visualize most of
entiate it from inappropriate urination and identify the the urethra.
possible cause (trauma, prolonged recumbency).
Urodynamic procedures.
Physical examination. ● These are not readily available in veterinary practice.
● Abdominal palpation reveals a distended bladder. ● Cystometry, urethral pressure profilometry,
● If detrusor dysfunction is neurological in origin, uroflowmetry and electromyography can provide
other signs of neurological disease such as useful objective information about detrussor and
hindquarter paralysis are commonly seen. urethral function.
Neurologic examination. ● Cystometrography showing large filling volumes,
● Neurologic deficits in the limbs suggest a neuro- and lack of sustained contractile peaks indicate
logic cause for the incontinence. detrussor atony.
● Loss of anal tone, perineal sensation and tail func- ● Urethral pressure profilometry can identify ure-
tion indicate a sacral spinal cord lesion. thral incompetence and urethral hypertonicity.
● Ophthalmological signs (mydriasis) may suggest
Urinalysis is useful in detecting the presence of inflam-
the incontinence is associated with dysautonomia. mation and infection.
Observe micturition. Blood tests including serum urea, creatinine and elec-
● This should always be done.
trolyte concentrations can be done to detect renal failure.
● Assess the urine stream passed.
● Note change in bladder size and residual urine vol- Biopsy a soft tissue mass, if detected.
ume after voiding.
Detrusor dysfunction is suspected on the basis of the Treatment
history, physical examination, and the exclusion of a
Immediately correct any life-threatening conditions,
mechanical obstruction to urine outflow.
such as postrenal renal failure, and fluid and electrolyte
Catheterize the urinary bladder to determine patency. imbalance.
● If an obstruction is detected, survey and contrast
Correct the primary cause, if possible.
radiographs are often necessary to further charac-
terize the obstruction. If the obstruction is due to a Always treat urinary tract infections first before
urethrolith, survey abdominal radiographs are nec- attempting pharmacologic manipulation.
essary to determine if other uroliths are present in
For bladder atony.
the urinary tract (kidney, ureter and bladder).
● To facilitate smooth muscle recovery, the residual
● If an obstruction is not detected, retrograde urethrog-
urine volume needs to be kept small by frequent
raphy and contrast cystography may be needed to
manual expression, intermittent catheterization or
exclude soft tissue masses in the bladder and urethra.
temporary indwelling urinary catheter placement.
If mechanical obstruction is ruled out, subjectively ● Use pharmacologic manipulation, such as parasym-
evaluate urethral resistance by palpating the urinary pathomimetics (bethanechol chloride, a cholinergic
bladder and applying constant, firm digital pressure agonist, 1.25–2.5 mg/cat orally every 8–12 hours) to
on the urinary bladder. The degree of pressure applied increase detrusor contractility and an alpha-adrener-
should not cause undue discomfort or pain to the cat. gic antagonist (phenoxybenzamine, 0.25 mg/kg
orally every 12 hours) to minimize urethral resist- migration of the metanephric ducts (which become the
ance, if necessary. Parasympathomimetic drugs are ureters) was abnormal.
most likely to be effective when some neurologic
Ectopic ureters usually terminate in the urethra and
innervation is still present. Drug doses may be
less frequently in the vagina.
increased incrementally, if needed, every 4–5 days,
but patients should be carefully monitored for Approximately 50% are unilateral.
potential side effects (lacrimation, salivation,
Because of the close relationship of the mesonephros
abdominal cramps, vomiting, diarrhea).
and the metanephros and development of other urogen-
For increased urethral resistance or detrussor–ure- ital organs, other anomalies such as cystic (bladder)
thral dyssynergia. hypoplasia, renal hypoplasia, hydronephrosis and
● The direct-acting skeletal muscle relaxant, dantro- megaureter may also occur.
lene sodium (0.5–2 mg/kg orally 12 hourly or
Acquired ureteral ectopia may occur due to a vagino-
1 mg/kg IV) may be effective in reducing striated-
ureteral fistula developing as a sequel to cesarian and
muscle resistance.
ovario-hysterectomy.
● The alpha-adrenergic antagonist (phenoxybenza-
mine) may be effective in reducing smooth-muscle
resistance. Clinical signs
● Benzodiazepines such as diazepam (valium 2–5 mg
Congenital ureteral ectopia has been infrequently
PO tid) may reduce striated-muscle resistance.
reported in cats and there appears to be no breed or sex
Laboratory investigation, including plasma urea, creati- predisposition.
nine and electrolyte concentrations and urinalysis,
Usually reported in cats less than 18 months of age.
should be done to determine the degree of post-renal
azotemia and to identify if hematuria, pyuria and/or Signs depend on the site of termination of the ectopic
infection are present. ureter(s) and the presence of other congenital or
acquired abnormalities.
Prognosis Continuous or intermittent dribbling of urine is typ-
ical.
Prognosis in neurologic cases is guarded and generally
depends on the chronicity and severity of the neuro- Cats with bilateral ectopic ureters may or may not
logic lesion, response to medical therapy and the ease urinate normally, depending on how much urine
of manually maintaining an empty urinary bladder. refluxes back into the bladder.
Incontinent cats with unilateral ureteral ectopia urinate
ECTOPIC URETER(S)* normally.
Urine scalding may result in vaginal discharge, phi-
Classical signs
mosis (contraction of the prepucial orifice), and
● Young cat. perivulvar or periprepucial dermatitis.
● Continuous dribbling of urine.
Soiled hair may discolor.
● Wetness around the perineal area.
● Perineal dermatitis. The urinary bladder on abdominal palpation is not
distended (in contrast to urine retention with overflow).
Abdominal palpation may reveal an abnormal kidney(s).
Pathogenesis
Secondary bacterial urinary tract infections are
A congenital anomaly where one or both ureters fail common and may result in intermittent bouts of hema-
to terminate normally in the trigone of the urinary turia, cystitis and/or ascending pyelonephritis. With
bladder. Ectopic ureter occurs because the origin or bilateral ectopia, renal failure may occur.
Diagnosis Ureteronephrectomy may be considered when the

affected kidney is diseased and the contralateral kidney
A history of urinary incontinence since birth or is normal.
when acquired as a kitten indicates congenital
ureteral ectopia. Onset of signs following recent Renal infarction by ligation of the renal blood vessel
abdominal surgery at any age would suggest acquired may be considered in azotemic cats with unilateral
ureteral ectopia. ureteral ectopia.
Clinical signs which are suggestive are: Continued incontinence after surgery may be due to
● Urinary incontinence without urinary bladder concomitant urethral incompetence or reduced bladder
distention. capacity due to disuse. If the latter, bladder capacity
● Incontinence despite normal urination (unilateral usually improves with time.
ectopic ureter). Secondary bacterial infections are not uncommon and
Radiographic techniques such as excretory urogra- antimicrobials based on culture and sensitivity tests
phy/pneumocystography and retrograde urethrography should be administered.
or vaginourethrography provide information on the site
of ureteral termination, renal size and ureteral shape.
Prognosis
● One or both ureters fail to terminate normally in the
urinary bladder. Following surgical correction, prognosis is generally
● Other anomalies, such as cystic and renal hypopla- good with immediate cessation of urinary incontinence.
sia, hydronephrosis and megaureter may be seen.
Cats with ectopic ureters that terminate in the vagina
Vaginoscopy may reveal the ectopic ureteral orifice if are more likely to be continent after surgery.
the ureter enters the vagina.
Reimplantation of dilated ureters into the bladder may
Ultrasonography may help to demonstrate the abnor- result in increased vesicoureteral reflux that can predis-
mal termination of the urethra or vagina. pose to ascending pyelonephritis.
Biochemistry
● Serum urea and creatinine estimations can be used URETHRAL STRICTURE*
to evaluate renal function.
● Urea and creatinine are more likely to be elevated Classical signs
with bilateral ureteral ectopia, especially if chronic.
● Elevations indicate both kidneys are diseased from
● Distended bladder.
ascending pyelonephritis or an associated congeni-
● Dysuria.
tal renal anomaly.
Urinalysis and bacterial culture can identify the pres-
ence of secondary infection. Pathogenesis
Congenital urethral strictures are occasionally seen in
Differential diagnosis young cats.
Urinary retention with overflow (overflow inconti- Acquired strictures are more common and occur sec-
nence) is differentiated from ectopic ureter by finding a ondary to trauma, inflammation or iatrogenic causes
distended bladder on palpation. following catheterization or surgery.

Vesico-ureteral transplantation is the treatment of Typical signs are incontinence associated with a dis-
choice when the kidney function is normal and the tended bladder (overflow incontinence) and dysuria
ureter is not markedly abnormal. (difficulty urinating) with a narrow urine stream.
Diagnosis Clinical signs

Diagnosis is via radiography using retrograde ure- Normal or small urinary bladder.
thrography.
Intermittent leakage of small volumes of urine, often
Following catheterization of the urethera using an while the cat is sleeping or relaxed.
open-ended cat catheter, contrast is injected (1–2 ml)
If congenital in origin, other anomalies, such as vaginal
while the radiographs are taken. Avoid over-distending
aplasia and cystic hypoplasia are commonly present.
the urinary bladder.
Many FeLV-positive cats with urinary incontinence
Urodynamic procedures such as urethral pressure
may also have anisocoria, reproductive disorders,
profilometry may be used to identify focal urethral
weight loss, vomiting and ptyalism suggesting a multi-
obstructions.
focal autonomic dysfunction. In cats with FeLV-asso-
ciated incontinence, digital palpation of the urinary
Treatment bladder often elicits a urine flow.
Treatment depends on location and size of the stricture. In cats with urethral incompetence due to neoplasia,
Extrapelvic strictures may be managed by urethros- abdominal palpation may reveal a mass at the bladder
tomy, whereas, intrapelvic strictures may require ure- neck. Others signs, such as dysuria and hematuria are
thral resection and anastomosis. often present.
URETHRAL INCOMPETENCE*
Classical signs Diagnosis
● Small urinary bladder. Diagnosis is based on history and clinical signs of leak-
● Intermittent dribbling of urine. age of small amounts of urine, often when sleeping, and
a normal or small bladder.
Ophthalmological signs (anisocoria) may suggest the
Pathogenesis incontinence is associated with FeLV infection.
Incontinence occurs because of reduced urethral outflow A positive FeLV test.
resistance during urine storage. This results from lost or
reduced urethral smooth or striated muscle tone. Retrograde contrast vaginourethrography in female cats
with urethral hypoplasia shows marked urethral short-
Reported causes of urethral incompetence include: ening and other anomalies, such as vaginal aplasia and
● Pelvic and pudendal nerve damage following cystic hypoplasia.
trauma (cystotomy, perineal urethrostomy) and
rarely neoplasia (acquired urethral incompe- Cystography or retrograde urethrography may reveal a
tence). mass at the bladder neck. Biopsy is necessary for a
● Dysraphism in Manx cats.
definitive diagnosis.
● Urethral hypoplasia has been reported in young Urodynamic procedures, including urethral pressure pro-
female cats (congenital urethral incompetence). filometry can be used to identify urethral incompetence.
● A relationship between incontinence and feline
leukemia virus (FeLV) infection is suspected.
● Reproductive hormone-responsive incontinence Differential diagnosis
has been reported in two female cats following Hypercontractile bladder (urge incontinence) is charac-
ovariectomy and suspected in three neutered terized by frequent conscious urination and a small
males. bladder.
Treatment Diagnosis
Bladder neck reconstructive surgery may be considered Physical examination reveals urine leakage from the
in cats with urethral hypoplasia. umbilical region.
Alpha-adrenergic agonists, such as phenyl-
propanolamine (1.5–2.2 mg/kg PO 8–12 h) and Differential diagnosis
ephedrine (2–4 mg/cat PO 8–12 h) may be used to
Exstrophy of the bladder. The bladder wall and abdom-
alleviate the incontinence. Once the incontinence is
inal wall are not fully formed and are joined, with leak-
controlled, the dosage can be reduced and/or the
age of urine to the exterior.
frequency lengthened.
High doses of oral estrogen therapy were reportedly
Treatment
effective in two cats that developed urinary incontinence
following ovariectomy. However, at such doses nympho- Surgical correction and antimicrobial therapy for sec-
mania and toxic bone marrow effects may occur. ondary infection.
Testosterone propionate (5–10 mg intramuscularly),
given to three neutered male cats suspected of repro- Prognosis
ductive hormone-responsive incontinence, gave vari-
Good.
able success.
SPINAL DYSRAPHISM
Prognosis
Response to drug therapy in severely affected animals Classical signs
is often poor.
● Young cat.
PATENT URACHUS ● Distended urinary bladder.
● ± Hindquarter abnormalities.
Classical signs
● Immature cat. Pathogenesis
● Dribbling urine from the umbilicus.
Incomplete closure of the neural tube during early
● Omphalitis.
prenatal development leads to malformation of the
● Ventral dermatitis.
sacral spinal cord segments and disruption of nerve
pathways responsible for micturition, resulting in loss
Pathogenesis of detrusor responsiveness and urethral sphincter
control.
Patent (persistent) urachus occurs when the entire ura-
chus between the urinary bladder and the umbilicus Sacrocaudal dysgenesis in Manx cats is due to a semi-
remains functionally patent after birth. lethal, autosomal dominant gene.

Kittens show urine leakage from the umbilicus. Signs occur in young cats (< 6 months of age).
A patent urachus is often associated with omphalitis Severity of the clinical signs vary and may include
(inflammation of the umbilicus), ventral dermatitis abnormalities of urination, defecation and hindlimb
and signs of urinary tract infection. gait.
Typically there is urinary incontinence (dribbling

COLO-UROCYSTIC FISTULA
urine) with a distended urinary bladder that is eas-
ily expressed.
Classical signs
Perivulvar or periprepucial dermatitis.
● Dribbling urine in young cat.
Other signs commonly seen include fecal inconti-
Clinical signs
nence, constipation, locomotor disturbances of the
hindlimbs (plantigrade stance, hopping gait) and Colorocystic fistula has been reported in a male domes-
abnormal hindquarter conformation. tic shorthaired kitten.
This anomaly may result from incomplete division of
the cloaca during embryogenesis.
Diagnosis
Signs were of persistent urine dribbling and cystitis in
Diagnosis is based on age, breed and clinical signs.
a young cat.
Survey radiographs may confirm vertebral abnormal-
ities of the caudal spine.
Diagnosis
Contrast myelography may demonstrate the presence
of meningoceles. The abnormality predisposes to urinary incontinence
and urinary tract infection.
Urodynamic procedures.
● Cystometrography may show large filling volumes Diagnosis can be established by contrast urography.
and lack of a sustained contractile peak, consistent
with detrussor atony.
● Urethral pressure profilometry can identify urethral Treatment
incompetence.
Treatment is surgical correction of the fistula while pre-
serving the colonic and urinary bladder function.
Most other congenital abnormalities do not produce the
classical combination of dribbling urine from the ECTOPIC UTERINE HORNS
penis/vulva and distended easily expressible bladder in
a young cat. Classical signs
● Urinary incontinence.
Treatment
Treatment depends on the severity of the clinical signs. Clinical signs
Therapy should be directed at minimizing or overcoming Ectopic uterine horns terminating into the urinary blad-
overflow incontinence by manual bladder compression der have been reported in a young female domestic
(provided there is not excessive urethral sphincter tone) shorthaired cat showing signs of persistent urinary
and appropriate treatment of urinary tract infections. incontinence and cystitis.
Prognosis Diagnosis
Poor in severe cases. Diagnosis based on contrast cystography.
Affected cats may voluntarily pass a small amount of

EXSTROPHY
urine with difficulty.
Classical signs Typically there is a large flaccid urinary bladder (detru-
sor atony), which is easily manually expressed.
● Urine dribbles from abdominal defect.
Other clinical signs usually predominate, such as an
acute onset over 24–48 h of depression and anorexia,
Clinical signs gastrointestinal signs (dysphagia, regurgitation, vomit-
ing, tenesmus, diarrhea, constipation), mydriasis, pro-
Very rare disorder in cats characterized by ventral mid-
lapsed third eyelids, dry mucous membranes and
line defects in the ventral abdominal wall, urinary blad-
bradycardia.
der, intestines and external genitalia.
Easily differentiated from other causes of incontinence
as urine dribbles from the abdominal defect.
Diagnosis
Diagnosis Diagnosis is based on clinical examination findings of
a flaccid bladder associated with acute onset of depres-
Diagnosis is based on clinical signs. Exstrophy should sion and gastrointestinal and ocular signs.
be differentiated from patent urachus.
Radiographic signs are of megesophagus and a dis-
tended urinary bladder.
FELINE DYSAUTONOMIA
Ophthalmological examination reveals reduced tear
Classical signs production, dilated poorly responsive pupils in a visual
cat, and prolapsed third eyelids.
● Distended bladder. Urodynamic procedures include the following:
● Cystometry and urethral pressure profilometry may
● Gastrointestinal and ocular signs.
be used to objectively evaluate detrussor and ure-
thral function.
● Cystometrograms can be used to show large filling
Pathogenesis
volumes, and lack of a sustained contractile peak
Feline dysautonomia is an autonomic polyganglionopa- indicates detrussor atony.
thy (Key–Gaskell syndrome). ● Urethral pressure profilometry can be used to iden-
Autonomic ganglia (sympathetic and parasympathetic) tify urethral incompetence.

are affected resulting in detrusor atony and urethral
sphincter incompetence.
Overflow incontinence occurs as a result. Treatment
Bethanecol is effective in inducing urination in some
cases, although it should not be used in cats with slow
Clinical signs
resting heart rates, as profound bradycardia and cardiac
Mainly seen in young cats. arrhythmia may occur.
RECOMMENDED READING
Barsanti JA, Finco DR, Brown SA. Diseases of the lower urinary tract. In: Sherding RG (ed) The Cat Diseases and
Clinical Management. Churchill Livingstone, Melbourne, 1994, pp 1769–1823.
Lane IF. Disorders of micturition. In: Osborne CA, Finco DR (eds) Canine and Feline Nephrology and Urology.
Williams and Wilkins, Baltimore, 1995, pp 593–717.
Lane IF, Barsanti JA. Urinary incontinence. In: August JR (ed) Consultations in Feline Internal Medicine. WB
Saunders Company, Sydney, 1994, pp 373–382.
13. The cat with discolored urine
Joseph William Bartges
KEY SIGNS
● Red, pink, orange, brown, black, white, blue or colorless urine.
MECHANISM?
● Urine color other than yellow including red, orange, white, blue, brown and black is abnormal.
Red, brown or orange urine suggests blood, hemoglobin, myoglobin or bilirubin.
Cloudy or white urine suggests pus, lipid or crystals.
Pale yellow or colorless urine is associated with dilute urine and increased urine volume.
Blue or green urine is uncommon, and is usually associated with excretion of drugs or toxins.
WHERE?
● Urogenital tract – urine is formed in the kidney and is usually yellow.
Pigments that are filtered by the glomerulus may alter urine color.
Blood cells may alter urine color if added to urine after formation.
WHAT?
● Red, pink, orange, brown or black urine***

Diseases causing discolored urine
MECHANICAL
● Urolithiasis causing hematuria*** (p 209)
*Occurs in 15–30% of cats with lower urinary tract disease; *struvite most common in young cats;
*calcium oxalate is most common in middle-aged or older cats; *nephroliths are often composed
of calcium oxalate.
NEOPLASIA
● Neoplasia causing hematuria* (p 210)
*urinary tract neoplasia is rare in cats; *renal neoplasia is often associated with renomegaly;
*hematuria may be the only clinical sign.
continued
205
continued
METABOLIC
● Coagulopathy or thrombocytopenia causing hematuria (p 212)
*coagulopathy and thrombocytopenia are rare in cats; *evidence of bleeding at other sites is often-
present, although hematuria may be the only clinical sign; *coagulation testing should be per-
formed in cats with undiagnosed hematuria.
● Bilirubinuria** (p 211)
*bilirubinuria is always abnormal in cats; *it may result from prehepatic, hepatic, or post-hepatic
causes; *most common causes are hepatic disease.
● Hemoglobinuria (p 212)
*associated with hemolysis; *hemolytic anemia is uncommon in cats; *myoglobinuria; *results from
muscle breakdown; *may occur secondary to polymyopathy, but uncommon.
INFECTIOUS
● Urinary tract infection causing hematuria** (p 209)
*bacterial UTI occurs in 1–2% of cats < 10 years of age, but may occur in >45% of cats >
10 years; * E. coli is the most common organism isolated from cats with bacterial UTI; *urine
should be collected by cystocentesis to adequately assess bacterial UTI.
IDIOPATHIC
● Idiopathic lower urinary tract disease causing hematuria*** (p 208)
*Most common cause of lower urinary tract disease in cats less than 10 years. Clinical signs
include hematuria, stranguria, pollakiuria, and inappropriate urination; *urethral obstruction may
occur in male cats.
TRAUMA
● Trauma causing hematuria* (p 210)
*Trauma to any part of the urinary tract may result in hematuria; *evaluate for other signs of
trauma; *if hematuria is secondary to trauma, assess integrity of urinary tract.
● Cloudy white or white urine** (p 206)
● Crystalluria*** (p 213)
*Commonly associated with urolithiasis, matrix-crystalline urethral plug formation in males;
*struvite and calcium oxalate most common; *struvite and urate more common in kittens; *may or
may not be pathologic.
● Pyuria** (p 214)
*Signifies inflammation, which is often but not always associated with bacterial UTI; *may result
from lower or upper urinary tract diseases.
●Lipiduria (p 214)
*May be normal; * may be an indication of lipid metabolism disorders.
13 – THE CAT WITH DISCOLORED URINE 207
● Pale yellow or colorless urine*** (p 207)

● Dilute urine*** (p 215)
*Occurs with polyuric states; *most common causes of PU/PD are renal failure, diabetes mellitus,
and hyperthyroidism; *other clinical signs may be present and relate to an underlying disorder.
● Blue or green urine (p 207)
*Drug discoloration; *occurs with some drugs or dyes especially methylene blue.
INTRODUCTION – Blood (hematuria) is present when centrifuged or

settled urine is clear with a red sediment at the bot-
tom of the tube, or there are > 10–20 red cells/HPF
MECHANISM? on microscopic examination of sediment.
Urine that is anything other than yellow is abnormal. – Hemoglobin is present if the urine remains pink
● Normal urine is typically transparent and yellow
after centrifugation or on settling, few red cells
or amber on visual inspection. (< 10 RBC/HPF) are evident on microscopic
● Two pigments, urochrome and urobilin, impart the
examination of the sediment, and there is clini-
yellow color. cal and hematologic evidence of hemolytic ane-
● The intensity of the yellow color is in part related to
mia. Plasma has a reddish discoloration.
the volume of urine collected and concentration of – Myoglobin is present if the urine remains pink
urine produced. after centrifugation or on settling, few red cells
● Significant disease may exist when urine is normal
are evident on microscopic examination of the
in color. sediment, and there is clinical and biochemical
evidence of muscle damage. Plasma is clear.
Abnormal urine color is caused by the presence of
several endogenous or exogenous pigments, and indi- Clinical signs associated with discolored urine will
cates a problem. aid in diagnosis.
● Hematuria (red or pink urine) indicates urinary
● Pink, red, brown, orange or black urine suggests
the presence of blood, hemoglobin, myoglobin or tract disease (upper or lower) or bleeding disorders.
bilirubin. – Signs that suggest the cause is lower urinary
● Cloudy or white urine suggests the presence of
tract disease are stranguria, pollakiuria and
pus, lipid or crystals. dysuria (urine may be pink, red, brown, orange
● Pale yellow or colorless urine is associated with
or cloudy in color).
decreased urine concentration and increased – Signs that suggest hematuria is from upper uri-
urine volume. nary tract disease include polyuria and polydip-
● Blue or green urine is uncommon, and is usually
sia (urine is usually pale yellow or colorless,
associated with excretion of drugs or toxins. however, cloudy or red urine may occur).
– A bleeding disorder is indicated by evidence of
Owners may observe discolored urine in the litter box bleeding from other sites.
or in areas of inappropriate urination. – Hemoglobin in urine suggests intravascular
Examination of urine sediment (for red blood cells) and hemolysis. Marked hemoglobinuria may
plasma or serum color will aid diagnosis. occur in kittens with neonatal isoerythrol-
ysis. Hemoglobinuria rarely occurs with
Whole blood, hemoglobin and myoglobin all give a Hemobartonella infection and immune-medi-
positive reaction on the blood test pad on dipsticks. ated anemia, which present mainly as extravas-
● These can be distinguished as follows: cular hemolysis.
– Signs that suggest intravascular hemolysis and

WHAT?
hemoglobinuria include acute illness, fever,
pale mucous membranes, +/− jaundice, +/− Hematuria is the most common cause of discolored
splenomegaly, or acute lethargy and death in urine. This is most often associated with idiopathic
1–3-day-old kittens. lower urinary tract disease and less frequently with
– Hemoglobinuria and bilirubinuria may be both urolithiasis.
present with intravascular hemolysis.
● Myoglobinuria (red or brown urine) suggests acute
muscle damage. In cats this is most often associated DISEASES CAUSING DISCOLORED
with ischemic myopathy secondary to an aortic URINE
thrombosis, muscle injury from trauma or ischemia
(e.g. entrapment in window), or snake bite (espe-
cially Australian tiger snake). RED, PINK, ORANGE, BROWN
– Muscle damage with leakage of myoglobin is OR BLACK URINE
suggested by signs of muscle pain, biochemical
evidence of muscle damage (increased creatine Red, pink, orange, brown or black urine suggests the
kinase) and other historical and clinical signs of presence of hematuria (frank blood), hemoglobin, myo-
trauma, thrombosis or snakebite. globin or bilirubin. Red or pink urine is most com-
● Bilirubinuria (dark yellow urine) suggests marked monly associated with hematuria.
erythrocyte breakdown (hemolytic anemia), hepatic Cats with discolored urine may or may not have signs
disease or bile duct obstruction. of lower urinary tract disease (stranguria, pollakiuria,
– Bilirubinuria is most often associated with dysuria, urination in inappropriate places).
hepatic disease including cholangiohepatitis
complex, hepatic lipidosis, neoplasia and feline Systemic illness may or may not be present.
infectious peritonitis. Mucous membranes may be pale or yellow if associ-
– Occasionally it occurs when Hemobartonella- ated with hyperbilirubinemia or anemia.
associated hemolysis is severe enough to cause
jaundice. Diagnosis is aided by examination of urine sediment
– Clinical signs are varied depending on the cause for red and white blood cells, and plasma or serum
of bilirubinuria. Serum and plasma are also jaun- color.
diced.
● Cats with hematuria from upper urinary tract dis-
ease or hemoglobinuria, myoglobinuria or biliru- IDIOPATHIC LOWER URINARY TRACT
binuria may be systemically ill. DISEASE CAUSING HEMATURIA***
● Mucus membranes may be pale or yellow if urine (IDIOPATHIC FELINE LOWER URINARY
discoloration is associated with hyperbilirubinemia TRACT DISEASE, IDIOPATHIC
or hemolytic anemia. CYSTITIS–URETHRITIS COMPLEX, FELINE
● Some cats with abnormal urine may have no other UROLOGIC SYNDROME, INTERSTITIAL
clinical signs. CYSTITIS)
Classical signs
WHERE?
● Stranguria, pollakiuria, inappropriate
Discolored urine is produced in the urinary tract. It may
urination and hematuria are present.
result from urinary tract disease (most common), a sys-
● Occurs most commonly in cats less than 10
temic bleeding disorder, or from excretion of pigments
years of age.
from the plasma.
Careful history and physical examination may help to See main reference on page 176 for details on idio-
determine if the discoloration is clinically significant. pathic lower urinary tract disease.

Clinical signs are similar to other causes of lower uri- If uroliths are located in the lower urinary tract,
nary tract disease: hematuria, pollakiuria, stranguria stranguria, pollakiuria, inappropriate urination,
and urination in inappropriate places. hematuria and/or urethral obstruction may occur.
Most commonly occurs in cats less than 10 years of If uroliths are located in the upper urinary tract, renal
age; average age is 2–4 years. pain, hematuria or uremia (if bilateral) may be present.
Occurs with even frequency in male and female cats. Uremia is present with urethral obstruction or bilateral
ureteral obstruction.
May be associated with urethral plug formation and
obstruction in male cats. Clinical signs may also be absent with uroliths.
Diagnosis Diagnosis
Must be differentiated from other causes of lower uri- Microscopic examination of urine sediment reveals
nary tract disease such as urolithiasis and bacterial uri- RBCs.
nary tract infection.
Crystalluria may or may not be present. If present, they
In cats less than 10 years of age, it occurs in 55–70% may aid in estimating mineral composition (see page
of cases of lower urinary tract disease; in cats 213 for description of crystal appearance).
greater than 10 years of age, it occurs in 5–10% of
Most common mineral composition includes struvite
cases of lower urinary tract disease.
(magnesium ammonium phosphate hexahydrate) and
Diagnosis is made by excluding other causes of calcium oxalate; urate (purine), cystine, calcium phos-
lower urinary tract disease. phate, and drug metabolites have also been observed to
occur.
Urinalysis reveals hematuria (>5 RBC/hpf) without a
urinary tract infection; white blood cells are usually Struvite and calcium oxalate uroliths are usually radio-
present at < 5–10/hpf and urine culture is negative. dense; urate and cystine are usually radiolucent and
require contrast radiography or ultrasonography to
Crystals may or may not be present on urine sediment
identify.
examination.
Radiographs and ultrasonography of the lower urinary
tract are usually normal; however, bladder wall thick-
ening or intraluminal blood clots may be present. URINARY TRACT INFECTION CAUSING
HEMATURIA**
Cystoscopy often reveals small mucosal hemorrhages
called glomerulations, without identifying other dis- Classical signs
eases processes.
● Hematuria, stranguria, pollakiuria, and/or
inappropriate urination (urinary bladder
infection).
UROLITHIASIS CAUSING HEMATURIA***
● Urinary tract infection may occur
secondary to another disease, and other
Classical signs
clinical signs may be present.
● Stranguria, pollakiuria, inappropriate ● Asymptomatic or associated with fever,
urination and/or urethral obstruction. renal pain, or uremia (upper urinary tract
● Renal pain, hematuria, or uremia if uroliths infection).
present in upper urinary tract.
See main reference on page 187 for details on urinary
See main reference on page 184 for details on urolithiasis. tract infections.
Clinical signs TRAUMA CAUSING HEMATURIA*

Bacterial urinary tract occurs in approximately
1–2% of cats less than 10 years of age that have Classical signs
lower urinary tract disease, 40–50% of cats greater ● Hematuria.
than 10 years of age that have lower urinary tract dis- ● History of trauma may be present.
ease, and in approximately 20% of cats with renal ● Evidence for other trauma-induced injury
failure. (such as broken bones, diaphragmatic
Bacterial urinary tract infection is more common than hernia, dyspnea, etc.).
other infectious agents and usually involves the lower
urinary tract.
Clinical signs
Less common infectious agents causing hematuria
include feline infectious peritonitis (FIP). Evidence for trauma such as broken bones, dyspnea,
pneumothorax, shredded nails, lacerations, etc., are
Urinary bladder is most common site of urinary tract often present.
infection. Clinical signs include hematuria, stran-
guria, pollakiuria and/or inappropriate urination; History of traumatic episode, such as being hit by a
however, some cats may be asymptomatic. car or attacked by a dog is often present.
If the upper urinary tract is involved, fever, renal pain Shock may be present.
and/or uremic signs may be present. Hematuria is present if the urinary tract is injured due
Bacterial urinary tract infection may occur secondary to trauma (hemorrhage may be from upper urinary
to diseases that alter normal host defense mechanisms tract, lower urinary tract or both).
such as renal failure, diabetes mellitus, urolithiasis or
neoplasia; therefore, additional clinical signs may Diagnosis
relate to the underlying disease.
Hematuria (numerous RBCs) is found on urinalysis.
● Hemorrhage may be from the lower urinary
tract, the upper urinary tract or both.
Diagnosis ● It is important to determine if the urinary tract is
intact. This may require an excretory urogram to
Urinalysis may reveal pyuria (> 5 WBC/hpf), bac-
evaluate the upper urinary tract and/or contrast ure-
teriuria, hematuria (> 5 RBC/hpf), and/or protein-
throcystography to evaluate the lower urinary tract.
uria; however, a bacterial urinary tract infection
– Unexplained azotemia or uroabdomen (abdominal
may be present with an inactive urinary sediment
fluid with composition of urine, i.e. creatinine con-
on microscopic examination, especially in cats with
centration > plasma) is an indication for contrast
concurrent disease(s).
radiography and possibly surgical intervention.
An aerobic culture and sensitivity should be performed
Evidence for other organ systems being traumatized
on a urine sample collected by cystocentesis.
aids diagnosis.
● This allows identification of the organism as well as
selection of the appropriate antimicrobial for treat-
ment.
● Nitrite and leukocyte test pads present on some dip-
NEOPLASIA CAUSING HEMATURIA*
sticks are not reliable and should not be used.
● Urine may be stained with Wright’s stain or
Classical signs
Gram stain to aid in identification of bacteria and ● Hematuria, pollakiuria, stranguria and/or
to assist in selecting an appropriate antibiotic until inappropriate urination may be present.
culture results are returned.
Classical signs—Cont’d BILIRUBINURIA**

● Hematuria may be only clinical sign if
upper urinary tract involved. Classical signs
● Urine is dark yellow.
See main reference on page 191 for details on blad- ● Mucous membranes and skin are icteric.
der/urethral neoplasia and page 250 for details on renal
neoplasia. See main reference on page 421 (The Yellow Cat or Cat
With Elevated Liver Enzymes) for details on the
icteric cat.
Clinical signs
If the neoplasm involves the lower urinary tract, clini- Clinical signs
cal signs may include hematuria, stranguria, pollak-
Urine is dark yellow or brown from presence of
iuria and/or inappropriate urination.
bilirubin.
If the neoplasm involves the upper urinary tract,
Cat may be weak and icteric.
hematuria may be present; renomegaly may be pal-
pated. Mucous membranes are pale if associated with
hemolytic anemia.
Abdominal palpation may reveal hepatomegaly, hepatic
Diagnosis masses or the liver may not be palpable.
Most common lower urinary tract neoplasms Bilirubinuria may be associated with vomiting,
include transitional cell carcinoma and lym- anorexia, diarrhea and/or neurologic signs (seizure,
phoma. hypersalivation, tremors).
● Neoplastic cells may be present on microscopic
examination of urine sediment. Diagnosis
● A bladder or urethral mass may be detected by
ultrasonography, contrast urethrocystography, ure- Bilirubinuria is diagnosed by a color change on the
throcystoscopy or cystotomy. bilirubin pad on a urine dipstick.
● Definitive diagnosis is made by fine-needle aspira- ● Bilirubinuria is always abnormal in a cat.
tion, biopsy or excision of mass. ● The bilirubin test pad may change color if the
urine is heavily pigmented as with hematuria.
Most common upper urinary tract neoplasms include
lymphoma and carcinoma. Bilirubinuria may occur because of prehepatic, hepatic
● Renomegaly is usually present; lymphoma often or posthepatic causes of excess bilirubin in the plasma.
involves both kidneys. ● Bilirubinemia and bilirubinuria occur when the
● Neoplastic cells may be present on microscopic hepatic capacity to process bilirubin is over-
examination of urine sediment. whelmed by marked hemolysis. Hemolysis is asso-
● Survey abdominal radiography may reveal ciated with anemia that is usually regenerative, and
renomegaly. most commonly caused by Hemobartonellosis or
● Renal ultrasonography may reveal a discreet renal immune-mediated mechanisms.
mass or diffuse hyperechogenicity if lymphoma is ● Bilirubinuria also occurs when the capacity of
involved. the liver to process bilirubin is reduced, causing

● Definitive diagnosis is made by fine-needle aspira- bilirubinemia. There are many causes for hepatic-
tion, biopsy or nephrectomy. related icterus, but hepatic lipidosis, cholangio-
hepatitis complex, feline infectious peritonitis ● Marked thrombocytopenia is present if it is the

and lymphosarcoma are most common. cause of the bleeding disorder or if associated with
● ALT, GGT and/or alkaline phosphatase activities DIC.
are abnormal. ● Coagulation tests are prolonged if associated with
● Liver function tests, such as provocative serum bile rodenticide poisoning or clotting factor deficiency.
acid concentrations or blood ammonia concentra-
Hematuria is present; however, white blood cell counts
tions, are abnormal.
are usually < 5–10/hpf.
● Abdominal radiography and ultrasonography may
reveal focal or diffuse hepatomegaly with abnormal
echotexture. HEMOGLOBINURIA
● Liver biopsy or fine-needle aspiration is necessary
to confirm the underlying disease. Classical signs
Bile duct obstruction (posthepatic cause of bilirubine- ● Urine is red or pink.
mia and bilirubinuria) is associated with cholestatic ● Mucous membranes may be pale if
icterus, and is most commonly associated with pancre- associated with anemia.
atitis, pancreatic or duodenal neoplasia, or sludge bile
syndrome. See main reference on page 532 for details (The
● Alkaline phosphatase activity is usually Anemic Cat) on hemolytic anemia.
extremely elevated relative to other liver enzyme
activities.
Clinical signs
● Enlarged bile duct may be observed by abdominal
ultrasonography. Hemoglobinuria indicates severe intravascular
hemolysis has occurred.
Urine is usually red or pink due to excretion of hemo-
COAGULOPATHY OR THROMBOCYTOPENIA
globin, which has exceeded the saturation limit of the
CAYSING HEMATURIA
carrier plasma protein (haptoglobin).
Classical signs Pale mucous membranes may be present and the cat
may be weak or may collapse due to anemia.
● Hematuria may occur.
● Tachypnea and tachycardia may be present.
● Other evidence of hemorrhage is usually
present. Other signs suggestive of intravascular hemolysis and
hemoglobinuria include acute illness, fever, pale
See main reference on page 487 (The Bleeding Cat) for mucous membranes, +/− jaundice, +/− splenomegaly or
details on coagulopathies. acute lethargy.
Marked hemoglobinuria is most common in kittens
Clinical signs with neonatal isoerythrolysis. Kittens are normal at
birth but develop acute lethargy or death in the first 1–3
Hematuria may be the only clinical sign, but hemor-
days of life. In adult cats, hemoglobinuria is very
rhage may occur from other orifices or in body cavities;
rarely associated with Mycoplasma haemofilis or
petechiations may be present.
immune-mediated anemia.
There may be a history of exposure to an anticoagulant
toxin.
Diagnosis
Pale mucous membranes.
Although urine is red or pink, RBCs are not observed
on microscopic examination of urine sediment.
Diagnosis
Hemoglobinuria may be differentiated from myoglo-
Anemia due to blood loss is present. binuria by examination of plasma or serum; plasma
or serum is pink with hemoglobinuria but clear with Evidence of cardiac disease is usually present with aortic-
myoglobinuria. saddle thrombus.
Anemia may be present. Snake bite may be complicated by a coagulopathy and
● Plasma and serum are pink. hemolysis, resulting in hemoglobinuria, hematuria, as
● May be Coombs positive if associated with well as myoglobinuria.
immune-mediated hemolytic anemia.
CLOUDY WHITE OR WHITE URINE
MYOGLOBINURIA Cloudy or white urine suggests the presence of pus,
lipid, or crystals.
Classical signs
Diagnosis is aided by microscopic examination of urine
● Urine is red or brown. sediment for pyuria, crystalluria or lipiduria.
● Muscle weakness or pain present.
Consideration of the clinical signs aids diagnosis. Signs
See main reference on page 950 (The Cat With General- of lower urinary tract disease or systemic illness may or
ized Weakness) for details on snake bite, and page 915 may not be present.
(The Weak and Ataxic or Paralyzed Cat) for details on
aortic thrombosis.
CRYSTALLURIA***
Clinical signs
Classical signs
Myoglobinuria is most commonly associated with
● White or cloudy urine.
aortic thrombosis or snake bite. Rarely, toxoplasmo-
● May or may not be associated with
sis results in myoglobinuria or bilirubinuria in young
urolithiasis.
cats.
Urine is red, brown, or black. See main reference on page 184 (The Cat Straining to
Urinate) for details on urolithiasis.
Muscle weakness or pain is present.
Vomiting, anorexia, or other polysystemic signs may be
present. Clinical signs
Arrhythmia or heart murmur may be present if an Crystalluria may result in white or cloudy urine if
aortic saddle thrombus is present secondary to underly- the crystalluria is marked or the urine is concentrated.
ing cardiomyopathy. Crystalluria may occur with or without urolithiasis, and
uroliths may be present without crystalluria.
Diagnosis ● Uroliths in the lower urinary tract may be associ-
Urine is red, brown or black. ated with hematuria, stranguria, inappropriate uri-
nation, pollakiuria or urethral obstruction.
No RBCs observed on microscopic examination of ● Uroliths in the upper urinary tract may be associ-
urine sediment. ated with hematuria or renal pain.
● Uroliths may not be associated with clinical signs.
Plasma and serum are normal in color.
Hyperkalemia and metabolic acidosis is often present
if due to muscle injury. Diagnosis
There is evidence for other organ dysfunction if myo- Crystals are identified on microscopic examination of
globinuria is associated with toxoplasmosis, including urine sediment.
dyspnea, anemia, vomiting, diarrhea, neurological ● Struvite crystals are typically “coffin-lid”-shaped
signs or jaundice. or amorphous, and occur in a neutral to alkaline pH.
● Calcium oxalate crystals are typically “dumb- immunodeficiency virus infection, or neoplasia
bell”-shaped (monohydrate) or are “square- (see page 228, The Cat With Inappropriate
shaped with an ‘X’ in the center” (dihydrate), and Urination).
occur in an acidic pH. ● Occasionally pyuria occurs without an infection.
● Urate crystals are typically yellow or brown and
Inflammation of the lower urinary tract is usually
amorphous, and occur in an acidic pH.
associated with stranguria, dysuria, pollakiuria
● Cystine crystals are six-sided, and occur in an
and/or inappropriate urination; however, clinical
acidic pH.
signs may be absent.
● Other crystals include other minerals (calcium
phosphate), normal metabolites (leucine, bilirubin, Inflammation of the kidneys/ureters may be associ-
tyrosine) or drugs (iodinated contrast media, sulfa- ated with systemic illness (fever, vomiting, renal pain
containing antibiotics). and/or anorexia).
Crystals may be present as artifact.
● Crystals may form due to a change in pH or tempera-
Diagnosis
ture after collection; struvite crystals commonly
form in healthy cats if the urine is allowed to cool to Urine is white or cloudy.
room temperature or colder (as with refrigeration).
Microscopic examination of urine sediment reveals
● Crystals may also occur if the urine sample is
increased numbers of WBC (typically > 50–100/hpf).
allowed to evaporate.
● Normal urine contains < 3–5 WBC/hpf.
● For accurate interpretation, a complete urinalysis
● The significance of cell counts should be consid-
including microscopic examination of sediment
ered in association with the urine specific gravity.
should be done on a freshly collected sample in
order to avoid artifact. Nitrite and leukocyte test pads present on some urine
dipsticks are not reliable and should not be used.
PYURIA**
Classical signs LIPIDURIA

● Cloudy white or white urine.
Classical signs
● Stranguria, pollakiuria if inflammation
involves lower urinary tract. ● White urine.
● Fever, vomiting, renal pain if inflammation ● Not usually associated with a systemic
involves upper urinary tract. disease although may be associated with
lipid metabolism abnormalities.
See main reference on page 187 (The Cat Straining to
Urinate) for details on bacterial cystitis and page 225 (The See main reference on page 425 (The Yellow Cat or
Cat With Inappropriate Urination) for pyelonephritis. Cat With Elevated Liver Enzymes) for details on
hepatic lipidosis and page 569 (The Cat With Hyper-
lipidemia).
Clinical signs
Pyuria is indicative of inflammation.
● This is usually associated with an infectious Clinical signs
process.
Lipiduria may result in white urine.
– Bacterial infection is most common.
– Funguria is rare and is usually associated with a Lipiduria is not usually associated with clinical signs;
decrease in the host defense mechanisms such as it appears to be normal in some cats particularly those
diabetes mellitus, urolithiasis, chronic antibiotic that are obese and consuming normal or increased
administration, feline leukemia virus or feline amounts of dietary fat.
It may be present with lipid metabolism disorders such Diagnosis

as idiopathic hyperlipidemia, inherited hyperchylomi-
cronemia and idiopathic feline hepatic lipidosis. Urine is pale yellow or colorless.
Urine specific gravity is isosthenuric (1.008–1.014) or
hyposthenuric (< 1.008).
Diagnosis
Pale yellow or colorless urine may be normal with con-
Lipid droplets identified on microscopic sediment sumption of a large quantity of water, consumption of a
examination. low-protein diet or administration of fluids or agents
Lipid droplets may be stained using Sudan IV. that induce diuresis.
Pale yellow or colorless urine should be considered
abnormal if present with azotemia or dehydration.
PALE YELLOW OR COLORLESS URINE
DILUTE URINE*** BLUE OR GREEN URINE
Classical signs DRUG DISCOLORATION

● Polyuria and polydipsia are usually
present. Classical signs
● Most common causes of polyuria in cats ● Blue or green urine.
are renal failure, diabetes mellitus and ● History of administration of drugs
hyperthyroidism. especially methylene blue.

With Polyuria and Polydipsia). Clinical signs
A number of drugs and dyes cause blue or green urine
but few are used in cats.
Clinical signs
Blue or green urine occurs in cats following methylene
Pale yellow or colorless urine implies increased urine blue use. In humans amitriptyline and riboflavin have
volume; therefore, polyuria and polydipsia are usu- been reported to cause blue or green urine.
ally present.
Polysystemic signs such as vomiting, weight loss and
Diagnosis
anorexia may be present with some diseases (renal fail-
ure and diabetes mellitus) and increased appetite may Careful questioning of the owner will usually identify
occur with hyperthyroidism and diabetes mellitus. the drug causing the urine discoloration.
RECOMMENDED READING
Bartges JW. Discolored urine. In: Ettinger SJ, Feldman EC (eds) Textbook of Small Animal Internal Medicine.
Philadelphia, WB Saunders, 2000, pp 96–99.
Bartges JW. Diseases of the urinary bladder. In: Birchard S, Sherding R (eds) WB Saunders Manual of Small Animal
Practice. Philadelphia, WB Saunders, 2000, pp 943–957.
Lulich JP, Osborne CA, Bartges JW, et al. Canine lower urinary tract disorders. In: Ettinger SJ, Feldman EC (eds)
Textbook of Small Animal Internal Medicine. Philadelphia, WB Saunders, 2000, pp 1747–1781.
Osborne CA, Lulich JP, Kruger JM (eds) Feline lower urinary tract disorders. Vet Clin North Am Small Anim Pract
1996; 26.
Osborne CA, Lulich JP, Bartges JW (eds) The ROCKet science of canine urolithiasis. Vet Clin North Am Small Anim
Pract 1999; 29.
14. The cat with inappropriate urination
Joseph William Bartges
KEY SIGNS
● Urination in inappropriate places.
MECHANISM?
● Urination occurs outside the litter box in inappropriate places.
Urine may or not be of normal consistency and composition.
Inappropriate urination occurs as a result of lower urinary tract diseases (urgency, irritation),
polyuric states (inability to retain large volume of urine), incontinence (uncontrolled urination),
or behavioral problems.
In addition to inappropriate urination, clinical signs are variable depending on the underlying
disease, if present.
WHERE?
● Urogenital tract.
WHAT?
● Most cats with inappropriate urination have an underlying disease process.
Many lower urinary tract diseases are associated with inappropriate urination.
Inappropriate urination may also be associated with polyuric states or behavioral problems.

Diseases causing inappropriate urination
DEGENERATIVE
● Hormonally responsive incontinence (p 227)
Incontinence is uncommon in cats; cats unconsciously urinate especially when sleeping.
ANOMALY
● Congenital anatomic diseases of the bladder or urethra (p 226)
Congenital bladder and urethral diseases are uncommon; usually stranguria, pollakiuria or com-
plete inability to urinate is observed in addition to inappropriate urination.
continued
217
continued
● Incontinence (p 227)
Incontinence resulting from congenital disease is uncommon. Affected cats may continuously pass
small drops of urine.
METABOLIC
● Polyuric states (p 224)
Any disease associated with increased urine volume may result in cats urinating inappropriately if
they are not able to adequately retain urine and use the litter box. Examples include chronic renal
failure, diuretic therapy, diabetes mellitus and hyperthyroidism.
● Urolithiasis** (p 222)
Signs of lower urinary tract disease including pollakiuria, stranguria and hematuria are usually
present, although uroliths may be present without clinical signs; may cause urethral obstruction.
NEOPLASTIC
● Neoplasm involving urethra and/or urinary bladder (p 225)
Pollakiuria, stranguria and hematuria usually present; may be associated with recurrent bacterial
urinary tract infections or urethral obstruction.
● Meningioma (p 227)
May be associated with proprioceptive deficits, alteration of spinal reflexes and alteration of men-
tation: however, only clinical sign may be urinary incontinence.
PSYCHOLOGICAL
● Behavioral*** (p 219)
Inappropriate urination without clinical, biochemical or radiological evidence for an underlying
disease involving the urinary bladder or urethra; may be associated with other behavioral problems
or develop as a consequence of lower urinary tract disease.
INFECTIOUS
● Bacterial urinary tract infection** (p 225)
Pollakiuria, dysuria and hematuria are usually present; bacterial urinary tract infections are uncom-
mon in cats and usually occur secondarily to another disease.
● Fungal urinary tract infection (p 228)
Cat may be asymptomatic or show pollakiuria, stranguria, hematuria and inappropriate urination;
often occurs secondary to an underlying disease or immunosuppressive process.
● Viral urinary tract infection (p 226)
May result in secondary bacterial or fungal urinary tract infection (FeLV, FIV), or hypothesized to
be one of the causes of idiopathic lower urinary tract disease.
IDIOPATHIC
● Non-obstructive idiopathic lower urinary tract disease**** (idiopathic cystitis,
feline urologic syndrome, interstitial cystitis, idiopathic FLUTD)*** (p 222)
Cats show pollakiuria, hematuria, stranguria and inappropriate urination without an identifiable
cause.
14 – THE CAT WITH INAPPROPRIATE URINATION 219
IATROGENIC
● Catheterization of the urinary bladder or urethra* (p 224)
History of catheterization for relief of urethral obstruction, bladder disease or for diagnostics.
TRAUMATIC
● Trauma to urethra and/or urinary bladder*** (p 223)
History of trauma or physical examination findings of trauma (fractures, skin abrasions, uroab-
domen, etc.). Cats may be able to urinate even when the urinary bladder is compromised.
● In young cats, idiopathic lower urinary tract dis-

INTRODUCTION ease is the most common cause of lower urinary
tract disease occurring in 50–70% of cases.
MECHANISM? – Urolithiasis is the second most common cause
occurring in 15–25% of cases.
Inappropriate urination is defined as cats urinating in
– Bacterial urinary tract infection, trauma, neoplasia
inappropriate places (typically outside of a litter box)
and incontinence are uncommon in young cats.
or at inappropriate times. ● In cats older than 10 years, bacterial urinary
Lower urinary tract disease is the most common cause tract infection is the most common cause of lower
of inappropriate urination, and signs such as pollaki- urinary tract disease, occurring in 35–50% of cases.
uria, stranguria and/or hematuria, are usually present. – Urolithiasis occurs in 10–15% of cases.
– Idiopathic disease, trauma, neoplasia and
Inappropriate urination may also occur with inconti-
incontinence are uncommon causes.
nence, polyuric states and an inability to retain urine
appropriately, or as a behavioral problem. Inappropriate urination, however, may occur without
– Inappropriate urination may be a behavioral prob- signs of lower urinary tract disease.
lem that is learned while the cat is suffering from ● It may occur with incontinence.
another lower urinary tract disease, such as idio- ● It may occur with polyuric states.
pathic lower urinary tract disease or urolithiasis. ● It may be behavioral.
● Cats are inherently fastidious creatures and do not
Diagnosis is based on historical information, physical
normally soil where they live.
examination findings and results of laboratory and radi-
● Male cats may urinate outside of the litter box to
ological evaluation.
mark their territory.
● Female cats usually do not mark territory; how-
ever, they may do so if they are, or become, the DISEASES CAUSING INAPPROPRIATE
dominant cat in the household. URINATION
BEHAVIORAL***
WHERE?
Classical signs
Brain, bladder and urethral sphincter (mucosa, muscle,
nerves). ● Behavioral elimination problems are the most
● If pollakiuria, stranguria and hematuria are present, common behavior complaints of owners.
it localizes the disease to the lower urinary tract. ● Cats may urinate outside of the box.
● Behavioral urination problems may include
inappropriate urination or urine marking.
WHAT? ● Underlying medical problems may result in
a behavioral component causing
Most commonly, inappropriate urination occurs with inappropriate urination.
Pathogenesis Diagnosis
House-soiling problems are the most common behavior Underlying medical problems must be ruled-out
complaints made by cat owners. for a diagnosis of a behavioral problem, although
behavioral urination problems may occur in conjunc-
Urine house-soiling problems include inappropriate
tion with or following an underlying medical condition.
urination and urine marking.
● Inappropriate urination involves elimination of A behavioral history should be performed once medical
urine outside the litter box at locations unaccept- problems have been eliminated.
able to the owner. ● The owner should be asked to keep a daily record of
– Inappropriate urination usually occurs on the number of eliminations in each litter box and
horizontal surfaces outside the litter box. the number of eliminations outside the litter box
– Any age, breed or gender cat may be affected. with the location noted.
– Location of inappropriate urination is variable. ● Information should also be obtained concerning the
– Inappropriate urination often results from a care of the litter box by the owner.
problem with the litter box including, unwill- ● It is beneficial to ask the owner to make a map of
ingness by the cat to use certain types of litter, the interior of the home, with sites of elimination
infrequent cleaning, change in litter consistency and litter boxes marked so patterns can be visually
or amount and a deterrent to using the litter box identified.
because of other cats in the household. ● If multiple cats are in the household or if it is
● Urine marking involves the use of urine in the uncertain as to where a cat may be urinating
act of olfactory communication, which may inappropriately, fluorescein dye (0.3 ml SQ, 0.5 ml
occur independent of the act of urination. PO, or six fluorescein strips in gel capsules given
– Urine spraying occurs more frequently in PO) may be administered; any urine that is found
males than in females, and in intact animals outside the litter box during the next 24 hours can
compared with neutered animals. be checked for fluorescence using a Wood’s light.
– Urine marking may act as a means for cats to
Urine marking is typically characterized by a cat passing
communicate their presence so that other cats
small amounts of urine in different places (“spraying”).
will avoid using the same space at the same time.
● Owners may or may not observe this behavior.
– Urine marking may be indicative of a high level
● In a multi-cat household, more than one cat may
of arousal, often associated with the presence
exhibit this behavior.
of other cats inside or outside of the house.
● Although isolation of cats in a household may iden-
– Urine marking often involves surfaces other
tify the individual, urine marking may cease when
than horizontal ones (such as drapes, walls
separated from housemates.
and furniture); however, it may involve hori-
● Fluorescein dye as described before may also be
zontal surfaces similar to inappropriate urination.
used to identify offenders.
– Urine marking is not usually associated with a
medical condition. Differential diagnosis
Clinical signs Inappropriate urination may or not occur second-
ary to a medical disorder.
Inappropriate urination occurs when the cat urinates a
● Diseases associated with polyuria, such as renal
normal amount of urine assuming a normal posture
failure and diabetes mellitus, may result in inap-
consciously outside of the litter box; inappropriate
propriate urination, because the cat finds the litter
fecal elimination may also occur. Urinalysis may or
excessively wet.
may not be normal.
● Causes of lower urinary tract disease, such as
Urine marking involves passing small amounts of urine on urolithiasis or idiopathic disease (non-obstructive
surfaces other than horizontal to mark a territory that a cat FLUTD or interstitial cystitis), result in inappropri-
inhabits or is passing through; urinalysis is normal. ate urination.
● Incontinence associated with a congenital or – Make the location where the cat marks aversive
acquired anatomical problem may be interpreted as to the problem cat.
inappropriate urination. – An odor deterrent such as citrus spray may be
effective.
Urine marking must be differentiated from inappropri-
– Spray synthesized facial pheromone (the F3
ate elimination.
fraction) at the site(s).
● This can usually be accomplished on the basis of
● Behavior modification consists of positive interac-
historical information and a good behavior history.
tions with the cat in scheduled play or grooming
● Underlying medical problems rarely result in
times.
urine marking.
– Avoid punishment because it may increase the
cat’s fear and anxiety.
● Pharmacologic treatment of urine marking attempts
Treatment to attenuate the cat’s arousal and/or anxiety in
response to social or environmental situations.
The goal of treatment of inappropriate urination is to
– Benzodiazepines have been used for their anxi-
enhance the appeal and accessibility of the litter box
olytic property.
and to decrease the availability and appeal of alter-
– They may not only decrease anxiety and fear, but
nate sites.
they produce mild sedation.
● The litter box should contain a litter that is pre-
– Dosage of diazepam is 1–4 mg/cat q 12–24 h
ferred by the cat and kept clean.
PO.
● A litter box may be used in the area where inap-
– Side effects include sedation, muscle relaxation,
propriate urination has occurred.
increased appetite and paradoxical excitation;
– Once the cat begins to use this litterbox, it may
hepatic necrosis has been reported to occur
be moved slowly to a site more acceptable to the
rarely in cats.
owner.
– Other benzodiazepines have not been thor-
– Deterrents such as an unacceptable substrate,
oughly evaluated in cats.
e.g. plastic covers or odor may be used at the
– Alprazolam may be given at 0.125–0.25 mg
inappropriate site.
PO q 12 h or 0.05–0.1 mg/kg PO q 8 h.
● Positive reinforcement when the cat uses the
– Dosage for clonazepam is 0.016 mg/kg PO q
appropriate litter box is better than negative rein-
6–24 h.
forcement when the cat inappropriately elimi-
– Clorazepate dosage is 0.55–2.2 mg/kg PO q
nates.
12–24 h.
● Pharmacologic therapy is not usually necessary;
– Flurazepam has been used primarily as an
environmental therapy is much more effective
appetite stimulant at 0.2–0.4 mg/kg PO as
with behavioral inappropriate urination.
needed.
● Owners’ compliance can be a problem, and owners
– Triazolam may also be tried at 0.03 mg PO q 12 h.
should maintain records of the cat’s elimination
– Azaperones have serotonergic and dopamin-
patterns; owners also need positive reinforcement.
ergic mechanisms.
Treatment of urine marking can be accomplished by – Buspirone has been shown to be efficacious
environmental, behavior, surgical and pharmaco- for the treatment of urine marking.
logical methods. – Dosage is 5–7.5 mg PO q 12 h, or 2–10 mg PO
● Environmental treatment involves deterring the cat q 12–24 h, or 0.5–1 mg/kg PO q 12–24 h.
from urine marking. – The drug has no potential for abuse and does not
– Restrict the cat from areas where spraying cause sedation.
occurs. – It may take 1–3 weeks to show an effect.
– Block the indoor cat’s view of outdoor cats. – Side effects include idiosyncratic changes in
– Reduce the number of cats outside or inside the social behavior and mild gastrointestinal side
house. effects.
– Tricyclic antidepressants are used commonly

NON-OBSTRUCTIVE IDIOPATHIC LOWER
to treat behavioral disorders.
URINARY TRACT DISEASE*** (IDIOPATHIC
– Amitriptyline is used most commonly although
CYSTITIS, FELINE UROLOGIC SYNDROME,
clomipramine has been used.
INTERSTITIAL CYSTITIS, IDIOPATHIC
– Dosage for amitriptyline is 2.5–10 mg PO q 24
FLUTD)
h or 0.5–1 mg/kg PO q 24 h, and for
clomipramine, it is 1–5 mg PO q 12–24 h.
Classical signs
– Side effects include sedation and possible anti-
cholinergic effects. ● Inappropriate urination, hematuria,
– Selective serotonin reuptake inhibitors act selec- stranguria and pollakiuria.
tively on the serotonin neurotransmitter system. ● Signs are usually transient lasting between
– Fluoxetine and paroxetine have been used to 3 and 7 days.
treat urine marking.
– Dosage for fluoxetine is 0.5 mg/kg PO q 12 h or See main reference on page 176 for details (The Cat
1–2.5 mg PO q 24 h, and for paroxetine, 0.5 Straining to Urinate) on idiopathic lower urinary tract
mg/kg PO q 24 h or 1.25–2.5 mg PO q 24 h. disease.
– Fluoxetine may take 3–4 weeks before an effect
is observed; paroxetine has a shorter half-life Clinical signs
and is quicker acting.
– Side effects include vomiting, diarrhea, nausea, Inappropriate urination, pollakiuria, stranguria and
inappetence, sleep disturbances and irritability. hematuria commonly occur.
– Historically, progestational compounds have been Idiopathic disease is more common in cats younger
used to treat urine marking; however, because than 10 years of age.
severe side effects such as diabetes mellitus may
occur, other pharmacotherapy should be used. Clinical signs typically last between 3 and 7 days.
● Surgical treatment can affect the incidence of
urine marking. Diagnosis
– Castrate intact males.
The diagnosis of idiopathic lower urinary tract disease
– Olfactory transaction has been used rarely and is
is based on clinical signs and exclusion of other causes
reserved for cats that are refractory to all other
of lower urinary tract disease.
forms of therapy.
● Urinalysis reveals hematuria (> 5 RBC/hbf).
● Pyuria and bacteruria are not present (i.e. < 5
Prognosis WBC/hbf).
● Abdominal radiography and ultrasonography, and
Prognosis for behavioral inappropriate urination is
contrast urethrocystography are normal or only
good; however, owner compliance is necessary.
show mild thickening of the bladder wall.
Prognosis for urine marking is good; however, cats that
Complete blood cell counts and serum biochemical
are refractory to treatment often become unacceptable
analysis are normal, and FeLV and FIV are negative.
as indoor pets and are put outdoors or are euthanized.
Prevention
UROLITHIASIS**
Inappropriate urination may be prevented by treating
underlying medical problems and by appropriate care Classical signs
of the litter box.
● Inappropriate urination is usually
Urine marking may be prevented by castrating cats associated with stranguria and hematuria.
when kittens, by minimizing stress in the environ-
ment, and by early treatment of the problem. See main reference on page 184 for details on urolithiasis.
Clinical signs TRAUMA TO URETHRA AND/OR URINARY

Inappropriate urination due to urolithiasis is usually asso- BLADDER**
ciated with stranguria, pollakiuria and hematuria.
Classical signs
Most uroliths occur in middle-aged to older cats.
● Inappropriate urination, hematuria,
Urethral obstruction may also occur, therefore, post- pollakiuria and stranguria.
renal uremia may also be present (vomiting, anorexia, ● Other signs of trauma, such as fractures
oral ulceration). and skin abrasions, may be present.
If urate uroliths develop in association with a portal
vascular anomaly, tremors, seizures, salivation, depres- See main reference on page 189 for details on trauma to
sion and stunted growth may also be observed. Signs the lower urinary tract.
are usually present before 2 years of age.
Clinical signs
Diagnosis Inappropriate urination, hematuria, pollakiuria
and stranguria may be present because of trauma to
Diagnosis is based on radiography and/or ultrasonogra-
the urinary bladder or urethra.
phy of the urinary tract.
● Because uroliths composed of struvite and cal- Other signs of trauma, such as fractures and skin abra-
cium oxalate account for more than 85% of uro- sions, may be present.
cystoliths, they are often observed on survey
Trauma to the caudal abdomen may result in rupture or
radiography. Contrast cystography will help iden-
perforation of the urinary bladder.
tify rediolucent uroliths.
● Post-renal uremia may be present.
– Uroliths composed of cystine, urate and xan-
● Only a small quantity or no urine at all may be
thine are not usually radiodense.
passed despite attempts at urination.
– Uroliths composed of drug metabolites are not
● Abdominal effusion may be present due to urine
usually radiodense.
leakage from the damaged bladder.
● Ultrasonography may reveal presence of urocys-
toliths, but not urethroliths.
Diagnosis
Urinalysis may reveal abnormalities.
● Crystalluria may or may not be present. Microscopic examination of urine reveals an inflamma-
● Hematuria is often present, but not always. tory reaction.
● Bacterial urinary tract infection may occur, but is
Serum biochemical analysis may reveal azotemia.
usually secondary to presence of uroliths.
Contrast cystography is necessary to determine the
Serum biochemical analysis is usually normal.
integrity of the urinary bladder.
● Approximately 35% of cats with calcium oxalate
● Ultrasonography may reveal abdominal effusion.
uroliths are hypercalcemic.
● Survey abdominal radiography may have decreased
● Urate uroliths associated with hepatic disease may
contrast due to abdominal effusion.
also be associated with increases in liver enzyme
● Abdominocentesis may reveal urine.
activity, increased blood ammonia concentration,
and increased bile acid concentrations (pre- or post- Other laboratory parameters may be abnormal depend-
prandial). ing on the extent of the trauma.
● Cats normally are not observed to drink very much,

POLYURIC STATES**
particularly if consuming canned diets. Cats eating a
mix of canned and dry food drink < 20 ml/kg/24 h.
Classical signs
● Owners may notice cats drinking out of water
● Polyuria, polydipsia and inappropriate sources, such as sinks and bowls, when the cat has not
urination. done so previously. Water intake of > 100 ml/kg/24
● ± Systemic signs such as anorexia or h is abnormal, even if cats are eating dry food.
polyphagia, vomiting, weight loss, poor
Serum biochemical analysis and serum thyroxine con-
hair coat quality and/or diarrhea.
centrations should be performed, in addition to a com-
plete urinalysis, in all cats that may have polyuria and
polydipsia to aid in localizing the problem further.
With Polyuria and Polydipsia) on chronic renal failure,
page 236 for details on diabetes mellitus, and page 304
for details (The Cat With Weight Loss and a Good CATHETERIZATION OF THE URINARY
Appetite) on hyperthyroidism. BLADDER OR URETHRA*
Clinical signs Classical signs

Polyuria and polydipsia may result in the cat being ● Inappropriate urination, stranguria,
unable to adequately retain urine resulting in inappro- pollakiuria and hematuria.
priate urination.
See main references on page 187 for details on bacter-
History of drinking and urinating a greater volume then
ial urinary tract infection and page 181 for details on
normal (polyuria and polydipsia).
urinary catheretization.
Inappropriate urination may occur because of the inability
to retain larger quantity of urine.
Clinical signs
Other clinical signs are variable depending on the
The urethra or urinary bladder mucosa may be
underlying disease process.
traumatized during catheterization performed to
● The most common causes of polyuria and polydip-
clear an obstruction from the urethra or for diagnostic
sia in cats are renal failure, diabetes mellitus and
procedures; therefore, there is a history of urinary
hyperthyroidism.
catheterization.
– Renal failure may be associated with inap-
petance anorexia, vomiting, poor body condition Indwelling urinary catheters may predispose to
and oral ulcers. bacterial urinary tract infection.
– Diabetes mellitus may be associated with weight
Inappropriate urination, stranguria, pollakiuria and hema-
loss despite a good appetite; vomiting and anorexia
turia may occur following catheterization of the urinary
may occur if associated with ketoacidosis.
tract if mucosal damage occurs, or if a secondary bacter-
– Hyperthyroidism may be associated with weight
ial infection occurs. Occasionally a urethral or urinary
loss despite polyphagia, poor body condition
bladder diverticulum is formed by traumatic catheteriza-
and intermittent vomiting.
tion, predisposing to recurrent bacterial infection.
● Other causes of polyuria and polydipsia may occur,
but are less common.
Diagnosis
Diagnosis
The diagnosis is made based on clinical signs and a his-
Polyuria is confirmed by a low urine specific gravity tory of urethral catheterization.
(<1.030).
A urinalysis and urine culture should be performed
Polydipsia may be difficult to confirm in cats because to rule-in or rule-out an iatrogenic bacterial urinary
measurement of fluid intake may be difficult. tract infection.
If a polypropylene catheter is placed too far into the ● Alkaluria (pH > 7) may occur with urease-
urinary bladder, perforation may occur. producing bacteria, such as Staphylococcus spp.
● Post-renal azotemia may be found on serum bio- and Mycoplasma spp.
chemical analysis. ● Urine culture is necessary to identify the species of
● Abdominal effusion, if present, will have a com- bacteria and its antibiotic sensitivity pattern.
position similar to urine. – Urine should be collected by cystocentesis.
● Contrast cystography is necessary to confirm the – Nitrite and leukocyte esterase test pads on urine
perforation although abdominal ultrasonography or dipsticks are not reliable indicators of bacterial
survey abdominal radiography will demonstrate urinary tract infection, and should not be used.
abdominal effusion if present.
Abdominal radiography or ultrasonography, or contrast
studies of the urinary tract may be necessary to detect
anatomic defects, and uroliths or neoplasms, that pre-
BACTERIAL URINARY TRACT INFECTION*
dispose the cat to a bacterial urinary tract infection.
Classical signs Systemic diseases resulting in dilute urine, such as
renal failure or diabetes mellitus, or in immunosup-
● Inappropriate urination occurs together
pression, such as FeLV, FIV or diabetes mellitus, may
with pollakiuria, stranguria and hematuria.
result in a bacterial urinary tract infection.
See main reference on page 187 for details (The Cat Drugs resulting in a diuresis, such as furosemide, or
Straining to Urinate) on bacterial urinary tract infection. in immunosuppression, such as corticosteroids, may
predispose to bacterial urinary tract infection.
Clinical signs Urethral catheterization may result in iatrogenic bac-
terial urinary tract infection, particularly if antibiotics
Bacterial urinary tract infections often occur as a con-
are administered concurrently.
sequence of an underlying disease of the urinary
bladder, polyuric states or immunosuppressive
states; therefore, other clinical signs may be present. NEOPLASM INVOLVING URINARY
● Any disease that disrupts the cat’s normal defenses BLADDER OR URETHRA
may result in a bacterial urinary tract infection.
● Systemic illness may be seen if the underlying dis- Classical signs
ease process is a systemic disease such as diabetes
● Inappropriate urination may occur with
mellitus, chronic renal failure, FeLV or FIV infection.
pollakiuria, stranguria and hematuria.
Urination in inappropriate places usually occurs ● Typically occurs in cats older than 10 years.
together with signs of pollakiuria, stranguria and
hematuria. See main reference on page 191 for details on neoplasia.
● Clinical signs of other lower urinary tract diseases
are similar to those observed with bacterial urinary Clinical signs
tract infections.
Although uncommon, lower urinary tract neoplasia
typically occurs in cats older than 10 years.
Diagnosis
Inappropriate urination associated with neoplasia
Diagnosis is made by examination of urine. may occur with other signs of lower urinary tract dis-
● Pyuria (> 5 WBC/hpf) and bacteruria are often ease such as stranguria, pollakiuria and hematuria.
observed on microscopic examination of urine, but
Urethral obstruction may occur if neoplasm occurs at
a bacterial urinary tract infection may be present
the trigone region, urethra or prepuce.
with an inactive urinary sediment on microscopic
examination, especially in older cats with concur- If urinary outflow obstruction occurs, signs of post-renal
rent disease(s). uremia may occur (vomiting, anorexia, depression).
Diagnosis FeLV and FIV may be associated with other clinical

signs including gingival disease, infections of other
Some urinary bladder neoplasms may be palpated on organs, liver disease or renal disease.
abdominal palpation; urethral neoplasm may be pal-
pated on rectal examination. Clinical signs of lower urinary tract disease, if idio-
pathic in nature (interstitial cystitis), usually resolve in
Transitional cell carcinoma of the urinary bladder is 5–7 days, although a protracted course of clinical signs
the most common lower urinary tract neoplasm; may occur.
other types of neoplasia that may occur include squa-
mous cell carcinoma, lymphoma, fibrosarcoma, and
leiomyoma or leiomyosarcoma. Diagnosis
Ultrasonography and/or contrast urethrocystography Hematuria may be observed with or without bacteruria
may be necessary to identify the neoplasm. and pyuria.
Diagnosis may require biopsy or fine-needle aspiration FeLV and FIV testing should be performed on cats
of the mass. with lower urinary tract disease or recurrent bacterial
● Occasionally, neoplastic cells may be found on urinary tract infections.
microscopic examination of urine sediment. Viral particles have been observed by electron
● Fine-needle aspiration may be accomplished by
microscopy in some matrix-crystalline plugs retrieved
palpation or by ultrasound guidance. from male cats with urethral obstruction.
● Cystoscopy may also be used to identify and aspi-
rate or biopsy a mass.
● It may be necessary to obtain a biopsy using surgery. CONGENITAL ANATOMIC DEFECTS
OF BLADDER OR URETHRA
VIRAL URINARY TRACT INFECTION Classical signs

● Inappropriate urination usually occurs with
Classical signs other clinical signs such as pollakiuria,
● Lower urinary tract signs including stranguria and possibly hematuria.
inappropriate urination, pollakiuria, ● Usually evident as a young kitten.
stranguria and hematuria.
See main references on page 201 for details (The
See main references on page 187 for details (The Cat Incontinent Cat) on patent urachus and page 198 for
Straining to Urinate) on hemorrhagic cystitis and page details on ectopic ureters.
225 for details on bacterial urinary tract infection.
Clinical signs
Clinical signs Inappropriate urination is first observed at an early age.
It may not be noticed until the kitten is older and litter
FeLV or FIV infections may result in bacterial uri- box training is undertaken.
nary tract infections.
Pollakiuria, stranguria and/or hematuria may also be
A cell-associated herpesvirus and a urotropic cali- present.
civirus have been hypothesized to be a cause of idio-
pathic lower urinary tract disease in cats resulting in Defects of the bladder or urethra may be associated with
hemorrhagic cystitis (non-obstructive feline lower uri- other congenital anomalies, especially of the vagina.
nary tract disease, interstitial cystitis).
Diagnosis
Inappropriate urination may occur with other clinical
signs of lower urinary tract disease including hema- Diagnosis is made by historical information concerning
turia, stranguria and pollakiuria. age of cat, physical examination of the urinary tract,
and radiology including contrast studies and ultra-

INCONTINENCE (INCLUDING
sonography of the lower urinary tract.
HORMONALLY RESPONSIVE
Many congenital anomalies are possible, but congenital INCONTINENCE)
anomalies are uncommon in cats.
● Patent urachus and ectopic ureters are the most Classical signs
common congenital anomalies.
● Unconscious urination usually occurs when
● Other anomalies include, but are not limited to:
asleep.
– Bladder agenesis.
● Cats with congenital disease may
– Bladder duplication.
continuously pass small drops of urine
– Vaginal defects such as septal defects.
whether awake or asleep.
– Urethral dysgenesis.
– Urethral strictures.
– Bladder and urethral diverticulae.
Incontinent Cat) on incontinence.
MENINGIOMA Clinical signs

Classical signs Incontinence may be due to an underlying congenital or
acquired anatomic problem.
● Inappropriate urination.
● Neurological deficits (altered mentation, Incontinence is urination that is uncontrolled or uncon-
abnormal proprioception or spinal sciously done.
reflexes). ● Unconscious urination usually occurs when
asleep.
See main reference on page 914 for details on menin- ● Cats with congenital disease may continuously
gioma. pass small drops of urine whether awake or

asleep.
Clinical signs Pollakiuria, dysuria and stranguria may also occur if a

secondary bacterial urinary tract infection occurs.
Meningiomas may be associated with urinary incon-
tinence and inappropriate urination. Urinalysis is usually normal unless a secondary bacterial
urinary tract infection is present.
Inappropriate urination is usually due to incontinence
related to a spinal cord meningioma but may be asso-
ciated with cerebral meningioma. Diagnosis
Other neurologic deficits, such as proprioceptive deficits Diagnosis is usually made on the basis of historical and
or abnormal spinal reflexes, may or may not be present. physical examination findings.
Typically occurs in old cats > 10 years. Incontinence must be differentiated from consciously
controlled inappropriate urination as might be
observed with bacterial urinary tract infection, urolithi-
Diagnosis asis, bladder or urethral neoplasia or other causes of
Diagnosis is difficult.
● With lower urinary tract disease, cats
● Meningiomas involving spinal cord may require
appear to have urgency or discomfort when
myelography for diagnosis.
urinating.
● Meningiomas that occur intracranially require com-
– Hematuria and/or pyuria with or without crystal-
puterized tomography or magnetic resonance imag-
luria is usually present.
ing for diagnosis.
– Laboratory and radiological evaluation may be
Laboratory evaluation is normal. abnormal.
● With incontinence, these signs are not present, Diagnosis

instead cats urinate without being aware that they
are doing so. Diagnosis of funguria is based on results of urinalysis
– Urinalysis is typically normal. and urine cultures.
● Microscopic examination of urine sediment reveals
budding yeasts or elongated hyphae, and inflamma-
tion.
FUNGAL URINARY TRACT INFECTION ● Urine culture is necessary to definitively diagnose
fungal urinary tract infections.
Classical signs – The absolute number of fungal organisms does
● Usually asymptomatic. not correlate with infection; however, fungi are
● Pollakiuria, stranguria, hematuria and not normal inhabitants of the urinary bladder.
inappropriate urination may occur. – A cystocentesis sample should be evaluated.
● Systemic clinical signs may be present. – Use of fungal culture media facilitates isola-
tion and identification of the organism.
Other diagnostic tests should be directed at identify-
Pathogenesis
ing abnormalities in local or systemic host defenses.
Fungal urinary tract infections are often associated ● Serum biochemical analysis may reveal azotemia
with impaired systemic or local host defenses such consistent with renal failure, or hyperglycemia
as glucosuria, indwelling urinary catheters, consistent with diabetes mellitus.
urethrostomy and urolithiasis. ● FeLV and FIV testing should be performed.
● Abdominal radiography, including contrast studies,
Cats with immunosuppressive diseases such as FeLV
and ultrasonography are necessary to determine if
and FIV infection are also at risk for development of
an abnormality of the lower urinary tract is present
fungal urinary tract infections.
such as urolithiasis or neoplasia.
Candida and Torulopsis are normal saprophytic inhab-
itants of the gastrointestinal tract and are the most com- Differential diagnosis
mon fungi observed to occur in urine.
Any disease of the lower urinary tract may present with
similar signs.
Clinical signs
Most common diseases with similar signs are non-
Fungi are not normally found in urine of healthy animals. obstructive idiopathic lower urinary tract disease and
● Cats with funguria may be asymptomatic.
urolithiasis. Differentiation is based on finding yeast
● However, clinical signs of systemic disease may be
or hyphae in the urine. Urolithiasis may occasionally
present. be concurrent with fungal infection.
Symptomatic fungal urinary tract infections are associ-
ated with pollakiuria, hematuria, stranguria and Treatment
inappropriate urination if the infection occurs in the
Some patients have asymptomatic funguria.
lower urinary tract, or fever, inappetence, vomiting
● No treatment may be necessary as some sponta-
and septicemia if it occurs in the upper urinary tract.
neously clear the fungi if predisposing factors can
Rarely, bezoars (fungal balls) may form. be resolved.
● Bezoars are clusters of intertwined fungal ● Urinary catheters should be removed or used
hyphae which may aggregate. intermittently.
● Bezoars may be present in patients with symptomatic ● If possible, antibacterial and immunosuppressive
or asymptomatic fungal urinary tract infections. medication should be discontinued.
● They are sources of persistent funguria. ● Alkalinization of urine may aid in clearing of
● Large bezoars may result in urethral obstruction. the fungal urinary tract infection.
– Candida species survive poorly at alkaline pH. – Ketoconazole and itraconazole are not very
– Alkalinization therapy has not been very suc- effective because they have limited urinary
cessful. excretion.
– Potassium citrate may be administered at – Fluconazole may be a viable alternative.
50–75 mg/kg PO q 12 h. – This imidazole is smaller, more water soluble,
– Sodium bicarbonate may also be used at 12 and less protein bound than other commonly
mg/kg PO q 8 h. used imidazoles.
– Active fluconazole is excreted primarily in urine.
More aggressive treatment is warranted in patients that
– Use a dosage of 50–100 mg/cat PO with food.
have symptomatic fungal urinary tract infections.
● Intravesicular clotrimazole
● An attempt should be made to correct predispos-
– Instillation of 1% clotrimazole intravesicularly
ing risk factors.
has been successful in treating fungal cystitis.
● Antifungal drugs should also be used.
– Instillation can be accomplished by anesthesia or
– Flucytosine has a narrow range of antifungal
sedation and urinary catheterization or by cysto-
activity, limited primarily to yeast-like fungi
centesis.
such as Candida, Torulopsis and Cryptococcus.
– Three to four treatments may be necessary.
– Flucytosine is deaminated to 5-fluorouracil in
fungal cells which interrupts intracellular pro-
tein synthesis resulting in death of the cell. Prognosis
– Flucytosine is excreted largely unchanged in
Prognosis for asymptomatic funguria in cats is
urine which makes it a good first-line treatment.
unknown.
– Dosage is 200 mg/kg/day PO divided into three
● Funguria may spontaneously resolve.
or four sub-doses.
● Funguria may also progress to symptomatic infec-
– Resistance may occur.
tion or to bezoar formation.
– Flucytosine should be continued 2–3 weeks
● Some animals may have persistent asymptomatic
beyond clinical resolution of fungal urinary
funguria without discernible harm.
tract infection.
● Amphotericin-B is also effective in the treatment Symptomatic funguria carries a variable prognosis.
of fungal urinary tract infection and can be used ● If systemic fungal infection is present, prognosis
with flucytosine or an imidazole. is guarded.
– Occurrence of nephrotoxicity is a major disad- ● If fungi are limited to the lower urinary tract, the
vantage to its use. prognosis is fair; however, complete clearance of
– Amphotericin-B disrupts fungal cell membranes the fungal urinary tract infection may be diffi-
making it effective. cult.
– Resistance is uncommon.
Bezoar formation may require surgical removal if it
– Dosage is 0.1–0.25 mg/kg IV (administered in
causes urethral obstruction or persistent or recurrent
30 ml of 5% dextrose in water over 15 min) q
funguria, and it cannot be disrupted by medical means.
48 h for up to 6 weeks. It may be also given sub-
cutaneously (see page 26, The Cat With Signs
of Chronic Nasal Disease). Prevention
– Amphotericin B may also be administered by irri-
Because fungal urinary tract infection usually occurs as
gation into the urinary bladder.
a result of a problem with local or systemic host
– A concentration of 200 mg of amphotericin-B
defenses, identification and correction of risk factors
per liter of sterile water is recommended.
may prevent it from occurring.
– This solution is infused at 5–10 ml/kg into the
urinary bladder lumen daily for 5–15 days. Urine from cats with indwelling urinary catheters should
● Imidazole derivatives may be used as treatment be examined periodically, particularly if the animal is
for funguria. receiving antibiotics or immunosuppressive therapy.
RECOMMENDED READING
Bartges JW. Diseases of the urinary bladder. In: Birchard S, Sherding R (eds) Saunders Manual of Small Animal
Practice. Philadelphia, WB Saunders, 2000; 943–957.
Lulich JP, Osborne CA, Bartges JW, et al. Canine lower urinary tract disorders. In: Ettinger SJ, Feldman EC (eds)
Textbook of Small Animal Internal Medicine. Philadelphia, WB Saunders, 2000, pp 1747–1781.
Lulich JP, Osborne CA. Fungal urinary tract infections. In: Kirk RW, Bonagura JD (eds) Current Veterinary Therapy
XI. WB Saunders, Philadelphia, 1993, pp 914–919.
Osborne CA, Lulich JP, Kruger JM (eds). Feline lower urinary tract disorders I and II. Vet Clin North Am Small
Anim Pract 1996; 26 (2, 3).
Simpson BS. Feline housesoiling part I: Inappropriate elimination. Compend Contin Educ Pract Vet 1998; 20:
1319–1329.
Simpson BS. Feline housesoiling part II: Urine and fecal marking. Compend Contin Educ Pract Vet 1998; 20:
1331–1339.
Toll J, Ashe CA, Trepanier LA. Intravesicular administration of clotrimazole for treatment of Candiduria in a cat with
diabetes mellitus J Am Vet Med Assoc 2003; 223:1156–1158.
15. The cat with polyuria and polydipsia
Jacquie Rand
KEY SIGNS
● Drinking more than normal.
● Increased frequency of urination and increased volume and/or nocturia.
● Urinating outside litter box.
MECHANISM?
● Polyuria and polydipsia usually occur in cats because of an inability to concentrate urine.
WHERE?
● Kidney (the kidney controls urine production, but it is influenced by many other organs).
WHAT?
● Most cats with polyuria and polydipsia (PU/PD) have renal failure, diabetes mellitus or hyper-
thyroidism.

Diseases causing polyuria and polydipsia
DEGENERATIVE
● Chronic renal failure*** (p 235)
Inappetence or anorexia, weight loss, PU/PD, vomiting, increased or decreased renal size.
METABOLIC
● Diabetes mellitus*** (p 236)
Usually older than 6 years of age, PU/PD of 1–12 weeks duration, weight loss, polyphagia or inap-
petence, may have been previously obese.
● Hyperthyroidism*** (p 242)
Older than 7 years of age, weight loss, polyphagia or inappetence, palpable cervical mass, vomit-
ing, tachycardia, restlessness.
● Diabetes insipidus* (p 243)
Central form is rare, nephrogenic form is common, and associated with renal failure, hyperthy-
roidism, pyometra, etc. Urine specific gravity often <1.007.
continued
231
continued
● Hyperadrenocorticism (p 251)
Very rare; poorly controlled diabetes mellitus which may be insulin resistant, poor hair coat,
weight loss despite higher than normal doses of insulin, thin fragile skin that bruises easily.
● Acromegaly (growth hormone-producing tumor, hypersomatotrophism) (p 254)
Very rare. Often associated with poorly controlled diabetes mellitus, which is usually insulin
resistant, often requiring very high doses of insulin. Typically there is a large blocky cat with
weight gain, enlarged tongue, widely spaced teeth, cardiomegaly and thickened soft palate.
● Hypoadrenocorticism (p 252)
Very, rare; lethargy, depression, anorexia, and weight loss are most frequent. Less frequent signs
include vomiting, polyuria and polydipsia.
● Hyperparathyroidism P (p 256)
A rare cause of hypercalcemia in cats. Usually results from a solitary adenoma, but can be from
solitary or bilateral adenocarcinoma or hyperplasia. Older cats (mean age 13 years) and Siamese
are overrepresented. Clinical signs are of hypercalcemia and more than half of the cats have a
palpable parathyroid mass.
● Primary hyperaldosteronism (p 256)
Rare cause of polyuria and polydipsia. Typically occurs in older cats (10–20 years) and is associ-
ated with an adrenal mass. Signs are of intractable hypokalemia and hypertension, and include
muscle weakness, cervical ventroflexion, inappetence, weight loss, blindness and polyuria and
polydipsia.
● Primary sex hormone-secreting adrenal tumor (p 258)
Very rare cause of polyuria, polydipsia. Progesterone-producing tumors result in signs indistin-
guishable from hyperadrenocorticism. Typically there is thin fragile skin that bruises easily,
patchy symmetrical alopecia, secondary skin infections such as demodicosis and polyuria,
polydipsia from poorly controlled diabetes mellitus.
● Pheochromocytoma (p 257)
Very rare cause of polyuria, polydispsia. Typically occurs in older cats (> 8 years of age) and
associated with an adrenal mass. Signs are vague and include polyuria and polydispsia. Systemic
hypertension is characteristic, and presents as sudden blindness from retinal hemorrhage or reti-
nal detachment, or dyspnea from heart failure. Diabetic cats may be insulin resistant.
● Polycythemia
Dark pink or purple mucosae, bleeding, PU/PD, neurological signs including abnormal behavior
and seizures.
● Hypokalemia* (p 244)
Lethargy, inappetence, weakness, ventroflexion of neck, stiff/stilted gait, impaired renal function.
PU/PD are not prominent signs unless associated with chronic renal failure or hyperthyroidism.
NEOPLASTIC
● Neoplasia (renal neoplasia or. lymphoma) (p 250)
PU/PD results from either renal neoplasia causing chronic renal failure, or lymphoma causing hyper-
calcemia (very rare in cats).
15 – THE CAT WITH POLYURIA AND POLYDIPSIA 233
● Hypercalcemia (p 245)
Associated with renal failure, lymphoma or squamous cell carcinoma, primary hyperparathy-
roidism, cholecalciferol rodenticide, infectious disease, diabetes mellitus, hyperthyroidism, liver
disease or idiopathic. Vomiting, weight loss, inappetence and in some cats, signs associated with
calcium oxolate urolithiasis (dysuria and inappropriate urination) may be present. In some cats,
signs are those of the primary disease process, e.g. renal failure or lymphoma.
PSYCHOLOGICAL
● Psychological polydipsia
This syndrome is not yet reported in cats.
INFLAMMATION INFECTIOUS (BACTERIAL)
● Pyelonephritis
Chronic form causes chronic renal failure with weight loss, inappetence. The acute phase may be
associated with fever, lethargy and pain on palpation of the kidneys. Bacteriuria, pyuria, casts
(especially WBC casts) may be present during the active infection, and occasionally leukocytosis
occurs.
● Cystic endometrial hyperplasia/pyometra complex (p 259)
Causes nephrogenic diabetes insipidus and PU/PD; vaginal discharge, inappetence, and weight
loss.
INFECTIOUS (IMMUNE)
● Chronic renal failure (glomerulonephritis or amyloidosis) (p 235)
Causes chronic renal failure and associated signs of PU/PD, weight loss, inappetence, lethargy, and
in the later stages, vomiting.
TREATMENT
● Drug induced* (p 244)
Drugs such as diuretics, phenobarbitol, amphotericin, gentamicin, thyroxine, corticosteroids, and
megestrol acetate may be associated with PU/PD through a number of mechanisms.
INTRODUCTION ● The solute load in the renal tubule is higher than

the capacity to reabsorb it, resulting in osmotic
diuresis. This is characterized by isotonic urine
MECHANISM? with a SG 1.007–1.030. This occurs in the follow-
Polyuria and polydipsia in cats usually occurs ing circumstances:
because of a primary inability to concentrate urine. – Glomerular filtration of an absorbable solute in
This is referred to as primary polyuria and leads to excess of the renal tubular ability to reabsorb
compensatory polydipsia. Although not reported in it, e.g. glucose in diabetes mellitus. This may
cats, the kidney may also be overloaded with water also occur when the glomerular filtration rate
from primary polydipsia, termed psychogenic poly- (GFR) is reduced, as the increased solute load on
dipsia. Mechanisms for primary polyuria are as the remaining functioning nephrons may over-
follows: whelm their absorptive capacity.
– Glomerular disease resulting in leakage of – Renal insensitivity to ADH (nephrogenic dia-

albumin and other poorly absorbable solutes betes insipidus). Renal cells may not respond to
into the renal tubule. adequate concentrations of ADH because of
– Impaired tubular reabsorption of glomerular insufficiency of functioning nephrons, compet-
filtrate solutes such as urea, creatinine, and itive inhibition for ADH receptors, or bacterial
phosphorus as occurs in renal failure and endotoxins. Altered cellular concentrations of
Fanconi syndrome. Ca++, Mg+, prostaglandin E, and corticosteroids
– Diuretics which act as a non-absorbable interfere with ADH receptor binding and render
solute, e.g. Mannitol. renal cells unresponsive to ADH (e.g. hyper-
● The medullary osmotic gradient is compromised, adrenocorticism, hypercalcaemia). Endotoxins
which decreases the concentrating ability of the such as E. coli render nephrons insensitive to
kidney, producing urine with a SG of 1.007–1.030. ADH (e.g. in pyometra–endometritis complex).
Causes include:
Polyuria should be differentiated from pollakiuria,
– Interference with the NaCl pump in the loop
which is increased frequency of urination of small
of Henle. This leads to a decrease in reabsorp-
quantities of urine, and is typically associated with
tion of ions, which is followed by a decrease in
bladder disease, especially cystitis. Inappropriate urina-
medullary hyperosmolality. These effects result
tion associated with behavioral disorders should also be
in the reduced movement of water out of the
differentiated from polyuria.
lumen of the distal tubules and collecting ducts
and hence an increased excretion of water and
solutes. Diuretics such as furosemide act via this
WHERE?
mechanism.
– Rapid fluid flow through the tubules or rapid Primary polyuria is most common, and occurs when the
blood flow through the vasa recta washes out ability to concentrate urine is decreased. Polydipsia is
the high concentration of solutes within the compensatory for polyuria.
medulla interstitium, referred to as medullary
Polyuria commonly results from structural and
washout. This impairs the countercurrent sys-
functional renal pathology, such as:
tem, which normally generates a hyperosmotic
● Loss of functioning nephrons.
environment in the renal medulla interstitium to
● Increased solute loading per nephron.
promote the movement of water out of the lumen
● Disruption of the medullary countercurrent system.
of distal tubules and collecting ducts. Medullary
● Decreased renal responsiveness to ADH.
washout can occur secondary to marked
polyuria, for example from diabetes insipidus, or Polyuria may also be influenced by many other organs
following diuretic use. and non-renal etiologies.
– Disruption to urea recycling through the body
Primary polydipsia (psychogenic polydipsia) has not
decreases the urea concentration in the
been reported in the cat.
medullary interstitium and hence decreases
medullary osmolality. Disruption to urea cycling
can be the result of decreased tubular response to
WHAT?
antidiuretic hormone (ADH) leading to the
reduced permeability of collection ducts to urea, Renal disease (acute and chronic renal failure), dia-
or from decreased plasma urea concentration betes mellitus, hyperthyroidism and nephrogenic
(cirrhosis, protein depletion). Urine specific diabetes insipidus are the most common causes of
gravity is 1.007–1.030. polyuria and polydipsia.
● Collecting ducts become impermeable to water.
Hyperadrenocorticism, hypoadrenocorticism, acromegaly
This is characterized by urine with a SG
and central diabetes insipidus are uncommon causes.
1.001–1.006, and is due to either:
– Deficiency of ADH (central diabetes insipidus). Psychogenic polydipsia has not been reported.
Dehydration is commonly present because of inade-

DISEASES CAUSING POLYURIA AND quate water intake to balance the excessive fluid loss in
POLYDIPSIA urine.
Ocular signs related to hypertension are common, e.g.
CHRONIC RENAL FAILURE*** scleral or conjunctival injection, hyphema or retinal
hemorrhage, retinal edema, retinal vessel tortuosity,
Classical signs retinal detachment.
● Inappetence, anorexia, weight loss. Terminally, seizures, stupor or coma may occur.
● Lethargy.
● Vomiting. Small and/or irregular kidneys may be palpable but
● Polyuria, polydipsia. occasionally kidneys are enlarged (associated with
● Small ± irregular kidneys, occasionally amyloid deposition, neoplasia or cystic kidneys).
enlarged kidneys.
Diagnosis
See main reference on page 333 for details (The Thin,
Inappetent Cat). Increased blood urea (BUN) and creatinine
(azotemia) concentrations together with a urine spe-
cific gravity of 1.007–1.030 (usually 1.007–1.015) is
considered presumptive evidence of renal failure.
Clinical signs
Other findings that may or may not be present are
Inappetence or anorexia is the most common sign and the following:
occurs in 80% of cats.
Hyperphosphatemia
Weight loss is frequent, together with poor body con- ● Serum phosphorus concentration increases when
dition. glomerular filtration rate (GFR) is below approxi-
mately 20% of normal, and tends to parallel BUN
Lethargy or depression are common signs.
concentration.
Polyuria and polydipsia are reported by owners in
Hypokalemia (< 3.5 mmol/l) occurs in 20% of cats.
40% of cats. Nocturia or urination in inappropriate
● Clinical signs of inappetence and generalized
places may also be observed and must be differentiated
muscle weakness (such as wobbliness, inability to
from other causes including behavioral.
jump, stiff, stilted gait and ventroflexion of the
Weakness occurs in nearly 50% of cats and is often neck) may occur when potassium < 3 mmol
associated with hypokalemia. Cats may appear reluc- (mEq)/L.
tant to jump or unsteady with jumping, and be less ● Respiratory muscle failure and death may occur at
active. < 2 mmol (mEq)/L.
Constipation is common and results from dehydration. Hyper- and hypocalcemia are infrequent abnormali-
ties, and result from derangements of calcium metabolism
Vomiting is less common, and if present, is usually
associated with renal secondary hyperparathyroidism.
intermittent and often low grade.
● Most cats have normal or low calcium; 10–20%
Diarrhea is rare, but very occasionally is hemorrhagic have mild to moderate hypercalcemia (≤ 3.1
from uremic enterocolitis. mmol/L, 12.5 mg/dl).
Halitosis, ulcers on the oral mucosa or tongue, brown- Acidosis is common (approximately 80% of cats),
ish discoloration of dorsal surface of tongue, or slough- and is evident as decreased bicarbonate and increased
ing of anterior of tongue may occur in advanced anion gap.
disease.
Normochromic, normocytic, non-regenerative ane-
Pale mucous membranes from anemia may be evident. mia is common when chronic renal failure is advanced.
● It occurs mainly from erythropoietin deficiency, but Pathogenesis

other factors contribute, such as decreased red cell
lifespan. Most diabetic cats appear to have type 2 diabetes mel-
litus, previously called adult-onset diabetes or non-
Proteinuria is typically mild to moderate (1.5–2 times insulin-dependent diabetes.
increase in protein excretion occurs). ● Type 2 diabetes is characterized by decreased
Radiographs of kidneys may show small irregular kid- insulin secretion, insulin resistance and amyloid
neys; size may be normal or increased in some cats deposition in the pancreatic islets.
especially if renal failure is due to amyloid, neoplasia Risk factors include old age, male gender, obesity,
or polycystic kidneys. physical inactivity, confinement indoors, Burmese breed
Ultrasound examination frequently shows small (in Australia, New Zealand and UK), and repeated or
hyperechoic kidneys. long-acting steroid or megestrol acetate administration.
At diagnosis, endogenous insulin secretion is usually
very low.
Differential diagnoses ● This is probably because of the combined effects of:
Pre-renal azotemia. This occurs secondary to dehy- – Impaired insulin secretion associated with the
dration or circulatory collapse; azotemia results from beta cell defect causing type 2 diabetes.
reduced renal blood flow; typically urine specific – Amyloid deposition in the islets which replaces
gravity is ≥ 1.035, in contrast to renal failure where SG beta cells.
is < 1.035. – Suppression of insulin secretion by glucose toxicity.
Pre-renal azotemia together with concomitant pri- Glucose toxicity is defined as suppression of insulin
mary disease that affects renal concentrating ability secretion by persistently (> 24 h duration) high
can mimic renal failure, e.g. a dehydrated cat with central blood glucose.
● Suppression of insulin secretion by glucose toxicity
or nephrogenic diabetes insipidus may have azotemia
with a urine specific gravity < 1.035. is initially functional and reversible, later it
results in structural changes in beta cells. With
time (weeks) changes become irreversible, and
Treatment beta cells are lost.
See main reference on page 336 for details. Some cats (5–20%) have other specific types of dia-
betes. Their diabetes results from another disease
Correct dehydration, reduce uremia, and improve qual- process causing decreased insulin secretion or impaired
ity of life. insulin action (insulin resistance).
● Pancreatic neoplasia is a significant cause of dia-
betes in cats referred to specialists, accounting for
as many as 18% of cases recorded at referral insti-
DIABETES MELLITUS***
tutions in USA.
● Pancreatitis is commonly associated with feline
Classical signs
diabetes (50% of diabetic cats have pancreatitis
● Older than 6 years of age, most > 8 years of lesions at necropsy).
age. – In most cats, pancreatitis is not severe enough to
● Moderate to marked PU/PD, usually of 2–8 cause diabetes alone, but probably contributes to
weeks duration. loss of beta cells.
● Weight loss, but may be normal weight, ● Hyperadrenocorticism and growth hormone-
obese or underweight. producing tumors (acromegaly) are rare causes of
● Polyphagia or inappetence. other specific types of diabetes associated with
insulin resistance.
Clinical signs If persistent hyperglycemia is present in a sick cat,

begin treatment with insulin, even if it is not clear if
Earliest signs are polyuria and polydipsia; nocturia the hyperglycemia is illness-associated. Illness-
and urinary incontinence may occur. associated stress hyperglycemia rarely results in
Weight loss occurs and is accompanied by increased blood glucose concentrations higher than 19
appetite. mmol/L (342 mg/dl).
● At the time of diagnosis, some cats are under- ● Plasma betahydroxybutyrate > 1 mmol/L (10
weight, some normal weight and others are obese. mg/dl) is indicative of diabetes mellitus. However,
some diabetic cats have normal plasma betahydrox-
At diagnosis, some cats have decreased appetite and ybutyrate.
are depressed, others are polyphagic. – A urine dipstick may be used in serum or
Lethargy or depression may be present. Other cats are heparinized plasma to detect ketonemia. A posi-
alert at presentation. tive test indicates ketonemia. It detects mainly
oxaloacetate rather than the predominant ketone
Muscle wasting and weakness are often present and in cats, β-hydroxybutyrate.
may be evidenced as reluctance or inability to jump.
Dehydration is common in cats that are lethargic and
inappetent. Differential diagnoses
Vomiting occurs in one third of cats, but is usually Stress hyperglycemia from struggling or illness.
infrequent. Beware of misdiagnosis in cats with stress hyper-
glycemia from illness or struggling, which also have
Hepatomegaly from hepatic lipidosis, and occasionally concomitant disease that produces similar signs to dia-
jaundice may be present. betes mellitus, e.g. renal failure or hyperthyroidism.
Rear limb weakness or plantigrade posture (hocks ● In stress hyperglycemia associated with struggling,
touching the ground) occur occasionally secondary to blood glucose concentration is generally < 12
diabetic neuropathy. mmol/L (216 mg/dl) within 4 h if the cat is hospi-
talized and further struggling does not occur.
Acetone odor on breath may be evident on average 5 ● Stress hyperglycemia associated with illness may
days before ketonuria is detected. persist for several days and exceed 20 mmol/L (360
Poor unkempt scurfy hair coat. mg/dl). If in doubt, treat these cats with insulin and
closely monitor blood glucose.
Diagnosis Hyperthyroidism may produce similar signs, i.e. old

cat with weight loss, polyphagia and polyuria/polydip-
In most cats, blood glucose greater than 20 mmol/l sia. Generally the polydipsia in hyperthyroidism is less
(360 mg/dl) is diagnostic of diabetes. pronounced. Glucose may be elevated but less than 20
If blood glucose is 12–20 mmol/l (216–360 mg/dl), the mmol/L (360 mg/dl), from stress and insulin resistance.
presence of typical clinical signs (polyuria, polydipsia, Elevated thyroxine concentration is diagnostic.
polyphagia with weight loss), significant glycosuria,
and increased plasma fructosamine or betahydroxy- Treatment
butyrate or ketonuria must be used to differentiate dia-
betes from stress-induced hyperglycemia. General principles
● Plasma fructosamine > 406 umol/L is indicative of
diabetes mellitus. However, some diabetic cats have For initial management, most cats have better
a normal fructosamine concentration, and occasion- glycemic control using insulin rather than oral hypo-
ally, non-diabetic sick cats have mildly increased glycemic agents.
fructosamine concentrations. ● Insulin is more potent in decreasing blood glu-
● Persistent hyperglycemia over 24 h is highly sug- cose; this enables beta cells to overcome the effects
gestive of diabetes, but may also occur with illness. of glucose toxicity.
Approximately 5–30% of cats have good glycemic betic cats, because it lowers blood glucose and insulin
control using oral hypoglycemic drugs which stimu- requirement, and may increase the diabetic remission
late insulin secretion. The sulfonylurea, glipizide, is the rate.
most widely used oral hypoglycemic drug for cats.
Underweight and normal bodyweight cats need a
Oral hypoglycaemic drugs are most useful as sole treat- high-quality, calorie-dense feline diet that is palatable.
ment when:
Obese cats should have their weight reduced by
● Beta cells are not markedly suppressed by glucose
1–2%/week (see page 454 The Cat With Abdominal
toxicity (e.g. blood glucose is < 16 mmol/L (< 290
Distention or Abdominal Fluid for treatment details).
mg/dl)) or
Use a high-protein, low-carbohydrate diet.
● The owner refuses to give insulin injections.
Transient diabetes.
Lente and NPH (Isophane) insulin must be given
● Approximately 20–90% of diabetic cats will
twice daily in all cats; most cats (up to 90%) require
undergo remission of their diabetes in 1–4 months,
ultralente twice daily.
if good glycemic control is achieved.
● In general, lente and NPH insulin have too short
● Remission is more common in diabetic cats
a duration of action to achieve excellent glycemic
recently treated with insulin-antagonistic drugs,
control in cats, although clinical control is often
such as megestrol acetate or long-acting steriods.
good, and signs of diabetes resolve in the majority
● Excellent glycemic control facilitates diabetic remis-
of cats.
sion, by enabling beta cells to recover from glucose
● For approximately 4 hours twice a day there is min-
toxicity. Excellent glycemic control is aided by use
imal exogenous insulin action when using these
of long-acting insulin, especially glargine adminis-
insulins. This means that most diabetic cats have
tered twice daily, and a low-carbohydrate diet.
episodes of hyperglycemia > 16 mmol/L (> 288
● Remission rates increase with increasing dura-
mg/dl) twice daily, which exacerbates glucose toxi-
tion of action of insulin, and highest rates are
city, and makes diabetic remission less likely than
obtained using glargine. PZI produces higher
when using longer-acting insulins.
remission rates than lente insulin, when both are
Long-acting insulins such as glargine, detemir and administered twice daily.
PZI in most cats provide better glycemic control and
Hypoglycemia kills cats.
higher remission rates than lente, NPH and ultralente,
● Teach owners to recognize signs (dazed drunken
and best results are obtained when they are adminis-
look, dilated pupils, wobbliness, weakness, head
tered twice daily.
or body tremors, twitching, seizures or coma).
Because of the small doses used in cats, 40 U/ml Signs may occur with little warning in cats that
insulin is preferable to 100 U/ml insulin. However, have apparently excellent clinical control of their
expected duration of action is more important than con- diabetes.
centration. Using 0.3 ml insulin syringes is advanta- ● The owner should immediately start treatment with
geous when using 100 U/ml insulin. Syringes with 1⁄4 u honey, or a glucose syrup designed for human dia-
gradations are available. betic patients, given per os. If the cat is seizuring,
rub honey or syrup into the gums, or give per rec-
Beef or pork insulins have a longer duration of
tum using the lubricated insulin syringe, if the nee-
action than human insulin. Most insulins for veterinary
dle can be removed.
use are pork or beef/pork mixes. Human-use insulin is
– Cats with severe signs require intravenous glu-
either identical to amino acid sequence in human
cose or glucagon.
insulin, or has substitutions to alter duration of action.
– Give 50% dextrose at 0.5–1.0 ml/kg IV.
Eating does not need to be coordinated with insulin – If intravenous access is not possible, 50% dex-
administration, because the postprandial increase in trose (0.5–1.0 ml/kg) or corn syrup (0.25–0.5
blood glucose is very prolonged (18+ h) in cats. Evidence ml/kg) administered per os, or rubbed on the
suggests that a high-protein, low-carbohydrate diet gums may be effective, but glucagon 0.25–1.0
(6–12% of calories from carbohydrate) is best for dia- mg IM is superior. Glucagon must be followed
by intravenous dextrose once seizures have Monitoring urine glucose is very useful. This can be
stopped to maintain blood glucose. accomplished using poorly absorbent litter material
● Re-evaluate the cat; usually the insulin dose needs such as silicon beads or shredded paper, which allows
to be decreased by 50–70%. Some cats will no collection of urine for testing with a dipstick, or a litter
longer require insulin, because their diabetes is in box glucose detector system such as Glucotest (Purina)
remission. which is added to the box filler, and reacts to urine with
● It is important to check if the cat is being inad- color changes to indicate the level of glucosuria. Some
vertently overdosed. This can occur when differ- owners are able to train the cat to tolerate a dipstick
ent syringes have been dispensed with a different applied to the urine stream during urination.
volume per gradation than was previously used. For Alternatively, some of the urine-soaked litter can be
example, for many brands of syringes, the grada- mixed with water and tested with a dipstick after strain-
tions on a 1 ml 100 U/ml syringe represent 2 U, ing through a cloth.
whereas on a 0.5 ml syringe represent 1 U. If ● Weekly urine glucose monitoring is helpful for
owners are switched to 1 ml syringes, the dose may detecting diabetic remission, especially in cats
be inadvertently doubled, if the same number of treated with lente, NPH or ultralente insulin. Cats
graduations is used to dose the insulin. Similarly, with negative urine glucose should be evaluated for
a switch from syringes designed for U100 insulin to remission.
those for U40 insulin may result in an inadvertent ● With the long duration of action of glargine, there
2.5 times increase in dose. should be minimal periods when blood glucose is
> 14 mmol/L (240 mg/dl), and hence stable cats
Treatment of “healthy” diabetic cats.
should almost always be 0 or 1+ for urine glucose.
● If the cat is not very depressed or dehydrated, start
A value 2+ or greater likely indicates that an
lente, ultralente, PZI or insulin glargine subcu-
increase in dose is required.
taneously.
● Because cats treated with lente, NPH or ultralente
– Use an initial dose of 0.25 U/kg ideal body
insulin usually have hyperglycemia within 6–8 h
weight q 12 h, if blood glucose is between
after insulin administration, which persists until the
12–19 mmol/L (220–350 mg/dl).
next dose, it is not recommended to use urine glu-
– Use an initial dose of 0.5 U/kg ideal body
cose measurements to increase the dose of these
weight q 12 h, if blood glucose is 20 mmol/L
insulins.
(360 mg/dl) or more.
Monitoring fructosamine or glycated hemoglobin
Glycemic control should be monitored using clini-
concentration can be a useful indicator of glycemic
cal parameters (water intake, urine glucose con-
control in cats susceptible to stress hyperglycemia, if
centration, body weight), and at each major
the owner is unable to measure water intake.
recheck, measurement of glucose concentration
Fructosamine concentrations > 500–550 μmol/L (nor-
every 2 h (lente, ultralente) or 4 h (PZI, glargine).
mal < 400 μmol/L) or glycated hemoglobin > 3–4%
Water drunk, urine glucose and blood glucose con-
(normal < 2.6%) are consistent with poor glycemic
centrations are the most useful parameters for
control.
adjusting insulin dose.
● Water drunk of ≤ 20 ml/kg/24 h on canned food or Adjusting insulin dose.
≤ 60 ml/kg/24 h on dry food indicates exemplary ● In general, increase the dose by 1⁄ 2–1 U/cat q 12 h
glycemic control. every 1–4 weeks to achieve a nadir glucose con-
● Water drunk is a better indicator of mean blood glu- centration of 7–9 mmol/L (126–162 mg/dl). Once
cose and level of clinical control than is fruc- clinical signs have resolved, and the blood glucose
tosamine concentration. is relatively controlled, a nadir of 5–6 mmol/L can
● Water drunk should be measured at home on at be achieved. Rebound hyperglycemia is a common
least two consecutive days prior to measurement of consequence of aiming for a low nadir too early in
blood glucose concentration. Ideally, an owner the stablization process, especially if using lente,
should keep a daily diary of water drunk. ultralente or NPH insulin.
If using lente, NPH or ultralente insulin, adjust – If cat has been treated with insulin for more than
dose based on nadir (lowest) glucose concentration 2 weeks, and total dose is 1 U/cat q 12 h or less,
and clinical signs. Do not use pre-insulin blood glu- and pre-insulin glucose is ≤ 10 mmol/L (≤ 180
cose concentration to increase the dose, only to mg/dl, withhold insulin and check subsequent
decrease the dose. There is little appreciable insulin blood glucose concentrations to determine if the
action after 8–12 h, so for most cats on these insulins, cat is in diabetic remission.
the pre-insulin glucose concentration cannot be – If nadir glucose concentration < 3 mmol/L (< 54
decreased by increasing insulin dose. In general, aim mg/dl) decrease dose by 1 U/cat/injection.
for a glucose nadir of 7–9 mmol/L (126–162 mg/dl) – If clinical signs of hypoglycemia develop, then
in the first 1–2 months. Later a nadir of 5–6 mmol/L reduce dose by 50%.
(90–108 mg/dl) can be achieved in cats that are well ● Insulin dose may be maintained, increased or
controlled. decreased depending on the water intake, urine
glucose, clinical signs and length of time the cat
If using glargine or PZI, adjust the dose based on
has been treated with insulin.
nadir (lowest) glucose and pre-insulin glucose con-
– If pre-insulin glucose concentration 11–14
centration (concentration immediately before next
mmol/L (198– 252 mg/dl) or
insulin injection).
● If nadir 3–4 mmol/L (54–72 mg/dl) clinical param-
The following criteria can be used for adjusting eters are essential for adjustment of insulin dose.
insulin dose.
Most cats are well controlled on:
● Indications for increasing dose of insulin (recom-
● 0.2–0.9 U/kg q 12 h of lente insulin (median dose of
mendations assume insulin is being given twice
porcine lente was 0.5 U/kg q 12 h); only 10–15%
daily):
require 1 U/kg or more. Most cats are controlled on
– If pre-insulin glucose concentration is > 12
2–3 U/cat q 12 h.
mmol/L (216 mg/dl), then increase dose by
● 0.3–1.2 U/kg q 12 h of PZI (average dose of PZI is
0.5–1 U/cat/injection provided nadir glucose is
0.9 U/kg q 12 h); only about 10% of cats require
also high (glargine and PZI only)
more than 2 U/kg q 12 h. Most cats are controlled
AND / OR
on 4–5 U/cat q 12 h .
– If nadir glucose concentration is > 10 mmol/L
● 0.25–0.5 U/kg q 12 h of glargine (average dose is
(180 mg/dl) then increase dose by 0.5–1
< 0.5 U/kg q 12 h). Most cats are controlled on 1–2
U/cat/injection. For well controlled cats after
U/cat q 12 h, only a few cats require doses of 4–6
several weeks of therapy, an upper cut–point of
U/cat q 12 h, and the requirement for these high
> 7 mmol/L (126 mg/dl) can be used.
doses may resolve within weeks.
– If water intake is > 40 ml/kg on wet food or
● Using glargine, cats with exemplary control have
> 100 ml/kg on dry food and glargine or PZI are
nadir glucose concentrations of 4–7 mmol/L
being used, then increase dose by 0.5–1
(72–126 mg/dl) and peak glucose concentrations of
U/cat/injection. Dose may need to be increased
≥ 11 mmol/L (200 mg/dl).
or decreased if water intake is excessive when
using lente insulin. Diabetic remission usually occurs in the first 4
● Indications for maintaining the same dose: months of therapy, and occurs most often in the first
– If pre-insulin glucose concentration is ≥ 10–12 month of treatment in cats on glargine. Impending
mmol/L (≥ 240–360 mg/dl) remission is suggested by a negative urine glucose
AND/OR measurement, and a pre-insulin blood glucose concen-
– If nadir glucose concentration is 5–9 mmol/L tration of < 12 mmol/L (216 mg/dl). Decrease insulin
(90–162 mg/dl). For well controlled cats aim for dose gradually to 0.5–1 U q 12 h or even q 24 h. If
a nadir of 4–7 mmol/L (72–126 mg/dl). urine glucose is still negative and pre-insulin blood
● Indications for decreasing the dose of insulin: glucose is still low on a minimal dose of insulin, stop
– If pre-insulin glucose concentration is ≤ 10 insulin and monitor blood glucose for 12–24 h. If it
mmol/L (≤ 180 mg/dl) decrease dose 0.5 remains low, send the cat home on a low-carbohydrate
U/cat/injection. diet and re-evaluate in 1 week. The owner should
closely monitor water intake and urine glucose, and if ● Dilute regular insulin with saline or manufac-
either increase, the cat should be reassessed immedi- turer’s diluent to increase accuracy of dosing. Give
ately and reinstituted if blood glucose ≥ 10 mmol/L 0.2 U/kg intramuscular initially, then continue with
(180 mg/dL). hourly injections at 0.1 U/kg.
● Adjust the dose up or down to achieve a decrease
Treatment of “sick” diabetic cats in glucose of 3–6 mmol/L (54–110 mg/dl) per hour.
Fluids are as important as insulin in dehydrated ● Once blood glucose is 16 mmol/L (288 mg/dl),
diabetic cats. give 0.1–0.4 U/kg every 4–6 h to achieve a blood
● Balanced electrolyte solutions or 0.9% sodium glucose of 11–14 mmol/L (200–252 mg/dl) in the
chloride is the best initial fluid depending on the first 24 h.
initial potassium concentration, with 0.9% sodium
For intravenous dosing of insulin:
chloride preferred in hyperkalemic cats.
● Use an infusion pump and add 25 IU of regular
● Once initial fluid and electrolyte deficits are cor-
insulin to a 500 ml bag of 0.9% saline, to produce
rected, use 0.45% NaCl with 30–40 mEq (mmol)/L
an insulin concentration of 0.05 IU/ml.
of KCl added.
● Infuse the insulin/saline mix using a pump into the
Serum potassium rapidly falls with treatment and maintenance fluid line via a Y piece, at an initial
potassium supplementation should be immediately rate of 1 ml/kg/h (0.05 IU/kg/h). Be sure to flush
instituted in fluids and orally, if potassium concentra- both sets of tubing before beginning the infusion, as
tion is initially normal. Cats with hyperkalemia at pres- insulin adheres to plastic.
entation usually require potassium within 12–24 h. ● When blood glucose reaches 180 mg/dl (10
● Supplement potassium in intravenous fluids at mmol/L), decrease the insulin infusion to 0.5
20–80 mmol/L (or mEq/L); do not exceed 0.5 ml/kg/h. At the same time replace the maintenance
mmol//kg/h. fluids with 0.45% NaCl supplemented to contain
● Supplement potassium orally using potassium glu- 2.5% dextrose and 30 mmol/L KCl.
conate 2–3 mmol (or mEq), q 8–24 h.
With either intramuscular or intravenous therapy, aim
Serum phosphorus falls rapidly with treatment. for a glucose drop of 54–72 mg/dl/h (3–4 mmol/L/h)
Hypophosphatemia causes hemolysis, muscle weak- and do not exceed a decrease of 108 mg/dl/h (6
ness and neurological signs. To supplement phosphate mmol/L/h). In the first 24 h, aim for a glucose con-
and potassium in intravenous fluids, give potassium as centration of 11–14 mmol/L (200–252 mg/dl). Long-
50% potassium dihydrophosphate and 50% potassium term adaptations to chronic hyperglycemia have
chloride. occurred, and glucose should not be normalized for
24–48 hours.
Bicarbonate is rarely required, because acidosis
improves rapidly with fluids and insulin therapy. If If glucose falls below 8 mmo/L (144 mg/dl) in the
bicarbonate is < 10 mmol/L (10 mEq/L), it can be first 24 h, add 50% dextrose to intravenous fluids to
added to the intravenous fluids using the formula: Body make a 5% solution.
weight × 0.4 × [12 – patient’s bicarbonate].
Continue regular insulin until dehydration is cor-
Cats which have normal hydration or are only mildly rected, and then swap to subcutaneous glargine, PZI,
dehydrated and not in shock can be started immedi- lente, or ultralente insulin administered q 24 h.
ately on insulin given subcutaneously (0.25 U/kg if
glucose is < 20 mmol/L (360 mg/dl); 0.5 U/kg ideal
body weight if glucose is ≥ 20 mmol/L).
Subcutaneous insulin is poorly absorbed in signifi- Prognosis
cantly dehydrated cats. These cats need intramus- Prognosis is relatively good. Reported median survival
cular or intravenous insulin. time is 17 months, considering the average age at diag-
For intramuscular dosing of insulin: nosis is 10–13 years.
Prevention ● Weight loss (95–98% of cats).

● Polyphagia (65–75%), decreased appetite
Obesity, physical inactivity and repeated long-acting (19–28%).
steroid or megestrol acetate administration are pre- ● Hyperactive, restless, aggressive (68–81%),
ventable risk factors for type 2 diabetes. lethargy (15–25%).
Individuals predisposed to type 2 diabetes by low ● Tachycardia (57–65%), heart murmur (10–54%).
insulin sensitivity (as evidenced by increased fasting ● Polyuria/polydipsia (45–55%).
glucose concentrations) or reduced beta cell function ● Vomiting (33–50%), diarrhea (30–45%).
(evidenced as impaired glucose tolerance) should not ● Panting (13–28%).
become obese, and may benefit from a high-protein, ● Muscle weakness/tremors (15–20%).
low-carbohydrate diet. An enlarged thyroid gland or glands are palpable in
more than 80% of cats.
HYPERTHYROIDISM*** ● These are located anywhere from the larynx to the
thoracic inlet.
Classical signs ● Most are 0.5–1 cm in size, although occasionally
they are up to 3 cm.
● Weight loss.
● Hyperactive, restless, aggressive.
● Polyphagia. Diagnosis
● Tachycardia.
● Polyuria/polydipsia. Increased plasma total thyroxine (T4) concentration
(> 64 nmol/L (5 μg/dl)) is considered diagnostic of
See main reference on page 304 for details (The Cat hyperthyroidism.
With Weight Loss and a Good Appetite). 2–10% of hyperthyroid cats have a total T4 concentration
between 26–64 nmol/L (2–5 μg/dl), and require addi-
Clinical signs tional testing for diagnosis.
Polyuria/polydipsia is present in approximately 50% In mild (early) hyperthyroidism, total T4 may be within
of hyperthyroid cats, and may be the major presenting the normal range.
complaint. Severe concurrent illness will also suppress total T4
● Renal blood flow and glomerular filtration rate are
concentration.
increased in hyperthyroidism, leading to an
increased water and solute load on the renal tubule. If clinical signs suggest hyperthyroidism or a mass is
This may exceed the tubular reabsorptive capacity palpable in the neck, but total T4 is normal, either:
and cause medullary washout. In hyperthyroid ● Repeat total thyroxine measurement in 1–3 weeks,
humans, impaired concentrating ability is present. or

● Because of the advanced age in many hyperthyroid ● Measure free T (best option, but must use assay
4
cats, concurrent renal failure is also common. validated for cats), or
● Perform a T (triiodothyronine) suppression test
3
Typically, a disease of old cats, as the average age is (hyperthyroid cats have little or no suppression), or
12–13 years. It is very rare in cats < 8 years of age. ● Perform a TRH stimulation test (hyperthyroid cats
Weight loss is present in nearly all cats. have no increase in total T4 after TRH).
Urine specific gravity ranges from 1.006–1.060 in
Two major presenting forms occur; either restless, hyperthyroid cats.
hyperactive, and polyphagic (approximately 80% of
cats), or depressed and anorexic (10–30% of cats). Approximately one third of hyperthyroid cats have
mild to moderate azotemia. Many of these cats have
Signs suggest cardiac, GIT or renal disease.
underlying renal failure, but others have pre-renal
Typical signs of hyperthyroidism: azotemia associated with thyrotoxic cardiac failure.
Increased protein catabolism may also contribute to the ● The most frequent known causes are head
azotemia. trauma, neoplasia, hypothalamic-pituitary mal-
formations (e.g. cystic structures), or following sur-
gery to the hypothalamic-pituitary area.
Inappetant Cat).
● Rarely, central diabetes insipidus occurs in kittens,
suggesting a congenital form.
Nephrogenic diabetes insipidus occurs when the
Renal failure and diabetes mellitus both cause weight renal tubules are unresponsive to vasopressin.
loss with PU/PD in aged cats. The PU/PD is more pro-
Unresponsiveness to vasopressin may result from prob-
nounced in diabetes and occurs with glycosuria. In
lems either at the receptor or with postreceptor mecha-
renal failure, appetite is usually reduced rather than
nisms, including inadequate hypertonicity of the renal
increased as in hyperthyroidism. The apathetic form of
medulla.
hyperthyroidism may be difficult to distinguish clini-
● Primary (familial) nephrogenic DI has not been
cally from renal failure but measurement of urea, crea-
reported in cats.
tinine and thyroxine usually distinguishes these
● Secondary (acquired) nephrogenic DI is com-
diseases.
mon.
– It occurs with renal failure, hyperthyroidism,
Treatment pyelonephritis, pyometra, hypercalcemia,
hypokalemia and drugs.
There are three treatment options: chronic administra-
tion of antithyroid drugs, surgical thyroidectomy,
radioactive iodine. See main reference on page 347 Clinical signs
for details (The Thin Inappetant Cat).
Polyuria and polydipsia occur ranging from mild to
severe, depending on cause, and is often present for
DIABETES INSIPIDUS* weeks to months.
Nocturia or urinary incontinence may result because
Classical signs
of the large volume of urine produced.
● Any age cat.
Weight loss may occur as a result of the underlying dis-
● Mild to marked polyuria and polydipsia,
ease, or when the water intake is huge.
often present for weeks to months.
● Nocturia or urinary incontinence may Neurologic signs may occur if DI is associated with a
occur. hypothalamic-pituitary neoplasia, e.g. stupor, disorien-
● Urine specific gravity is typically < 1.007, tation, ataxia, seizures, circling.
but in some dehydrated cats may be
1.007–1.020.
Diagnosis
Urine specific gravity is usually < 1.007, and often
Pathogenesis 1.001 or 1.002 in classical DI.
● Urine specific gravity may be 1.007–1.020 if the
Diabetes insipidus (DI) occurs in two forms, central
cat is very dehydrated, or has partial DI.
and nephrogenic.
● Partial DI frequently occurs with acquired nephro-
Central diabetes insipidus is very rare in cats, and genic DI such as renal failure, hypercalcemia,
occurs when vasopressin (antidiuretic hormone, ADH) hypokalemia, pyometra and pyelonephritis.
secretion from the hypothalamic-pituitary system is ● Urine, hematologic and serum biochemistry
inadequate. analyses must be performed to exclude causes of
● Central DI is most commonly idiopathic (i.e. no acquired nephrogenic DI. Renal failure, hyperthy-
cause identified on necropsy). roidism, pyelonephritis, pyometra, hypercalcemia,
hyperadrenocorticosteroidism, hypokalemia and If central DI, administer synthetic vasopressin

drugs causing PU/PD (see page 244) must be ruled (desmopressin, DDAVP, SC, intranasal or conjuncti-
out. val). Thiazide diuretics are less expensive, but less
effective than desmopressin.
Trial synthetic vasopressin (DDAVP) therapy to
determine if PU/PD resolves. Pretreatment water
intake is measured for 2–3 days, and then again follow- Prognosis
ing DDAVP therapy. A greater than 50% reduction of
Prognosis depends on cause. The best prognoses occur
water intake suggests central or partial nephrogenic DI,
with reversible nephrogenic DI (e.g. hyperthyroidism)
but is rarely indicated.
and non-neoplastic central DI.
A modified water deprivation test can be performed
if the cat is not dehydrated, azotemic and laboratory
DRUG INDUCED*
tests do not indicate nephrogenic DI.
● Ignoring these contraindications may kill the
Classical signs
cat, or make renal failure worse. The cat must be
carefully monitored. ● PU/PD following initiation of drug therapy.
● Rarely is a water deprivation test required in
feline medicine, because central diabetes
insipidus is very rare and psychogenic polydipsia Clinical signs
has not been reported.
Common drugs causing polyuria and polydispsia
● The main use of a water deprivation test is to deter-
include: diuretics, anticonvulsants (e.g. phenobarbital),
mine if the kidney can concentrate urine when
thyroxine, salt supplementation, sodium bicarbonate,
water is unavailable (indicating psychogenic poly-
amphotericin B (from renal toxicity and hypokalemia),
dipsia), and whether vasopressin therapy can
corticosteroids and megestrol acetate.
increase urine concentration (central or partial
nephrogenic DI) after medullary washout has Polyuria and polydipsia occur following initiation of
resolved with water deprivation. drug therapy.
● Only consider performing a water deprivation test if
Other clinical signs relate to the underlying disease
there is massive polyuria and polydipsia, urine SG
process.
is < 1.008, and nephrogenic diabetes inspidus has
been ruled out.
● Details of the test and interpretation are found in Diagnosis
many standard textbooks.
Diagnosis is rarely a problem. If polyuria and polydip-
sia occur with phenobarbital or thyroxine, check
Differential diagnosis dose is not excessive by measuring trough serum
It is important to differentiate central DI from second- concentration.
ary nephrogenic DI, which is much more common. Test Although cats are more resistant to the side effects of
for renal failure, hyperthyroidism, hyperadrenocor- corticosteroids, polyuria and polydipsia does occur, but
ticosteriodism, pyelonephritis, pyometra, hypercal- is usually less dramatic than in dogs.
cemia and hypokalemia.
Treatment HYPOKALEMIA*
Ensure water is freely available at all times. Classical signs

If nephrogenic DI, manage the underlying disease, ● Acute onset of muscle weakness, neck
e.g. renal failure, hyperthyroidism. Thiazide diuretics ventroflexion, a stiff, stilted gait, and
may be useful for reducing water consumption if the muscle pain.
underlying disease is not treatable.
Classical signs—Cont’d HYPERCALCEMIA

● Decreased activity and inappetence for (HYPERCALCEMIA ASSOCIATED WITH
weeks to months. MALIGNANCY, CHOLECALCIFEROL
● Dyspnea in severe cases. TOXICITY, CHRONIC RENAL FAILURE,
● Signs relating to the underlying disease, HYPERPARATHYROIDISM
e.g. polyuria and polydipsia in chronic AND IDIOPATHIC)
renal failure.
● Occurs in older cats and Burmese kittens. Classical signs
● Anorexia and lethargy.
See main reference on page 893 for details (The Cat ● Vomiting.
With Neck Ventroflexion). ● Weight loss.
● Dysuria, inappropriate urination,
pollakiuria, stranguria.
Clinical signs ● Respiratory signs.
● Lymphadenopathy.
Acute onset of weakness. However, decreased activity ● Palpable cervical mass.
and inappetence are often present for weeks to months
prior to presentation.
Pathogenesis
Ventral neck flexion, stiff, stilted gait, and a reluc-
tance to walk or jump are typical. Calcium is important for formation of bones and
teeth, and is essential for blood coagulation. It is
Larger muscle groups may appear sensitive or palpa- important for muscle function, including cardiac mus-
tion. cle, as well as nervous system function where it stabi-
Dyspnea occurs when the potassium is very low lizes nerve cell membranes. As a cation, it is important
(2.0–2.5 mmol/L), because of weakness of the respira- for cell membrane permeability.
tory muscles. It may occur after fluid administration Calcium is regulated in the body via:
because volume dilution and increased urinary potas- ● Gastrointestinal absorption.
sium loss induced by diuresis may lead to further wors- ● Renal excretion.
ening of the hypokalemia. ● Binding to plasma proteins.
● Tissue deposition, especially into bone.
Polyuria, polydipsia may result from hypokalemia or
be the result of the underlying disease causing Parathyroid hormone (PTH) and calcitriol (active
hypokalemia, such as renal failure or hyperthryoidism. form of vitamin D) maintain calcium homeostasis.
Serum calcium concentration regulates parathyroid
hormone secretion and their serum concentrations have
Diagnosis an inverse linear relationship.
● PTH is produced in the parathyroid gland and
Decreased serum potassium concentrations (usually
acts to increase serum calcium. It stimulates bone
< 3.5 mmol/L) in association with clinical signs are
resorption by increasing osteoclastic activity, which
required for diagnosis. The severity of signs varies
mobilizes calcium into the bloodstream. PTH pro-
between cats when potassium is 2.5–3.5 mmol/L.
motes renal reabsorption of calcium and excretion
Below 2.5 mmol/L and especially below 2.0 mmol/L,
of phosphorus.
signs are life threatening, with death occurring from ● Cholecalciferol (vitamin D) is a fat-soluble vita-
respiratory muscle failure.
min that is metabolized by the liver and kidney to
Serum creatine kinase (CK) may be elevated reflecting produce calcitriol (1,25 [OH]2 vitamin D), which
the mypoathy associated with hypokalemia. acts to increase serum calcium. Calcitriol enhances
intestinal calcium uptake and calcium resorption from the GIT. Phosphate retention also reduces
from bone. extracellular calcium.
● Calcitonin acts to decrease high calcium concen- ● Chronic stimulation of the parathyroid glands to main-
trations, but does not appear to be important in tain serum calcium concentrations in renal failure
small day-to-day corrections of calcium concentra- leads to hyperplasia (renal secondary hyperparathy-
tion, which is the role of PTH and calcitriol. roidism). In some cats, autonomous function devel-
Calcitonin decreases osteoclast activity and forma- ops because some hyperplastic cell lines are very
tion of new osteoclasts. deficient in calcitriol receptors. Calcitriol regulates
synthesis of calcium receptors, so these cells are also
Hypercalcemia occurs when there is some derangement
poorly sensitive to calcium concentrations, and pro-
of the interaction between parathyroid hormone, vita-
duce large amounts of PTH. Uremia also reduces
min D and organs such as the gut, bone, kidneys and
formation of calcium receptors in parathyroid gland
parathyroid glands.
cells, leading to inappropriate PTH secretion.
Malignancy (lymphoma and squamous cell carci-
The diuretic phase of acute renal failure may also be
noma), renal failure and primary hyperparathy-
associated with hypercalcemia via other mechanisms.
roidism are the most common causes of hypercalcemia
in cats. In many cats, the cause of the hypercalcemia Primary hyperparathyroidism is a less common
is not identified, and is termed idiopathic hypercal- cause of hypercalcemia, and is the result of an
cemia. autonomous adenoma producing excess PTH. It is usu-
ally a solitary functional adenoma, although bilateral
Hypercalcemia of malignancy is the most common
cystadenomas and solitary or bilateral adenocarcino-
cause of hypercalcemia in cats. It results from secretion
mas have been reported.
of locally acting or humorally acting osteoclast-activat-
ing substances. Vitamin D toxicosis may be acute and associated with
● In cats, lymphoma and squamous cell carcinoma cholecalciferol (vitamin D) rodenticides, or chronic
are most often associated with hypercalcemia but due to excess supplementation or plant ingestion. In
multiple myeloma and adenocarcinoma have also some countries, cholecalciferol rodenticides have been
been reported. withdrawn from the market because of their potential
● In some tumors, for example lymphoma, there is for irreversible nephrotoxicity in children.
autonomous secretion of a humorally acting PTH- ● Acute toxicity occurs at 5 g of bait/kg body
related protein, which activates osteoclasts, increases weight and hypercalcemia occurs within 24 h of
intestinal absorption and increases renal tubular ingestion.
reabsorption of calcium and excretion of phospho- ● At lower doses of vitamin D, the maximal effect on
rus. Endogenous PTH secretion is suppressed. calcium and phosphorus may not be evident for 1–2
● Some neoplastic cells invade bone or bone marrow weeks after ingestion.
and secrete products that act locally to activate ● Cats requiring supplementation with vitamin D and
osteoclasts, such as prostaglandins, osteoclast-acti- calcium following thyroidectomy are at risk of vita-
vating factor, calcitriol, interleukin-1, and PTH- min D toxicity and nephrocalcinosis, if calcium and
related protein or PTH. phosphorus is not monitored carefully.
● Some plants contain active metabolites of vita-
Chronic renal failure is the second most common
min D such as the houseplant Cestrum diurnum
cause of hypercalcemia in cats. A number of mecha-
(day-blooming jasmine). Solanum malacoxylon
nisms associated with chronic renal failure lead initially
and Trisetum flavescen also contain vitamin D
to reduced extracellular calcium. In a few cats, com-
metabolites.
pensatory mechanisms eventually result in hypercal-
cemia. Fungal and bacterial granulomatous disease is a rare
● Extracellular calcium concentration is decreased in cause of hypercalcemia. The inflammatory process
renal failure because reduced renal mass and hyper- may or may not directly involve the bone. The mecha-
phosphatemia reduce formation of calcitriol (active nism may involve local osteolysis or secretion of fac-
vitamin D), leading to reduced calcium absorption tors from inflammatory cells such as prostaglandins
and osteoclast-activating factors, which lead to bone Clinical signs

resorption.
Signs associated with hypercalcemia are com-
Hypoadrenocorticism is a very rare cause of hyper- pounded by signs of the underlying cause of hyper-
calcemia in cats (<2% of hypercalcemic cats). It is calcemia, such as malignancy, toxicity from
likely multifactorial, and in dogs is related to the sever- cholecalciferol-containing rodenticides and renal failure.
ity of hyperkalemia. Mechanisms include hyperpro-
teinemia from dehydration and increased renal In general there is no breed or gender predisposition,
resorption of calcium. although Siamese appear predisposed to primary
hyperparathyroidism.
Other rare associations with hypercalcemia include ● Cats with hypercalcemia have a wide range of ages
hyperthyroidism, diabetes mellitus, liver disease (1–19 years) reflecting the multitude of causes, but
(hepatic lipidosis, bilary fibrosis), and bone marrow mean age is 9 years old.
diseases (myelodysplasia, myelofibrosis). ● Renal, gastrointestinal or neuromuscular signs
Idiopathic hypercalcemia is common in cats, and has occur, and in part may reflect the underlying cause.
been postulated to be associated with acidifying diets, Lethargy, anorexia and/or weight loss are typical of
which increase bone turnover of calcium, but hypercal- hypercalcemia, regardless of the cause.
cemia was not corrected by partial parathyroidectomy
or a non-acidifying diet. Many features are similar to Polyuria and polydipsia occur in up to 25% of cats
familial benign hypercalcemia reported in humans with hypercalcemia, and may be associated with inap-
which is associated with a mutation in the calcium- propriate urination.
sensing receptor. Signs of lower urinary tract disease, including
Chronic over-supplementation with calcium in dysuria and pollakiuria, occur in approximately 20%
the diet increases the intestinal absorption of cal- of cats. In a high proportion of cats, this is associated
cium. It also stimulates bone resorption and results with calcium oxalate urolithiasis of the urinary blad-
in hypercalcemia and dystrophic calcification. der. Renal, ureteral, urethral or urolithiasis may also
Because the ability to excrete the increased filtered occur.
load of calcium is impaired in cats with renal failure, Vomiting occurs in 20–30% of cats with hypercal-
older cats are more sensitive to excess supplementa- cemia, including cats with idiopathic hypercalcemia.
tion. Dietary over-supplementation is rarely seen
because of the widespread use of balanced commer- Constipation or diarrhea are infrequently reported.
cial diets. Neuromuscular weakness evidenced as a reluctance to
Sequalae to hypercalcemia include: jump, or unsteadiness with jumping is less common.
● Chronic renal failure. High levels of calcium are Shaking, tremors, seizures, stupor and coma have the
toxic to the renal tubular cells, mineralize renal potential to occur with extremely high calcium concen-
tissue and interfere with ADH action causing renal trations, and are reported in dogs with cholecalciferol
failure and polyuria/polydipsia. Hypercalcemia can toxicity. Cats tend to ingest less toxin and these signs
also lead to calcium oxalate urolithiasis of the kid- have not been reported.
ney, ureter, bladder or urethra and result in signs of
lower urinary tract disease (LUTD). Cardiac arrhythmias may occur if serum calcium is
● Reduced excitability of smooth muscle results in
more than 4.5 mmol/L (18 mg/dL). Prolongation of PR
altered gastrointestinal function. Chronic vomiting interval and shortening of QT interval may be evident
is a common sign of hypercalcemia. on ECG.
● Depressed skeletal muscle contractility and Acute cholecalciferol toxicity is associated with
weakness, and altered cardiac contractility and lethargy, anorexia and polyuria/polydipsia within
arrhythmias occur with high calcium concentra- 24 h of ingestion. Vomiting may occur, but the hemateme-
tions. sis and bloody stool seen in dogs have not been reported.
Toxicity is less frequently reported and signs are less hyperphosphatemia, and a history of recent exposure
severe in cats than dogs. to rodenticide. Polyuria/polydipsia, vomiting and pain
Lower levels of cholecalciferol toxicity result in on palpation of the kidneys may also be present. PTH
PU/PD, inappetence and lethargy and low-grade and PTH-rP concentrations would be expected to be
vomiting, and clinically may be indistinguishable low if the cat is not dehydrated, but have not been
from acute or chronic renal failure. reported. Later there may be evidence of mineraliza-
tion of abdominal and other soft tissues. Toxicity
Physical examination findings are dependent on the
needs to be distinguished from other causes of hyper-
cause of hypercalcemia. Lymphadenopathy, abdomi-
calcemia and hyperphosphatemia (renal failure and
nal organomegaly or dyspnea may be evident in cats
hypoadrenocorticism) on the basis of history, signs
with lymphosarcoma. Cats with squamous cell carci-
and ionized calcium (often normal or decreased in
noma-associated hypercalcemia most often have
renal failure).
tumors of the head and neck. In contrast to dogs, a pal-
pable cervical mass is present in about 40% of cats with Chronic renal failure (renal secondary hyper-
primary hyperparathyroidism. parathyroidism) is associated with normal to elevated
PTH concentrations and low to undetectable PTH-rP
assay, hyperphosphatemia, but ionized serum calcium
Diagnosis
is usually normal or decreased. In contrast, ionized
Serum calcium concentration greater than 3 mmol/L serum calcium is increased with other causes of hyper-
(12 mg/dl). calcemia.
● The serum calcium concentration does not fluctuate
Idiopathic hypercalcemia is increasingly being identi-
with age in cats as it does in dogs, where a healthy
fied in cats (mean age 5 years). Typically cats are
puppy can have higher calcium and phosphorus lev-
hypercalcemic with normal or slightly low serum phos-
els.
phorus concentration, and have normal serum
A non-lipemic fasted blood sample is required for concentrations of PTH, calcitriol and 25-hydroxyc-
measurement of serum calcium, phosphorus, urea holecalciferol. Gross and histologic morphology of the
nitrogen and creatinine concentrations to differentiate parathyroid glands is normal. Subtotal parathyroidec-
between several of the causes of hypercalcemia. tomy does not resolve the hypercalcemia.
Hypercalcemia of malignancy is a relatively com-
mon cause of hypercalcemia in cats and is most often
secondary to lymphoma and squamous cell carcinoma,
but may be from multiple myeloma or adenocarcinoma. Clinical signs of hypercalcemia (anorexia, lethargy,
Serum phosphorus concentration is below the midpoint vomiting, weight loss) are typical of many diseases,
of the reference range, unless renal failure is present. and serum biochemistry analysis is necessary to detect
Diagnosis of neoplasia-associated hypercalcemia is hypercalcemia.
based on documenting increased PTH-related protein
If PU/PD is present in addition to anorexia, vomiting
(PTH-rP) and suppressed PTH concentration in serum,
and weight loss, chronic renal failure would be the
or finding the primary tumor and demonstrating resolu-
most likely differential diagnosis based on clinical
tion of hypercalcemia with successful tumor therapy.
signs. Most cats with chronic renal failure are not
Primary hyperparathyroidism is rare in cats. It is hypercalcemic and of those that are, ionized calcium is
associated with anorexia and lethargy, an inappropri- usually normal or low.
ately high PTH concentration relative to the hypercal-
Chronic renal failure with secondary hypercalcemia
cemia. Serum phosphorus is below the midpoint of the
is usually differentiated from other causes of hyper-
reference range unless renal failure is present, and in
calcemia causing secondary renal failure by the pres-
some cats, a palpable cervical mass is evident.
ence of anemia, small kidney size on palpation or
Cholecalciferol poisoning is associated with acute ultrasound, and normal or low ionized calcium in
depression and anorexia, marked hypercalcemia and chronic renal failure. Cats with chronic renal failure
and secondary hypercalcemia also tend to have lower ● Prednisone at 2 mg/kg PO q 12 h also increases
calcium concentrations, higher phosphorus concentra- renal loss of calcium.
tions, lower urine specific gravity and higher levels of ● If available, salmon calcitonin should be adminis-
azotemia than cats with renal failure induced by hyper- tered until serum calcium levels normalize. Begin
calcemia. with 4–6 IU/kg SC q 2–3 h, and increase the dose
up to 10 IU/kg if the lower doses are not effective.
– Monitor serum calcium, hydration status and
Treatment renal function via urine output.
– Complications include soft tissue mineraliza-
Severe hypercalcemia is a medical emergency as car-
tion, renal failure, seizures and arrhythmias.
diac arrhythmias may occur if serum calcium is more
than 4.5 mmol/L (18 mg/dl). Cats with primary hyperparathyroidism are best
treated with surgical removal of the parathyroid ade-
Hypercalcemia with concurrent hyperphosphatemia is
noma and short-term vitamin D and calcium therapy
associated with metastatic calcification and nephro-
over 2–3 months to prevent post-operative hypocal-
toxicity when the calcium (mg/dl) × phosphorus
cemia.
(mg/dl) product is > 60–80.
● Hypervitaminosis D and hypercalcemia of renal Cats with renal failure causing hypercalcemia,
failure are both associated with a high Ca × P prod- should be started on a low phosphorus diet. If phos-
uct and require early treatment to minimize further phorus is not decreased into the middle of the normal
nephrotoxicity. range, add a phosphate binder.
● Once phosphorus is < 1.9 mmol/L; (normal range,
Fluids containing 0.9% NaCl should be used for vol-
0.7–1.8 mmol/L) or < 6 mg/dl (normal range,
ume expansion to dilute plasma calcium and to induce
2.2–5.6 mg/dl), begin low-dose calcitiol therapy
sodium diuresis, which causes calcium loss in urine.
(2.5 ng/kg PO q 24 h) to decrease progression of
Avoid calcium-containing fluids.
renal failure.
Diuretics (furosemide) promote renal sodium diuresis ● Calcitriol decreases PTH concentrations by
and hence renal calcium loss. inducing formation of the calcium receptor on the
● Thiazide diuretics are contraindicated as they can parathyroid gland cells membrane. In renal fail-
cause calcium retention. ure, calcium sensing is impaired because of the
effect of uremia on formation of calcium recep-
Corticosteroids promote renal calcium loss, and
tors. This results in inappropriate PTH secretion.
decrease bone resorption and intestinal absorption of
By increasing calcium sensing, PTH secretion is
calcium, but should only be used once the diagnosis of
decreased, resulting in decreased serum calcium
lymphoma is excluded, as they can conceal the diagnosis.
concentration.
Vitamin D toxicosis requires intensive therapy to ● PTH is a uremic toxin. It contributes to CNS
reduce calcium levels and may require therapy to con- depression and EEG abnormalities, appetite sup-
trol seizures and arrhythmias. pression and anemia associated with uremia. It
● Reduce GIT absorption using an emetic and acti- also promotes progression of chronic renal fail-
vated charcoal with a saline or osmotic cathartic. ure. Low-dose calcitriol has been shown to slow the
Do not use emetics in convulsing patients. progression of renal failure and decrease signs of
– Xylazine (Rompun) can be used as an emetic in chronic renal failure.
cats (1.1 mg/kg IM or SC). ● At phosphorus concentrations ≥ 1.9 mmol/L;
– Charcoal 1–4 g/kg combined with saline (5 ml (normal range, 0.7–1.8 mmol/L) or 6 mg/dl (normal
per 1 g of charcoal) as a suspension in water ≤ 5.6 mg/dl), calcitriol loses its effectiveness to
should be administered orally or by gastric tube suppress PTH secretion. Using higher doses of cal-
if ingestion occurred within 3–4 h. citriol in the face of hyperphosphatemia risks wors-
● Reduce hypercalcemia using the diuretic ening progression of the renal failure, due to
furosemide (2–5 mg/kg PO q 8 h). mineralization of renal tissue. It is essential to
monitor calcium and phosphate regularly when Restrict access to cholecalciferol-based rodenticides.
using calcitriol therapy.
Avoid diets or dietary supplements that are unusually
● See Chronic renal failure in The Thin Inappetent
high in vitamin D, such as liver or cod-liver oil.
Cat (page 336) for details of treatment of chronic
renal failure.
NEOPLASIA (RENAL NEOPLASIA
In cats with idiopathic hypercalcemia, dietary mod-
OR LYMPHOMA)
ification may be partially or fully effective in a minor-
ity of cats. Dietary modification is worth trying
Classical signs
initially, as the only other reported therapy to be effec-
tive is long-term corticosteroids. ● Inappetence, weight loss and lethargy.
● Dietary modifications reported to have variable suc- ● Enlarged kidney/s or abdominal mass on
cess include use of a high-fiber diet (Hills w/d) to palpation.
reduce availability of calcium for intestinal absorp- ● ± Vomiting.
tion, or use of a less-acidifying diet (Hills k/d) to ● ± Polyuria, polydipsia.
reduce bone turnover. ● ± Dysuria, inappropriate urination,
● Prednisone (2–3 mg/kg PO q 24 h) has been pollakiuria, stranguria.
reported to be partially or fully effective in normal- ● ± Respiratory signs.
izing both total and ionized serum calcium in the ● ± Lymphadenopathy.
small number of cats reported, however therapy was ● ± Palpable cervical or abdominal mass.
required long term (> 12 months).
Clinical signs
Prognosis
Neoplasia is a cause of polyuria in cats.
If hypercalcemia is unresponsive after aggressive treat-
ment, the prognosis is poor. Lethargy, anorexia and/or weight loss are typical,
regardless of the cause.
In contrast to dogs, cats are reported to have a good
prognosis following ingestion of cholecalciferol-con- Renal, gastrointestinal, respiratory or neuromuscular
taining rodenticide, if appropriate fluid and diuretic ther- signs may occur, and in part reflect the underlying cause.
apy are instituted. Hypercalcemia associated with lymphoma is rare in
cats but does occur (see page 245, Hypercalcemia).
Hypercalcemic cats may have polyuria and polydipsia
Prevention
which may be associated with inappropriate urination,
Do not use calcium-containing intestinal phosphate and/or have signs of lower urinary tract disease,
binders. including dysuria and pollakiuria, which is commonly
associated with calcium oxalate urolithiasis.
Be aware of the risk of hypercalcemia and soft tissue
calcification when using calcium supplementation Vomiting may occur associated with the underlying
and calcitiol therapy in hypocalcemia. neoplasm, hypercalcemia or uremia.
Avoid inappropriately high doses of calcitriol or Other signs include unilateral or bilateral renal enlarge-
other vitamin D preparations, and monitor calcium ment on palpation, or an abdominal, cervical or tho-
and phosphate concentrations carefully when using racic mass.
these products. Moderately increased ionized calcium
does not contraindicate use of calcitriol in chronic renal
Diagnosis
failure, as low doses of calcitriol (2.5 ng/kg q 24 h) do
not significantly increase intestinal calcium absorption. Serum creatinine and urea concentrations may be
Increased serum phosphate concentration is a con- increased if the neoplasia is associated with renal
traindication for calcitriol use. failure.
Urine specific gravity is usually dilute. tion and doses greater than 1.5 U/kg q 12 h are often
required. Poor glycemic control is often still present
Identification of a mass on palpation or imaging.
despite higher than normal doses of insulin.
Biopsy and histology is required for a definitive diag-
nosis. Thin, fragile skin that bruises easily is a common
sign. Some cats have extremely fragile skin, and nor-
mal grooming, or lifting the skin for injection or
HYPERADRENOCORTICISM
restraint results in severe skin tears.
Classical signs Poor unkempt hair coat, patchy alopecia, or skin
infections including demodicosis may be evident.
● Diabetes mellitus.
● Polyuria and polydipsia. Potbelly, which may be reported by the owner as weight
● Weight loss. gain or abdominal enlargement.
● Fragile skin and poor hair coat.
Muscle wasting.
See main reference on page 324 for details (The Cat Hepatomegaly.
With Weight Loss and a Good Appetite).
Other concomitant infections may occur, e.g. bacterial
cystitis, pyothorax.
Pathogenesis
Hyperadrenocorticism is a rare disease in cats.
Diagnosis
Usually occurs in middle-aged to older cats (average
Diagnosis is based on consistent clinical signs and an
age 10–11 years).
abnormal dexamethasone suppression test, i.e. fail-
Pituitary-dependent form is most common (approxi- ure of cortisol to suppress below 41 nmol/L
mately 75–80% of cases); a functional adrenocortical (1.5 μg/dl) at both 4 and 8 h after IV dexamethasone.
tumor is less frequent (20–25%). ● Because up to 20% of normal cats do not suppress
using 0.01 mg/kg dexamethasone, a higher dose is
Clinical iatrogenic hyperadrenocorticism is less pro-
recommended in cats, i.e. 0.1 mg/kg.
nounced in cats as they are more resistant to the effects ● It is important not to stress the cat when doing this
of excess exogenous glucocorticoids than dogs. PU/PD
test.
may occur with exogenous steroids, but is less dramatic ● Cats with pituitary-dependent hyperadrenocorti-
than in dogs.
cism may fail to suppress, or exhibit suppression at
Chronic insulin resistance from excess endogenous 3–4 hours followed by “escape” of suppression at 8
steroid may result in diabetes mellitus. hours. The latter pattern is diagnostic for pituitary-
dependent disease, and makes further testing
unnecessary.
Clinical signs
A normal urine cortisol:creatinine ratio is useful for
Polyuria, polydipsia is typical, which may be marked
excluding hyperadrenocorticism, but lacks specificity
(>120 ml/kg/24 h) if concurrent diabetes is present.
for diagnosis.
Weight loss occurs as a result of poorly controlled dia-
The corticotropin (ACTH) stimulation test is best
betes.
used to differentiate endogenous from iatrogenic hyper-
Lethargy is common. adrenocorticism, rather than as a diagnostic test for
hyperadrenocorticism, because 15–30% of cats with
Many of the common signs are attributable to poorly
hyperadrenocorticism have a normal response.
controlled diabetes mellitus (although not all cats with
hyperadrenocorticism have diabetes). The diabetes The combined dexamethasone suppression/ACTH
tends to be insulin resistant. Normal doses of insulin stimulation test has been used successfully to diag-
often produce a minimal decrease in glucose concentra- nose hyperadrenocorticism in cats. The combined test
does not appear to be more advantageous than the Transsphenoid hypophysectomy may be available in
ACTH stimulation and dexamethasone suppression some referral centers.
tests evaluated separately.
Differentiation of pituitary-dependent from adrenal Prognosis
tumors is based on abdominal ultrasound (one
Prognosis is guarded to grave. Cats that have adreno-
enlarged adrenal if adrenal tumor) and ACTH concen-
cortical tumors surgically removed have the longest
tration. Normal to increased ACTH concentrations
survival.
support a diagnosis of pituitary-dependent disease.
Low concentrations support adrenal disease. This test
must only be used after hyperadrenocorticism is con-
HYPOADRENOCORTICISM
firmed, because normal cats often have low ACTH con-
centrations.
Classical signs
Differential diagnosis ● Very rare disease.
● Lethargy, depression, anorexia and weight
Other causes of poorly controlled diabetes need to be
loss.
considered, e.g. excessive insulin dose, too short a
● Dehydration, hypothermia, ± weakness or
duration of action of insulin, hyperthyroidism and
collapse.
acromegaly.
● ± Bradycardia.
Some cats appear to have poorly controlled diabetes ● ± Vomiting.
based on persistently high blood glucose concentra- ● ± Polyuria and polydipsia.
tions measured in hospital, but have good control of ● ± Waxing and waning illness, that responds
clinical signs (e.g. stable weight and water intake < 60 to fluids or glucocorticoids.
ml/kg). These cats have stress hyperglycemia associ-
ated with visits to the veterinarian. In contrast, cats
with undiagnosed hyperadrenocorticism and dia- Pathogenesis
betes usually have persisting clinical signs of dia-
Hypoadrenocorticism results from a deficiency of glu-
betes, despite insulin therapy.
cocorticoids and/or mineralocorticoids produced by
the adrenal gland.
Treatment
It can be classified as either primary or secondary
Medical therapy produces inconsistent results, but is adrenocortical insufficiency.
useful in improving the presurgical condition of the cat. ● Primary adrenocortical failure occurs rarely in
● Drugs which have produced improvement in some cats as a naturally occurring disease, and is pre-
cats are ketaconazole (15 mg/kg q 12 h) and sumed to result from immune-mediated destruc-
metyrapone (65 mg/kg q 12 h). tion of the adrenal cortices.
● Trilostane and L-depronyl have been used in dogs ● Secondary adrenocortical failure involves only a
successfully, but there is comparatively little infor- deficiency of glucocorticoid secretion as a result
mation available on their use in cats. Trilostane of reduced secretion of pituitary ACTH.
ameliorates clinical signs of hyper adrenocorticism ● Spontaneously occurring secondary hypoadreno-
in cats based on the studies published. corticism has not been reported in cats.
● Iatrogenic secondary hypoadrenocorticism can be
Surgical adrenalectomy (unilateral for adrenal
demonstrated with an ACTH stimulation test after
tumor and bilateral for pituitary-dependent hyper-
withdrawal of potent glucocorticoids or progestins,
adrenocorticism) provides the best response.
especially after long-term use. However, clinical
● Begin glucocorticoids, fluids and antibiotics just
signs are rarely seen.
before surgery.
● Fatal post-operative complications are relatively Glucocorticoid (cortisol) deficiency impairs the
common. body’s response to stressful situations.
Mineralocorticoid (aldosterone) deficiency directly Polyuria and polydispia are reported in 30% of cats.
affects renal function and the body’s ionic and water
Partial adrenal deficiency is characterized by episodic,
homeostasis.
non-specific gastrointestinal signs and lethargy or
● Loss of aldosterone secretion results in impaired
depression, which occur particularly at times of stress-
renal conservation of sodium and chloride and
ful events (travel, boarding, surgery).
excretion of potassium, leading to hyponatremia,
hypochloremia and hyperkalemia. A waxing and waning course of illness is typical.
● The loss of sodium and chloride reduces the extra-
A history of previous response to steroids or fluids is
cellular fluid volume, resulting in hypovolemia,
common.
hypotension, reduced cardiac output and decreased
renal perfusion.
● Hyperkalemia has deleterious effects on myocardial
electrical activity. Diagnosis
For clinical signs to develop there must be a loss of at Diagnosis is based on clinical signs plus a
least 85–90% of the adrenal cortices. sodium:potassium ratio of < 24:1.
Disease progression varies in severity depending on Definitive tests are an ACTH stimulation test com-
the degree of stress and the adrenocortical reserve. bined with measurement of ACTH concentration.
● Synthetic ACTH (Controsyn, Organon) adminis-
An Addisonian crisis is the most severe presentation
tered at 0.125 mg/cat IM with blood samples col-
of hypoadrenocorticism. This is the result of severe
lected at 0, 30 and 60 minutes or IV with samples
hyponatremia and hyperkalemia, which are the precur-
collected at 0, 60 and 90 minutes or ACTH gel (2.2
sors for hypovolemia, prerenal azotemia and cardiac
mg/kg) IM with samples at 0, 60 and 120 minutes.
arrhythmias. ● Cortisol concentration pre- and post-ACTH < 55
nmol/L (2 μg/dl) is diagnostic.
Clinical signs ● Elevated ACTH concentration differentiates spon-
taneous primary hypoadrenocorticism from iatro-
Very rare disease in cats.
genic steroid administration, because the cause of
Most common in young to middle age 1–9 years (aver- the spontaneous disease is lack of cortisol response
age, 6 years old). to ACTH.
In general, signs are similar to those in dogs. It often Hyponatremia occurs in cats, and is usually accompa-
presents with only vague clinical signs of lethargy, nied by hypochloremia.
anorexia and weight loss. Vomiting and diarrhea are
Hyperkalemia occurs in 90% of cats, but is less
less common signs in cats, as are changes in the elec-
marked (< 7.6 mmol/L or mEq/L) than in dogs.
trocardiogram associated with hyperkalemia.
Azotemia, hyperphosphatemia and dehydration
Signs may be present for only a few days or up to 4
occur in nearly all cats.
months prior to diagnosis.
Urine specific gravity < 1.030 was present in 70% of
Lethargy or depression are frequent signs.
cats.
Anorexia and weight loss are also common.
On physical examination, most cats (>50%) are dehy-
drated, hypothermic or depressed.
Renal failure is much more common, and also typi-
Weakness, weak femoral pulses, and slow capillary
cally presents with azotemia and urine specific gravity
refill are common although, unlike dogs, collapse and
of < 1.030, and can have similar signs. The ACTH
bradycardia are rare.
stimulation test is normal in renal failure and the cats
Vomiting may be reported. tend to be older.
Chronic glucocorticoid or megestrol acetate admin- nisone (0.25–1 mg/cat PO q 12 h) or methylpred-

istration may result in a similar ACTH stimulation test nisolone (10 mg IM q 1 month).
result. The cortisol increase is suppressed in the ACTH
Stressful events may warrant an increase in medication
stimulation test. However, ACTH concentration is also
dose.
suppressed, and electrolytes are normal.
An Addisonian crisis needs to be differentiated from
Prognosis
other critical conditions such as diabetic ketoacidosis,
necrotizing pancreatitis and septic shock. Prognosis is good with appropriate treatment, provided
the hyperkalemia and electrolyte imbalance is cor-
Mild hypoadrenocorticism displays signs that are rela-
rected in time. Cats with adrenal insufficiency will have
tively non-specific, and are often seen in other gas-
a normal life expectancy provided they are treated
trointestinal and renal diseases.
appropriately.
Treatment Prevention
An acute Addisonian crisis is a medical emergency. Secondary adrenocorticism caused by rapid withdrawal
of chronic corticosteroid therapy can be prevented via
Immediate correction of hypotension, hypov-
staged withdrawal of steroids and progestins, which
olemia, electrolyte imbalances and metabolic acido-
allows adrenal gland function to recover from chronic
sis via fluid administration is essential. Use isotonic
suppression.
fluids (0.9% NaCl) at 40 ml/kg/h IV initially for the
first 1–4 hours. Once dehydration is corrected, reduce
the fluid rate to 60–90 ml/kg/day, using the higher
ACROMEGALY (HYPERSOMATOTROPISM;
fluid rate if the cat is not eating.
GROWTH HORMONE-PRODUCING TUMOR)
● Potassium supplementation in fluids is contraindi-
cated, but if the only fluids available immediately
Classical signs
have potassium, use them.
● Poorly controlled, insulin-resistant
Provide an immediate source of glucocorticoids.
diabetes mellitus requiring high doses of
● Prednisolone sodium succinate (4–20 mg/kg, IV) or
insulin.
dexamethasome (0.1–2.0 mg/kg, IV or IM).
● Polyuria, polydipsia, polyphagia.
● Mineralocorticoids should be replaced using oral flu-
● Weight gain despite poorly controlled
drocortisone acetate (0.05–0.1 mg/cat PO q 12 h) or
diabetes.
DOCP (deoxycorticosterone pivalate, 2.2 mg/kg, IM
● Large, blocky or coarse body and head.
q 25 days). In Australia, the long-acting form in oil for
● Enlarged tongue, widely spaced teeth,
intramuscular injection is an acetate product (DOCA).
thickened soft palate.
● If the cat is in shock, higher doses of glucocorti-
● Cardiomegaly.
coids may be warranted.
Despite appropriate therapy, lethargy, anorexia and See main reference on page 322 for details (The Cat
weakness may persist for 3–5 days, unlike the rapid With Weight Loss and a Good Appetite).
response in dogs.
Pathogenesis
In the long term, glucocorticoid and mineralocorti-
coid replacement is required lifelong. Use either flu- Very rare disease.
drocortisone acetate (0.05–0.1 mg/cat PO q 12 h) or
Caused by a functional adenoma of the pars distalis
DOCA (2.2 mg/kg, IM q 25 days) for mineralocorti-
which produces excess growth hormone.
coid replacement long term. Some cats require addi-
tional glucocorticoid replacement long term or at times Excess growth hormone results in soft tissue and bone
of stress, which can be provided using prednisolone/pred- overgrowth from the chronic hypertrophic actions of
the hormone. These anabolic actions are mediated by Diagnosis

insulin-like growth factor-1, a growth factor synthe-
sized in the liver and also locally in the growth plate of Diagnosis is based on clinical signs and increased
bones. The effects of excess growth hormone are plasma concentrations of insulin-like growth factor-
chronic and insidious. 1 (> 1200 U/L).
Acute catabolic actions of growth hormones result in Growth hormone concentrations can be measured
fat breakdown (lipolysis) and glycolysis. Hyperglycemia with an assay developed for dogs, available at some
results from increased gluconeogenesis in the liver and research laboratories. Demonstration of persistently
decreased glucose uptake into tissues as a result of elevated GH concentrations, which do not increase
insulin resistance. Long term, the marked insulin resist- with stimulation from GHRH or clonidine, support the
ance results in diabetes mellitus. diagnosis, but is not readily available to most practi-
tioners.
Insulin resistance may be extreme with insulin doses
between 20–130 U/day required to control blood glucose. A pituitary mass on CT or MRI scan supports the
diagnosis, and is useful for monitoring response to irra-
Clinical signs diation therapy.
Cats are typically middle aged to elderly, with a pre-

dominance of males. Differential diagnosis
All cats reported have diabetes mellitus, and in most Other causes of poorly controlled insulin-resistant
cats, their diabetes is poorly controlled and insulin- diabetes need to be distinguished from acromegaly.
resistant. Normal doses of insulin produce no or mini- When insulin resistance is extreme and insulin dose
mal decrease in glucose concentration, and in many exceeds 20–30 U/cat/injection without causing hypo-
cats, very large doses of insulin are required to produce glycemia, the likely cause is acromegaly. Most other
an acceptable glucose-lowering effect. causes of insulin resistance produce less extreme
Polyphagia, polyuria and polydipsia are associated insulin resistance and very high doses of insulin pro-
with poorly controlled diabetes. duce severe hypoglycemia.
Typically, there is weight gain despite poorly con- Hyperadrenocorticism causes poorly controlled
trolled diabetes, although sometimes weight loss is insulin-resistant diabetes. Typically, insulin doses
present. required to control hyperglycemia are much lower
than for acromegaly. In contrast to acromegaly, cats
A large, blocky or coarse body is typical, and cats with hyperadrenocorticism have weight loss. Other
often have coarse facial features. General coarsening of signs suggestive of hyperadrenocorticism are a poor
body type is evident when the cat is compared to pic- hair coat and fragile skin, which may tear with
tures taken several years before. restraint for blood sampling or insulin injection. Many
Acromegalic cats often have thickened enlarged have a potbelly (may also be present in acromegaly)
tongues, sometimes widely spaced teeth and a thick- and hepatomegaly.
ened soft palate. Displacement of lower canine teeth Other causes of apparent insulin resistance such as
forward (prognathia inferior) may occur. excessive insulin dose resulting in rebound hyper-
Cardiomegaly is often evident on radiographs and glycaemia or use of an insulin of insufficient dura-
occasionally congestive heart failure occurs resulting in tion of action result in poorly controlled diabetes, but
dyspnea. clinical signs of acromegaly are absent.
Degenerative arthritis may occur resulting in stiffness

on rising and walking. Periosteal reaction is evident Treatment
around the joints on radiographs.
Cobalt radiation has been used successfully, and may
Renal failure occurs in some cats. result in resolution of the diabetes in some cats.
Pituitary ablation using cryosurgery may be effective nary tract signs including dysuria, inappropriate uri-
(refer to current literature). nation, pollakiuria and stranguria (23%), and weak-
ness and/or muscle tremors (14%).
The long-acting somatostatin analog, octreotide has the
potential to lower GH concentrations, but its use has A palpable parathyroid mass is present in more than
not been reported in cats. half the cats.
Diagnosis
Prognosis
A presumptive diagnosis is based on finding hypercal-
Without specific treatment for the GH excess, the long-
cemia and demonstrating a parathyroid mass on pal-
term prognosis is poor; most eventually die with con-
pation or cervical ultrasound.
gestive heart failure, renal failure or neurologic signs
from the expanding pituitary tumor within 1–2 years. PTH concentrations are inappropriately high for the
Short-term prognosis is reasonable, provided sufficient calcium concentration, and are in the normal range or
doses of insulin are administered to control hyper- increased.
glycemia and resolve the clinical signs of diabetes
A definitive diagnosis is by surgical removal of the
mellitus.
parathyroid mass and normalization of serum calcium
concentrations. Vitamin D and calcium are usually admin-
istered following surgical removal to prevent life-threaten-
HYPERPARATHYROIDISM
ing hypocalcemia (see page 248, Hypercalcemia).
Classical signs
PRIMARY HYPERALDOSTERONISM
● Anorexia and lethargy.
● Vomiting.
Classical signs
● Weight loss.
● Dysuria, inappropriate urination, ● Weakness, cervical ventroflexion.
pollakiuria, stranguria. ● Inappetence and weight loss.
● Weakness, tremors. ● Polyuria, polydipsia.
● Palpable cervical mass. ● Blindness.
See main reference on page 245 for details of hypercal-

cemia (The Cat With Polyuria and Polydipsia). Pathogenesis
Primary hyperaldosteronism is a very rare cause of
Clinical signs polyuria and polydipsia, and results from an aldos-
terone-secreting adrenal tumor.
Primary hyperparathyroidism is an uncommon
cause of hypercalcemia, and is usually the result of an Aldosterone stimulates reabsorption of sodium in
autonomous adenoma producing excess PTH. It is usu- the distal tubule and collecting ducts. To maintain elec-
ally a solitary functional adenoma, although bilateral trical and osmotic neutrality, chloride, bicarbonate and
cystadenomas and solitary or bilateral adenocarcino- water are reabsorbed, and potassium and hydrogen ions
mas have been reported. are excreted. Hyperaldosteronism results in hypokalemia,
metabolic alkalosis, and systemic hypertension from
Affected cats are typically old (average age 13 years)
the sodium and water reabsorption.
and Siamese cats are over-represented.
Clinical signs are of hypercalcemia and include
Clinical signs
anorexia and lethargy (50% of cats), gastrointesti-
nal signs including vomiting, diarrhea or constipation Affected cats are typically old, ranging from 10–20
(27%), polyuria and/or polydipsia (24%), lower uri- years.
Clinical signs are mainly of hypokalemia including

PHEOCHROMOCYTOMA
muscle weakness, ventroflexion of the neck, inappe-
tence and weight loss, or of hypertension and include
Classical signs
blindness from hypertensive retinopathy. Other signs
include ataxia, abdominal enlargement and polyuria ● Polyuria, polydipsia.
and/or polydipsia with two of the five reported feline ● Signs of systemic hypertension (blindness,
cases also having diabetes mellitus. dyspnea from heart failure).
Diagnosis
Pathogenesis
Serum creatinine kinase activity is increased reflecting
Pheochromocytoma is a rare tumor, that develops
hypokalemic myopathy.
from the medullary region of the adrenal gland, or
Urine specific gravity is usually dilute. occasionally as an extra-adrenal mass.
A presumptive diagnosis is based on finding persistent Functional tumors may produce adrenaline (epineph-
hypokalemia despite supplementing with high doses rine), noradrenaline (norepinephrine) and occasion-
of potassium, and intractable hypertension in an eld- ally other hormones such as dopamine.
erly cat. The finding of an adrenal mass and increased
Signs result from either elevated catecholamine con-
aldosterone concentrations help confirm the diagnosis.
centrations or from a mass effect of the tumor, metas-
tasis or local invasion.
Excessive catecholamine concentrations may produce
Pheochromocytoma may also cause hypertension in severe hypertension and associated signs such as reti-
an elderly cat and be associated with an adrenal mass. nal hemorrhage and detachment.
Other causes of hypertension in elderly cats including Polyuria and polydipsia may result directly from the
hyperthyroidism and renal disease need to be ruled excessive catecholamine concentrations, hypertensive
out. renal damage or from insulin resistance. In diabetic cats
with unexplained insulin resistance, pheochromocy-
toma is a rare potential cause.
Treatment
Clinical signs can be improved or resolved with potas-
sium supplementation and antihypertensive Clinical signs
therapy. Affected cats are typically old, ranging from 10–20
● Use potassium gluconate solution, tablets or pow-
years.
der (4–10 mmol (mEq)/cat PO q 24 h in divided
doses. See treatment of hypokalemia in The Cat Clinical signs are vague and diagnosis pre-mortem is
With Generalized Weakness (page 946) and The rare. Signs include polyuria and/or polydipsia. In dia-
Cat With Neck Ventroflexion (page 895). betic cats, pheochromocytoma may result in poor
● Use amlodipine (0.625 mg or 1/4 of a 2.5 mg glycemic control associated with insulin resistance.
tablet, PO q 24 h) for hypertension. Some cats with Sudden blindness with evidence of retinal hemorrhage
severe hypertension may require doses as high as and detachment has been reported as well as congestive
1.25 mg PO q 12 h. Titrate dosage carefully, based heart failure.
upon blood pressure determinations.
● Trilostane has been used in humans with hyperal-
dosteronism, but its use has not been reported in Differential diagnosis
cats.
Primary hyperaldosteronism may also cause hyper-
Long-term resolution involves surgical removal of the tension in an elderly cat and be associated with an adre-
adrenal mass. nal mass. Typically there is hypokalemia, which is
difficult to control, and increased aldosterone concen- one cat was reported to have an estradiol- and testos-
trations. terone-secreting tumor.
Other causes of hypertension in elderly cats including The few cats reported were middle-aged to older cats
hyperthyroidism and renal disease need to be ruled out. (aged 7–14 years).
Hyperadrenocorticism may be associated with an In humans and dogs, progesterone binds to cortisol-
adrenal mass and polyuria, polydipsia, but can be ruled binding proteins displacing cortisol and resulting in
out based on clinical signs and a low dose dexametha- increased concentrations of free cortisol. Progesterone
sone test. is also a potent insulin antagonist.
Cats with progesterone-secreting tumors have clinical
Diagnosis
signs indistinguishable from hyperadrenocorticism,
An index of suspicion is required to make a presump- including concurrent diabetes mellitus.
tive diagnosis. Systemic hypertension together with an
adrenal mass, in the absence of signs of hyperadreno-
Clinical signs
corticism or hypokalemia are suggestive of pheochro-
mocytoma. In cats with a progesterone-secreting tumor, skin and
hair coat changes are the most common signs. Thin,
The mass can be imaged with ultrasound, MRI or CT.
fragile skin that bruised easily, an unkempt greasy
Biopsy may establish a definitive diagnosis.
hair coat, non-pruritic symmetrical alopecia, and skin
A definitive diagnosis based on demonstration of infections including demodicosis were the most com-
increased plasma or 24 h urinary catecholamine excre- mon signs reported.
tion is rarely performed.
Polyuria, polydipsia is typical, and in the majority of
cats was attributable to poorly controlled diabetes
Treatment mellitus.
Clinical signs can be improved using alpha (phenoxy- Weight loss occurs as a result of poorly controlled dia-
benzamine) blockers, and if needed beta blockers (e.g. betes.
atenolol).
One cat with an estradiol- and testosterone-secreting
Long-term resolution involves surgical removal of the tumor, developed behavioral changes including
adrenal mass, but perioperative care is critical, and aggression, had vulval hyperplasia, urine with a strong
includes use of preoperative alpha blockers for 1–2 “tom-cat” smell and an unkempt hair-coat.
weeks prior to surgery. Surgery is best performed
where a specialist anesthetic service is available.
Diagnosis
Diagnosis of a progesterone-secreting tumor is
PRIMARY SEX HORMONE-SECRETING
based on consistent clinical signs, an abnormal dex-
ADRENAL TUMOR
amethasone suppression test (0.1 mg/kg), i.e. basal
cortisol concentrations are low–normal, but there is
Classical signs
failure of cortisol to suppress below 41 nmol/L (1.5
● Fragile skin and poor hair coat. μg/dl) at both 4 and 8 h after IV dexamethasone,
● Polyuria and polydipsia. increased basal progesterone concentrations and evi-
● Poorly controlled diabetes mellitus. dence of an adrenal mass on ultrasound. Alternatively,
as with dogs, basal cortisol may be low-normal and
suppress normally following dexamethasone.
Pathogenesis
● Cortisol concentrations were below the reference
Rarely, adrenal tumors secrete sex hormones. The range after ACTH stimulation, but that occurs in
most common is a progesterone-secreting tumor, and 50% of cats with hyperadrenocorticism.
The cat with an estradiol- and testosterone-secreting

CYSTIC ENDOMETRIAL
tumor, had bilaterally enlarged adrenal glands, and
HYPERPLASIA/PYOMETRA COMPLEX
basal estradiol and testosterone concentrations were
markedly elevated.
Classical signs
A skin biopsy shows changes consistent with an
● Low-grade inappetence and lethargy.
endocrinopathy.
● Vaginal discharge or distended uterus
palpable.
● ± Fever.
● ± Polyuria, polydipsia.
Hyperadrenocorticism is the most likely differential
diagnosis and may appear identical clinically and on See main reference on page 269 for details of acute
hormonal testing to a progesterone-secreting tumor, pyometra/metritis (The Cat With Depression, Anorexia
except for the absence of markedly increased basal or Dehydration).
progesterone concentrations.
Other causes of poorly controlled diabetes need to be
considered, e.g. excessive insulin dose, too short a Clinical signs
duration of action of insulin, hyperthyroidism and
acromegaly. Chronic cystic endometrial hyperplasia/pyometra
complex presents with vaginal discharge, and cats
Other causes of a poor hair coat need to be considered. may have polyuria and polydipsia as a presenting sign.
Pyrexia is rare.
Treatment Stump pyometra is rarely a cause of polyuria, poly-

dipsia; it more often presents as vaginal discharge.
Aminoglutethimide (AGT; approximately 6 mg/kg q
12 h PO) was used successfully for 1–2 months in some Chronic cystic endometrial hyperplasia/pyometra com-
cats to control signs prior to surgery. plex occurs in intact cats of any age, regardless of
● Aminoglutethimide inhibits the enzyme, which whether they have previously had kittens.
converts cholesterol to prenenolone during synthe- Copious vaginal discharge (watery or thick) is most
sis of adrenocortical steroids. common.
● Mammary gland enlargement following treatment
has been reported in a male cat. Low-grade inappetence may be present for weeks or
months.
Trilostane resulted in a temporary improvement in the
cat with the estradiol- and testosterone-secreting Weight loss, lethargy, unkempt appearance and
tumor. mild dehydration may be evident.
Surgical removal of the adrenal tumor is the treat- Depression, listlessness, ± mild dehydration. Cats are
ment of choice once signs have been controlled usually not pyrexic.
medically. Surgery resulted in long-term survival Polyuria, polydipsia occurs in some cats.
and resolution of clinical signs including diabetes
mellitus.
Diagnosis
Prognosis
Clinical signs that are highly suggestive of cystic
Prognosis is good for cats that respond to medical ther- endometrial hyperplasia/pyometra complex are vaginal
apy and undergo successful surgical removal of the discharge and listlessness in an intact cat, plus a dis-
adrenal mass. tended uterus on radiograph. Radiographically,
cystic endometrial hyperplasia/pyometra can only be Ultrasonography readily distinguishes between preg-
distinguished from a pregnant uterus after approxi- nancy and pyometra 21 days after last breeding date.
mately 42 days, when calcification of the fetal skeleton
Increased white cell count and/or left shift are found
is visible.
in some cats.
RECOMMENDED READING
Chastin C, Panciera D, Waters C, Savary K, Price G, Vaden S. Hypercalcemia in cats: a retrospective study of 71
cases (1991–1997). Small Anim Endocrinol 2000; 10(3): 9.
Feldman EC, Nelson RW. Hypercalcemia and primary hyperparathyroidism. In: Canine and Feline Endocrinology
and Reproduction, 2nd edition. Philadelphia, Saunders, 1996, pp 455–497.
Gunn Moore D. Feline Endocrinopathies. In: Advances in feline medicine. Vet Clin North Am Small Anim Pract
2005; 35(1): 171–210.
Martin GJ, Rand JS. Current understanding of feline diabetes: Part 2, treatment. J Feline Med Surg 2000; 2: 3–17.
Midkiff A, Chew D, Randolph J, Center S, DiBartola S. Idiopathic hypercalcemia in cats. J Vet Intern Med 2000;
14(6): 619–626.
Nelson WN. Diabetes mellitus. In: Ettinger SJ (ed) Textbook of Veterinary Internal Medicine, 5th edition.
Norman EJ, Mooney CT. Diagnosis and management of diabetes mellitus in five cats with somatotrophic abnormal-
ities. J Feline Med Surg 2000; 2(4): 183–190.
Rand JS, Marshall R. Diabetes mellitus in cats. In: Advances in feline medicine. Vet Clin North Am Small Anim
Pract 2005; 35(1): 211–224.
Rand JS, Martin GJ. Management of feline diabetes mellitus. Vet Clin North Am 2001; 31(5): 881–913.
Reusch CE. Hypoadrenocorticism. In: Ettinger SJ (ed) Textbook of Veterinary Internal Medicine, 5th edition.
Philadelphia, Saunders, 2000, pp 1488.
Rijnberk A. Acromegaly. In: Ettinger SJ (ed) Textbook of Veterinary Internal Medicine, 5th edition. Philadelphia,
Saunders, 2000, pp 1370–1379.
PART 5
Cat with acute illness
16. The cat with acute depression,

anorexia or dehydration
Anthony Abrams-Ogg
KEY SIGNS
● Acute lethargy, depression or listlessness.
● Acute inappetence or anorexia.
● Dry mucous membranes, skin tenting.
MECHANISM?
● Depression, anorexia and dehydration are non-specific signs that frequently occur together and
accompany most diseases.
● Depression may result from a primary neurologic disorder or be secondary to diseases of
other organs.
● Reduced eating behavior may be due to primary anorexia, secondary anorexia due to an
underlying disorder, pseudoanorexia and physiologic anorexia.
● Dehydration occurs when drinking cannot compensate for water losses.
WHERE?
● Disorders of any organ system may cause acute depression, anorexia or dehydration.
WHAT?
● The most common causes of acute depression, anorexia and dehydration without other more
specific signs are pancreatitis, hepatopathies and poisoning.
261
262 PART 5 CAT WITH ACUTE ILLNESS

Diseases causing acute depression, anorexia or dehydration
METABOLIC
● Acute anemia** (p 270)
Acute anemia of any cause will result in depression, anorexia and dehydration. Pale mucous mem-
branes are typical, with or without splenomegaly or icterus. Polypnea may be evident, and fever
may be present if due to Mycoplasma haemofelis (Haemobartonella felis).
● Acute renal failure* (p 278)
This is usually due to renal ischemia or nephrotoxins, and results in progressive depression and
anorexia, vomiting, and polyuria, oliguria or anuria. Acute exacerbation of chronic renal failure
may also occur.
● Urethral obstruction*** (p 267)
Progressive depression and anorexia occur. Dysuria may not be witnessed and non-specific signs
predominate due to acute uremia. A turgid bladder is evident on palpation.
● Hepatic encephalopathy (p 297)
In young cats this is usually due to a porto-systemic shunt. In mature cats this is usually due to
hepatic lipidosis. Intermittent disorientation and ptyalism are the most common signs.
● Diabetic ketoacidosis* (p 292)
Insulin deficiency and dehydration lead to hyperglycemia and ketoacidosis. This may occur
acutely without a history of weight loss and polyuria/polydipsia. Depression and anorexia are the
main signs and a history of infrequent vomiting may be present.
● Acute hypoglycemia (p 296)
This is usually due to insulin overdose. Lethargy, disorientation, trembling, ataxia and dilated
pupils are often present. Signs may progress to coma or seizures if not treated.
● Acute hypokalemia** (p 271)
Hypokalemia has numerous causes including chronic renal failure, post-obstructive diuresis, intra-
venous fluid therapy with potassium-poor fluids, furosemide therapy, vomiting, hyperaldostero-
nism (rare) and the treatment of diabetic ketoacidosis. Anorexia may contribute to hypokalemia,
which in turn may exacerbate anorexia and depression.
● Hypophosphatemia* (p 295)
Severe hypophosphatemia may complicate the treatment of diabetic ketoacidosis and enteral ali-
mentation of an anorexic cat, causing increased depression and anorexia and hemolysis.
● Hypoparathyroidism* (p 295)
Hypoparathyroidism is usually caused by parathyroidectomy during thyroidectomy. Idiopathic
hypoparathyroidism is uncommon. Hypocalcemia results in anorexia and depression that may
progress to muscle fasciculations and seizures.
● Hypernatremia (p 298)
Hypernatremia should be considered in a critically ill cat with progressive depression not attributa-
ble to other causes.
16 – THE CAT WITH ACUTE DEPRESSION, ANOREXIA OR DEHYDRATION 263
● Acute heart failure* (p 292)

Non-specific signs of lethargy and inappetence may occur prior to dyspnea. An arrhythmia, mur-
mur and/or a weak pulse may be evident. Abnormal lung sounds consistent with edema or pleural
fluid may be auscultated.
NEOPLASTIC
Many tumors may cause acute signs, and non-specific signs of lethargy and inappetence often
appear prior to specific signs.
● Central nervous system neoplasia (p 297)
The tumor may acutely affect alertness or appetite. Other neurologic signs may or may not be
present.
NUTRITIONAL
● Unpalatable food* (p 294)
Primary anorexia may occur due to a change in the diet. History of a diet change, together with normal
physical examination findings are suggestive.
● Alternate food source* (p 294)
Physiologic anorexia may occur after consumption of an unknown source of food.
PHYSICAL
● Separation or situation anxiety** (p 270)
Change in environment and routine may cause primary anorexia and depression. Withdrawal or
hiding may occur.
● Environmental stress* (p 294)
Temperature extremes may cause primary anorexia and inactivity.
INFLAMMATION
● Fever*** (p 267)
Acute fever and its underlying disorder may cause acute depression, anorexia and dehydration.
Localizing signs may or may not be present.
● Pancreatitis* (p 272)
Non-specific signs of depression and/or anorexia dominate the clinical picture. Unlike the dog, vomiting and
abdominal pain are not consistent findings.
● Gastrointestinal foreign body and inflammation*** (p 268)
Non-specific signs often predominate and vomiting and diarrhea may or may not be witnessed.
Occasionally, a linear foreign body is evident wrapped around the base of the tongue.
● Esophageal foreign body and inflammation (p 299)
Regurgitation and gagging may not be witnessed, and non-specific signs may predominate.
● Acute intranasal, oral or pharyngeal inflammation ** (p 269)
Sneezing, nasal discharge and stertor may not be witnessed initially and non-specific signs predominate
including depression, anorexia and pyrexia. Careful examination may reveal a mild serous ocular
continued
continued
discharge or tongue ulceration. Acute oral and oropharyngeal inflammation will cause pseudoanorexia.
The associated pain and underlying condition may cause non-specific signs. Salivation and halitosis may
be evident.
● Central nervous system inflammation (p 297)
Acute meningitis or encephalitis may initially be characterized by non-specific signs. Careful neurologi-
cal examination may reveal cranial nerve or proprioceptive deficits.
INFECTIOUS
Viral:
● Panleukopenia** (p 272)
Non-specific signs of extreme lethargy and anorexia usually appear prior to the onset of vomiting.
Diarrhea may occur 1–2 days after vomiting begins. Fever may or may not be present.
● Feline leukemia virus infection (p 299)
Occasionally the only signs of infection are acute depression, anorexia and dehydration.
Bacterial:
● Bacterial sepsis** (p 269)
Depression, anorexia and fever are typical of bacterial infection, although fever may not be present,
especially in severe sepsis, and hypothermia may herald impending septic shock. Evidence of an inter-
nal site of infection may or may not be present on physical examination.
Parasitic:
● Toxoplasmosis* (p 293)
Lethargy, anorexia and fever are early signs. Dyspnea is present in the majority of cats, and is associated
with increased respiratory sounds over the chest. Neurological signs, icterus, uveitis or evidence of other
specific organ involvement may or may not be apparent.
Idiopathic:
● Primary anosmia (p 299)
Reduced sense of smell may cause anorexia. Primary anosmia may be idiopathic or neurologic.
Toxic:
● Acute poisoning and envenomation* (p 283)
Poisoning with ingested substances or animal venoms commonly causes acute non-specific signs,
although more specific signs are often present as well. Depending on the toxin, these signs include sali-
vation, vomiting, diarrhea, polypnea, arrhythmias, pale mucous membranes, hypothermia, tremors
(which may cause hyperthermia), excitability and other behavioral changes, seizures and profound gen-
eralized weakness.
● Ethylene glycol poisoning* (p 287)
Acute depression in acute ethylene glycol toxicosis is due to direct central nervous system effects.
Depression is due later to acute renal failure. Other signs include ataxia, vomiting, tremors, polyuria,
painful and swollen kidneys and seizures.
● Lily poisoning* (p 290)

Acute depression occurs following ingestion. Later depression is due to acute renal failure. Other signs
include vomiting, polyuria, oliguria or anuria and painful and swollen kidneys.
● Snake bite envenomation* (p 291)
Acute weakness caused by snake venom neurotoxins may present as acute depression. Other signs
depend on the specific snake toxins, which include procoagulants, hemolysins, nephrotoxins, myotoxins
and local cytotoxins.
●Drug therapy*** (p 268)
Many drugs can cause anorexia.
Traumatic
● Trauma*** (p 266)
Trauma may cause primary and secondary depression, anorexia and dehydration. External signs of
trauma may be subtle or obvious. Shorn nails are often evident. A fractured jaw and tongue lacera-
tions or puncture wounds cause pseudoanorexia and impede drinking.
● Pain*** (p 268)
Pain may contribute to the depression and anorexia seen in many of the disorders listed in all cate-
gories above. Other signs of pain include vocalization (spontaneous and evoked by palpation),
defensive aggression evoked by palpation, lameness, hunched posture (abdominal pain) and reluc-
tance to move.
● Depressed and critically sick cats may still purr, and

INTRODUCTION the presence of purring should not be interpreted as
an indication of mild illness.
MECHANISM? Anorexia refers to a reduced appetite. Anorexia may be
complete or partial. (“Inappetence” is commonly used to
Depression, anorexia and dehydration are non-
refer to partial anorexia. In this chapter “anorexia” will be
specific signs that frequently occur together and
used to refer to a reduced appetite regardless of severity.)
accompany most diseases.
● Primary anorexia is due to anosmia, behavioral
● The severity of the signs varies with the primary
factors or neurologic disorders.
disease and the temperament of the animal.
● Signs may be stable or progressive.
– The smell of food is important to appetite stimu-
● Various non-specific (e.g. acute phase response)
lation, especially in cats.
– Behavioral (psychologic) factors causing
and specific (e.g. uremia) mechanisms may be
anorexia include fear, change in routine and
involved, depending on the primary disease.
unpalatable food.
Depression refers to dullness, lethargy and withdrawal – Central neurologic disorders may impair the
from contact (hiding). The animal is less responsive, but appetite center in the hypothalamus.
not to the extent that it would be considered stuporous ● Secondary anorexia occurs when a primary dis-
or comatose. Depression may result from a primary neu- ease process affects the cytokine, endocrine and
rologic disorder or be secondary to diseases of other neurologic control of appetite.
organs. Weakness, behavioral factors (e.g. anxiety), and – Most disorders may result in secondary anorexia
depression of the reticular activating system may con- by various mechanisms.
tribute to depression due to non-neurologic disorders. – This is the most common cause of anorexia in cats.
● Anorexia may also be due to pseudoanorexia and

physiologic anorexia. DISEASES CAUSING ACUTE
– In pseudoanorexia the animal has a normal DEPRESSION, ANOREXIA OR
appetite but is reluctant to eat because of oral DEHYDRATION
pain. (If there is a non-painful disorder of pre-
hension, the presenting complaint will be dys- TRAUMA***
phagia not anorexia.)
– In physiologic anorexia the animal is satiated Classical signs
after eating. This may mimic true anorexia if the
animal has an unknown source of food. ● Shorn nails, dirty haircoat, dyspnea, pale
mucous membranes, weak pulses,
Dehydration refers to a reduction in body water other lameness or inability to walk.
than that present in the transcellular compartment ● Fractured mandible, broken canine teeth,
(third space, i.e. the gastrointestinal tract, pleural cav- scleral hemorrhages, neurologic signs
ity and peritoneal cavity). It occurs when the animal (head trauma).
does not drink and absorb sufficient quantities of
water to replace physiologic or pathologic losses.
Thirst may be reduced by analogous mechanisms that
reduce appetite.
Clinical signs
Cats with generalized trauma may be depressed and
anorexic for a number of reasons including shock,
WHERE?
hypovolemia, dyspnea, pain from soft tissue contusions
Disorders of any organ system may cause acute and fractures, herniations and concussion.
depression, anorexia or dehydration. The focus of this
Pseudoanorexia may occur from fractures of the jaw
chapter is diseases where the owner complaint is typi-
and teeth and lacerations to the tongue.
cally that the cat is suddenly quiet and/or refusing to eat
or drink. Specific signs are often not reported and are
not obvious on physical examination. Meticulous and
repetitive history-taking and physical examinations may
Diagnosis
be needed to detect subtle signs and development of new External signs of trauma are not always obvious.
signs as the disease progresses. Laboratory assessment Although shorn nails are usually evident, this sign may
and imaging are often required to establish a diagnosis. be absent. For example, nails may not be shorn on ice
Acute pyrexia and acute anemia as causes of depression, following motor vehicle trauma in the winter. Subtle
anorexia and dehydration are discussed in The Pyrexic signs of trauma include dried blood around the external
Cat (page 364) and The Anemic Cat (page 526). The nares, blood against the tympanic membranes, bite
reader should also refer to The Cat With Stupor or wounds or lacerations to the ventral surface of the
Coma (page 821), The Cat With Seizures, Circling tongue, and pain on palpation of the pelvis of a cat with
and/or Changed Behavior (page 795), and The Cat With normal ambulation.
Generalized Weakness (page 941). In the absence of a
specific diagnosis, treatment should be supportive.
WHAT? Other causes of acute depression.
The focus of this chapter is diseases of acute onset, as
opposed to acute exacerbation of chronic diseases. In
most cases the cat will be in good body condition.
Treatment
Intravenous fluids and transfusions to treat hypov-
The most common causes of acute depression, anorexia
olemia.
and dehydration without other more specific signs are
pancreatitis, hepatopathies and poisoning. Surgical and conservative management of injuries.
Injuries to the oral cavity may necessitate placement of

URETHRAL OBSTRUCTION***
an esophagostomy or gastrostomy tube for nutritional
support.
Classical signs
FEVER*** ● Straining to urinate (owner reports

“constipation”).
Classical signs ● Progressive depression and anorexia.
● Depression, anorexia. See main reference on page 179 for details (The Cat
● Elevated body temperature. Straining to Urinate).

Clinical signs
Pyrexic Cat).
Straining to urinate, vocalizing, growling when handled,
difficulty walking, vomiting.
Clinical signs Progressive depression and anorexia.
Febrile cats may be presented for acute depression and
Pain on abdominal palpation and a turgid bladder are
anorexia.
evident.
Other clinical signs will depend upon cause of fever.
Whitish, chalky material may be seen blocking the ure-
thral orifice or around the prepucial/perineal area and
the cat may be excessively licking the area.
Diagnosis
Progressive weakness and bradycardia may occur.
Fever must be distinguished from hyperthermia as a
result of environmental stress, activity or anxiety.
Diagnosis
To identify the cause of the fever see The Pyrexic Cat
(page 364). Palpation of a turgid bladder is diagnostic. Rarely, spon-
taneous relief of obstruction occurs before examination.
Urinalysis typically reveals blood and struvite crystals.
Blood work reveals elevated urea, creatinine, potassium
Other causes of acute depression and anorexia with and phosphorus.
superimposed hyperthermia mimicking a febrile condi-
tion must be differentiated.
If the owner has only noted non-specific signs, then
Treatment most other causes of acute depression must be consid-
ered. The diagnosis is usually straightforward on the
Treatment of the underlying cause is of primary
basis of physical examination.
importance.
If antipyretic agents are not contraindicated, reduc-
Treatment
ing the fever will usually improve the well-being and
appetite of the cat. Dipyrone is the superior agent, Intravenous fluids and correction of hyperkalemia (see
but has been discontinued in some countries. Acute renal failure, below).
Ketoprofen and meloxicam may be used at standard
Urethral catheterization.
doses.
Management of urethral spasm, detrusor atony.
Hyperthermia is treated by placing the cat in a cool
environment. Dietary management.
Antiemetic agents will decrease nausea, and thereby

GASTROINTESTINAL FOREIGN BODY AND
reduce depression and anorexia.
INFLAMMATION***
Classical signs
DRUG THERAPY***
● Vomiting and diarrhea.
● Anorexia and depression. Classical signs
● Anorexia.
With Signs of Acute Vomiting), page 713 (The Cat
With Signs of Acute Small Bowel Diarrhea), page 765 Clinical signs
(The Cat With Signs of Large Bowel Diarrhea), page
792 (The Constipated or Straining Cat). Anorexia is a side effect of many drugs, including
antibiotics, anti-thyroid medications and anti-cancer
agents. Anorexia typically develops within the first
Clinical signs week of therapy.
Cats with acute gastritis, acute gastroenteritis or acute Vomiting and diarrhea are the most common concurrent
gastrointestinal foreign bodies typically have vomiting signs.
and diarrhea. However, these signs may be intermittent,
so that only non-specific signs such as anorexia and Some drugs also cause oral irritation.
depression are reported by the owners.
Variable more specific findings include abdominal Diagnosis
pain, vomiting following abdominal palpation, Rule out other causes of anorexia.
dilated loops of intestine and an intestinal mass.
A linear foreign body may be evident around the base Improved appetite upon withdrawal of the drug.
of the tongue.
PAIN***
Diagnosis
If only non-specific signs are reported, observation for Classical signs
vomiting and diarrhea may be of value. ● Depression, anorexia and localizing sign of
Rule out extra-intestinal causes of vomiting and diar- pain.
rhea with routine laboratory work.
Diagnostic imaging is required to identify foreign Clinical signs
material and intestinal obstruction.
Pain may contribute to the depression and anorexia
seen in many disorders. Other signs of pain include
Differential diagnosis vocalization (spontaneous and evoked by palpation),
Pancreatitis. defensive aggression evoked by palpation, lameness,
hunched posture (abdominal pain) and reluctance to
Other causes of acute vomiting and diarrhea. See The Cat move.
With Signs of Acute Vomiting (page 630) and The Cat
With Signs of Acute Small Bowel Diarrhea (page 697).
Diagnosis
Treatment A cat with acute depression and anorexia should be

carefully examined for signs of pain, which may help
Treatment of the underlying cause. identify a causative disorder.
Ulcers and foreign material in the oral cavity are usu-

ACUTE INTRANASAL, ORAL
ally obvious, except for those under the tongue.
OR PHARYNGEAL INFLAMMATION
Anesthesia is often required for thorough evaluation of
the tongue and oropharynx.
Classical signs
● Partial or complete anorexia and Differential diagnosis
depression.
Other causes of acute depression need to be ruled out.
● Sneezing, nasal discharge.
● Stertor.
Treatment
● Halitosis, ptyalism.
Foreign material should be removed by extraction or
See main reference on page 5 for details (The Cat With lavage.
Acute Sneezing or Nasal Discharge), page 32 (The Cat
Antibiotics (e.g. ampicillin or amoxicillin at standard
With Stridor).
doses) are indicated when secondary bacterial infection
is evident with viral, foreign body, corrosive or uremic
Clinical signs ulceration.
Cats with foreign material (e.g. kitty litter, plant mate-

rial) in the nose or nasopharynx may be acutely depressed BACTERIAL SEPSIS**
and refuse to eat. Typically there is an acute onset of
sneezing or serous nasal discharge. Foreign material in the Classical signs
nasopharynx may result in stertorous respiration. ● Acute anorexia and depression.
Cats with acute viral rhinitis may also be depressed ● Fever and localizing signs of infection.
and anorexic, but these cats usually have a fever. ● Hypothermia and bradycardia with severe
Anosmia may contribute to anorexia; so may concur- sepsis.
rent oral inflammation with calicivirus infection.
Conjunctivitis may be present. See main reference on page 112 for details (The Fading
Kitten and Neonate).
Cats with oral and oropharyngeal foreign bodies
(e.g. needle) will be acutely depressed and refuse to eat.
More specific signs include halitosis, ptyalism, unusual Clinical signs
jaw motions, gagging, pawing at the mouth and ster- Cats with a bacterial infection usually have a fever and
torous respiration. localizing signs of infection, in addition to depression
Oral ulcers, acute anorexia and salivation may occur and anorexia.
following exposure to a corrosive substance. ● Sepsis is defined as presence of a systemic inflam-
matory response syndrome (SIRS) due to a dissem-
Uremic ulceration contributes to anorexia in cats with inated bacterial infection. Signs of SIRS include
renal failure. high fever or hypothermia; tachycardia or bradycar-
dia; polypnea; and moderate to marked neutrophilia,
neutropenia or left shift.
Diagnosis ● Severe sepsis is defined as sepsis accompanied by
Acute viral rhinitis is usually diagnosed on the basis organ dysfunction, hypoperfusion or hypotension.
of clinical findings. ● Septic shock is defined as severe sepsis with
hypotension that is refractory to adequate fluid
Foreign material may be evident adhered to the external resuscitation.
nares. The nasal cavity may be examined for foreign mate-
rial by means of an otoscope, rigid endoscope or radi- Febrile responses may be blunted in older cats, and
ographically. The nasopharynx may be examined under the severity of infection may be underestimated based
anesthesia with a dental mirror or flexible endoscope. on the magnitude of the fever.
In some cases fever is absent, and this should not be

ACUTE ANEMIA**
used to rule out bacterial infection. Septic cats without
a fever are more likely to have severe sepsis and
Classical signs
impending septic shock.
In some cats, the localizing signs of infection are not
● Acute onset of anorexia, depression and
readily detectable on physical examination. This most
physical inactivity.
often occurs when there is primary neutropenia
and secondary infection.
● Severe sepsis or septic shock should always be con-
Anemic Cat).
sidered in the differential diagnoses of cats with
acute depression and anorexia without more spe-
cific signs.
Clinical signs
● Other common signs of severe sepsis are bradycar-
dia, pale mucous membranes, weak pulses, polyp- The degree of depression, anorexia and dehydration cor-
nea, diffuse abdominal pain and icterus. relates with the severity and acuteness of the anemia.
Tachypnea and tachycardia may be evident.
Diagnosis Pale mucous membranes with or without splenomegaly
or icterus.
A complete blood count may reveal neutrophilia
and a left shift. Alternatively, neutropenia may be If the anemia is due to infectious causes, e.g.
present from primary bone marrow failure (e.g. Mycoplasma haemofelis (Haemobartonella felis), the
FeLV infection) or exhaustion of marrow granulo- cat may be pyrexic.
cyte reserve.
Meticulous physical examination, serum chemistries,
Diagnosis
diagnostic imaging and fine-needle aspiration will help
localize the infection (e.g. deep subcutaneous abscess, Routine hematology will confirm anemia.
pyometra, pyelonephritis, peritonitis, pyothorax, pneu-
The cause of the anemia can usually be determined by
monia).
routine work-up (see The Anemic Cat).
In the absence of a fever and localizing signs, all other
Pale mucous membranes due to shock.
causes of acute depression and anorexia should be con-
sidered.
Treatment
Treatment Treat the cause of anemia; transfusion. See The Anemic
Treatment is supportive pending a diagnosis. Cat.
Systemic antibiotic therapy and local treatment of

infection if indicated (e.g. drainage of abscess). SEPARATION OR SITUATION ANXIETY**
Empirical therapy with broad-spectrum, bactericidal
antibiotics (e.g. cefazolin plus gentamicin, cefoxitin) Classical signs
should be started at standard doses in depressed ● Withdrawal or hiding and/or anorexia.
neutropenic cats.
Pathogenesis line, clomipramine) or selective serotonin re-uptake

inhibitors, together with environmental changes may
Removal of significant persons, or other pets from be effective (see The Cat With Anxiety-Related
the cat’s environment, or removal of the cat from famil- Behavior Problems, page 1014, for doses). Other treat-
iar surroundings may trigger separation or situation ments that have been used (but some may have undesir-
anxiety. able side effects) include hydroxyzine, phenobarbital,
Introduction to new persons, pets or surroundings megesterol acetate, prednisone, diazepam, oxazepam,
may also trigger anxiety. cyproheptadine at standard doses and catnip.
Dependency can develop with some treatments.
The cat’s personality is an important risk factor.
Nasoesophageal, esophagostomy or gastrostomy
Separation/situation anxiety may exacerbate second- tube feeding or parenteral nutrition should be insti-
ary anorexia and depression in a hospitalized cat. tuted for hospitalized cats if anorexia persists for more
than 3 days.
Clinical signs
Variable withdrawal, inactivity, anorexia and dehydra- Prognosis
tion. The ability of the cat to adapt is dependent upon per-
Other behavioral signs may occur, such as aggression sonality.
to other pets or persons, and inappropriate elimination. Hepatic lipidosis may complicate primary anorexia,
No signs of another disorder causing depression and especially in an obese cat anorexic for more than two
anorexia. weeks.
Weight loss is dependent on degree and duration of

anorexia. Complete anorexia will result in detectable ACUTE HYPOKALEMIA**
lumbar muscle wasting within one week.
Classical signs
Diagnosis ● Ventroflexion of the neck
● Stilted forelimb gait.
History of change in environment.
Ruling-out other causes of depression and anorexia. Pathogenesis
Hypokalemia results from insufficient potassium
Differential diagnosis intake and/or excessive urinary or gastrointestinal
Other causes of depression and anorexia. potassium loss and/or translocation from extracellular
to intracellular fluid.
Treatment Hypokalemia may be seen in numerous disorders

including chronic renal failure, post-obstructive diure-
No treatment is necessary if signs are mild and it is sis, intravenous fluid therapy with potassium-poor flu-
likely that the cat will adapt. ids, furosemide therapy, vomiting, hyperaldosteronism
Return cat to previous environment if possible. (rare) and the treatment of diabetic ketoacidosis.
Anorexia may contribute to hypokalemia, which in turn
Offer a variety of foods, warm the food, increase may exacerbate anorexia and depression.
palatability of food with clam juice, or canned tuna or
salmon juice.
Clinical signs
Anxiolytic and/or appetite-stimulant drugs or herbal
remedies may be useful if anorexia or anxiety cannot be Lethargy, muscle weakness, anorexia – increasing
quickly resolved. Tricyclic antidepressants (amitripty- risk with decreasing potassium level.
Ventroflexion of the neck and stilted forelimb gait. Clinical signs

Severe muscle weakness may lead to respiratory mus-
cle failure (rare). Most common in cats 2–6 months of age.
Polyuria and polydipsia – this is usually due to the Typically, there is acute onset of depression and
underlying disorder, but hypokalemia may impair con- anorexia. Vomiting then appears, followed by the onset
centrating ability (hypokalemic nephropathy). of fetid and often bloody diarrhea in 1–2 days. Cats
may stand hunched-up, sometimes with the face over a
Arrythmias – increasing risk with decreasing potas- water bowl, but refuse to drink. Dehydration develops
sium level. with vomiting and diarrhea.
Diagnosis Pain is often evident on abdominal palpation, and loops

of intestine may be thickened and contain excess gas
Serum potassium level < 3.5 mmol/L. and fluid.
Ruling-out other causes of depression, weakness and Affected kittens are initially febrile, but if signs are
anorexia. severe, this progresses rapidly to hypothermia. Coma
and death usually follow in a few hours.
Other causes of depression, weakness and anorexia Diagnosis
related to the primary disorder.
Diagnosis is usually suspected when there are consis-
Other causes of cervical ventroflexion include thiamine tent clinical signs in a kitten or cat with no history of
deficiency and other causes of muscle weakness vaccination.
(including motor neuron disease and myasthenia
gravis, which do not cause anorexia). Complete blood count reveals severe neutropenia and
lymphopenia. Fecal tests for parvovirus antigen are
Treatment sometimes useful.
Potassium-rich intravenous fluids. See Diabetic

ketoacidosis in The Cat With Polyuria and Polydipsia. Differential diagnosis
Cats with mild hypokalemia (3.0–3.5 mmol/L) may be No other disease mimics classic severe panleukopenia,
treated as outpatients with potassium gluconate, 1.0–3.0 and this should be the first differential diagnosis in any
mEq/kg/day q 8 h, followed by a maintenance dose of 1.0 unvaccinated kitten presented for acute depression.
mEq/kg/day q 12 h once serum potassium has normalized.
Many other diseases mimic mild panleukopenia clini-
Prognosis cally. However, leukopenia is usually present, even in
mild cases, which supports the diagnosis.
The prognosis for correction of hypokalemia is good
and overall prognosis is determined by the underlying
disorder. Treatment
Intravenous fluids and bactericidal antibiotics (e.g.
PANLEUKOPENIA** ampicillin plus gentamicin, cefoxitin) at standard doses
are required.
Classical signs
● Acute depression, anorexia, dehydration,
and fever in kittens or unvaccinated cats. PANCREATITIS*
● Vomiting usually precedes diarrhea.
Classical signs
See main reference on page 650 for details (The Cat ● Acute depression and anorexia.
With Signs of Acute Vomiting).
The pathogenesis of acute pancreatitis is believed to be

Pathogenesis
similar to that in other species:
Pancreatitis is typically classified based on post- ● Premature zymogen activation occurs within the
mortem pancreatic histopathology. Classification pancreas leading to local inflammation, circulating
schemes vary in different reports, but in general the pancreatic enzymes, and systemic inflammatory
degree of fibrosis and mononuclear cell infiltration cor- response syndrome (SIRS). Potential sequelae
relates with chronicity. include hypotension, disseminated intravascular
● Acute pancreatitis is characterized by variable coagulation (DIC), pulmonary edema, pleural effu-
neutrophil infiltration, edema, hemorrhage, acinar sion, pulmonary thromboembolism, encephalopathy,
necrosis and peripancreatic fat necrosis, inflamma- systemic lipodystrophy, acute renal failure and multi-
tion (steatitis) and saponification. In one series of organ failure.
40 cats, acute pancreatitis was categorized as necro- ● Neither bacterial infection of the inflamed pancreas
tizing pancreatitis (some with fibrosis) and suppu- nor bacteremia appears to be common in naturally
rative pancreatitis. occurring pancreatitis.
● Both acute and chronic pancreatitis can be severe
and no clinical, laboratory or diagnostic imaging
Clinical signs
finding reliably distinguishes the two.
Cat may be of any age, with no sex or breed predilec-
Pancreatitis may occur with or without concurrent
tion, except perhaps for Siamese cats.
disorders. In the absence of a concurrent condition,
a specific cause is usually not identified. Duration of clinical signs prior to presentation varies
● Identified causes of acute pancreatitis include pan- from several days to more than 3 weeks. Both acute
creatic neoplasia, hypothermia, virulent systemic and chronic pancreatitis may present with acute signs,
feline calicivirus strains, ascending bacterial but cats presenting with a longer clinical history are
infection, toxoplasmosis, abdominal trauma and more likely to have pancreatic fibrosis.
organophosphate intoxication. Ingestion of a high-
Clinical findings are often more subtle than expected
fat meal is not a cause, unlike in dogs. Pancreatic
for the degree of pancreatic injury. This may explain in
flukes (Eurytrema procynonis) and liver flukes
part the delay in presentation to a veterinarian.
(Amphimerus pseudofelineus) have been associ-
ated with chronic, but not acute, pancreatitis. The Depression and/or anorexia are the most common
cat has been used extensively as an experimental historical signs and may be the only signs present. The
model of acute pancreatitis, but the methods of most common physical abnormalities are dehydra-
inducing pancreatic inflammation have little rele- tion and hypothermia (68% in one study). Fever is
vance to the etiology of naturally occurring disease. uncommon.
● Associated disorders include hepatic lipidosis,
Other inconsistent signs include weight loss, vomit-
cholangiohepatitis, inflammatory bowel disease,
ing, diarrhea, cranial abdominal pain, cranial abdomi-
diabetes mellitus, diabetic ketoacidosis and acute
nal mass, abdominal distention due to ascites, dyspnea,
renal failure. Cause and effect between these condi-
ataxia and disorientation and shock. Polydipsia may be
tions and pancreatitis is not known, but the disor-
present, but is usually due to concurrent diabetes melli-
ders are probably related. Other concurrent
tus. Systemic lypodystrophy is a rare complication of
disorders include chronic renal diseases and neo-
acute pancreatitis, characterized by subcutaneous nod-
plasia, which may be related to age rather than pan-
ules that may ulcerate.
creatitis. If a concurrent disorder is not identified,
pancreatitis is more likely to be acute based on
histopathology. Diagnosis
● Obesity is not an independent risk factor, but is a
Because clinical and laboratory findings are non-spe-
risk factor for conditions associated with pancreati-
cific, diagnosis requires a high index of suspicion.
tis, such as hepatic lipidosis and diabetes mellitus.
Cats with pancreatitis may be thin, but it is not clear Pancreatitis should be considered in any cat with
if this is a risk factor or consequence of anorexia. unexplained acute depression. Acute pancreatitis
should also be considered in any critically ill cat devel- – Elevated fTLI is not specific for pancreatitis.
oping pleural effusion, ascites or hypothermia. Elevations may also be seen in inflammatory
bowel disease, intestinal lymphoma and renal
Laboratory findings are variable and are most valu-
failure.
able in ruling out other causes of depression and
– fTLI is not as widely available as other laboratory
anorexia.
tests, and delays in reporting reduce its utility.
Hematology abnormalities include: ● The measurement of trypsinogen activation peptide
● Mild non-regenerative anemia. may be useful in the future.
● Neutrophilia, with or without a left shift (inflam- ● Feline pancreatic lipase immunoreactivity (fPLI)
matory leukogram). appears to be a very sensitive test for acute pancre-
● Neutropenia. atitis, but is currently not widely available.
● Lymphopenia (stress leukogram). ● Abdominal fluid is usually a modified transudate
● Thrombocytopenia (consumption). but may be a non-septic exudate. Pleural fluid is
usually a modified transudate.
Serum biochemistry abnormalities include eleva-
tions in liver enzymes (with a tendency to be higher in Diagnostic imaging findings are also variable.
chronic pancreatitis), bilirubin, cholesterol, urea and
Abdominal radiography is most useful in ruling out
creatinine, and decreases in potassium, calcium and
other causes of vomiting.
albumin. Lower concentrations of ionized calcium
● Radiographic findings are often normal and do not
have been associated with a poor prognosis in acute
rule out pancreatitis.
pancreatitis. Low serum cobalamin levels may be
● If abnormalities are present, they are similar to
present.
those of acute pancreatitis in dogs: decreased
Blood glucose concentration may be increased, normal cranial abdominal contrast (due to effusion), a
or low. Mild coagulation abnormalities may be present. mass effect (displacement of organs) in the right
● Serum amylase and lipase levels are infrequently cranial quadrant due to the swollen pancreas), and
elevated in naturally occurring pancreatitis (poor localized dilation of loops of intestine (due to
sensitivity). ileus).
– Serum amylase levels may be elevated by dehy-
Abdominal ultrasonography is more useful than radi-
dration, and amylase and lipase levels may be
ography. Ideally high-resolution equipment should be
elevated by renal failure. An elevated lipase
used. (Abdominal ultrasonography, fTLI and fPLI are
level in the presence of normal renal function is
the best non-invasive tests for pancreatitis.)
probably highly specific for pancreatitis.
● Normal findings do not rule out pancreatitis
– There may be a greater likelihood of detecting
(reported sensitivity is 11–80%).
an elevated lipase level if measured immediately
● Abnormalities with a high specificity for pancre-
after the onset of clinical signs.
atitis include pancreatic regular or irregular
– In one model of experimental pancreatitis, amy-
enlargement, pancreatic hypoechogenicity, hypere-
lase levels actually decreased from baseline val-
chogenicity of peripancreatic fat (may be difficult
ues during the first week of illness.
to appreciate), dilation of the pancreatic duct in the
– Decreased lipase level usually rules out pancre-
left lobe and accumulation of peritoneal fluid
atitis in the dog; it is not known if this is also true
around the pancreas. Less specific changes include
for the cat.
dilated common bile duct and gall bladder, cranial
– The utility of measuring amylase and lipase in
abdominal mass effect, generalized peritoneal effu-
peritoneal effusion has not been evaluated in
sion and mesenteric lymphadenopathy. If a
clinical cases.
pancreatic mass is identified, it is most likely a neo-
● A more useful laboratory test is feline trypsin-like
plasm, followed by a pseudocyst. Pancreatic abscesses
immunoreactivity (fTLI).
are rare. Hepatic parenchymal and gastrointestinal
– fTLI is a more sensitive test than amylase or
changes may also be present because of associated
lipase for pancreatitis, but a normal value does
conditions.
not rule out pancreatitis.
● CT-scanning has low sensitivity. The diagnostic util-

severe in acute renal failure and will not normalize
ity of magnetic resonance imaging is not known.
with rehydration. Acute renal failure may be a com-
Some cases have had no changes.
plication of acute pancreatitis.
Thoracic radiographs should be obtained in dyspneic
Liver disease.
cats to rule out pleural effusion, which may be caused
● Elevations in liver enzymes, bilirubin and choles-
by pancreatitis. Dyspnea may rarely be due to pul-
terol may characterize both pancreatitis and liver
monary thromboembolism.
diseases. Furthermore, hepatic lipidosis and cholan-
Definitive ante-mortem diagnosis requires biopsy giohepatitis are common concurrent disorders with
obtained by exploratory laparotomy or laparoscopy. acute pancreatitis. It is often difficult to establish if
The pancreas may appear grossly normal (or show only one disorder preceded the other, and to establish if
nodular hyperplasia in the older cat). one is more responsible for clinical signs. Moderate
to marked liver enzyme elevations are suggestive of
A cat with pancreatitis may be a poor anesthetic risk.
primary hepatic disease, and a disproportionate ele-
Acute exacerbation of pancreatitis occasionally occurs
vation of ALP compared to ALT and GGT is sug-
following biopsy.
gestive of hepatic lipidosis. Elevations in serum bile
Inflammation may be irregularly distributed in dogs acids in the absence of cholestasis confirm the pres-
and multiple biopsies are recommended; the situation ence of hepatocellular dysfunction. Elevated
may be the same in cats. plasma ammonia levels are diagnostic for hepatic
encephalopathy. Marked coagulation abnormalities
Ultrasound-guided fine-needle aspiration may be
are suggestive of liver disease. Abdominal ultra-
used to biopsy pancreatic masses. Amylase and lipase
sound examination of cats with liver disease is rec-
should be measured in cystic fluid – levels above
ommended in an effort to detect pancreatitis. If
serum levels support a diagnosis of pseudocyst; lev-
laparotomy is performed to obtain a liver biopsy,
els equivalent to serum levels do not rule out a
then a pancreatic biopsy should also be obtained,
pseudocyst.
and vice versa.
Diabetic ketoacidosis (DKA).
● Confirmation of DKA requires demonstration of
Acute anemia. hyperglycemia, ketonuria or ketonemia, and
● Some cats with acute pancreatitis will have pale acidosis. DKA may be confused with pancreatitis
mucous membranes from shock. Routine haema- because urine test strips measure oxaloacetate or
tology will confirm severe anemia. Anemia is usu- acetone, which may be produced in minimal quan-
ally only mild in pancreatitis. tities by cats, and cats with pancreatitis may be
hyperglycemic. Several drops of hydrogen perox-
Urethral obstruction.
ide may be added to the urine sample in an effort
● A painful turgid bladder is palpable. Rarely the
to convert β-hydroxybutyrate to oxaloacetate to
obstruction has spontaneously resolved by the time
increase the concentration of oxaloacetate in
the cat is presented for examination. In the latter
urine. Alternatively, β-hydroxybutyrate may be
case, diagnosis is established by history, prepucial
measured in serum using a point-of-care test, or
crystal deposits, urinalysis and azotemia.
the urine test strip may be used to detect oxaloac-
Acute renal failure. etate in heparinized plasma. Using a standard
● Both acute renal failure and pancreatitis may urine test strip, a negative plasma test rules out
cause depression, anorexia, dehydration, vomiting, ketosis, and a positive urine test rules in ketosis,
azotemia and reduced urine production. In acute in cats. It should be remembered that acute pan-
renal failure urine will be isosthenuric to minimally creatitis and DKA may occur concurrently. Acute
concentrated, while in acute pancreatitis urine pancreatitis, DKA and hypoglycemia should
should be well-concentrated, unless there is pre- always be considered in an acutely depressed dia-
existing chronic renal failure. Azotemia is more betic cat.
Hypoglycemia. Severe sepsis without an externally obvious source

● Cats with acute pancreatitis may be hypoglycemic, of infection.
but it is not known if this contributes to depression. ● Septic cats may not have a fever. Meticulous phys-
Clinical hypoglycemia usually results from insulin ical examination, serum, chemistries, diagnostic
overdose. This is confirmed by measuring blood imaging and fine-needle aspiration will help local-
glucose levels and by prompt resolution of clinical ize the infection (e.g. deep subcutaneous abscess,
signs following intravenous dextrose or intramus- pyometra, pyelonephritis, peritonitis, pyothorax,
cular glucagon. Portable glucose meters have a ten- pneumonia).
dency to measure falsely low values, so a diagnosis
Toxoplasmosis.
of hypoglycemia should be reconsidered if the cat
● Acute systemic toxoplasmosis typically affects kit-
does not respond to intravenous glucose or
tens or immunosuppressed cats, causes a fever,
glucagon. Lack of response to sugar solutions
and uveitis is a common finding. Confirmation is by
rubbed on the gums or given by stomach tube does
measuring serum IgM antibodies or demonstrating
not rule out hypoglycemia, because most absorp-
rising serum IgG antibodies.
tion of glucose occurs in the small intestine.
Ethylene glycol poisoning.
Acute gastritis/gastroenteritis.
● The diagnosis of acute poisoning relies on history
● This is a differential diagnosis for cats with pancre-
of ingestion or a high index of suspicion. Both cats
atitis that are vomiting. Indeed, some cases diag-
with pancreatitis and cats with acute ethylene gly-
nosed with acute gastritis probably have acute
col poisoning may have acute depression without
pancreatitis. If signs are mild, then distinguishing
other signs, but cats with acute ethylene glycol
the two diseases is not important, because both are
poisoning should be isosthenuric, while cats with
similarly treated (short-term withholding of food
pancreatitis should have well-concentrated urine,
and fluid therapy). The most useful test for distin-
unless there is a concurrent disorder causing dilute
guishing the two is abdominal ultrasound examina-
urine, such as chronic renal failure. Metabolic aci-
tion. Abdominal radiography will help rule out
dosis, increased anion gap and increased osmolal
foreign material and obstruction as a cause of acute
gap will be more severe than in pancreatitis.
vomiting.
Definitive diagnosis relies on measuring ethylene
Acute heart failure. glycol in serum or urine or seeing oxalate crystals
● Potential overlapping signs of acute heart failure in urine or in a kidney biopsy.
and pancreatitis include pale mucus membranes, ● In the later stage of poisoning (renal failure), kid-
hypothermia, weak pulses, tachycardia, bradycar- neys may be firm and painful on palpation, and the
dia, dyspnea and vomiting. Clinical findings of a bladder is usually small because of anuria. The ele-
heart murmur, irregular heart rate, and pulmonary vations in urea and creatinine will be marked.
crackles, and radiographic findings of pulmonary
Lily poisoning.
edema and cardiomegaly help establish the diagno-
● The diagnosis of acute poisoning relies on history
sis of heart failure. (Note that both heart failure and
of ingestion or a high index of suspicion. Cats in the
pancreatitis may be associated with pleural effu-
acute stage of lily poisoning should have poorly
sion.) Definitive diagnosis of cardiomyopathy
concentrated urine, while cats with pancreatitis
requires echocardiography.
should have well-concentrated urine, unless there is
Panleukopenia. a concurrent disorder causing dilute urine, such as
● Severe panleukopenia usually affects immature chronic renal failure.
cats while pancreatitis usually affects mature cats. ● In the later stage of poisoning (renal failure), kid-
A complete blood count will usually reveal severe neys may be firm and painful on palpation, and
neutropenia. Depression and vomiting are early the bladder is usually small because of anuria.
signs. Marked diarrhea typically develops later, The elevations in urea and creatinine will be
but may not be evident at the time of presentation. marked.
Acetaminophen (paracetamol) poisoning. The remainder of therapy is largely supportive.

● Probing for a history of ingestion, and careful
Fluid therapy to correct dehydration and hypotension.
observation for appearance of brown mucous
● If crystalloid solutions are insufficient, or pul-
membranes, and facial and paw edema, will
monary or peripheral edema is present, colloid
establish the diagnosis.
solutions should be considered (e.g. plasma, dex-
Anticoagulant rodenticide poisoning. trans, hetastarch, pentastarch).
● A careful search for subcutaneous or internal
Nutritional support.
bleeding will help establish that a bleeding disorder
● The optimal approach is not known. The tendency
is present. Clotting times are likely to be normal to
to withhold food based on treatment of acute pan-
minimally elevated in acute pancreatitis, and
creatitis in dogs is tempered by the overlap between
markedly prolonged in rodenticide poisoning. Note
acute and chronic pancreatitis in cats, the presence
that markedly prolonged clotting times and vitamin K
and risk of hepatic lipidosis in cats, the observation
deficiency have been recognized in chronic pancre-
that most cats are not vomiting, and the observation
atitis.
that feeding does not appear to aggravate pancreati-
Snake bite envenomation. tis in cats.
● A high index of suspicion should be maintained for ● Cats that are willing to eat should be fed. Food
cats at risk because of geographical location and should be withheld for 2–3 days for cats that are
season. For North American snakes with cytotox- vomiting. For anorexic cats that are not vomiting,
ins, a thorough physical examination should reveal an appetite stimulant may also be considered –
a bite wound; there may be associated tissue necro- these include cyproheptidine (may cause unusual
sis. For Australian snakes, acute onset of weakness behavior), intravenous diazepam and oral oxazepam
and depression are early findings. Dilated pupils at standard doses.
with slow or absent papillary light reflexes, ataxia ● Parenteral nutrition may be used if available,
and elevated creatine kinase concentration or evi- especially for cats that are vomiting.
dence of a bleeding tendency are frequent findings. ● If exploratory laparotomy is used to make a diagno-
Paresis may progress to flaccid paralysis. sis, a jejunal feeding tube should be placed. This
is best placed as a jejunostomy tube. Transpyloric
Trauma.
tubes may also be used, either threaded through a
● Subtle external signs of trauma include car grease
gastrostomy tube, or as a nasojejunostomy tube, but
on the fur, shorn nails, dried blood around the exter-
preliminary experience is that such tubes tend to
nal nares, blood seen on otoscopic examination,
back out into the stomach.
small scleral hemorrhages and lacerations on the
● If laparotomy is not performed, a gastrostomy or
ventral surface of the tongue.
esophagostomy tube may be placed once the cat
The above differential diagnoses are applicable to cats has stopped vomiting. Endoscopic placement of a
with acute onset of signs. Other than liver diseases, most transpyloric tube is difficult.
of the above differential diagnoses will not be applicable ● If it is desired to avoid anesthesia, a nasoesophageal
to cats with pancreatitis with a longer duration of clini- tube should be used.
cal signs and weight loss. For cats with pancreatitis and ● The optimal diet is not known. Low-protein, low-
subacute or chronic signs, the primary differential fat and high-carbohydrate diets are recommended
diagnoses are neoplasia, chronic renal failure, and for dogs, but may not be appropriate for cats,
inflammatory bowel disease. Concurrent diabetes mel- especially if there is concurrent diabetes melli-
litus may confuse the clinical picture. See The Thin, tus, and may not be sufficiently calorie-dense.
Inappetent Cat (page 355). Another problem is that the fat content on an
energy basis is not provided for many foods.
A food with a moderate fat content is a reason-
Treatment
able initial choice, which includes most commer-
Address the inciting cause if one is identified. cial cat foods.
● Supplemental B vitamins should be considered. laparotomy reveals abnormal pancreatic tissue. For
Specifically, cobalamin treatment should be given cats with a non-surgical presumptive diagnosis of pan-
(0.5–1 mg SC q 2–3 weeks) if serum level is low. creatitis, similar to dogs, surgery should be consid-
● Antiemetics. Metoclopramide, ondansetron, prochlor- ered if the cat is not improving with conservative
perazine and chlorpromazine given at standard management, if there are worsening pancreatic
doses may be used to control vomiting. The latter changes on ultrasound examination, or if peritoneal
two should not be given if the cat is hypotensive. effusion is an exudate, but there are no firm guidelines.
● Analgesics. Although many cats do not show evi- Closed therapeutic abdominal lavage may also be con-
dence of abdominal pain, it is likely present, and sidered if peritoneal effusion is an exudate. Therapeutic
may contribute to depression. Opioid analgesics abdominocentesis should be considered if there is
should be considered at standard doses. large-volume ascites, and it should definitely be per-
● Antibiotics are not indicated in most cases. formed if there is a problem secondary to a volume
Antibiotics are recommended if there is a marked effect (e.g. dyspnea from diaphragmatic compression),
inflammatory leukogram or fever (blood culture is but the benefit of the procedure on the course of the
recommended), or evidence of pancreatic infec- disease is not known.
tion on biopsy (pancreatic and liver biopsies
should be cultured). Empirical choices include
ampicillin, cefazolin and cefoxitin at standard Prognosis
doses.
The true prognosis is not known because of under-
● Corticosteroids should only be used if needed to
diagnosis, mortality due to concurrent disorders, and
treat a concurrent disorder (e.g. inflammatory
euthanasia because of the prevailing attitude that feline
bowel disease). They may be considered if the cat is
pancreatitis carries a poor prognosis. Prognosis is
presented in shock, but the value of such therapy
related to the severity of the pancreatitis.
has been overstated.
● Fresh-frozen plasma (10–20 ml/kg) has been Cats with mild acute pancreatitis probably have a
advocated in acute pancreatitis to replenish coagu- good prognosis, while cats with severe pancreatitis and
lation factors and anti-thrombin III consumed in an associated disorder have a poor prognosis. Chronic
DIC, and to replenish α-macroglobulins, which are pancreatitis may be subclinical.
involved in clearing pancreatic enzymes from the
In one series of 13 cats with acute pancreatitis and
circulation. There is no evidence of a beneficial
hepatic lipidosis, recovery rate was 20%, versus 50%
effect in humans, and there are too few reports in
for cats with hepatic lipidosis alone. In another series of
dogs or cats to make an assessment. Transfusions
40 cats with severe acute pancreatitis, all cats died or
are expensive, and any benefit is probably as a col-
were euthanized. Successful management of acute pan-
loid solution. (It should be noted that α-macroglob-
creatitis has been anecdotally reported and reported in
ulins and anti-thrombin III are stable in regular
individual case reports and small case series.
plasma. The main difference in regular plasma and
fresh-frozen plasma are the concentrations of factor
VIII and von Willebrand’s factor. Fresh-frozen
ACUTE RENAL FAILURE*
plasma is potentially more beneficial in DIC only if
the aPTT is prolonged.)
Classical signs
● Dopamine 5 μg/kg/min as a constant rate infusion
is beneficial in experimental acute pancreatitis ● Progressive depression and anorexia.
when given within the first 12 hours of injury, but ● Vomiting.
not after that time. Most cats with naturally occur- ● Polyuria, oliguria or anuria.
ring disease are presented after 12 hours, and it is
unknown if there is any benefit.
● Vitamin K – see The Bleeding Cat (page 499). Pathogenesis
Surgical debridement of grossly necrotic tissue and Acute renal failure is a syndrome characterized by an
abdominal lavage may be performed if a diagnostic abrupt reduction in glomerular filtration rate and result-
ant dysregulation of water, acid–base and electrolyte ● Intratubular obstruction from desquamated tubular
balance, and accumulation of uremic toxins. Acute epithelial cells.
renal failure may be non-oliguric (polyuric), oliguric or ● Tubular backleak, where filtrate leaks across the
anuric. injured tubular epithelium and is thus shunted
● Oliguria is defined as < 0.27 ml/kg/h, and anuria directly to the peritubular capillaries.
< 0.08 ml/kg/h and these definitions may be used ● Reduced glomerular permeability.
as guidelines for cats.
The central pathophysiologic event in acute renal fail- Clinical signs
ure is acute tubular necrosis. This is initiated by
The salient historical findings are acute depression
altered hemodynamics (ischemia), nephrotoxins or
and anorexia, which are progressive in nature. Most
miscellaneous primary renal diseases. In some cases
cats will vomit; diarrhea may also occur.
more than one mechanism is involved.
● Ischemia may be caused by hypotension (e.g. Physical examination findings are variable.
prolonged anesthesia, shock), thromboembolism Hypothermia typically develops within 24–48 hours
(e.g. cardiomyopathy), or acute hydronephrosis of the development of oliguria or anuria. Bradycardia
(e.g. prolonged urethral obstruction). may be present.
– Hemodynamically mediated acute renal failure ● Body condition is normal in a cat without pre-exist-
may be caused by the same factors that cause ing chronic renal failure or other disorder-promot-
pre-renal azotemia, but the reduced perfusion of ing weight loss.
the kidney is so profound that it leads to acute ● Renal size is normal to large in a cat without pre-
tubular necrosis. existing renal disease, and kidneys may be painful
● Nephrotoxins include ethylene glycol and lilies; mer- on palpation. Kidneys are likely to be small in cats
cury, lead and other heavy metals; aminoglycoside with chronic renal failure. Kidneys may also be
antibiotics and amphotericin B; NSAIDs, and enlarged in FIP, lymphoma, polycystic kidney dis-
cholecalciferol (vitamin D3) rodenticides. The ease, chronic hydronephrosis and amyloidosis, but
mechanism of NSAID nephrotoxicity is ischemia are not painful. It should be noted that hydration
from vasoconstriction. The chemotherapeutic status and the quantity of peri-renal fat affects renal
agents doxorubicin, epirubicin and carboplatin are size on palpation. Kidneys may feel larger upon
also nephrotoxic, although the clinical importance rehydration.
of this appears to be low. ● The bladder is small with oliguria and anuria,
● Primary renal diseases do not commonly cause may be large with polyuria, and is large and turgid
acute renal failure in the cat. Glomerulonephritis, with urethral obstruction. Owners should be
amyloidosis, feline infectious peritonitis, bacterial queried as to when the cat was last seen to urinate.
pyelonephritis and bilateral renal lymphoma may ● Halitosis and oral ulceration and dehydration are
cause renal failure with a more acute clinical course common findings.
than typical chronic renal failure due to age-related
chronic tubulointerstitial disease, but true acute
Diagnosis
renal failure is rare. It is most likely to occur with
acute bacterial pyelonephritis. Acute exacerbation The diagnosis of acute renal failure is based on:
of chronic renal failure (“acute on chronic renal ● Acute onset of clinical signs.
failure”) may also occur; the mechanism in most ● Elevated serum urea, creatinine and phosphorus
cases is probably ischemia. levels.
● Increased (polyuria), or reduced (oliguria/anuria)
Acute oliguric renal failure is classically divided into
production of inappropriately concentrated
initiation, oliguric, polyuric and recovery stages.
urine.
The oliguric stage is maintained by various factors, – In cats with pre-renal azotemia, urine specific
including: gravity should be > 1.035 unless there is another
● Arteriolar vasoconstriction. mechanism present for reducing specific gravity
(e.g. therapy with a diuretic). In acute renal Other variable serum biochemistry abnormalities
failure, urine is usually isosthenuric or mini- include hyperglycemia, hyperkalemia, hyponatremia,
mally concentrated. Some cats with chronic hypocalcemia and decreased bicarbonate (total CO2).
renal failure maintain adequate urine concentrat-
Other variable urinalysis findings include glucosuria,
ing ability, but this does not appear to happen in
proteinuria, tubular casts, crystaluria, pyuria and bac-
acute renal failure.
teruria.
– If urine specific gravity was not measured prior
to initiating fluid therapy, monitoring serum bio- Diagnostic imaging of the kidneys, urinalysis, urine
chemistry abnormalities will help in distinguish- culture and kidney biopsy may be needed to rule in and
ing pre-renal from renal azotemia. If azotemia is rule out causes of renal failure. See Ethylene glycol
pre-renal in origin, it will normalize within poisoning and Lily poisoning, below.
24–48 hours upon rehydration and/or correc- ● Renal biopsy may also help determine the severity
tion of hypotension, whereas renal azotemia will and reversibility of the injury, but there is poor
remain elevated during this period (although it correlation between histopathologic findings and
may improve). renal function.
– In animals with pre-renal azotemia, urine pro-
duction will increase as the animal becomes
rehydrated and/or hypotension is corrected. The
volume of urine produced and time to do so will
depend on the rate of fluids. Because these ani- Pre-renal azotemia and reduced urine production.
mals are usually acutely dehydrated, rehydration Causes of acute depression, anorexia, dehydration and
is typically performed quickly, so within a few vomiting may cause pre-renal azotemia and reduced
hours urine production is expected. A method to urine production. These causes include acute gastritis,
rapidly detect oliguria or anuria is to give gastroenteritis and pancreatitis. In acute renal failure,
a 10 ml/kg bolus of intravenous fluids over 10 urine will be isosthenuric to minimally concentrated,
minutes. This should cause sufficient volume while in the other disorders urine should be well-
expansion and increase in blood pressure to ini- concentrated, unless there is pre-existing chronic
tiate urine production within 10–30 minutes. If renal failure. Azotemia is more severe in acute renal
there is no urine produced after 30 minutes, failure and will not normalize with rehydration. Acute
another fluid bolus may be considered. If there renal failure may be a complication of a primary dis-
is no urine production after two fluid boluses, order, due to the progression from pre-renal to renal
then it is likely that intrinsic oliguric renal fail- azotemia.
ure is present. Ideally blood pressure should be
Pre-renal azotemia and increased urine production.
measured to confirm that reduced urine produc-
● Both acute renal failure and diabetic ketoacidosis
tion is not due to persistent hypotension that is
may cause acute depression, polyuria, vomiting,
still causing pre-renal azotemia. A normotensive
dehydration, hyperglycemia and glucosuria, and
cat receiving maintenance fluid therapy should
both may be preceded by a history of chronic
produce urine at 0.5–2 ml/kg/h.
polyuria and polydipsia (due to chronic renal failure
– The diagnosis of acute oliguric/anuric renal fail-
and diabetes mellitus, respectively). Diabetic
ure is usually straightforward. Acute non-oliguric
ketoacidosis is confirmed by detecting ketones in
renal failure is more difficult to distinguish from
the blood or urine. Acute renal failure is also an
subacute chronic renal failure and acute-on-
uncommon complication of diabetic ketoacidosis.
chronic renal failure.
Cats with diabetic ketoacidosis may have concur-
A hemogram typically reveals hemoconcentration and rent chronic renal failure.
a stress leukogram. Cats with acute-on-chronic renal ● Other disorders that cause polyuria and polydipsia
failure may have anemia, and this finding is highly in the cat include hyperthyroidism (common), and
suggestive of pre-existing chronic renal failure. The hepatic encephalopathy and central diabetes
anemia may not be evident until the cat is rehydrated. insipidus (rare) (see The Cat With Polyuria and
Polydipsia, page 231). Dehydrated animals with Monitor for changes in respiratory pattern and
such a condition will appear to be in renal failure auscultate lungs frequently for evidence of pul-
because of concurrent azotemia and poorly concen- monary edema. Observe extremities and inter-
trated urine (SG < 1.035). mandibular space for subcutaneous edema.
● Cats with hypovolemia from hypoadrenocorticism ● Normal saline, lactated Ringer’s or other balanced
may also present with pre-renal azotemia, hyper- electrolyte solutions.
phosphatemia and poorly concentrated urine. – Rehydration. The goal of initial fluid therapy is
to correct dehydration and achieve 3–5% vol-
Post-renal azotemia. The conditions will result in
ume expansion. Replace fluid deficits over 4–6
azotemia, hyperkalemia and reduced urination.
hours. An initial fluid bolus may be given in an
● Urethral obstruction. A painful turgid bladder is
effort to overcome renal arteriolar vasoconstric-
palpable. Rarely the obstruction has spontaneously
tion. Use 10 ml/kg over 10 minutes in cats with
resolved by the time the cat is presented for exami-
anuria or rapidly progressive oliguria, and 7–10
nation. In the latter case, diagnosis is established by
ml/kg/h for 4–6 hours if there is increased
history, preputial crystal deposits, urinalysis and
concern for pulmonary edema or oliguria is less
azotemia. Note that prolonged urethral obstruction
severe.
may rarely lead to acute renal failure.
● Ruptured bladder. The bladder is not palpable or, The goal of fluid therapy after rehydration is to main-
rarely, is palpable but small, and abdominal fluid is tain 3–5% volume expansion above normal hydra-
present. Creatinine or potassium concentrations tion. More aggressive fluid therapy will not “flush out”
higher in the abdominal fluid than that of serum are or “open up” the kidneys, and overzealous treatment
strongly suggestive of uroperitoneum. A ruptured will result in pulmonary edema. Fluid rate must be
bladder may be confirmed by a positive contrast adjusted based on body weight, central venous pres-
cystogram. See page 464, The Cat With Abdominal sure, PCV and total protein levels and urine output.
Distention or Abdominal Fluid. ● In cats with anuria or oliguria, place a urinary
catheter and attach to a closed collection bag.
Always palpate the bladder whenever checking
Treatment
urine production because the catheter may kink.
Remove or correct the primary cause. Avoid any The urine should be cultured periodically to
nephrotoxic drugs. monitor for urinary tract infection.
● In cats with polyuria, while a urinary catheter may
Administer intravenous fluid therapy.
be used, frequent palpation of the bladder and meas-
● Weigh the cat prior to fluid therapy and monitor
urement of voided urine by weighing the litter pan is
weight throughout treatment. Weight is one of the
usually adequate to estimate urine production.
most important markers of hydration status. Daily
weight loss of 0.5–1% is expected in anorexic Monitor electrolytes and acid–base status (initially
animals, and this should be taken into account three times daily) and adjust fluids accordingly.
when judging hydration based on weight. ● Hyperkalemia is a potentially life-threatening
● Establish a jugular catheter if possible. This will complication of acute renal failure. Signs of signif-
facilitate fluid therapy, repetitive blood sampling icant hyperkalemia include bradycardia and weak-
and measurement of central venous pressure. ness, which may progress to shock and a moribund
– If direct measurement of central venous pressure state. ECG findings include loss of P waves, spiked
is not possible, observe the jugular veins. T waves, and shortened Q–T interval.
Progressive distention of these veins and/or ● Mild hyperkalemia (above reference range to 6.5
increase in the jugular pulse indicates rising cen- mEq/L) may not require immediate treatment. If no
tral venous pressure. The medial saphenous clinical signs are present, one or more of the fol-
veins may also be observed while the hind legs lowing treatments will usually suffice: reducing
are raised and lowered. Decreased emptying potassium concentration in the fluids, changing flu-
and increased refilling of the medial saphe- ids to a more alkalinizing fluid, adding 5% dextrose
nous veins indicates volume expansion. to the fluids, and furosemide (see below).
● Moderate hyperkalemia (6.5–8.0 mEq/L) should

it is best used in conjunction with insulin to min-
always be treated promptly.
imize exacerbation of hyperosmolality.
● Severe hyperkalemia (> 8.0 mEq/L) may be life-
– Enhance potassium secretion. Give furosemide
threatening and usually requires aggressive treat-
as discussed below. This may be used in the
ment. The higher the potassium level and the worse
management of mild hyperkalemia, or subse-
the clinical signs, the more rapid and aggressive
quent to emergency management of moderate to
should be the treatment. Treatments include:
severe hyperkalemia, but it will not act rapidly
– Dilution of potassium concentration by rapid
enough to correct hyperkalemia that is causing
infusion of intravenous fluids (60 ml/kg/h).
clinical signs, especially in the presence of olig-
Potassium-free solutions have the most dilu-
uria or anuria where the drug may not promote
tional effect. Saline is beneficial for this reason
urine production.
although it is acidifying. Note that life-threaten-
ing hyperkalemia in acute renal failure is most Diuretics.
likely to occur in anuric animals, which may not – If anuria or oliguria persists after fluid
tolerate a large fluid bolus. replacement, administer furosemide 2 mg/kg.
– Protect the heart against the membrane effects If diuresis does not occur within 30 minutes,
of hyperkalemia with 10% calcium gluconate, repeat once. Furosemide will not improve
0.5–1.0 ml/kg IV, over 5–15 minutes. This glomerular filtration rate, but diuresis may
should be given if there is a life-threatening reduce tubular blockage and tubular back-
arrhythmia. Monitor the ECG during therapy. leak, and a polyuric animal is easier to manage
– Translocate potassium from the blood into the than an oliguric one. If diuresis does occur, treat-
intracellular fluid. Usually only one of the fol- ment may be given two to three times a day if
lowing treatments is necessary. needed to maintain diuresis. Fluid requirements
– NaHCO3, 0.5 mEq/kg IV over 5 minutes, fol- will be increased. Constant-rate infusions of
lowed by another 0.5 mEq/kg over the next furosemide have been used in the management
30–60 minutes. This treatment is best reserved of acute renal failure in dogs but there is limited
for cats with HCO3− or total CO2 < 12 mmol/L, experience with cats. Constant rate infusions of
if measurements are available. furosemide at 0.25 mg/kg/h have been used in
– Dextrose: Severe hyperkalemia or moderate the management of congestive heart failure in
hyperkalemia with clinical signs – give 50% dex- cats and may be considered in the management
trose, 1.0–2.0 ml/kg IV (ideally diluted 1:1 with of acute renal failure.
sterile water or saline), over 30–60 minutes. ● Osmotic diuretics.
Moderate hyperkalemia without clinical signs – – If furosemide fails to induce a diuresis, con-
add 5–10% dextrose to the fluids (100–200 ml sider using 10–20% dextrose as an osmotic
50% dextrose/L). Monitor blood glucose. Note diuretic, 25–50 ml/kg over 1–2 hours. Monitor
that dextrose may also serve as a diuretic. urine for glucosuria indicating adequate dosage.
– Insulin-dextrose: regular insulin 0.1–0.5 units/kg Diuresis should occur within 60 minutes of com-
IV followed by 2–4 ml of 50% dextrose/unit of pleting infusion. If diuresis results, the treatment
insulin given (ideally diluted 1:1 with sterile may be repeated every 8–12 hours.
water or saline) and then followed by adding – Mannitol may also be used as an osmotic
2.5% dextrose to the fluids (50 ml of 50% dex- diuretic at a dose of 0.25–0.5 g/kg over 10 min-
trose/L of fluids). Monitor blood glucose. Note utes. Diuresis should occur within 60 minutes of
that NaHCO3 and dextrose should be avoided if completing infusion. If diuresis results, the treat-
effective serum osmolality is > 330 mOsm/kg. ment may be repeated every 4–6 hours. Mannitol
(Effective osmolality is calculated as [1.86(Na+ + is a more potent osmotic agent than dextrose, but
K+)] + glucose + 9, with all units in mmol/L.) If can only be eliminated by renal excretion, and
the cat is hyperosmolar and dehydrated, increase carries a higher risk of causing pulmonary
the fluid rate. If dextrose therapy is needed, then edema.
– Osmotic diuretics should not be used in the Opioid analgesics should be considered at standard
presence of hyperosmolality (e.g. ethylene gly- doses for cats with swollen and painful kidneys or oral
col poisoning, diabetic ketoacidosis), dehydra- ulceration.
tion or overhydration.
Peritoneal dialysis, pleural dialysis, hemodialysis or
Monitor urea, creatinine and phosphorus levels (ini- transplantation should be considered for cats with
tially once daily). anuria or severe oliguria.
● A rapid fall in serum urea and creatinine levels
in the first 24–48 hours of fluid therapy indicates
Prognosis
that there was a substantial pre-renal component
to azotemia. Mild decreases in urea and creatinine There are few reports of acute renal failure in cats due
levels during the following week are usually due to to causes other than ethylene glycol or lily poisoning
mild ongoing volume expansion and the cat should (see below). Most cats with hemodynamically medi-
be watched closely for over-hydration. Decreases ated non-oliguric acute renal failure and cats with
in urea and creatinine levels due to improved pyelonephritis will probably recover with appropriate
renal function usually take 10–14 days to appear. critical care, but may have residual or worsened
After renal function improves and then stabilizes, chronic renal failure. In general, the prognosis for
fluids may be tapered. Urea and creatinine levels non-oliguric renal failure is better than for oliguric or
will rise when fluids are tapered. anuric renal failure. Without dialysis, the prognosis is
typically considered poor if there is persistent olig-
Obtain minimum blood sample sizes. Frequent blood
uria or anuria.
sampling may lead to anemia and hypoproteinemia that
will affect use of PCV and total protein values to moni-
tor hydration. Anemia may require correction by trans- Prevention
fusion.
Minimize prolonged renal hypoperfusion. Correct fluid
Dopamine is not recommended as its effects are uncer- deficits and hypotension promptly in cats with chronic
tain in cats and its benefit in acute renal failure in renal failure.
humans is being questioned.
Begin intravenous fluids preoperatively in elderly cats
Antiemetics. Prochlorperazine, chlorpromazine, undergoing surgery, to prevent acute exacerbation of
yohimbine, metoclopramide and ondansetron may be chronic renal failure.
used to control vomiting. Metoclopramide is a less
Minimize exposure to ethylene glycol and lilies. Use
effective antiemetic in the cat than in the dog. It is elim-
aminoglycosides and other nephrotoxic drugs judi-
inated via the kidney so an initial dose of 0.2 mg/kg, SC,
ciously and avoid in elderly cats and in cats with
twice daily is recommended (dose range 0.2–0.5 mg/kg
three times a day). It may also be given by constant rate
infusion at a dose of 0.005–0.02 mg/kg/h (lower end of
the range recommended initially). Prochlorperazine and
ACUTE POISONING AND EVENOMATION*
chlorpromazine may cause hypotension.
Gastrointestinal protectants. Ranitidine and famoti- Classical signs
dine (H2 blockers) are eliminated via the kidney (about
● Acute depression.
2/3–3/4 of the dose) so an initial dose of 0.5 mg/kg IV
● Other specific signs: weakness, tremor, GIT
once daily is recommended. Sulcralfate 0.25–0.5 g PO
signs.
three times a day may be used if it does not increase
vomiting.
Nutritional support. This may include nasoesophageal With Salivation) and page 481 (The Bleeding Cat) and
or esophageal feeding in cats that are not vomiting, page 381 (The Pyrexic Cat), page 812 (The Cat With
and parenteral nutrition. Seizures, Circling and/or Changed Behavior for
bromethalin, lead, methaldehyde, strychnine, organo- sion). Chlorpyrifos may cause a delayed toxicosis
phosphates, carbamates, organochlorines, pyrethrins, characterized by cervical ventroflexion and marked
pyrethroids), page 833 (The Cat With Stupor or Coma for hind limb ataxia.
lead), page 850 (The Cat With a Head Tilt, Vestibular ● Pyrethrins, pyrethroids (phenothrin, etofenprox,
Ataxia or Nystagmus for blue-tailed lizard), page 861 and especially permethrin) and rotenone: signs
(The Cat With Tremor or Twitching for hexachlorophene, include hypersalivation, vomiting and agitation from
organophosphate) and pages 947, 950 (The Cat With oral irritation and tremors, ataxia, and seizures from
Generalized Weakness for OP, snakes, spiders, ticks). systemic toxicoses.
● Organochlorines (e.g. lindane): signs include
ataxia, tremors and seizures.
Clinical signs
Slug and snail bait.
Acute depression and anorexia are signs of most poi- ● Metaldehyde: signs include hypersalivation, vom-
sonings and envenomations and are not listed with every iting, diarrhea, tachycardia, polypnea, mydriasis,
poison below. Other common signs include hypersaliva- ataxia, excitability, hyperesthesia and marked mus-
tion, vomiting, diarrhea, polypnea, arrhythmias, pale cle tremors progressing to convulsions, with result-
mucous membranes, hypothermia, tremors (which may ant hyperthermia.
cause hyperthermia), excitability, agitation and other
Analgesics.
behavior changes, seizures, and generalized weakness.
● Acetaminophen: signs include depression,
Rodenticides. anorexia, salivation, vomiting, abdominal pain,
● Anticoagulants: signs include pale mucous mem- polypnea, dark mucous membranes, edema of the
branes and signs referable to localized bleeding. face and paws, and dark discolored urine. See page
Acute depression may be the only initial sign of 595, The Cat With Salivation.
internal bleeding, occurring prior to pale mucous ● Aspirin: signs include hematemesis, melena,
membranes. See page 522, The Bleeding Cat. polypnea and fever.
● Cholecalciferol: signs include vomiting, diarrhea ● Ibuprofen and other non-selective NSAIDs: signs
and polydipsia. include depression, hematemesis, melena, diarrhea,
● Bromethalin: signs include mydriasis, paresis, abdominal pain, polydipsia (renal failure), and
tremors, hyperthermia, excitability and seizures. seizures and coma with very high doses.
● Strychnine: signs include muscle stiffness, extensor
Plants (partial list).
rigidity and opisthotonus, and tetanic seizures that may
● Lilies: signs are described in a separate heading below.
be initiated by physical, visual or auditory stimulation.
● Marijuana: signs include acute depression, ataxia,
Anthelmintics. hypothermia and polyphagia.
● Ivermectin: signs include tremors, abnormal ● Azaleas and oleander: signs include arrhyth-
behavior, ataxia, blindness, bradycardia, hypother- mias, shock and acute heart failure.
mia, seizures and coma. ● Daffodils: signs include vomiting, hypothermia,
● Piperazine: signs include weakness, tremors, hypotension and bradycardia.
ataxia, behavior changes, seizures and vomiting and ● Many other plants result in oropharyngeal and gas-
diarrhea. trointestinal irritation. English ivy (Hedera helix)
and Cyclamen species may cause severe, poten-
Insecticides.
tially life-threatening, vomiting (including
● Organophosphates and carbamates: signs vari-
hematemesis) and diarrhea.
ably include systemic parasympathetic (mus-
● Pine (water in Christmas tree reservoir): signs
carinic) signs (salivation, lacrimation, urination,
include vomiting, abdominal pain and icterus.
defecation, miosis, dyspnea, bradycardia); sympa-
thetic (ganglionic) signs (tachycardia, mydriasis); Heavy metals.
neuromuscular (nicotinic) signs (muscle stiffness, ● Lead: Anorexia may be the only sign. Other signs
tremors, weakness, paralysis); and CNS choliner- include vomiting, diarrhea, abdominal pain,
gic signs (hyperactivity, seizures, marked depres- excitability, seizures and blindness.
Miscellaneous. ● Toad poisoning: Bufo marinus (cane toad) is

● Ethylene glycol: signs are described in separate found mostly in South America, southeast
headings below. United States and Hawaii, and Australia. Bufo
– Venlafaxine is a human antidepressant medica- alvarius is found is the southwest United States
tion (serotonin and noradrenaline reuptake and northern Mexico. Signs of poisoning include
inhibitor). It is an emerging toxicosis in that it is profuse salivation, vomiting, arrhythmias,
one of the few human medications that cats vol- hindlimb weakness, a fixed trance-like stare and
untarily ingest. Clinical signs include vomiting, collapse.
polypnea, tachycardia, ataxia, mydriasis and agi- ● Poisonous lizards: Gila monster (Heloderma sus-
tation. pectum) and Mexican beaded lizard (Heloderma
– Glow-in-the-dark items contain dibutyl (n- horridum) are found in the southwest United States
butyl) phthalate as a luminescent. It is extremely and Mexico. Envenomation occurs during a tena-
unpalatable and when a cat bites into a glow-in- cious bite with chewing action. Signs of envenoma-
the-dark item it causes marked hypersalivation, tion include painful bite wound, salivation,
frothing, head-shaking, agitation, hyperactivity, lacrimation, urination, defecation, and loss of voice.
aggression and other behavioral changes. The Ingestion of a blue-tailed lizard skink (Eumece
luminescent is of low toxicity and a sufficient egregius) found in the southeast United States may
quantity to cause systemic toxicosis would not cause vestibular signs.
be ingested.
– Liquid potpourri causes poisoning when there
is accidental skin contact and the product is Diagnosis
licked off. The product may contain essential oils
History is often critical to the diagnosis of intoxica-
(irritants and central nervous system depres-
tion.
sants), and/or cationic detergents (corrosives)
that cause more severe signs. Cutaneous and oral Definitive diagnosis can be made by measuring poison-
cavity signs vary from erythema to ulceration. ous principles in vomitus, serum or urine.
Marked hyperthermia may accompany oral
Anticoagulant rodenticide: prolonged prothrombin,
inflammation and precede ulceration. Gastro-
activated partial thromboplastin times, and activated
intestinal signs include dysphagia (esophagitis)
clotting time.
and vomiting, hematemesis, melena, and abdom-
inal pain (gastritis). Esophageal and gastrointesti- Cholecalciferol rodenticide: hypercalcemia and
nal ulceration and perforation may occur. hyperphosphatemia.
Envenomation. Black widow spider (Latrodectus) envenomation:
● Tick bite paralysis: Cats do not appear to be marked elevation in creatinine kinase and aspartate
affected by North American ticks. Ixodes holocy- aminotransferase, and myoglobinuria.
clus in Australia causes rapidly progressive motor
weakness, megaesophagus, mydriasis, tach-
yarrhythmias and dyspnea (various causes).
● Spider bites: Latrodectus spp. (black widow spi- Other causes of acute depression are differential diag-
der in North America, red back spider in Australia) noses. Other differential diagnoses should be consid-
live in warm and temperature regions in all conti- ered for the more specific signs (e.g. hypocalcemia as a
nents. Cats are very sensitive to the venom. Signs of cause of tremors).
envenomation include loud vocalization from pain;
restlessness and polypnea; salivation, vomiting and
Treatment
diarrhea; and muscle tremors and spasms that
progress to flaccid paralysis. The most effective treatments vary with the toxin, and
● Wasp and bee stings: Local angioedema and pain consultation with a toxicology service is recom-
are common signs. Anaphylaxis is rare. mended.
Minimize further absorption (cutaneous and gas- Activated charcoal is an effective absorbent for
trointestinal decontamination). many poisons including vitamin K antagonist
● Bath the cat if there is poison on the skin (e.g. per- rodenticides, ethylene glycol, alkaloids, organophos-
methrin) phate and other insecticides, acetylsalicylic acid,
● Remove the source of the poison. NSAIDS and barbiturates. It is not effective with
● Irrigate oral cavity if there is poison in the mouth most caustic or corrosive agents.
(e.g. after mouthing a Bufo toad). If clinical signs ● Catharsis is used to promote elimination of the
are due to unpleasant taste or oral irritation (hyper- toxin in the stool. It should always be used follow-
salivation, agitation +/– vomiting) after milk or liq- ing the use of activated charcoal and should not be
uid from a can of tuna. used in the presence of diarrhea. Catharsis may
● Induction of emesis. Xylazine 0.44 mg/kg IM reli- have to be repeated every 4–6 hours as with
ably causes vomiting in 5–20 minutes. The effect activated charcoal. Catharsis using non-absorbed
can be reversed with yohimbine 0.1–0.5 mg/kg IV. salts or sugars will cause dehydration that must be
If xylazine is not available, or for induction of vom- addressed with fluid therapy.
iting at home, use fresh 3% hydrogen peroxide, – Salts: sodium sulfate (Glauber’s salts, pre-
2 ml/kg PO, or syrup of ipecac, 3–6 ml/kg diluted ferred) or magnesium sulfate (Epsom salts), 1/2
1:1 with water, PO or by gavage (i.e. via stomach level teaspoon per kg in 5–10 volumes of tepid
tube). Vomiting should occur within 10–30 min- water, by gavage. Magnesium sulfate may cause
utes. Hydrogen peroxide and syrup of ipecac treat- central nervous system depression, should not be
ments may be repeated once if the initial treatment repeated, and must be used cautiously in renal
is ineffective. failure. These salts are the preferred cathartics in
● Induction of emesis is absolutely contraindicated lead poisoning as lead will precipitate as unab-
in the presence of a caustic or volatile poison, sorbable lead sulfate.
impaired gag reflex, laryngeal paralysis, extreme – Sugars: sorbitol 70% solution (preferred) or
weakness or unconsciousness, and is relatively con- lactulose, 3 ml/kg. The most practical prod-
traindicated in the presence of seizures or dyspnea. uct to use in the non-specific treatment of poi-
● If induction of emesis is ineffective or con- soning is a commercial product that combines
traindicated, perform gastric lavage. Establish activated charcoal and sorbitol in a suspen-
light general anesthesia if the cat is not uncon- sion.
scious and place a cuffed endotracheal tube extend- – Colonic lavage (“high enema”), 20 ml/kg tepid
ing 2–3 cm beyond the teeth. Position the cat with water.
the head and thorax slightly lowered. Pass a tube
Enhance elimination.
the same size or slightly larger than the endotra-
● Diuresis. Diuresis will hasten renal elimination of a
cheal tube into the stomach, deliver 5–10 ml/kg
toxin only if it is reabsorbed by the renal tubules,
tepid water, and aspirate with a 60 ml syringe or
e.g. ethylene glycol. Diuresis may be achieved with
aspiration bulb. Repeat the procedure 10–15 times.
fluid therapy, furosemide, mannitol or dextrose (see
Kink the stomach tube as it is removed from the
Acute renal failure, page 282).
stomach. Addition of activated charcoal at the dose
● Ion trapping. A toxin must be unionized to be
below to the lavage solution will increase its effec-
reabsorbed by the renal tubules. Elimination of
tiveness.
acidic toxins (e.g. aspirin) may be hastened by
● Solid poisons (e.g. lead) may be removed by
alkalinizing the urine using sodium bicarbonate.
endoscopy or gastrotomy/enterotomy.
Elimination of alkaline toxins (e.g. strychnine)
● Absorption of remaining poison. Give a slurry of
may be hastened by acidifying the urine using
activated charcoal by gavage, 1–5 g/kg dissolved
saline or ammonium chloride.
in 3–5 ml of tepid water/g charcoal, after induction
● Peritoneal dialysis or hemodialysis.
of emesis or when gastric lavage is complete.
Treatment may need to be repeated every 4–6 hours Specific therapy.
for 2–3 days because the poison may return to the ● Anticoagulant rodenticide – vitamin K (see page 509,
intestinal tract by enterohepatic circulation. The Bleeding Cat).
● Cholecalciferol rodenticide – treatment of hyper- It tastes sweet to humans, and is palatable to cats. The
calcemia (saline, furosemide, calcitonin, pred- minimum lethal dose of undiluted ethylene glycol in
nisone, ± biphosphonates). cats is only 1.4 ml/kg.
● Organophosphates and carbamates – atropine
Ethylene glycol is rapidly absorbed from the intes-
(both), pralidoxime chloride (organophosphates
tinal tract.
only).
● Peak plasma concentration is achieved 1 hour
● Acetaminophen – acetylcysteine, ascorbic acid,
post ingestion in a fasted cat. Food probably delays
transfusion (see page 596, The Cat With Salivation).
peak plasma concentrations, but by at most 1–2
● Aspirin and NSAIDs – Treatment of gastric ulcera-
hours.
tion (H2 blockers, sulcralfate), treatment of acute
renal injury with fluids. Following absorption, ethylene glycol is excreted
● Lilies – see separate heading below. about 50% unchanged in the urine (peak urine con-
● Lead – CaNa2EDTA, D-penicillamine (contraindi- centration is achieved at 6 hours). Some passive reab-
cated if lead present in intestinal tract), succimer sorption occurs in the distal convoluted tubules and
(preferred treatment). collecting ducts. The other 50% is metabolized in
● Ethylene glycol – see separate heading below. the liver by alcohol dehydrogenase to glycoaldehyde,
● Venlafaxine – cyproheptadine 2–4 mg/cat PO or per which in turn is metabolized by aldehyde dehydroge-
rectum may counteract serotonin effects. nase to glycolic acid. Glycolic acid is further metabo-
● Ixodid tick paralysis and Lactrodectus spider lized to glyoxylic acid, which is then metabolized to
bites – specific antivenin (see pages 954, 975, The final metabolites including oxalic acid. Oxalic acid
Cat With Generalized Weakness). combines with calcium to form calcium oxalate crys-
tals. The serum half-life of ethylene glycol in
Treat arrhythmias, e.g. atropine for daffodil-induced
untreated cats is 2–5 hours.
bradycardia (see page 160, The Cat With Tachycardia,
● Acute tubular necrosis is caused by cytotoxic effects
Bradycardia or an Irregular Rhythm).
of glycolic, glyoxalic and oxalic acids. Deposition
Treat tremors and seizures – diazepam, methocarbamol, of crystals in the kidneys has a minor role.
phenobarbital, pentobarbital (see page 801, The Cat
With Seizures, Circling, and/or Changed Behavior).
Beware of hypothermia following correction of hyperther- Clinical signs
mia, which may cause renewed tremors.
Signs of acute ethylene glycol poisoning (<12 hours)
Treat agitation – consider acepromazine (ensure cat is are due to direct effects of the poison and metabolites
not hypotensive). on the central nervous system and gastrointestinal
tract, and include depression, ataxia, tremors, vom-
Supportive care.
iting, and a sweet odor to the breath. Polyuria
occurs due to osmotic diuresis. Polydipsia is uncom-
mon in cats.
ETHYLENE GLYCOL POISONING*
Later signs (> 12 hours) are due to acute renal failure
Classical signs and include progressive depression, anorexia, oral ulcer-
ation, hypothermia, painful and swollen kidneys,
● Acute depression and anorexia. seizures, oliguria and anuria.
Pathogenesis
Diagnosis
Ethylene glycol is a solvent used in paints, polishes,
inks and antifreeze, which is the most common source The diagnosis of acute poisoning relies on history of
of poisoning. It is a colorless liquid – the yellow-green ingestion or a high index of suspicion.
appearance of antifreeze is due to the addition of fluo- ● Acute ethylene glycol poisoning should be consid-
rescein. ered in any cat at risk with acute depression.

A hemogram typically reveals hemoconcentration and

a stress leukogram.
Both ethylene glycol and lily intoxication cause acute
A serum biochemistry profile will reveal decreased
depression and acute renal failure. The laboratory fea-
bicarbonate (total CO2) and an increased anion gap.
tures of lily poisoning have not been as well character-
Blood gases, if available, will reveal severe metabolic
ized as those of ethylene glycol poisoning therefore it is
acidosis with or without partial respiratory compensa-
difficult to use these to differentiate the two poisonings.
tion. Measured osmolality, if available, will be
Ethylene glycol poisoning is more likely in outdoor
increased in parallel with ethylene glycol concentra-
cats and lily poisoning in indoor cats. Vomiting is
tion, resulting in an increased osmolal gap. Other vari-
more consistent in lily poisoning and there is evidence
able findings are hyperglycemia (stress and reduced
of plants being chewed. Detectable serum or urine con-
metabolism by aldehydes), hypocalcemia (chelation
centrations of ethylene glycol, oxalate crystalluria,
by oxalic acid), and hypophosphatemia (binding by
and oxalates on kidney biopsy are diagnostic for
rust-inhibitors in antifreeze). In the later stage of poi-
ethylene glycol poisoning. If these findings are absent,
soning serum chemistry findings are typical of acute
other causes of acute renal failure must be ruled out.
renal failure.
● Both cats with pancreatitis and cats with acute
Urinalysis will reveal persistent isosthenuria to mini- ethylene glycol poisoning may have acute depression
mally concentrated urine and aciduria within 3 hours with or without vomiting, but cats with acute ethylene
of ingestion. Oxalate crystals are usually present at glycol poisoning will be isosthenuric, while cats with
some point during the acute phase of intoxication, and acute pancreatitis should have well-concentrated
may appear as early as 3 hours. Glucosuria and pro- urine. Azotemia, metabolic acidosis, increased anion
teinuria may be present. A Wood’s lamp may be used gap and increased osmolal gap will be more severe
in an effort to detect fluorescence from fluorescein in than in pancreatitis. Definitive diagnosis relies on
stomach contents and on the muzzle and paws. measuring ethylene glycol in serum or urine or seeing
However numerous products contain fluorescents and oxalate crystals in urine or a kidney biopsy.
absence of fluorescence does not rule-out exposure, so ● Both ethylene glycol poisoning and diabetic ketoaci-
the diagnostic utility of fluorescence may be limited. dosis may cause acute depression, polyuria, vomit-
Similarly examination of urine for fluorescence is ing, dehydration, hyperglycemia, azotemia, increased
likely of limited values as cat’s urine normally fluo- anion gap metabolic acidosis, and increased osmolal-
resces and a potential increase in fluorescence from a ity. The former is confirmed by detecting ethylene
small amount of excreted fluorescein may be difficult glycol in serum or oxalate crystals and the latter by
to detect. detecting ketones in the blood or urine. Ethylene
glycol poisoning invariably causes acute renal failure
Definitive diagnosis can be made by measuring ethyl-
(unless treated within 3 hours), while acute renal fail-
ene glycol in serum or urine, but cats are very
ure is an uncommon complication of diabetic ketoaci-
sensitive to ethylene glycol poisoning and may
dosis, although cats with diabetic ketoacidosis may
develop signs at concentrations below that detected
have concurrent chronic renal failure.
by the assays. Serum is preferred because concentra-
tion of the poison is higher than in urine. Ethylene Ethanol ingestion may cause depression, polyuria,
glycol is usually not detectable in serum or urine after ataxia and increased osmolality. Diagnosis relies on
72 hours. Propylene glycol (present in diazepam history of ingestion and measurement of ethanol in
injection) causes a false positive reaction in some the serum.
assays.
Certain abnormalities in the acute phase of ethylene
Ultrasound may reveal hyperechoic renal cortices. The glycol poisoning (depression, tremors, hypocalcemia)
kidney may feel very firm when advancing a percuta- may resemble acute hypoparathyroidism. Other his-
neous biopsy needle. torical and physical abnormalities, and the presence of
● Kidney biopsy will reveal acute tubular necrosis, hyperphosphatemia in the latter, will distinguish the
with the presence of oxalate crystals. two.
Treatment during therapy. Observe very closely for life-

threatening respiratory depression, which should
Immediate induction of emesis and activated char- prompt reduction of ethanol treatmet. Monitor
coal or gastric lavage if ingestion is witnessed. body temperature and rewarm if hypothermia
Ethylene glycol is rapidly absorbed and intestinal develops.
decontamination is unlikely to be of any benefit after ● Ideally monitor acid-base status. If pH < 7.25
two hours or once clinical signs have appeared. and/or HCO3– < 8 mmol/L, give NaHCO3 (mmol =
Prevent ethylene glycol metabolism. This may be 0.2 × kg × base deficit) over 4 hours IV. Repeat as
achieved using either ethanol or fomepizole as compet- necessary.
itive inhibitors of alcohol dehydrogenase. Treatment ● If intravenous therapy is not possible, give the
must be initiated within 3 hours of ingestion to prevent ethanol doses above intraperitoneally, and addi-
acute renal failure. The unmetabolized ethylene glycol tional fluids subcutaneously.
is eliminated via the kidneys. – If the cat cannot be hospitalized immediately for
● Cats are usually treated with ethanol; several pro- ethanol therapy, the owner can attempt to give a
tocols exist. Prepare 20% (20 g/100 ml, 200 mg/ml) 40% alcoholic beverage by mouth (e.g. rum,
ethanol my mixing 1 part of 95–100% ethanol with vodka), 2.5 ml/kg, although a cat is less likely to
4 parts saline. (An alternative is to mix 1 part vodka tolerate this than a dog.
[40% ethanol] with 1 part saline.) Give 3 ml/kg 20% ● Fomepizole (4-methylpyrazole) is the treatment of
ethanol (600 mg/kg) over 1 hour further diluted to a choice in dogs. The drug causes minimal central
minimum of 1 part 20% solution and 2 parts saline nervous system depression and does not increase
for a final ≈7% maximum concentration solution. serum osmolality or metabolic acidosis. Although
(Additional dilution is needed in these protocols as initially considered ineffective in cats, recent stud-
the ethanol solutions are hyperosmolar). This is fol- ies suggest that higher doses are effective.
lowed by a constant rate infusion of 20% ethanol, – Give 125 mg/kg 5% solution IV initial dose, fol-
0.5 ml/kg/hr (100 mg/kg/hr), in a minimum of lowed by 31.25 mg/kg IV at 12, 24 and 36 hours
2 ml/kg/hr saline (again for a final ≈7% maximum post-ingestion. The dose should be given over
concentration). (The dose may be increased with 15–30 minutes.
close monitoring up to 1.0 ml [200 mg]/kg/hr in Multiple B-vitamins containing pyridoxine and thi-
4 ml/kg/hr fluids.) Treatment is continued for 10 amine may enhance the metabolism of glyoxylic acid
hours after a negative serum ethylene glycol test, or to non-toxic metabolites and protect the nervous system
18 hours after correction of metabolic acidosis during ethanol therapy. Compatability of B-vitamins
without ongoing need for NaHCO3 treatment. An with ethanol solutions is not known, so administration
alternative protocol is to give 5 mL/kg 20% ethanol, via a separate IV line is recommended.
diluted into IV fluids, by constant rate infusion over
6 hours for 5 treatments, then over 8 hours for 4 See Acute renal failure, above.
treatments. (The serum half-life of ethylene glycol ● Most ingestion is not witnessed, and, without dial-
for cats receiving ethanol is 29 hours.) ysis, the prognosis for cats with oliguric or anuric
● Begin IV fluids (do not use Ringer’s or lactated renal failure is grave. Hemodialysis has been used
Ringer’s) at 1.5–3 times maintenance based on successfully to support cats through oliguric and
patient requirements and adjusted to account for anuric renal failure until tubular regeneration
volume delivered with ethanol solutions. Monitor occurred. Peritoneal dialysis may be considered,
hydration status, body weight, and urine output; especially if oliguria has not progressed to anuria,
observe respiration and auscultate lungs frequently as the chances for recovery of renal function are
to monitor for pulmonary edema. perhaps somewhat better with oliguria than with
● Ideally measure serum ethanol concentrations anuria.
and maintain at 100 mg/dL. Treatment will ● Renal transplantation may be considered in cats
increase central nervous system depression and with oliguric or anuric renal failure.
serum osmolality. The cat may become comatose
LILY POISONING* Diagnosis

The diagnosis of acute poisoning relies on history of
Classical signs ingestion or a high index of suspicion.
● Acute lily poisoning should be considered in any
● Acute depression and anorexia.
● Vomiting. cat at risk with acute depression and vomiting.
Indoor cats with access to newly introduced plants
are at highest risk.
Pathogenesis ● Vomitus should be examined for plant material.
Lily poisoning is caused by ingestion of plants in the Plants should be examined for evidence of having
genera Lilium and Hemerocallis, and all plants within been chewed.
these genera should be considered potentially toxic. A hemogram typically reveals hemoconcentration and
Plants with proven toxicity include the Easter lily a stress leukogram.
(L. longiflorum), tiger lily (L. tigrinum), rubrum lily
(L. speciosum), Japanese show lily (L. lancifolium), Acid-base and osmolality values in the acute phase of
Lilium hybrids and daylilies (all Hemerocallis spp.). poisoning have not been well characterized. In the later
Calla lilies (Zantedeschia aethiopia) and peace lilies phase of poisoning serum chemistry findings are typi-
(Spathyphyllum wallis) are not toxic. cal of acute renal failure, but there may be a dispro-
portionate elevation in creatinine compared to urea.
Leaves, flowers and stems are toxic; only small quan- Liver enzyme and creatinine kinase values may also
tities have to be ingested to result in intoxication. The increase.
flowers are most toxic.
Urinalysis will reveal isosthenuria to minimally con-
The toxic principles have not been fully characterized centrated urine. Glucosuria and proteinuria may be
and it is not known if Lilium and Hemerocallis toxins present.
are the same.
Ultrasound may reveal hyperechoic renal cortices.
Poisoning results in acute renal failure, which initially The kidney may feel very firm when advancing a per-
is non-oliguric. cutaneous biopsy needle.
Dehydration appears to be a critical factor in the pro- Kidney biopsy will reveal acute tubular necrosis and
gression of non-oliguric to oliguric renal failure. intact basement membranes. Low numbers of birefrin-
gent crystals may be present.
Clinical signs
Signs of acute lily poisoning (< 24 hours) are probably
due to direct effects of the uncharacterized poison and Other causes of acute renal failure.
include depression, anorexia, polyuria with or with- Other causes of acute vomiting.
out polydipsia, hypersalivation and acute vomiting. ● Both cats with acute pancreatitis and cats with
Hypersalivation and vomiting typically begin within acute lily poisoning may have acute depression and
3 hours of ingestion and lasts for 4–6 hours. Cases vomiting, but cats with lily poisoning will have
have been presented without a history of vomiting. minimally concentrated urine, while cats with
Polyuria typically begins within 12–30 hours and lasts acute pancreatitis should have well-concentrated
for 12–24 hours. Ataxia, tremors and seizures have also urine unless there is a concurrent disorder causing
been reported . dilute urine, such as chronic renal failure.
Later signs (> 24 hours) are due to acute renal failure
and include persistent depression and anorexia, Treatment
hypothermia, recurrent vomiting, painful and swollen Induction of emesis, activated charcoal and cathar-
kidneys, and polyuria, oliguria or anuria. sis if recent ingestion.
Prompt intravenous fluid therapy. This is critical for Elapidae also have hematoxins that activate and deplete
a good prognosis. clotting factors resulting in bleeding, myotoxins that
cause rhabdomyolysis, or hemolysins that cause
Dehydration is an important mechanism in the
intravascular hemolysis.
development of renal failure. Prompt initiation of
intravenous fluids will halt progression of non-oliguric Venoms from Viperidae are predominantly hematoxic,
to oliguric/anuric renal failure and hasten recovery. although some have neurotoxic properties. Edema ±
Deliver fluids at 2–3 times maintenance for a mini- bleeding/bruising around the bite is typical.
mum of 24 hours (48 hours preferred).
Venoms from Crotalidae are predominantly hematoxic,
Gastrointestinal decontamination and intravenous although some are potent neurotoxins. Acute depres-
fluid therapy within 6 hours of ingestion is likely to pre- sion may occur from hypotension or neurotoxicity.
vent renal failure. If such treatment is delayed for more
Venoms from most Colubridae are mild and clinical
than 18–24 hours, acute renal failure will likely occur.
reports of bites to cats lacking.
If renal failure occurs, see Acute renal failure, above.
● Hemodialysis and peritoneal dialysis have been
used to support cats through oliguric/anuric renal
Diagnosis
failure until tubular regeneration occurs. Without
dialysis, the prognosis for oliguric/anuric renal fail- Diagnosis is based on history of possible exposure to
ure is grave. Cats with non-oliguric acute renal fail- a snake and physical examination findings.
ure may develop chronic renal failure.
CBC may reveal hemoconcentration, echinocytosis and
thrombocytopenia. Serum chemistry profile may reveal
SNAKE BITE ENVENOMATION* hypokalemia and elevated CK, ALT, urea and creati-
nine levels. Urinalysis may reveal myoglobiunuria or
Classical signs hemoglobinuria and glucosuria.
● Flaccid paresis/paralysis with mydriasis
(most Elapidae, some Crotalidae and
Viperidae snakes). Differential diagnosis
● Bleeding tendency (some Elapidae and
See The Cat With Generlized Weakness (page 952) and
Viperidae snakes).
for differential diagnosis of neurologic signs and The
● Bite wound on cranial half of body ± local
Bleeding Cat (page 503) for differential diagnosis of
swelling or bleeding (Viperidae snakes).
hematologic signs.
See main reference on page 950 for details (The Cat Differential diagnoses for the local reaction include
With Generalized Weakness). angioedema from insect envenomation, animal bite
wounds, sharp and blunt trauma.
Clinical signs
Treatment
Cats are less likely to be bitten than dogs.
Keep the animal calm.
Venoms from Elapidae snakes (all Australian snakes)
are predominantly neurotoxic. Initial signs may be Supportive care. See page 953, The Cat With
acute depression and weakness. More specific signs Generalized Weakness.
include areflexic dilated pupils, dysphagia (salivation),
Specific antivenin therapy.
dyspnea (respiratory paralysis), hindlimb ataxia and
flaccid quadraplegia. Local reaction to the bite is mini- Transfusions for clinically significant hemostatic or
mal, and the bite wound is rarely located. Some hematologic abnormalities.
ACUTE HEART FAILURE* Clinical signs

Typically there is a history of weight loss, polyuria
Classical signs and polydipsia, together with a normal appetite or
● Acute dyspnea. polyphagia in the preceding weeks or months prior to
● Lethargy and inappetence. an acute onset of anorexia, vomiting, dehydration, and
depression. Other signs that may be evident with the
See main reference on page 124 for details (The Cat onset of depression include icterus and dyspnea.
Diagnosis
Clinical signs
Diagnosis requires demonstration of ketonemia or
Acute onset of depression, anorexia and dyspnea. In ketonuria, and hyperglycemia. Ketones may be
severe cases, collapse may occur, especially if stressed. falsely negative in urine because urine test strips
Pulmonary crackles, a heart murmur, arrhythmia and/or measure primarily oxaloacetate (and to a lesser
weak pulses may be found on physical examination. extent acetone), which may be present in concentra-
tions in urine below the limit of detection by the test
Some cats have a history of vomiting. strip in cats. Several drops of hydrogen peroxide
may be added to the urine sample in an effort to con-
Diagnosis vert β-hydroxybutyrate to oxaloacetate to increase
Pulmonary edema and cardiomegaly are evident on the concentration of oxaloacetate in urine. Alternatively,
radiographs. The radiographic appearance of pul- β-hydroxybutyrate may be measured in serum using
monary edema is variable in cats. a point-of-care test, or the urine test strip may be
used to detect oxaloacetate in heparinized plasma.
Furosemide may be given and radiographs repeated in Using a standard urine test strip, a negative plasma
one hour to see if the pulmonary changes have test rules-out ketosis, and a positive urine test
improved. Definitive diagnosis of cardiomyopathy rules-in ketosis, in cats. Finally, bicarbonate (total
requires echocardiography. CO2) concentrations in plasma may be used to
demonstrate acidosis.
Other causes of depression and dyspnea. See The Dys- Differential diagnosis
pneic or Tachypneic Cat (page 47).
Acute pancreatitis or sepsis (depression), hepatic lipi-
Treatment dosis or cholangiohepatitis (depression and icterus),
ethylene glycol or lily intoxication (depression and
Furosemide and nitroglycerin ointment at standard polyuria), acute heart failure (depression and dyspnea)
dosages. See details of additional treatment page 130 may all cause vomiting and dehydration and appear
(The Cat With Abnormal Heart Sounds and/or an similar to diabetic ketoacidosis.
Enlarged Heart).
Treatment
DIABETIC KETOACIDOSIS*
Intravenous fluids are required to correct dehydration
and electrolyte imbalances.
Classical signs
Regular insulin should be administered using intravenous,
● Polyuria, polydipsia, and weight loss.
intramuscular or subcutaneous administration protocols
● Recent onset of acute depression and anorexia.
depending on the status of the cat’s peripheral perfusion.
See main reference on page 236 for details (The Cat Appropriate antibiotics should be administered if urine
With Polyuria and Polydipsia). has evidence of bacteria or inflammation. Many diabetic
cats have urinary tract infection at the time of admis- Clinical signs
sion (culture urine).
Cats of any age may be affected, but 70% of cats are
less than 2 years of age.
NEOPLASIA*
Toxoplasmosis may affect any organ system resulting
Classical signs in a wide variety of clinical signs. Uveitis, pneumonia,
hepatitis and encephalitis are the most common syn-
● Usually chronic depression, anorexia and dromes. Most cats with systemic toxoplasmosis have a
weight loss. fever.
● Occasionally acute signs.
Lethargy, anorexia and fever are early signs.
Clinical signs Uveitis or other forms of intraocular inflammation are

present in about 80% of cases.
Neoplasia typically causes chronic signs, but depend-
ing on location and growth rate, a tumor may cause Dyspnea is present in the majority of cats, and associ-
acute signs, which may include acute depression, ated with increased respiratory sounds over the chest.
anorexia, and dehydration. Abdominal signs may occur associated with hepatitis
or pancreatitis and include abdominal pain on palpa-
Diagnosis tion, infrequent vomiting, and enlarged mesenteric
lymph nodes.
Routine history-taking, physical examination, and
diagnostic work-up is required to identify specific Neurologic signs are more common in older cats.
signs and localize organ involvement. Definitive diag-
nosis requires biopsy. Diagnosis
Acute systemic toxoplasmosis typically affects kittens,
Differential diagnosis or immunosuppressed cats, which usually have a his-
Other causes of acute depression and anorexia. tory of chronic disease.
Confirmation is by measuring serum IgM antibodies
Treatment or demonstrating rising serum IgG antibodies.
Surgery, radiation therapy, chemotherapy and other The organism occasionally may be seen in airway wash
treatment modalities may be indicated, depending upon cytology of cats with pneumonia.
the neoplasm.
NUTRITIONAL SUPPORT Rule out other diseases causing acute lethargy,
anorexia and fever, which in the cat are usually infec-
tious causes. Physical examination will often identify
TOXOPLASMOSIS*
localizing signs, which can be pursued diagnostically.
Classical signs
● Fever, anorexia and depression. Treatment
● Uveitis, dyspnea, icterus, or neurologic
Clindamycin at standard doses (10–12 mg/kg orally q
signs.
12 h for 4 weeks).
See main reference on page 432 for details (The Yellow Other drugs with potential efficacy include trimethoprim-
Cat or Cat With Elevated Liver Enzymes), page 375 sulfas, doxycycline, minocycline, azithromycin and clar-
(The Pyrexic Cat). ithromycin.
UPALATABLE FOOD* Clinical signs

Partial or complete anorexia is observed with respect to
Classical signs the cat’s normal food source.
● Partial anorexia. No weight loss or other signs of illness are apparent.
Change in diet to unpalatable food may precipitate Diagnosis is based on confirming that another food
total or partial anorexia. source is being used, e.g. neighbors, successful hunting.
Stale food or spoiled food may cause anorexia. Ruling out other causes of anorexia.
Clinical signs
Other causes of anorexia.
Complete or partial anorexia.
Treatment
Diagnosis
Eliminate the alternate food source if indicated.
History of change in diet.
History of feeding from a large, slowly consumed bag of ENVIRONMENTAL STRESS*
dry food, or providing several days of rations in one meal.
Ruling out other causes of anorexia. Classical signs
● Inactivity and/or anorexia.
Other causes of depression and anorexia. Pathogenesis
Hot weather may cause inactivity and withdrawal to
Treatment cool locations.
Resume previous diet or offer other more palatable Cold weather may cause withdrawal to warm locations.
food.
The cat may not be eating because of discomfort or
because of inactivity and withdrawal.
Prognosis
Excellent provided anorexia is not protracted in obese Clinical signs
cats resulting in hepatic lipidosis.
Variable withdrawal, inactivity, anorexia and dehydration.
ALTERNATE FOOD SOURCE* During hot weather periods the cat may be more active
than usual at night when it is cooler.
Classical signs No signs of another disorder causing depression and
● Partial anorexia. anorexia.
Diagnosis
Pathogenesis
History of temperature extremes.
The cat has another food source in addition to its usual
source, causing physiologic anorexia. Ruling-out other causes of depression and anorexia.
Differential diagnosis serum phosphorus level < 0.3–0.5 mmol/L, but has
occurred at higher levels.
Other causes of depression and anorexia.
Diagnosis
Treatment
Serum phosphorus level < 0.8 mmol/L.
Provide a thermoneutral environment.
Ruling out other causes of depression, weakness,
Place food in withdrawal location. anorexia and hemolysis.
Prognosis Differential diagnosis

This is usually a short-term problem with no adverse Other causes of depression, weakness and anorexia
consequences. related to the primary disorder.
HYPOPHOSPHATEMIA* Treatment
Classical signs Intravenous potassium phosphate or sodium phos-
phate. See Diabetic ketoacidosis in The Cat With
● Weakness. Polyuria and Polydipsia (page 236).
● Pallor and hemoglobinuria (hemolysis).
Transfusion with fresh red blood cells if hemolysis
occurs.
Pathogenesis
Hypophosphatemia results from insufficient phospho- Prognosis
rus intake and/or excessive urinary phosphorus loss The prognosis for correction of hypophosphatemia is
and/or translocation from extracellular to intracellular good and overall prognosis is determined by the under-
fluid. lying disorder.
Mild to moderate hypophosphatemia (serum phospho-
rus level 0.5–0.8 mmol/L) may be seen in numerous HYPOPARATHYROIDISM*
disorders where anorexia is a feature. It is seen most
often with hepatic lipidosis and chronic renal failure. Classical signs
Anorexia may contribute to hypophosphatemia, which
in turn may exacerbate anorexia and depression.
● Anorexia and depression.
● Muscle tremors and seizures.
Severe hypophosphatemia (serum phosphorus level < ● History of thyroidectomy.
0.5 mmol/L) is most likely to be seen in the treatment
of diabetic ketoacidosis and within 3 days of initiating
tube feeding in an anorexic cat. Clinical signs
Anorexia and depression are consistent findings.
Clinical signs Muscle tremors have been reported in 83%, and seizures
Lethargy, muscle weakness, anorexia – increasing in 50%, of cases of idiopathic hypoparathyroidism.
risk with decreasing phosphorus level.
Severe muscle weakness may lead to respiratory mus- Diagnosis
cle failure (rare).
Hypocalcemia (serum calcium level usually < 1.6
Pale mucous membranes, hemoglobinemia and hemo- mmol/L in the presence of normal serum albumin
globinuria from hemolysis – most likely to occur with level) and hyperphosphatemia.
History of thyroidectomy within the previous Other signs that are sometimes observed include mus-
2 weeks. cle tremors, vomiting, vocalizing, circling, panting,
diarrhea or urination.
Differential diagnosis Hypoglycemia is unlikely to stimulate eating behavior
in a cat; it is more likely to cause anorexia.
Acute poisoning is main differential diagnosis for
acute anorexia and depression progressing to muscle
tremors and seizures. Diagnosis
Hypoglycemia may cause similar signs. Clinical hypoglycemia usually results from insulin
overdose in a diabetic cat. This is confirmed by meas-
uring blood glucose levels and by prompt resolution of
Treatment
clinical signs following intravenous dextrose or intra-
Tremors or seizures: muscular glucagon.
● 10% calcium gluconate 0.5–1.0 ml/kg, or 10% cal-
Portable glucose meters have a tendency to measure
cium chloride 0.15–0.5 ml/kg, given IV over 10–15
falsely low values. A diagnosis of hypoglycemia should
min. Temporarily stop administration if bradycar-
be reconsidered if the signs do not improve once blood
dia, QT-interval shortening or vomiting occur. Both
glucose increases in response to intravenous glucose or
solutions are caustic (calcium chloride >> calcium
glucagon. Lack of response to sugar solutions
gluconate) if extravasated.
rubbed on the gums or given by stomach tube does
● If severe initial signs or recurrent signs, follow with
not rule out hypoglycemia, because most absorption
10% calcium gluconate 0.25–0.375 ml/kg/h CRI.
of glucose occurs in the small intestine. Cats with
Long-term management: severe signs such as coma may not respond if there is
● Vitamin D and oral calcium preparations – see The irreversible brain damage.
Cat With Tremor or Twitching (page 864).
● Cats with post-thyroidectomy hypoparathyroidism
typically regain parathyroid function within 2 Differential diagnosis
weeks to 6 months. Other causes of neurologic disease. See The Cat With
Stupor or Coma (page 821) and The Cat With Seizures,
ACUTE HYPOGLYCEMIA Circling and/or Changed Behavior (page 809).
Some poisonings may cause similar signs, e.g. vocaliz-
Classical signs ing, mydriasis, vomiting, diarrhea, polypnea, tremors,
● Acute depression in an insulin-treated cat. seizures and stupor (see Acute poisoning and enveno-
● Weak wobbly gait. mation, above).
● Muscle fasciculations. Hypocalcemia may also cause lethargy and anorexia
● Dilated pupils. progressing to muscle tremors and seizures.
See main reference on page 236 for details (The Cat Hypoglycemia may also be a finding in acute pancre-
With Polyuria and Polydipsia). atitis, porto-systemic shunts, hepatic lipidosis, cholan-
giohepatitis, and overwhelming sepsis, but it is usually
a marker of disease rather than a cause of clinical signs.
Clinical signs
Clinical signs of hypoglycemia most often occur in
Treatment
insulin-treated diabetic cats.
A Somogyi reaction should not be relied upon to rescue
Signs may be mild and include lethargy or increased
a cat from hypoglycemia.
somnolence, a weak wobbly gait and mydriasis, or be
more severe and include seizures, stupor or coma. Give 50% dextrose at 0.5–1.0 ml/kg IV.
If intravenous access is not possible, 50% dextrose Diagnosis

(0.5–1.0 ml/kg) or corn syrup (0.25–0.5 ml/kg) PO and
rubbed on the gums may be effective, but glucagon The cat with unexplained acute depression should be
0.25–1.0 mg IM is superior. Glucagon must be fol- carefully examined repetitively for neurological signs.
lowed by intravenous dextrose once seizures have
stopped and intravenous access is possible. Differential diagnosis
In the absence of specific neurologic signs, all other
causes of acute depression and anorexia should be con-
CENTRAL NERVOUS SYSTEM NEOPLASIA sidered.
OR INFLAMMATION
If neurologic signs develop, poisoning should be con-
Classical signs sidered.
● Acute depression and anorexia.

● Stupor, coma, and specific neurological Treatment
signs. Treat the underlying disease.
See main reference on page 795 for details (The Cat In the absence of a specific diagnosis, treatment should
With Seizures, Circling and/or Changed Behavior), page be supportive.
821 (The Cat With Stupor or Coma), page 835 (The Cat
With a Head Tilt, Vestibular Ataxia or Nystagmus), page HEPATIC ENCEPHALOPATHY
852 (The Cat With Tremor or Twitching) and page 941
(The Cat With Generalized Weakness). Classical signs
● Disorientation and ptyalism.
Clinical signs ● Intermittent central nervous system (CNS)
signs often associated with eating.
Acute meningitis, encephalitis or central nervous ● Usually in young cats (< 1 year).
system neoplasia may initially be characterized by ● Affected cats are often stunted in size.
non-specific signs such as acute onset of anorexia and
depression. See main reference on page 588 for details (The Cat
Depression may then progress to stupor, coma, behav- With Salivation) and page 425 (The Yellow Cat or Cat
ior change or other specific neurological signs. See The With Elevated Liver Enzymes).
Cat With Stupor or Coma, The Cat With Seizures,
Circling and/or Changed Behavior, and The Cat With a Clinical signs
Head Tilt.
Porto-systemic shunts usually cause signs in young
● Acute depression may be the only finding in a cat in
cats that are small in size. Copper-colored irises may be
the prodromal phase of clinical rabies, but fever
evident. Intermittent central nervous system signs
spikes are typical. The prodromal phase typically
including disorientation and behavioral changes, and
only lasts one to two days in cats before proceeding
occasionally seizures occur, often associated with eat-
to the furious phase (most often) or the paralytic
ing. Ptyalism may occur alone or associated with neu-
phase. Rabies is highly unlikely if there is persist-
rological signs. Occasionally urethral obstruction
ent depression and anorexia without the develop-
results from ammonium biurate uroliths. Prolonged
ment of other behavior changes or specific
post-anesthetic recovery may be reported.
neurologic signs.
● Acute depression is a consistent initial sign in Mature cats with hepatic lipidosis and cholangio-
pseudorabies (Aujesky’s disease, mad itch), but hepatitis typically have anorexia, weight loss, vomit-
typically progresses to severe pruritis, voice change ing and icterus. In severe cases, collapse, disorientation
and anisocoria with 1–2 days. and ptyalism may occur.
Diagnosis HYPERNATREMIA
Elevated plasma ammonia level confirms hepatic
encephalopathy; but a normal fasting concentration Classical signs
does not rule it out. ● Coma, twitching, seizures.
Porto-systemic shunts have variable hematologic and
biochemical findings, which may include low normal to
low MCV, low urea, albumin, glucose and cholesterol Pathogenesis
concentrations, and elevated globulin and bile acid con- Hypernatremia results from excessive sodium intake
centrations. Imaging may reveal a small liver and the and/or inadequate water intake and/or excessive water
shunt. Definitive diagnosis may require an exploratory loss.
laparotomy.
Hypernatremia in cats is most likely to occur in criti-
Hepatic lipidosis and cholangiohepatitis are typically ill cats receiving sodium-rich fluids that have con-
cally associated with increased ALT and/or ALP. A current sodium-poor water loss (e.g. diabetes mellitus,
disproportionate elevation of ALP compared to ALT head-trauma induced central diabetes insipidus).
and GGT is suggestive of hepatic lipidosis. Elevations
in serum bile acids in the absence of cholestasis con-
firm the presence of liver dysfunction. Coagulation Clinical signs
abnormalities may be present. Imaging may reveal an Acute progressive lethargy in a critically ill cat.
enlarged, hyperechoic liver. Definitive diagnosis relies
on liver biopsy. May progress to coma, twitching, and seizures.
Dehydration.
Differential diagnosis Weak pulse, prolonged capillary refill time and
The main differential diagnosis for ptyalism is oral cav- hypothermia may be present.
ity ulceration.
The main differential diagnoses for icteric depressed Diagnosis
cats are acute pancreatitis and diabetic ketoacidosis. Serum sodium level > 160 mmol/L.
The main differential diagnosis for transient depression Ruling out other causes of depression and anorexia.
and disorientation is poisoning.
Urine specific gravity < 1.035 may indicate diabetes
insipidus.
Treatment
Hepatic encephalopathy treatment includes lactulose,
enema, lactulose retention enema, correction of Differential diagnosis
hypokalemia, and antibiotics (neomycin, metronida- Other causes of depression and anorexia related to the
zole, ampicillin/amoxicillin). primary disorder causing critical illness.
Porto-systemic shunts can often be reduced or closed
by partial or complete surgical ligation or placement of
an ameroid constrictor. Treatment
Hepatic lipidosis requires nutritional support. Sodium-poor intravenous fluids. Hypernatremia

should be corrected at the same rate at which it devel-
Cholangiohepatitis treatment includes nutritional sup- oped, i.e. serum sodium concentration should be
port, antibiotics if an organism is cultured, and corcor- lowered rapidly in acute hypernatremia, and slowly in
ticosteroids if lymphocytic-plasmacytic inflammation chronic hypernatremia. Overly rapid correction of
is evident on biopsy. hypernatremia will result in signs similar to hyperna-
tremia. Idiogenic osmols form in hypernatremia to pro- anorexia and depression are reported by the owners.
tect the brain against dehydration; these osmols result Anorexia and depression may be due to esophageal pain.
in cerebral edema if serum sodium concentration is
lowered too quickly. Because the rate at which hyper- Diagnosis
natremia developed is often not known, a general
Diagnostic imaging or endoscopy is required to iden-
recommendation is to lower serum sodium level by
tify foreign material. The latter is required to identify
1–2 mmol/L/h.
esophagitis.
Assess percent dehydration and replace using 0.9%
saline over 4–8 hours if acute dehydration and over
PRIMARY ANOSMIA
8–12 hours if chronic dehydration.
Once the cat is rehydrated, calculate free water deficit: Classical signs
Deficit (L) = 0.6 × body weight (kg) × ([Na ÷ 140] – 1). ● Anorexia.
Give this volume over 12–24 h if the cat’s mentation is
normal, and over 24–48 h if mentation is abnormal. Clinical signs
Give furosemide 0.5 mg/kg IV if hypernatremia per- Anorexia and cat may sniff less.
sists and the cat is normally hydrated.
Diagnosis
Consider antidiuretic hormone therapy (e.g. DDAVP) if
there is diabetes insipidus (see The Cat With Polyuria History of olfactory tractotomy for inappropriate elim-
and Polydipsia, page 231). ination behavior.
No reaction to placement of noxious stimuli in front of
Prognosis nose.
The prognosis for hypernatremic cats with head trauma
is poor; the prognosis for uncomplicated correction of FELINE LEUKEMIA VIRUS INFECTION
hypernatremia with other disorders is good and overall
prognosis is determined by the underlying disorder. Classical signs
● Fever.
ESOPHAGEAL FOREIGN BODY AND ● Signs of secondary infections, hematologic
INFLAMMATION disorders, or neoplasia.
Classical signs
Clinical signs
● Regurgitation.
Feline leukemia virus infection usually causes fever;
● Anorexia and depression.
anemia and other hematologic disorders; immunosup-
pression leading to secondary infections; lymphoma,
See main reference on page 616 for details (The Cat With
myeloproliferative disorders, and fibrosarcomas and
Signs of Regurgitation (Acute or Chronic)).
neurologic disorders.
Occasionally the only sign of infection is acute depres-
Clinical signs
sion, anorexia and dehydration.
Cats with esophageal foreign bodies or esophagitis (e.g.
secondary to treatment with tetracyclines) are typically
Diagnosis
presented for regurgitation (or vomiting as perceived by
the owner), dysphagia or gagging. However, this may A feline leukemia virus test should be considered in the
be intermittent, so that only non-specific signs such as work-up of a cat with acute depression and anorexia.
RECOMMENDED READING
Akol KG, Wachabau RJ, Saunders HM, Hendrick MJ. Acute pancreatitis in cats with hepatic lipidosis. J Vet Intern
Med 1993; 7: 205–209.
Brady CA, Otto CM, Van Winkle TJ, King LG. Severe sepsis in cats: 29 cases (1986–1998). J Am Vet Med Assoc
2000; 217: 531–535.
Connally HE, Thrall MA, Hamar DW. Safety and efficacy of high dose fomepizole as therapy for ethylene glycol
intoxication in cats. Proceedings of the 8th International Veterinary and Emergency and Critical Care Symposium,
2002, p 777.
Ferreri JA, Hardam E, Kimmel S, Saunders HM, Van Winkle TJ, Robatz KJ, Washabau RJ. Clinical differentiation
of acute necrotizing from chronic nonsuppurative pancreatitis in cats: 63 cases (1996–2001). J Am Vet Med Assoc
2003; 223: 469–474.
Forman MA, Mark SL, De Cock HE, Hergesell EJ, Wisner ER, Baker TW, Kass PH, Steiner JM, Williams DA. Eval-
uation of serum feline pancreatic lipase immunoreactivity and helical computed tomography versus conventional
testing for the diagnosis of feline pancreatitis. J. Vet. Intern. Med., 2004; 18: 807–815.
Frenier SL, Dhein CR. Diagnosis and management of acute renal failure. In: August FR (ed) Consultations in Feline
Internal Medicine. Philadelphia, WB Saunders, 1991, pp 281–288.
Hill RC, Van Winkle TJ. Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. J Vet Intern Med
1993; 7: 25–33.
Holzworth J. Diseases of the Cat. W.B. Saunders, Philadelphia, 1987.
Mathews KA (ed) Veterinary Emergency and Critical Care Manual. 2 Edition, Guelph, Ontario, Lifelearn Inc., 2006.
Mathews KA. Acute renal failure: what’s new in treatment and prevention. Proceedings of the 8th International
Veterinary and Emergency and Critical Care Symposium, 2002, pp 399–403.
Rumbeiha WK, Francis JA, Fitzgerald SD, Nair MG, Holan K, Bugyei KA, Simmons H. A comprehensive study of
Easter lily poisoning in cats. J. Vet. Diagn. Invest., 2004; 16: 527–541.
Simpson KW, Michel KE. Medical and nutritional management of feline pancreatitis. Proceedings of the 18th Annual
Veterinary Medical Forum. American College of Veterinary Internal Medicine, 2000, pp 428–430.
Steiner JM. Diagnosis of pancreatitis. Vet Clin North Am Small Anim Pract 2003; 33: 1181–1195.
Tefft KM. Lily nephrotoxicity in cats. Comp Cont Edu Pract Vet 2004: 26: 149–156.
Temo K, Rudloff E, Lichtneberger M, Kirby R. Hypernatremia in critically ill cats: evaluation and treatment. Comp
Cont Ed Pract Vet 2004; 26: 434–444.
Wisner T. Top feline toxicities. Veterinary Information Network, 2005.
PART 6
Cat with weight loss or chronic
illness
17. The cat with weight loss and a good

appetite
Danièlle Gunn-Moore and James B Miller
KEY SIGNS
● Thin cat eating well.
● Weight loss and a good appetite.
MECHANISM?
● Weight loss with a good appetite occurs when the cat is unable to gain sufficient nutrition from
its diet.
WHERE?
● Diseases involving many body systems can lead to weight loss with a good appetite.
WHAT?
● In older cats the most common causes of weight loss with a good appetite are hyperthyroidism,
diabetes mellitus and inflammatory bowel disease. In younger cats, inflammatory bowel dis-
ease and intestinal parasites are the most common causes.
301
302 PART 6 CAT WITH WEIGHT LOSS OR CHRONIC ILLNESS

Diseases causing weight loss and a good appetite
METABOLIC
● Hyperthyroidism*** (p 304)
Usually seen in cats greater than eight years of age. Weight loss, good appetite, tachycardia, rest-
lessness and/or intermittent vomiting and diarrhea.
● Diabetes mellitus** (p 310)
Usually seen in older cats. Increased risk in fat cats and some Burmese. History of polyuria, poly-
dipsia and polyphagia, plus variable weight changes.
● Acromegaly (p 322)
Rare condition of older, typically males, cats. Slow increase in body size, especially affecting the head
and feet. Usually diabetic; so polyuric, polydipsic and polyphagic.
Rare condition of middle-aged and older cats. Poor coat condition and pot-bellied appearance. Often
diabetic; so polyuric, polydipsic and polyphagic.
● Glomerulonephritis (protein-losing nephropathy) (p 326)
Weight loss with a good appetite may be seen early in disease, accompanied by ascites, subcutaneous
edema, polydipsia and polyuria, ± vomiting and diarrhea.
NEOPLASTIC
● Alimentary lymphosarcoma* (p 317)
Usually older cats. Weight loss with variable appetite. History of acute, or more commonly, chronic
vomiting and/or diarrhea.
NUTRITIONAL
● Inadequate nutrition** (p 316)
Weight loss with a good appetite, few other signs. History of inadequate or inappropriate diet.
Seen in kittens from poor conditions or cats that have recently changed environment.
INFLAMMATORY
● Inflammatory bowel disease*** (p 307)
Can affect any age but most typically seen in middle-aged cats. Any combination of chronic weight loss,
● Chronic pancreatitis/exocrine pancreatic insufficiency* (p 318)
Typically seen in middle-aged to older cats with a history of episodic anorexia, lethargy, vomiting
and/or diarrhea. If also diabetic; polyuria and polydipsia.
● Lymphocytic cholangiohepatitis* (p 320)
Typically seen in younger to middle-aged cats. Often polyphagic, may have mild generalized lym-
phadenopathy. May be associated with inflammatory bowel disease.
INFECTIOUS
● Intestinal parasites** (p 314)
Usually seen in young cats from poorly cleaned multi-cat environments. Weight loss or failure to
gain weight, usually with a good appetite, may have diarrhea and/or vomiting.
17 – THE CAT WITH WEIGHT LOSS AND A GOOD APPETITE 303
INTRODUCTION WHAT?
The most common cause of weight loss with a good
MECHANISM? appetite is hyperthyroidism. Other common causes
include various malassimilation syndromes including
While weight loss is a common presenting problem in
combinations of inflammatory bowel disease, pancre-
feline medicine, weight loss in association with a
atitis and/or lymphocytic cholangiohepatitis (in combi-
good appetite is seen less frequently. This occurs
nation termed “triaditis”). Intestinal parasitism,
when the cat is unable to gain sufficient nutrition
diabetes and alimentary lymphosarcoma are seen
from its diet.
reasonably commonly, while hyperadrenocorticism,
This can result from inadequate nutrition (feeding acromegaly, protein-losing nephropathy and lymphang-
insufficient food or a diet of inadequate nutritional con- iectasia are seen very rarely.
tent), or an inability to derive nutrient from the diet.
Disorders which may occasionally present with weight
The latter can result from:
loss with a good appetite, but more typically present
● Inability to digest or absorb nutrients (malassim-
with a poor appetite are discussed elsewhere, e.g. con-
ilation syndromes), e.g. parasitism, inflammatory
gestive heart failure, congenital portosystemic shunts.
bowel disease, pancreatitis/exocrine pancreatic
insufficiency, lymphocytic cholangiohepatitis, ali-
mentary lymphosarcoma or lymphangectasia. DIAGNOSIS
● Inability to utilize absorbed nutrients – as seen
Initial diagnostic evaluation should include history,
with diabetes mellitus, or endocrinopathies which
physical examination, hematology, serum biochem-
result in diabetes, e.g. acromegaly or hyperadreno-
istry, serum thyroxin if > 8 years of age, urinalysis, and
corticism.
fecal examination for parasites.
● Increased utilization of absorbed nutrients
(hypermetabolic states), e.g. hyperthyroidism, Age of cat is an important consideration. Younger
pregnancy, lactation, congestive heart failure, cats are more likely to develop parasitism, inappropriate
excessive physical activity or neoplasia. nutrition, or protein-losing nephropathy. Middle-aged
● Excessive nutrient loss, e.g. diabetes mellitus, cats have a greater risk of hyperadrenocorticism, while
protein-losing nephropathy or lymphangectasia. older cats develop hyperthyroidism, diabetes mellitus,
alimentary lymphosarcoma or acromegaly. Inflammatory
bowel disease can affect cats of any age, but most typi-
cally affects middle-aged or older individuals.
WHERE? The history is essential. Determine the cat’s environ-
Weight loss with a good appetite may be seen when the ment (inside or outside, competition over food sup-
intestinal tract is unable to digest and/or absorb plies), what and how much is fed, whether nutritional
food (malassimilation syndromes, hyperthyroidism), requirements have changed (pregnancy, going outside
the body tissues are unable to utilize nutrition that in cold weather), or whether diabetogenic drugs have
has been absorbed (diabetes mellitus), the body loses been given.
essential nutrients through the intestines or kidneys
Other clinical signs are important to consider. These
(diabetes, protein-losing nephropathy, lymphangecta-
signs may result from underlying or concurrent disease
sia), or the demands of the body have been raised
processes. Polyuria and/or polydipsia are suggestive
beyond the level that the diet can supply (hyperthy-
of an endocrinopathy or protein-losing nephropathy.
roidism, pregnancy, lactation).
Vomiting and/or diarrhea are suggestive of enteric
Weight loss with a good appetite indicates a gastroin- disease, hyperthyroidism, lymphocytic cholangiohep-
testinal problem, renal problem or a problem- atitis or protein-losing nephropathy. Feces becoming
involving tissue metabolism (either metabolic bulky or fatty suggest malassimilation syndromes or
demands have increased, or the tissues are unable to hyperthyroidism, and increased aggression or restless-
utilize nutrients). ness are suggestive of hyperthyroidism.
Careful physical examination is essential for diag- exposure to allergens), genetic mutation, abnormal
nosis. Careful palpation of the ventral cervical region immune and/or hormonal responses.
is required to detect thyroid mass(es). Thorough ● 70% of the cats have both thyroid glands
abdominal palpation is essential to detect anterior affected.
abdominal pain (pancreatitis, hepatopathy), liver
1% of cases result from mild to moderately malig-
enlargement (diabetes-associated hepatopathy, hyper-
nant thyroid carcinoma.
adrenocorticism, lymphocytic cholangiohepatitis),
thickened bowel loops (inflammatory bowel disease, GIT signs may result from polyphagia, malabsorption
alimentary lymphosarcoma), mesenteric lym- or intestinal hypermotility.
phadenopathy (alimentary lymphosarcoma, occasion-
Polyuria/polydipsia may result from diuretic effects of
ally eosinophilic or suppurative inflammatory bowel
T4, increased renal blood flow, associated renal insuffi-
disease), ascites (lymphocytic cholangiohepatitis, pro-
ciency or compulsive polydipsia.
tein-losing nephropathy) or an enlarged uterus (late
pregnancy). General physical examination is impor- Cardiac effects result from a high output state, induced, in
tant to detect mild generalized lymphadenopathy part, by a demand for increased tissue perfusion to meet
(lymphosarcoma, lymphocytic cholangiohepatitis), an the needs of increased tissue metabolism. Cardiovascular
ill-kept coat (hyperthyroidism), a greasy coat (exocrine changes include left ventricular hypertrophy, left atrial
pancreatic insufficiency), alopecia and thin skin and ventricular dilation, increased myocardial contractil-
(hyperadrenocorticism), subcutaneous edema (pro- ity, and decreased peripheral vascular resistance. Other
tein-losing nephropathy), or extremities that appear contributors are the direct effect of thyroid hormones on
disproportionately enlarged (acromegaly). cardiac muscle and the nervous system.
Associated cardiac hypertrophy may cause congestive
DISEASES CAUSING SIGNS OF A THIN heart failure with tachycardia, a gallop rhythm, systolic
CAT WITH A GOOD APPETITE murmurs, dyspnea, apathy, hindlimb weakness due to
aortic thromboemboli or collapse.
HYPERTHYROIDISM*** Associated hypertension may be seen as ocular hemor-
rhage, or may cause clinical signs associated with cere-
Classical signs brovascular accidents, dementia and/or renal failure.
● Up to 85% of cats with hyperthyroidism may develop
● Older cats (usually > 8 years).
● Progressive weight loss, often with a systemic hypertension, either initially or even some
ravenous appetite. time after apparently successful treatment.
● May also show restlessness, a lack of
grooming, vomiting ± diarrhea, ± Clinical signs
polyuria/polydipsia.
Hyperthyroidism is the most common endocrinopa-
thy in cats; affecting ~1 in 300 pet cats.
Pathogenesis
It is seen mainly in older cats (>8 years of age); it is
99% of cases of hyperthyroidism result from benign occasionally seen in cats as young as 4 years, and has
nodular hyperplasia/adenoma. even been documented in an 8-month-old kitten.
● Disease results from autonomous secretion of thyrox-
There is no sex or breed predisposition, but Siamese
ine (T4) and triiodothyroxinine (T3). Negative feed-
cats appear to be under-represented.
back on the pituitary suppresses release of thyroid-
stimulating hormone (TSH) and normal thyroid Most cats have a history of weight loss and polyphagia.
tissue atrophies.
Weight loss usually occurs over several months.
● Cause is unknown but may involve diet (iodine
content, frequent changes, food additives), environ- 10–20% of cats will present with signs of inappetence
mental causes (in cat litter, toxins, pollution, with weight loss.
Cats may have a history of restlessness, aggression ● T4 concentrations varying during the day.
and a lack of grooming. ● Severe systemic illness causing a reduction in T4
(euthyroid sick syndrome).
Cats may also show tachycardia ± a gallop rhythm,
vomiting and/or diarrhea (feces may become bulky) If hyperthyroidism is suspected despite a high normal
and/or polyuria/polydipsia. T4 concentration:
● Retest the cat – either immediately, or in a few
GIT signs may result from polyphagia, malabsorption
weeks time.
or intestinal hypermotility.
● Check free T4 – by equilibrium dialysis.
Polyuria/polydipsia may result from diuretic effects of ● T3 suppression test – Collect blood sample, give
T4, increased renal blood flow, associated renal insuffi- 7 × 25 mg doses of T3 PO every 8 h, then collect
ciency or compulsive polydipsia. blood 2–4 h after the 7th dose (i.e. on day 3). An
increase in T3 concentration confirms successful
Associated cardiac hypertrophy may cause congestive
medication. Suppression of T4 concentration
heart failure with tachycardia, a gallop rhythm, systolic
(below 50% of baseline, <20 nmol/l [1.5 ug/dl]
murmurs, dyspnea, apathy, hindlimb weakness due to
does not usually occur in hyperthyroid cats.
aortic thromboemboli or collapse.
● Thyrotropin-releasing hormone (TRH) stimula-
Associated hypertension may be seen as ocular hemor- tion test – Collect blood, give 0.1 mg/kg TRH IV,
rhage, or may cause clinical signs associated with cere- then collect second blood sample 4 hours later.
brovascular accidents, dementia and/or renal failure. Assess both samples for serum T4 concentration.
● Up to 85% of cats with hyperthyroidism may have Stimulation to > 50% does not occur in hyperthy-
signs of systemic hypertension. roid cats. Side effects of TRH include transient
salivation, vomiting, tachypnea and defecation.
Many hyperthyroid cats are presented for their routine
● Thyroid-stimulating hormone (TSH) response
vaccination with no owner complaints.
test – The usefulness of this test has been ques-
tioned and TSH may be difficult to obtain.
Diagnosis ● Nuclear isotope scanning detects hyperactive thy-
roid tissue. Procedure is relatively safe and simple
Hyperthyroidism should be suspected when any older
to perform, but requires access to a licensed facility,
cat presents with weight loss, and especially when the
which is not always available.
weight loss is associated with a good appetite.
● Trial course of anti-thyroid therapy (see below)
However, inappetence should not rule out hyperthy-
of approximately 30 days is not without risk of
roidism.
toxic side effects.
Physical examination usually reveals a thyroid nodule
on either or both sides of the trachea in the ventral cer-
vical region (80–90%).
These include most other causes of weight loss with a
Tachycardia and/or a gallop rhythm are usually present.
good appetite. However, hyperthyroidism typically
Liver enzymes (ALT and/or SAP) are often raised. occurs in older cats and presents with polyuria, polydip-
Hepatopathy may be secondary to a direct toxic effect sia, vomiting and/or diarrhea, so diabetes, renal disease,
of thyroid hormones, hepatic lipidosis, malnutrition or malassimilation syndromes (including IBD, pancreati-
hepatic hypoxia resulting from cardiac failure. tis/exocrine pancreatic insufficiency, and early intestinal
lymphosarcoma), acromegaly and hyperadrenocorti-
Definitive diagnosis is based on detecting elevated
cism are perhaps the most important differentials.
serum concentrations of total T4 (and/or T3).
Some cats with hyperthyroidism have a T4 concen-
Treatment
tration that is within the normal range. This may be
due to: Hyperthyroidism can be treated medically, surgically,
● Early or mild hyperthyroidism. or with radioiodine (I131).
Prior to deciding which treatment to use the cat

and/or agranulocytosis, hepatopathy and, rarely,
should be assessed for concurrent disease, especially
immune-mediated hemolytic anemia (IMHA).
renal disease, systemic hypertension and heart dis-
– Frequent side effects. Up to approximately 20%
ease, all of which occur commonly in association with
of cats develop anorexia, vomiting, lethargy,
hyperthyroidism.
● The interplay between systemic blood pressure and
hepatopathy ± jaundice, cutaneous reactions (typ-
ically pruritus of the head and neck), bleeding
renal function is complex. While systemic hyper-
tendencies or, very occasionally, myasthenia
tension is detrimental to kidney function, a sudden
gravis, or IMHA.
fall in blood pressure or a reduction in glomerular
– Mild side effects may resolve despite continued
filtration rate (e.g. associated with a sudden fall in
treatment.
T4) can exacerbate renal dysfunction by causing a
sudden fall in renal blood flow. Changes in T4 need Other medical therapies include:
to be made gradually so there are no sudden ● Atenolol (selective β adrenoceptor blocking agent)
1
changes in renal blood pressure. may be added to reduce tachycardia, arrhythmias and
● By maintaining renal blood pressure, hyperthy- hypertension (6.25 mg/cat PO every 24 hours).
roidism can mask low-grade renal insufficiency. It ● Stable iodine helps to decrease T3 and T4 synthesis
is essential to check serum urea and creatinine con- and reduce thyroid gland vascularity, but the effect
centrations and urine specific gravity prior to induc- can be transient and inconsistent. Give potassium
ing irreversible reduction of T4 (i.e. by thyroidectomy iodide 30–100 mg/cat/day PO for 10–14 days prior
or I131 treatment). A short course of medical therapy to surgery using 100 g potassium iodide/100 ml
may reveal the presence of masked renal insuffi- solution, or potassium iodate ~20 mg/cat every 12
ciency. hours PO.
● Calcium or sodium ipodate is a radiopaque iodine
Medical therapy tends to be given to stabilize the cat
agent that reduces T3 concentrations. Its effect can
prior to surgical treatment, to check for masked renal
be transient, and it may be difficult to obtain (15
disease prior to thyroidectomy or I131 treatment, or
mg/kg PO every 12 hours).
when neither I131 nor surgery are possible.
Surgical thyroidectomy. The success depends on the
Methimazole and carbimazole block T3 and T4 syn-
stability of the patient, the expertise of the surgeon (a
thesis. It takes 1–3 weeks before a significant decrease
bilateral thyroidectomy is usually performed), and the
in T4 concentrations occur after beginning treatment.
● Carbimazole is broken down to methimazole
expertise of the anesthetist (e.g. do not give atropine).
● Successful response rate is > 95%. Ectopic overac-
in vivo. Bioavailability and volume of distribution
tive thyroid tissue is a cause of failure, as it is usu-
of methimazole is highly variable between cats.
● Dose for both is 1.25–5.0 mg PO every 8–24
ally missed at surgery.
● Reduce the risks of surgery by making the cat euthy-
hours initially, reducing to every 12–24 hours. If
roid prior to surgery (see Medical therapy, above).
the cat has concurrent renal insufficiency, start
● Surgical risks include anesthetic risks in older
with a low dose and monitor renal values as dose
patients (often with concurrent renal ± cardiac dis-
is gradually increased. Preliminary studies with
ease), iatrogenic damage to parathyroid tissue lead-
topical transdermal applications show promise.
● When cat and owner compliance is good, the suc-
ing to transient or permanent hypocalcemia, or to
the local nerves leading to laryngeal paralysis or
cessful response rate is approximately 85% with
Horner’s syndrome.
medical treatment.
● Poor compliance results from: Radioiodine (I131) is taken up by and destroys the
– The need for frequent medication. overactive thyroid tissue, but spares the normal
– The need for frequent blood samples to look tissue.
for possible side effects. Blood dyscrasias occur ● Successful response rate is > 95%, but it may take
in 2–10% of cats and include eosinophilia, lym- a few weeks, or occasionally months, for the nor-
phocytosis, leukopenia, thrombocytopenia mal tissue to recover function.
● Availability of facilities and length of stay in hospi- ● The hypersensitivity may result from a primary,
tal varies from 2 days to 4 weeks depending on possible genetic, disorder, or arise secondary to
country and state, as it often depends on the inter- mucosal injury incurred by a number of different
pretation of radiation safety laws. disorders including bacterial, viral, protozoal or
● Side effects are few and include transient dysphagia fungal infections, bacterial overgrowth, food
or dysphonia, or permanent hypothyroidism (~2%). hypersensitivity, drug administration, metabolic
disease, neoplasia, pancreatitis or cholangiohep-
atitis.
Prognosis
● Regardless of the initial cause of the hypersensitivity,
Without treatment, cats with hyperthyroidism will usu- it results in increased mucosal permeability which
ally die of concurrent renal disease, heart disease, liver allows luminal antigens to cross the mucosa, lead-
disease or systemic hypertension. ing to inflammation and further mucosal damage.
With treatment, prognosis varies from very good to
guarded, dependent on the presence of heart disease,
Clinical signs
renal disease and systemic hypertension, whether or not
any damage has become permanent prior to treatment IBD can occur in any age, sex or breed of cat. While
of the hyperthyroidism, and which treatment options it is most commonly seen in middle-aged to older cats,
are available. a third of cases occur in cats of less than 2 years of age.
Some purebred cats may be predisposed.
Prevention Clinical signs include any combination of progres-
sive weight loss, and/or vomiting and/or diarrhea.
Since it is not known what triggers the development of
hyperthyroidism, it is currently not possible to prevent Weight loss may result from malabsorption and/
its onset. or inappetence (which usually occurs late in the dis-
ease). Not all cases show significant enteric signs,
so some cats present with only weight loss and a
INFLAMMATORY BOWEL DISEASE*** variable appetite.
Vomiting is often intermittent and may occur every
Classical signs
few days to weeks, often accompanied by anorexia and
● Any age, sex or breed of cat. lethargy. Vomiting is rarely associated with feeding. It
● Any combination of progressive weight may contain froth, bile-stained fluid and food or, occa-
loss, vomiting and/or diarrhea. sionally, blood.
Diarrhea can vary in consistency from almost well
formed to liquid. Some cats may show evidence of
Pathogenesis
large bowel involvement with mucus and/or blood and
Inflammatory bowel disease (IBD) is a group of increased frequency.
chronic idiopathic gastrointestinal tract disorders that are
Clinical signs may wax and wane, and tend to vary
characterized by infiltration with inflammatory cells.
with the type and severity of inflammation.
The infiltration may consist of lymphocytes, plasma
cells, neutrophils, eosinophils and/or macrophages, Physical examination is often unremarkable, but
and the inflammation may involve the stomach, small may reveal a thin cat, palpably thickened intestines,
intestine and/or colon. enlarged mesenteric lymph nodes and/or abdominal
discomfort.
The etiology is probably multifactorial and appears
to involve host hypersensitivity responses to antigens Concurrent pancreatitis and/or cholangiohepatitis
within the bowel lumen or mucosa. Suspected antigens may result in jaundice, a palpably enlarged liver and/or
include food, bacteria, parasites or self-antigens. anterior abdominal discomfort.
When lymphangectasia is present, severe hypopro- ● Survey radiographs tend to be unrewarding, but
teinemia may lead to subcutaneous edema and/or may reveal gas- or fluid-filled loops of intestines.
ascites. Barium studies may reveal flocculation or per-
sistent adherence of the barium to the mucosa,
irregular mucosal surfaces or delayed transit
Diagnosis times.
● Ultrasound examination may reveal intestinal
Before a diagnosis of IBD can be made, all other
wall irregularity or echogenicity. It may also be
causes of enteropathy must be ruled out. These include
used to examine the mesenteric lymph nodes and
bacterial enteritis (Helicobacter spp., Salmonella spp.,
other intra-abdominal structures.
Campylobacter spp., Clostridium perfringens, E. coli),
● Serum folate and cobalamin levels may be
intestinal parasites (helminths, cestodes, protozoans),
reduced because of malabsorption.
fungal enteritis, GI neoplasia (lymphosarcoma, adenocar-
● Serum feline trypsin-like immunoreactivity
cinoma) and viral enteritis (feline leukemia virus, feline
(fTLI) and feline pancreatic lipase immunoreac-
immunodeficiency virus, feline coronavirus, feline pan-
tivity (fPLI) may be helpful in the diagnosis of
leukopenia). IBD is diagnosed by documenting
exocrine pancreatic insufficiency (EPI) and pancre-
histopathological evidence of GI inflammation and
atic inflammation, respectively.
excluding all of other causes of it.
● Breath hydrogen analysis and sugar permeability
Baseline laboratory tests include hematology, serum studies may be used to try to demonstrate malab-
biochemistry (including total T4 concentration in older sorption and/or small intestinal bacterial overgrowth
cats), FeLV and FIV tests, urinalysis, fecal culture for (SIBO)/antibiotic-responsive diarrhea.
pathogenic bacteria and a full examination for fecal
A dietary trial should be performed in all except very
parasites.
ill patients prior to more invasive investigation.
● Performing all of these investigations can be expen-
● Feed a single highly digestible source of protein for
sive so the investigation should, where possible, be
at least 3–4 weeks and see if the clinical signs
tailored to the patient, and many clinicians start
resolve.
with a dietary trial (see below).
● Since the investigations are being performed to rule It is inadvisable to carry out treatment trials with
out other causes of enteropathy they are frequently antibiotics or corticosteroids prior to making a
unremarkable. However, IBD may be associated definitive diagnosis.
with a number of non-specific findings: ● This delays making the correct diagnosis, and may
– Hematology may reveal an inflammatory cause complicating intestinal bacterial overgrowth
response; neutrophilia, eosinophilia, lymphope- (antibiotics) or potentiate secondary infections
nia or monocytosis. Microcytic anemia may (corticosteroids).
result from chronic blood loss associated with
Definitive diagnosis requires the collection of intes-
severe IBD.
tinal biopsies.
– Hyperglobulinemia may result from chronic
● Mucosal biopsies may be collected by endoscopy.
inflammation. Panhypoproteinemia may be
Unfortunately, it is not always possible to make a
seen with severe protein-losing enteropathies.
definitive diagnosis from these biopsies, so in some
– Increases in liver enzymes may result from
cases, full-thickness biopsies must be collected via
associated hepatic inflammation (see below).
laparotomy or laparoscopy.
Non-invasive screening tests may provide additional ● IBD often causes no gross mucosal changes, but
information. These include abdominal radiography, changes that may be seen include increased granu-
ultrasound examination, assessment of serum folate larity and friability, the presence of erythema, ulcer-
and cobalamine (B12) levels, examination of fecal ations, and/or mass lesions and poor distensibility.
smears for the presence of undigested fats or starch, fat ● Multiple biopsies should be taken since the
absorption tests, breath hydrogen analysis and sugar inflammatory infiltrates may not be spread dif-
permeability studies (where available). fusely throughout the gastrointestinal tract.
● When performing laparotomy or laparoscopy it is Treatment

advisable to collect biopsies of the mesenteric
lymph nodes, liver and, if possible, pancreas, as The basic aims of treatment are to remove the source of
well as from multiple intestinal sites. Part of the antigenic stimulation and to suppress the inflammatory
liver and/or mesenteric lymph node biopsy, and response within the GI tract.
● Treatment typically involves dietary manage-
bile aspirated from the gall bladder can be sent for
culture. ment, ± metronidazole, ± prednisolone.
● Treatment should be tailored to each patient.
● Collection of duodenal aspirates for quantitative
● Relapses warrant critical reassessment of the case,
culture may help to determine the bacterial load of
the small intestine. and often require repeated intensification of treat-
● Gastric biopsies should always be assessed for the ment and/or the addition of more potent immuno-
presence of Helicobacter spp. suppressive drugs.
● Histopathology reveals inflammatory cells The diet should contain a single highly digestible
infiltrating the lamina propria, plus variable source of protein, ideally that the cat has not eaten before.
degrees of epithelial abnormality and glandular ● The diet should preferably contain few food addi-
distortion. tives, be gluten-free, lactose-free, low residue, not
– Lymphocytic-plasmacytic IBD is the most too high in fat, and adequately supplemented with
common form of IBD in the cat. It may occa- vitamins and minerals, especially B vitamins and
sionally progress to intestinal lymphosarcoma. potassium.
– Granulomatous enterocolitis is less common, ● High-fiber diets may help when the large bowel is
and often presents as GI obstruction. affected.
– Eosinophilic IBD is rare. It may be associated ● No other foods should be fed concurrently.
with eosinophilia and/or hypereosinophilic syn- ● During the initial phase of treatment, when the
drome where tissues other than the GI tract are bowel is recovering, it may be preferable to feed
also affected. either a home-cooked diet, a “sacrificial protein”
– Suppurative IBD is usually associated with an which the cat will then not be fed again, or protein
infectious etiology. hydrolysate which has reduced molecular weight
– Other forms also exist and many cats have mixed protein and is supposed to be less antigenic. This
populations of inflammatory cells. should be fed for 1–2 months, after which time the cat
● Unfortunately, when lymphangectasia is present, can then be fed a commercial “hypoallergenic” diet,
severe hypoproteinemia may render these patients a or further protein sources can be gradually reintro-
poor anesthetic and surgical risk. It may therefore be duced. If feeding homemade diets long-term, great
necessary to make a presumptive diagnosis based on care should be taken to ensure they are balanced.
the presence of diarrhea, panhypoproteinemia and
lymphopenia in the absence of finding other diseases Metronidazole often forms the mainstay of treat-
on hematology, serum biochemistry, fecal evalua- ment. Its effect against anaerobic bacteria helps to
tion, abdominal ultrasound examination ± mucosal reduce secondary bacterial overgrowth. It is also effec-
biopsies. tive against protozoa (e.g. Giardia spp.), has positive
effects on brush border enzymes levels, and is
believed to alter the immune function of the GI tract,
perhaps by altering neutrophil chemotaxis and inhibit-
Differential diagnosis ing cell-mediated immunity. Administer 7.5–15 mg/kg
These include most of the other causes of weight loss PO q 8–12 hours for 2–4 weeks, then taper gradually
with a good appetite. However, since cats with IBD over 1–2 months. Some authors suggest that it is inad-
usually develop vomiting and/or diarrhea, other causes visable to give very prolonged courses.
of enteropathy, cholangiohepatitis, pancreatitis, Immunosuppressive agents:
hyperthyroidism and the other malassimilation syn- ● Immunosuppressive doses of corticosteroids are
dromes (including alimentary lymphosarcoma) should usually required. Administer prednisolone 2–4
be considered as important differentials. mg/kg q 12–24 hours PO, then taper over 1–3
months and maintain on every other day doses, if include vitamin E (50–200 IU/cat/day PO),
needed. Use of budesonide (1 mg/cat PO q 24 hours) vitamin A (1000–5000 IU/cat/day PO), vitamin C
instead of prednisolone may help to reduce sys- (50–80 mg/kg/day PO), zinc (7.5 mg/cat/day PO), and
temic signs of corticosteroid administration. N-acetyl glucosamine (125–1500 mg/cat/day PO).
● Other immunosuppressive agents may be consid-
ered. While they all have potential side effects and Prognosis
warrant regular monitoring chlorambucil (2–5
The prognosis depends on the nature and severity of the
mg/m2 PO up to once every 48 h) is often very
GI infiltration, and the presence of concurrent and/or
well tolerated. Other less favorable options
associated disease, such as pancreatitis or cholangio-
include cyclophosphamide (50 mg/m2 PO up to
hepatitis. In general, the prognosis for control is rea-
four times a week), cyclosporine (0.5–8.5 mg/kg
sonably good, but the condition cannot be cured, and
every 12–24 hours, indefinitely) or, in the cases of
many cats will need treatment for the rest of their life.
colonic disease, sulfasalazine (10–20 mg/kg/day
PO for 7–10 days). Prevention
Supportive therapies are often recommended. Since it is not known what triggers IBD to develop, it is
However, few have been assessed using controlled not currently possible to prevent its onset.
studies in cats.
● Tylosin may be effective for its antibiotic actions as
DIABETES MELLITUS**
well as other, as yet undefined, effects (5–20 mg/kg
every 6–12 hours PO). Classical signs
● Motility modifiers may give short-term palliative
relief in cases of very watery diarrhea (loperamide ● Usually seen in older, obese, neutered
0.04–0.2 mg/kg every 8–12 hours PO). male cats, and Burmese cats may be over-
● Metoclopramide may be useful for its anti-emetic represented.
and prokinetic effects (0.2–0.5 mg/kg PO up to four ● History of polyuria, polydipsia and
times a day, being given just prior to feeding, or as polyphagia.
a constant IV infusion 1–2 mg/kg over 24 hours). ● Possible initial weight gain, followed by
● Cisapride is a good prokinetic, but it is now more weight loss.
difficult to obtain (0.3–1.0 mg/kg every 8–12 hours
PO). Pathogenesis
● Cobalamin and folate may be needed as they are
often reduced by malabsorption (cobalamin Diabetes results from a variety of mechanisms that
125–250 μg/week SC or IM for 6–8 weeks then q cause an absolute or relative lack of insulin.
2–4 weeks [50–100 μg/cat/day PO]; folate 0.5–1.0 Classification of diabetes in cats is best made by cause,
mg/cat/day PO for 1 month). rather than whether or not they require exogenous
● Vitamin K1 is often required because fat malab- insulin.
sorption results in poor absorption of fat-soluble
vitamins like vitamin K, and this can result in Type 1 diabetes, previously called juvenile-onset dia-
abnormal hemostasis (0.5 mg/kg/day SC for 3–4 betes, is due to immune-mediated destruction of pan-
days, then once weekly). creatic islet beta cells. It appears to be very rare in cats.
● Glutamine may be given as an energy source for Type 2 diabetes results from impaired insulin secre-
the GI mucosal cells (250–5000 mg/cat/day PO, tion, and peripheral resistance to the action of insulin.
indefinitely). Hyperglycemia results from decreased glucose uptake
● Lactobacillus acidophilus may be given as a probi- in tissues and increased hepatic glucose production.
otic to help restore intestinal flora (50–500 M Many cats with diabetes appear to have type 2 diabetes.
organisms/cat/day PO until feces return to normal). ● This is often associated with accumulation of islet-
● Various nutritional supplements may be given for specific amyloid polypeptide (IAPP), which
their potential anti-inflammatory properties. These occurs in aggregates around pancreatic islets. While
IAPP is co-secreted and accumulates as amyloid in It can occur in any age, sex or breed of cat, but is seen
normal cats as they age, it accumulates more exten- most frequently in older obese neutered male cats.
sively in cats with diabetes. The accumulation of
In Australia, New Zealand and Great Britain, Burmese
islet amyloid eventually leads to loss of beta cells.
cats appear to be predisposed, with ~1 in 50 affected.
● Obesity is a significant risk factor for diabetes
because it results in peripheral insulin resistance. The most consistent signs are polyuria, polydipsia
Other specific types of diabetes, previously called type 3 and polyphagia. In the early stages these signs may go
or secondary diabetes, results from diseases which destroy unnoticed by the owners, possibly because of free
beta cells or cause marked insulin resistance, such as: choice feeding and outdoor toileting habits.
● Beta cell destruction due to pancreatitis or neopla-
Possible initial weight gain is followed by weight
sia. Pancreatitis may be more common than previ- loss.
ously thought, as >50% of diabetic cats have
evidence of past or current pancreatitis at necropsy Urinary tract infections are common, and cats may
(see below under pancreatitis/exocrine pancreatic present with signs of cystitis and/or renal failure.
insufficiency). The coat may be ill kept and a pot-bellied appearance
● Insulin resistance resulting from unrelated
may result from hepatomegaly.
endocrinopathies, e.g. acromegaly or hypera-
drenocortisim (see below under Acromegaly and Hindlimb weakness and a plantigrade stance due to dia-
Hyperadrenocorticism). betic neuropathy are seen quite frequently, but cataracts
● Insulin resistance from drug administration, e.g. occur rarely.
corticosteroids, megestrol acetate. Cats are frequently presented only when they become sys-
60–70% of cats with diabetes require exogenous temically ill with signs of anorexia, vomiting and/or diar-
insulin, at least temporarily. rhea, jaundiced and depression (see page 261, The Cat
With Depression, Anorexia or Dehydration).
10–80% of cats with diabetes may lose the need for
exogenous insulin. This may result from: Cases of diabetes that result from chronic pancreatitis
● Correction of ‘glucose toxicity’. Prolonged hyper- may have a history that includes episodes of depres-
glycemia causes impaired insulin and increased sion, anorexia, vomiting, diarrhea and/or abdominal
peripheral insulin resistance, termed glucose toxic- pain. Since diabetes is most likely to occur when most
ity. Exogenous insulin administration and reduction of the pancreatic mass has been destroyed, it may be
of hyperglycemia can result in resolution of this accompanied by signs of exocrine pancreatic insuffi-
toxicity and return of sufficient insulin secretion to ciency, evidenced by large quantities of voluminous
maintain normoglycemia. Long-acting insulin fatty feces and a voracious appetite (see below under
administered twice daily and a low-carbohydrate, pancreatitis/exocrine pancreatic insufficiency).
high-protein diet appear to facilitate this.
● Reduction of obesity which deceases insulin resist-
Diagnosis
ance.
● Resolution of pancreatitis. Diagnosis of diabetes mellitus is based on docu-
● Treatment of underlying disease, e.g. acromegaly or menting persistent fasting hyperglycemia (> 11
hyperadrenocortisim. mmol/l [200 mg/dl]) and glucosuria in a cat with
● Removal of diabetogenic drugs, e.g. progestogens appropriate clinical signs (polyuria, polydipsia and
(megestrol acetate) or exogenous corticosteroids. polyphagia).
Stress-induced hyperglycemia can result in glucose lev-
Clinical signs els above the renal threshold and hence glucosuria, so a
single documentation of these findings is not diagnos-
Diabetes is the second most common endocrinopathy
tic of diabetes.
in cats following hyperthyroidism. However, while it
used to affect ~1 in 400 pet cats, in Great Britain this has Allowing the cat to settle down then re-testing it after a
risen to ~1 in 200. few hours may help to determine whether or not the
hyperglycemia is stress-induced. Alternately, the owner calorie intake to no more than 75% of maintenance
can be asked to test the cat’s urine for the presence of requirements and monitoring for changes in insulin
glucose when it is at home. requirement. Aim for no more than 2% weight loss per
week.
Assessing serum fructosamine or glycosylated hemo-
globin concentrations will give an indication of how Dietary modification – all cats with diabetes benefit
high the blood glucose concentration has been during from being fed a well-balanced diet on a regular, con-
the preceding 2–3 weeks, and 1–2 months, respectively. sistent, feeding schedule.
● Obese cats may benefit from being fed a low-calorie,
Many cats with diabetes have mild to moderate
high-fiber diet to help them lose weight. However,
increases in serum concentrations of cholesterol and
a low-carbohydrate, high-protein diet may be more
liver enzymes. However, more severe changes such as
beneficial to minimize demand for insulin secretion
bilirubinemia, acidemia, uremia and electrolyte disor-
and minimize post-prandial hyperglycemia.
ders are unlikely to be present in a cat that is maintain-
● Non-obese cats benefit from being fed a low-car-
ing a good appetite, that is, a cat with uncomplicated
bohydrate, high-protein diet. The choice of diet
diabetes.
may be affected by concurrent illness, especially
Ketones may or may not be present in the urine. Their renal disease.
presence further confirms the diagnosis of diabetes. By ● Regular feeding is essential. Cats on once-daily
the time a cat has developed diabetic ketoacidosis it is insulin are usually fed just before their morning
unlikely to be maintaining a good appetite (see page 355, insulin, then again in the early evening. Cats on
The Thin, Inappetent Cat). twice daily insulin are usually fed just before both
insulin injections. Free-choice feeding can be bene-
ficial, but it is important to monitor the amount of
Differential diagnosis food eaten on a daily basis.
These include most of the other causes of weight loss Oral hypoglycemic agents act to increase insulin
with a good appetite. However, since cats with diabetes secretion, decrease peripheral insulin resistance, and/or
develop polyuria and polydipsia, hyperthyroidism and decrease absorption of glucose from the intestinal tract.
renal disease (particularly protein-losing nephropathies) They may successfully control some non-ketotic,
should be considered as important differentials, as should uncomplicated diabetic cats, either temporarily or
underlying causes of diabetes, such as acromegaly and longer term, particularly when given in conjunction
hyperadrenocorticism. with dietary modification. There are several different
types of drugs that have been shown to be at least some-
what effective in cats.
Treatment
● Sulfonylureas, e.g. glipizide (0.25 mg/kg PO q
Treatment consists of various combinations of 8–12 h, adjust dose as needed). Side effects include
weight loss, dietary modification, oral hypoglycemic vomiting, anorexia and hepatopathy. Periodic
agents and insulin administration. checks for serum biochemistry and hematology are
● While the signs of diabetes in obese cats may recommended. It may take a few weeks of medicat-
resolve with dietary modification alone, most cats ing to see the full effect of the drug.
need at least temporary medical intervention. ● Alpha-glucosidase inhibitors, e.g. ararbose
● Oral hypoglycemic agents may be successfully (12.5–25 mg/cat with meals). Side effects include
used in some cases of uncomplicated diabetes, or flatulence, soft feces and diarrhea.
once glucose toxicity has resolved following insulin ● Transition metals, e.g. vanadium (0.2 mg/kg/day
therapy. in food). Side effects include anorexia, vomiting,
● Insulin is required for most diabetics, at least ini- diarrhea and renal disease; chromium (200
tially. μg/cat/day PO). Side effects are unknown.
Obese cats usually benefit from weight loss. Insulin: There are a number of different types of insulin,
However, this should be done very gradually, restricting and the choice is often based on personal preference.
● Most cats with uncomplicated diabetes respond during a 12–24 h period. The level of the
well to once- or twice-daily subcutaneous admin- blood glucose at its nadir (lowest point) deter-
istration of lente, protamine zinc insulin (PZI) or mines whether or not the dose of insulin needs
glargine. to be changed, while the duration of insulin
● The source of the insulin does not appear to be action determines how frequently it needs to
important in cats, as anti-insulin antibodies do not be given.
cause many problems.
Water drunk measured at home on at least two con-
● The duration of action of the different preparations
secutive days is better correlated with mean blood
varies between cats (lente – peak 2–10 h, duration
glucose than is fructosamine concentration. If water
of action 6–16 h; PZI – peak effect at 3–12 h, dura-
intake is < 20 ml/kg on wet food or < 70 ml/kg on
tion of action 6–24 h; glargine peak effect at 16 h,
dry food, it indicates good glycemic control.
duration of action > 24 h). In general, PZI and
glargine are preferred because of their longer dura- At all times, but especially after altering the insulin
tion of action, improved glycemic control and dosage, the owners should be warned to look for signs
increased remission rates. of hypoglycemia (weakness, lethargy, shaking, ataxia,
● Start at ~0.25–0.5 IU insulin/kg/per injection, then collapse and coma). If these signs occur, the cat’s gums
adjust as necessary, usually by 0.5–1.0 IU per dose. should be rubbed with sugar water, jam or honey, and
See page 239, Diabetes mellitus in The Cat With immediate veterinary attention sort.
Polyuria or Polydipsia, for detailed criteria for ● Reasons for apparent insulin resistance include
adjusting the insulin dose. ineffective insulin (out of date, poor storage,
● The aim of therapy is to prevent the clinical signs of incomplete mixing), poor injection technique,
diabetes and, if possible, maintain blood glucose out-of-date urine test strips and insulin overdose
concentration between 5.5–14 mmol/l (100–250 leading to insulin-induced hyperglycemia. The
md/dl). Somogyi over-swing occurs when hypoglycemia
● It takes 2–3 days for glucose homeostasis to adjust induces counter-regulatory hormones such as epi-
after starting or altering insulin doses. Any changes nephrine and glucagon to induce hyperglycemia.
in dose should therefore be based on recurring True insulin resistance can result from recent
effects, not a single urine (or blood) glucose deter- weight gain, infection, acromegaly, hyperadreno-
mination. Owners can monitor water intake, urine corticism, hyperthyroidism, the administration of
glucose and ketone levels at home. Ideally glucose diabetogenic drugs, renal or hepatic insufficiency,
will be negative or trace, and ketones will be nega- anti-insulin antibodies or presence of certain
tive. Glucose curves can also be performed at home types of tumor.
by obtaining a drop of blood for glucose testing via
ear vein pricking.
– It is generally recommended that glucose curves Prognosis
be performed every 1–2 weeks until the diabetes
The prognosis is very variable. It depends on the
is stable. After this time they need be performed
owner’s commitment, the presence of concurrent and
less frequently, and the dosage can be adjusted
interacting disease and the ease of glycemic control. If
in response to changed clinical signs, ± serum
diabetes arises secondary to chronic pancreatitis it can
fructosamine concentrations.
be particularly difficult to control.
– The usefulness of glucose curves can be very
limited in easily stressed cats that become hyper-
glycemic whenever they are hospitalized.
Prevention
Anorexic cats may have a lower blood glucose
concentration in the hospital than at home when The risk of developing diabetes can be reduced by not
eating. allowing cats to become obese or physically inactive
– A glucose curve is performed by giving the cat and not giving long courses of diabetogenic drugs. A
its usual breakfast and dose of insulin, then low-carbohydrate, high-protein diet may also help to
determining blood glucose level every 1–2 h reduce the demand on beta cells to produce insulin.
● Lactational and prenatal infections do not occur.

INTESTINAL PARASITES**
● Rodents can act as transport hosts.
● Infection can cause cutaneous larva migrans in
Classical signs
humans.
● Usually in kittens or young adult cats.
Adult tapeworms live in the small intestine and both
● Weight loss or failure to gain weight,
D. caninum and T. taeninaeformis require an interme-
usually with a good appetite.
diate host to complete their life cycle. Gravid proglot-
● Diarrhea and/or vomiting may be present.
tids containing many eggs are released from the adult
worms. They may rupture within the intestines, or
Pathogenesis remain intact and pass out in the feces and be seen
around the cat’s anus.
Intestinal parasites that can infect cats and, at least
● Dog and cat fleas are the intermediate hosts for
occasionally, cause weight loss associated with a good
D. caninum.
appetite include nematodes (large ascarid roundworms
● Rodents are the intermediate hosts for T. taeni-
Toxocara cati and Toxascaris leonina), and hook-
naeformis.
worms (Ancylostoma braziliense, A. tubaeforme
and Uncinaria stenocephala), cestodes (tapeworms Isospora spp. live in intestine of cats and shed oocysts
Dipylidium caninum and Taenia taeninaeformis), and into the environment via the feces. Sporulated oocysts
protozoans (coccidians, Isospora felis, I. rivolta, and can be directly ingested by other cats.
Cryptosporidium parvum and flagellates Giardia ● Rodents harboring cyst stages can act as transport
lamblia and Tritrichomonas foetus). hosts.
● Infection and clinical disease is seen most com-
T. cati and Isospora spp. are the most common para-
monly in cats kept in large unhygienic groups.
sites of kittens. D. caninum, T. taeninaeformis and
G. lamblia are the most common parasites of adult cats. C. parvum lives in the small intestine and sheds
oocysts that can either break open to release sporo-
Adult T. cati live in the small intestine of cats. Eggs
zoites into the intestine resulting in chronic infection or
are passed into the environment with the feces to be
be passed out into the environment where they can
ingested by other cats, in which they migrate via the
remain viable for many months.
liver and lungs to the small intestine.
● Infection can cause severe disease in immuno-defi-
● Larvae can be transmitted lactationally to kittens,
cient humans.
but prenatal infection does not occur.
● Rodents can act as transport hosts. In cats, G. lamblia lives in the jejunum and ileum.
● Infection can cause visceral larva migrans in humans. Environmentally resistant cysts are shed in feces, con-
taminate drinking water or food, and are then ingested
Adult T. leonina live in the small intestine of cats.
by other cats.
Eggs are passed into the environment with the feces to
● Infection and clinical disease are seen most com-
be ingested by other cats where they mature in the
monly in cats kept in large unhygienic groups.
wall of the small intestine.
● Giardia spp. do not appear to be host-specific and
● Lactational and prenatal infections do not occur.
have a world-wide distribution in tropical and tem-
● Rodents can act as transport hosts.
perate areas.
● Does not cause visceral larva migrans in humans.
In cats, T. foetus lives in the colon and sheds flagellated
The prevalence of hookworms varies. Ancylostoma
protozoa into the feces. Infection and clinical disease
spp. prefer warm, humid climates, while U. steno-
are seen most commonly in young cats kept in large
cephala can live in colder climates. Severe hookworm
unhygienic groups.
infections are usually seen in warm, moist climates.
● Adults hookworms live in the small intestine of
Clinical signs
cats. Eggs are passed into the environment with the
feces and then hatch. They can be ingested by other The prevalence of intestinal parasites varies with geo-
cats or infect them by skin penetration. graphic location, the level of sanitation, whether or
not the cat is an indoor or outdoor animal, and Since some parasites can be transmitted lactationally
whether or not it hunts and eats its prey. (T. cati), and infections are frequently more severe in
young cats, all young cats should be evaluated for intes-
While infection is common, disease is seen most com-
tinal parasites or treated against the common parasites
monly in young cats living in poorly cleaned multi-
of the region.
animal environments.
Infection rarely causes systemic changes. However, hema-
In these situations, episodes of disease may be seen in
tology may reveal an eosinophilia and, in severe cases,
kittens or cats of similar ages, and may be preceded by
low serum proteins may be found on serum biochemistry.
a stressful event such as an environment change, addi-
tion of new cats, or weaning, etc. With the exception of tapeworm segments, most intes-
tinal parasites are not noticed in the feces.
Clinical signs vary but typically include diarrhea and
vomiting (especially with T. cati infections), but Fecal floatation techniques are used to diagnose most
anorexia is not often present. intestinal parasites (round worms, hook worms and
● Ascarids: In adult cats, infections are usually sub- Isospora spp.). However, special techniques may be nec-
clinical, but kittens and young cats may develop essary for some parasites, such as C. parvum (special
vomiting, small bowel diarrhea, a pot-bellied stains or, possibly, fecal antigen tests), Giardia spp. (direct
appearance, poor coat condition and a failure to saline fecal smears or fecal antigen tests), or T. foetus
thrive. (PCR, ‘In Pouch’ culture or direct saline fecal smears).
● Hookworms: Infections cause less disease in cats
Rather than confirming the presence of an infection
than dogs, and most disease is seen in young adult
with fecal tests, a therapeutic trial with a suitable drug
cats that live in poorly cleaned, crowded conditions.
may be considered.
A heavy infection can cause weight loss, poor coat
condition and melena.
● Tapeworms: Infections are usually subclinical, but Differential diagnoses
heavy infections can cause anal pruritus, vomiting,
Differential diagnoses include most of the other causes
diarrhea, weight loss and, occasionally, intestinal
of weight loss with a good appetite. Inadequate nutri-
obstruction.
tion becomes the most likely differential when there
● Isospora spp.: Infections rarely cause clinical dis-
are no signs other than weight loss. However, the vari-
ease in adult cats unless they are stressed or
able presence of gastrointestinal signs is more sug-
immunocompromised. In kittens, infections can
gestive of some of the malassimilation syndromes
range from subclinical through to severe hemor-
such as IBD, exocrine pancreatic insufficiency, or
rhagic diarrhea.
early alimentary lymphosarcoma.
● C. parvum: Infections are usually subclinical, but
can also cause acute or chronic small bowel diar-
rhea, or result in lymphocytic-plasmacytic duodeni- Treatment
tis.
Roundworms and hookworms may be treated with
● G. lambia: Infections can be subclinical, or cause
pyrantel pamoate (20 mg/kg/day – two doses need to be
acute, chronic or episodic small bowel diarrhea
given 2–3 weeks apart) or fenbendazole (20–50
where intestinal malabsorption may result in
mg/kg/day usually given for 3–5 days, then repeated 2–3
mucoid, soft, foul-smelling feces.
weeks later) which are both safe and effective in cats.
● T. foetus: Infections can be subclinical or cause
chronic large bowel diarrhea. Tapeworms may be treated with praziquantel
(3.5–7.5 mg/kg SC, PO) or epsiprantel (2.75 mg/kg
Diagnosis PO). One dose is effective against D. caninum and
T. taeninaeformis.
Intestinal parasites should be suspected in any cat, but
especially those coming from a poorly cleaned multi- Isospora spp. may be treated with trimethoprim/sul-
animal environment in a geographic region with a high fonamide (15 mg/kg q 12 hours PO for 10–14 days),
prevalence of intestinal parasites. plus improved sanitation.
C. parvum can be difficult to treat, but tylosin (10–15 Clinical signs

mg/kg q 12 hours PO for 28 days, but may need higher
doses), paromycin (125–165 mg/kg q 12 hours PO for Disease can be seen in any age, sex or breed of cat, but
5 days), or azithromycin (7–15 mg/kg q 12 hours PO is seen most commonly in kittens from poor envi-
for 5–7 days) may be effective. ronments.
Giardia spp. may be treated with fenbendazole (10–30 It may also be seen in pregnant or lactating queens,
mg/kg/day PO for 5 days) or metronidazole (10–25 or in cats that have recently changed environments:
mg/kg q 12–24 hours PO for 5–7 days). Repeated treat- e.g. changed from having a sedentary life in a warm
ment may be needed. The possibility of vaccination is environment, to having an active life in adverse weather
currently being studied. conditions.
T. foetus may be treated with ronidazole (10–30 mg/kg Affected cats show a generalized loss of body condi-
q 12 hours PO for 14 days). tion despite a good appetite.
They are usually bright and active until terminal stages
Prognosis of malnutrition.
If given the correct treatment, the prognosis for full There are few specific findings, but severe cases may
recovery is usually very good. show lethargy, muscle weakness, depression, diarrhea,
neurological signs, blindness and/or ascites.
Severe infections can occasionally result in permanent
intestinal damage and chronic clinical signs. Diagnosis
Resistant C. parvum, Giardia spp. and/or T. foetus Diagnosis is based on resolution of clinical signs fol-
infections can occasionally result in chronic disease. lowing correction of diet. If necessary, rule out other
likely differentials.
Prevention
Severe infections can usually be prevented by having a
good preventative worming policy, giving prompt and These include most other causes of weight loss with a
effective treatment to any animals found to be infected good appetite. However, given the lack of other clinical
or carrying these organisms, improving sanitation, and signs, the most likely differentials include intestinal
reducing stocking densities. parasites and some of the malassimilation syn-
dromes including IBD, exocrine pancreatic insuffi-
ciency, early alimentary lymphosarcoma.
INADEQUATE NUTRITION**
Treatment
Classical signs
Changing the diet to a suitable well-balanced diet is
● Seen in any age, sex or breed of cat, but usually all the treatment that is necessary. Very severe
mostly typically in kittens from poor cases may need supportive care and nursing.
environments.
● Weight loss, often in association with a Prognosis
voracious appetite.
● Few other signs until terminal stages of Provided that the malnutrition was not too severe or
malnutrition. prolonged, the prognosis for recovery is very good.
Prevention
Pathogenesis Cats should always be fed appropriate amounts of a
Disease due to inadequate nutrition is caused by feed- suitable well-balanced diet that has been designed to be
ing an inadequate or inappropriate diet. fed to cats.
ALIMENTARY LYMPHOSARCOMA* Diagnosis

Hematology may reveal non-specific changes includ-
Classical signs ing neutrophilia and lymphopenia. Lymphoblasts may
● Usually older cats. occasionally be seen in the circulation.
● Anorexia and weight loss, ± vomiting, ± Serum biochemistry may reveal panhypoproteinemia
diarrhea. and/or hyperbilirubinemia.
● Early in disease may have a good appetite.
Most cats test negative for FeLV infection.
Survey radiographs may reveal gas- or fluid-filled
Pathogenesis loops of intestines. Barium studies may reveal floccula-
Lymphosarcoma is the most common GI neoplasia tion or persistent adherence of the barium to the
of cats. mucosa, irregular mucosal surfaces, luminal narrowing
or intramural thickening.
Alimentary lymphosarcoma can occur isolated to the
intestine, or as part of multicentric disease. Ultrasound examination may reveal intestinal wall
irregularity, thickening, or altered echogenicity, and/or
It can occur as a focal lesion or diffuse intestinal enlarged mesenteric lymph nodes, liver or spleen.
thickening. It can arise in the stomach, small intestines
and/or colon, and involvement of the ileocolic junction Diagnosis is made by examination of a GI tract fine-
is common. needle aspirate or biopsy, with or without biopsies
● Concurrent involvement of mesenteric lymph
from mesenteric lymph nodes and/or other abdominal
nodes, liver and/or spleen is not uncommon. organs.
The cells may be lymphocytic, lymphoblastic, of B or Differentiating lymphocytic (small cell) alimentary
T cell origin or, occasionally, large granular lympho- lymphosarcoma from lymphocytic-plasmacytic IBD
cytes or globular leukocytes. can be very difficult.
Lymphoblastic lymphosarcoma are more likely than Determining which types of cells are involved can aid
lymphocytic lymphosarcoma to present as an abdomi- in treatment and prognosis (see below).
nal mass.
Alimentary lymphosarcoma may arise secondary to Differential diagnosis
chronic lymphocytic-plasmacytic IBD.
These include most of the other causes of weight loss
with a good appetite. However, since cats with alimen-
tary lymphosarcoma usually develop vomiting and/or
Clinical signs diarrhea, other causes of enteropathy, IBD, cholan-
Typically seen in older cats of any sex or breed. giohepatitis, pancreatitis, hyperthyroidism and the
other malassimilation syndromes should be consid-
History usually includes anorexia and weight loss, ered as important differentials.
but early in the disease the appetite may be good.
Vomiting and/or diarrhea may or may not be
present. Treatment
Some cats develop fever, ascites or jaundice, and at this Localized alimentary lymphosarcoma may respond to
stage they rarely maintain a good appetite. surgical resection and adjunct chemotherapy.
Physical examination typically reveals a thin cat ● Large masses involving the entire thickness of the
with a palpable abdominal mass(es) and/or thick- bowel wall should not be treated with chemother-
ened intestines. apy alone as this may result in gut perforation.
Diffuse lymphosarcoma are best treated with com- Pathogenesis

bination chemotherapy.
● Lymphoblastic lymphosarcoma and lymphosarcoma
Pancreatitis develops when there is activation of
affecting more than just the GI tract are best treated digestive enzymes within the pancreas, which results
with combinations of cyclophosphamide, vincristine in some degree of auto-digestion. While there are many
and prednisolone, ± doxorubicin, ± l-asparaginase possible causes of pancreatitis in cats, over 90% are
(see page 676, for protocols and doses). idiopathic.
● Lymphocytic lymphosarcoma may respond more In cats, the most common forms of pancreatic disease
favorably to a combination of only prednisolone are chronic non-suppurative (lymphocytic/plasma-
(10 mg/cat/day PO) and chlorambucil (2–5 mg/m2 cytic or, occasionally, eosinophilic) pancreatitis and
PO up to once every 48 h or 15 mg/m2/day for 4 suppurative (neutrophilic) pancreatitis, while acute
days PO, every 3 weeks). septicemic pancreatitis and exocrine pancreatic insuffi-
ciency (EPI) are seen less frequently.
Prognosis It is the presence of exocrine pancreatic insuffi-
The prognosis is guarded. The best prognostic indica- ciency that results in weight loss with a good, often
tors are response to therapy and the duration of the first ravenous, appetite.
● Primary exocrine pancreatic insufficiency is
remission.
uncommon in cats. However, exocrine pancreatic
Response rates to chemotherapy range from 30–70%, insufficiency secondary to chronic, often episodic,
with median remissions of 4–23 months. pancreatitis is being recognized more frequently.
● In exocrine pancreatic insufficiency the lack of pan-
Being FeLV positive or having lymphoblastic lym-
phosarcoma are negative indicators, while having creatic digestive enzymes leads to maldigestion and
lymphocytic lymphosarcoma is a positive indicator. malabsorption.
● Lymphoblastic lymphosarcoma has a complete In cats, pancreatitis is often seen in association with
remission rate of 18%, and median survival time of idiopathic inflammatory bowel disease (IBD),
2.7 months. cholangitis/cholangiohepatitis complex, or both
● Lymphocytic lymphosarcoma has a complete remis- (termed “triaditis”).
sion rate 69%, median survival time 22.8 months. ● This association may occur because the pancreatic
duct in some cats enters the common bile duct
Prevention before it opens into the duodenum. In other cats, the
pancreatic and bile ducts enter the duodenum sepa-
Since it is not known what triggers lymphosarcoma to rately.
develop, it is not currently possible to prevent its ● When disease occurs in the small bowel it may
onset. However, since lymphocytic IBD has been seen ascend the common bile duct and from there affect
to progress to lymphosarcoma, it would appear sensible the pancreas and the rest of the biliary tree, or it may
to try to control lymphocytic IBD as well as possible, to ascend both ducts from their opening in the duode-
try to prevent its progression. num. For the same reason, disease of the biliary tree
or pancreas may affect the other two regions.
● Regardless of which organ is affected first, the
CHRONIC PANCREATITIS/EXOCRINE
PANCREATIC INSUFFICIENCY* other two organs tend to become involved as
inflammatory mediators, infectious agents, bile
Classical signs and/or pancreatic secretions pass from one area to
another.
● Typically seen in middle-aged to older cats.
● History of episodic anorexia, lethargy, Clinical signs
● If also diabetic; polyuria and polydipsia. Chronic pancreatitis can occur in any sex or breed of
cat, and is typically seen in middle-aged or older cats.
Burmese cats in Great Britain may be predisposed to demonstrate undigested fat (Sudan III or IV stain) and
pancreatitis. starch (iodine stain), and fat absorption tests.
History and clinical signs of chronic pancreatitis tend Abdominal radiographs are usually unremarkable.
to be very variable and non-specific.
Ultrasound examination may reveal pancreatic
They usually include episodes of anorexia or variable enlargement, irregularity or heterogeneity, evidence of
appetite, with or without vomiting and/or diarrhea, peripancreatic fat necrosis, enlargement of mesenteric
weight loss and/or possible abdominal pain. lymph nodes, and/or evidence of post-hepatic biliary
obstruction (enlarged gall bladder, thickened bile or
Once exocrine pancreatic insufficiency develops the
tortuous common bile duct).
cat is usually thin, has a greasy coat and produces
large quantities of voluminous, fatty, foul-smelling Evaluation of serum trypsin-like immunoreactivity
feces or has severe diarrhea. (TLI) may be helpful.
● The species-specific assay must be performed on a
Cats with chronic pancreatitis may also develop
fasted serum sample.
episodic or persistent diabetes mellitus, which is seen
● Serum TLI may be increase with pancreatitis and
as polyuria and polydipsia.
decrease with exocrine pancreatic insufficiency.
When both exocrine pancreatic insufficiency and dia- ● While it consistently diagnoses exocrine pancreatic
betes occur concurrently the polyphagia can be pro- insufficiency, it often fails to confirm pancreatitis,
found. possibly because chronic inflammation has reduced
Physical examination is often unremarkable, but may the overall ability of the pancreas to produce TLI.
reveal anterior abdominal discomfort, a palpably irreg- Evaluation of serum pancreatic lipase immunoreac-
ular and enlarged pancreas, or hepatomegaly associated tivity (PLI) may be helpful.
with cholangitis/cholangiohepatitis complex. ● The species-specific assay must be performed on a
fasted serum sample.
Diagnosis ● Serum PLI may increase with pancreatitis and
Chronic pancreatitis is very difficult to diagnose. appears to be more sensitive than TLI.
Hematology and serum biochemistry may reveal non- A therapeutic trial with replacement pancreatic
specific changes. enzymes may be considered (see under treatment).
● Hematology may show neutrophilia, neutropenia ● Providing that any associated IBD and/or cholangi-
(associated with sequestration during acute exacer- tis/cholangiohepatitis complex has been addressed,
bation), monocytosis and/or a mild non-regenera- the response to treatment may be dramatic. However,
tive anemia. a positive response is not diagnostic of chronic pan-
● Serum biochemistry may show hyperglobuline- creatitis and/or exocrine pancreatic insufficiency.
mia, bilirubinemia and raised liver enzymes
(depending on the degree of associated cholangi- Pancreatic biopsy is required to confirm a diagnosis
tis/cholangiohepatitis complex), and/or hyper- of pancreatitis.
● Because triaditis is common, it is advisable to col-
cholesterolemia, hypertriglyceridemia and
hyperglycemia (often associated with concurrent lect liver and intestinal biopsies at the same time,
diabetes). Hypocalcemia may be associated with and send part of the liver biopsy and a sample of
severe disease. bile for culture.
● Serum amylase and lipase tests are rarely useful
in the diagnosis of pancreatitis in cats, although a Differential diagnosis
raised lipase level may be seen occasionally.
Serum cobalamin and folate levels are usually with a good appetite. However, since cats with chronic
decreased. pancreatitis and exocrine pancreatic insufficiency usu-
A number of older tests are very unreliable and are now ally develop diarrhea and/or vomiting, other causes of
rarely used. These include staining fecal smears to enteropathy, IBD, cholangiohepatitis, alimentary
lymphosarcoma, hyperthyroidism and the other Prognosis

malassimilation syndromes should be considered as
important differentials. Prognosis depends on the severity of damage. Many
cats live with low-grade smoldering pancreatitis for
Treatment many years, however, once exocrine pancreatic insuffi-
ciency and/or diabetes has developed the prognosis is
(For treatment of acute pancreatitis see page 277, The worse.
Cat With Depression, Anorexia or Dehydration)
In rare cases of congenital exocrine pancreatic insuffi-
Replace pancreatic enzymes by adding pancreatic ciency, the prognosis is good, as long as the cat receives
enzyme replacement to food (~ half a teaspoonful of pancreatic supplementation.
powder per meal, or to effect), or add fresh-frozen then
defrosted pig pancreas (~20–40 g per meal, or to effect).
Prevention
Immunosuppression: In the non-suppurative form of
pancreatitis, immunosuppressive doses of corticos- Since it is not known what triggers pancreatitis to
teroids may be needed to reduce ongoing inflammation develop, it is not currently possible to prevent its onset.
(prednisolone 1–4 mg/kg q 12–24 hours PO, then taper However, since chronic pancreatitis can progress to
over 1–3 months and maintain on every other day doses exocrine pancreatic insufficiency, it would appear sen-
if needed). Alternately, chlorambucil could be consid- sible to try to control it as well as possible to try to pre-
ered (2–5 mg/m2 PO up to once every 48 h). vent its progression.
Supportive therapies:
● Feed a highly digestible, “bland enteric diet”,
which is low in fat. Feed small meals frequently. LYMPHOCYTIC CHOLANGIOHEPATITIS*
● Cobalamin is often reduced by lack of pancreatic
intrinsic factor and malabsorption and should be Classical signs
supplemented (125–250 μg/week SC or IM for 6–8 ● Typically seen in middle-aged cats, and
weeks or 50–100 μg/cat/day PO). Persian cats may be over-represented.
● Vitamin K1 is often required because fat malab- ● Weight loss, inappetence, some cats may
sorption results in poor absorption of fat-soluble be polyphagic,
vitamins like vitamin K, and this can result in ● ± mild generalized lymphadenopathy,
abnormal hemostasis (0.5 mg/kg/day SC for 3–4 ● ± vomiting and/or diarrhea.
days, then once weekly). ● In some cats, is associated with IBD and/or
● Vitamin E may be given for its anti-oxidative prop- pancreatitis.
erties (50–200 IU/cat/day PO).
Surgical intervention may be required if complete
biliary obstruction occurs (cholecystotomy or cholecys- Pathogenesis
toduodenostomy), or if a focal pancreatic mass is The cholangitis/cholangiohepatitis complex com-
detected (partial pancrectomy to remove a pancreatic prises chronic non-suppurative (lymphocytic) cholangi-
pseudocyst, abscess, fibrotic mass or tumor). tis/cholangiohepatitis, suppurative cholangitis/cholan-
Diabetes that develops secondary to chronic pancreati- giohepatitis and biliary cirrhosis.
● The pathogenesis and interaction of the three condi-
tis can be very difficult to stabilize. Insulin require-
ments may vary widely because of the ongoing tions is poorly understood and it is highly probably
pancreatic pathology, and treatment is complicated fur- that each of these conditions incorporates a number of
ther when corticosteroids also need to be given. different diseases.
● Cholangitis describes inflammation of the biliary
It is essential to diagnose and treat any concurrent distract, while cholangiohepatitis describes inflamma-
ease (e.g. IBD and/or cholangitis/cholangiohepatitis tion of the peribiliary hepatocytes as well as the bil-
complex). iary tract.
● The only condition that may be associated with mon bile duct obstruction. Associated findings may
polyphagia is lymphocytic cholangitis/cholangio- include enlarged mesenteric lymph nodes, pancreatic
hepatitis. irregularity, and/or thickening of the duodenal walls.
Pathogenesis of lymphocytic cholangitis/cholangio- A definitive diagnosis is made by histopathological
hepatitis complex is unknown. It is probably immune- examination of a liver biopsy.
mediated, but is possibly associated with progression of ● A fine-needle aspirate is rarely diagnostic, so a per-
the suppurative form. It is often associated with IBD cutaneous needle biopsy or surgical wedge
and/or pancreatitis, and when all three occur biopsy is required. Blood clotting times and/or a
together it is termed “triaditis”. PIVKA test (protein induced by vitamin K absence
or antagonism) should be assessed first, and a
platelet count should be performed.
Clinical signs
● Typical gross findings include a very firm often
Cats of any age may be affected, but disease is seen rather irregular liver, and a thickened and dis-
most typically in middle-aged cats. Persian cats may tended gallbladder and common bile duct, which
have an increased risk. often contains inspissated bile. Enlarged mesenteric
lymph nodes, pancreatic irregularity and/or thick-
Clinical signs are usually chronic and insidious in
ening of the duodenal walls may also be present.
nature.
● If performing an exploratory laparotomy, it is sensi-
Affected cats are typically jaundiced, but bright, and ble to check the patency of the biliary outflow, then
are often polyphagic. collect biopsies from the mesenteric lymph nodes,
small intestines and pancreas as well as liver. Send
Vomiting and/or diarrhea may be present.
bile and part of the liver biopsy for culture.
Cats may have a palpably enlarged liver and mild ● Histopathology of the liver reveals lymphocytic
generalized lymphadenopathy. and/or plasmacytic periportal inflammation,
bile ductule hyperplasia, and periportal fibrosis.
Cats may show intermittent signs of systemic illness,
Very chronic cases may have biliary cirrhosis.
with fever, anorexia, weight loss, and vomiting.
Systemic signs are sometimes associated with second-
ary infections, typically of the liver and/or pancreas.
The disease may progress to causing chronic biliary cir-
rhosis with ascites, hepatic encephalopathy, and bleed-
with a good appetite. However, since cats with lympho-
ing tendencies.
cytic cholangitis/cholangiohepatitis complex often
develop vomiting and/or diarrhea enteropathies (includ-
Diagnosis ing IBD), pancreatitis, and the other malassimilation
syndromes should be considered as important differen-
Serum biochemistry often reveals mild to moderately
tials. In cases that develop ascites, the wet form of feline
(occasionally severely) increased liver enzymes,
infectious peritonitis (FIP) should also be considered.
increased bile acids, hyperbilirubinemia, hyperglobu-
This is because both conditions produce a protein-rich
linemia and hypoalbuminemia.
ascitic fluid and have similar biochemical and hemato-
Hematology may reveal mild anemia, lymphopenia or logical changes. However, the presence of polyphagia
lymphocytosis, monocytosis and/or thrombocytopenia. usually differentiates the two conditions as cats with FIP
Blood clotting times are frequently prolonged. are usually anorexic.
Ascitic fluid, if present, is typically high in protein.
Radiographs typically reveal hepatomegaly and occa- Treatment
sionally choleliths (gallstones), while ultrasound
Treatment is largely empirical.
examination may also show blotchy hepatic hypere-
chogenicity, “sludging” of bile, and evidence of com- Antibiotics, if needed:
● Ampicillin (10–40 mg/kg q 8 hours PO), amoxi- require euthanasia. Once severe fibrosis, cirrhosis or
cillin (11–22 mg/kg q 8–12 hours PO), or ascites has developed the prognosis is usually guarded.
cephalexin (10–35 mg/kg q 8–12 hours PO)
● Add metronidazole for its effect against anaerobes
and its immune-modulating effects (7.5–10 mg/kg Prevention
every 12 hours PO). Do not use higher doses, as
Since it is not known what triggers the development of
these can be hepatotoxic.
lymphocytic cholangitis/cholangiohepatitis complex, it
Immunosuppressive agents: is currently not possible to prevent its onset.
● Immunosuppressive doses of corticosteroids
(prednisolone 2–4 mg/kg q 12–24 hours PO), then
taper over 1–3 months, and maintain on every other ACROMEGALY
day doses if needed.
● Other immunosuppressive agents may be consid-
Classical signs
ered, e.g. methotrexate (0.13 mg/cat every 12 ● Rare condition of older, typically, male cats.
hours × 3 doses PO, repeated once weekly) or chlo- ● Slow increase in body size, especially
rambucil (2–5 mg/m2 PO up to once every 48 h). affecting head and feet.
Supportive therapies:
● Variable weight change with a good
● Ursodeoxycholic acid aids bile flow and is
appetite.
believed to have hepatoprotective effects (10–15
● Usually diabetic; so polyuric and polydipsic.
mg/kg q 24 hours PO).
● Vitamin K1 is often required because fat malab- Pathogenesis
sorption results in poor absorption of fat-soluble
vitamins like vitamin K and this can result in In cats, most cases of acromegaly are caused by the
abnormal hemostasis (0.5 mg/kg q 24 hours SC for development of a growth hormone-secreting tumor
3–4 days, then once every 7–14 days). within the pituitary gland.
● Vitamin E may be given for its anti-oxidative prop- Unlike the situation in the dog, increased levels of cir-
erties (50–200 IU/cat/day PO). culating progestogens or progesterone do not stimulate
● S-adenosylmethionine (SAMe) may be given for growth hormone secretion in the cat.
its hepato-protective and anti-oxidative properties
(18 mg/kg/day PO).
● Some authors suggest feeding either hypoallergenic
Clinical signs
or high-fiber diets. Acromegaly is seen most typically in older, male,
● Milk thistle, 7–50 mg/kg q24h PO. mixed-breed cats.
Surgery will be required where complete biliary Affected cats slowly increase in size, with somewhat
obstruction occurs (cholecystotomy or cholecystoduo- disproportionate enlargement and thickening of the
denostomy). head and feet.
● Growth of the jaw bones may result in obvious
It is important to address any associated or underlying
interdental spaces and/or prognathism.
conditions, such as IBD, pancreatitis, extrahepatic bile
● A mild increase in respiratory noise may result from
duct obstruction or cholecystitis.
increased soft tissue thickness around the airways.
● Distortion of the joints can lead to destructive
Prognosis arthritis.
Prognosis is very variable and often unpredictable. Acromegalic cats develop insulin-resistant diabetes
Some cases respond well and only need temporary because excess growth hormone causes peripheral
treatment, others require continued therapy to maintain insulin resistance. However, early cases may have
remission, while others progress relatively rapidly and unstable diabetes rather than being truly resistant.
● They therefore develop polyuria, polydipsia and ● Ultrasonography and, where available, computed
polyphagia. tomography (CT) or magnetic resonance imaging
● They may either gain or lose weight. (MRI) can also be used to detect organomegaly. CT
and MRI may be used to determine the location and
While all organs undergo growth and hypertrophy,
extent of the tumor within the brain.
hepatomegaly and renomegaly are the easiest to detect
on palpation. Enlargement of the abdominal organs
often results in a pot-bellied appearance. Differential diagnosis
Organ enlargement may lead to organ failure. The clin- Differential diagnoses include most of the other causes
ical signs will therefore reflect the particular organ sys- of weight loss with a good appetite. However, since all
tems that have been affected; e.g. cardiac hypertrophy cats with acromegaly develop diabetes with polyuria
and eventual congestive heart failure, liver failure and polydipsia, other causes of diabetes, hypera-
and/or kidney failure. drenocorticism, hyperthyroidism and renal insuffi-
ciency are the most important differentials.
Concurrent hypertension may result in clinical signs,
typically ocular hemorrhages, sudden blindness and/or
Treatment
neurological signs.
Only rarely do neurological signs result from the pitu- Acromegaly can be treated three ways; surgery,
itary tumor compressing and invading the hypothalmus. external-beam radiotherapy or medically.
● Surgical excision of the growth hormone-secret-
ing tumor is usually a rapid and effective treatment
Diagnosis for affected humans. However, the procedure has
Acromegaly should be considered in any large-sized rarely been performed in cats, and mapping of the
cat which develops insulin-resistant or unstable tumor is essential prior to considering surgery.
● In humans, external-beam radiotherapy is often
diabetes.
● Hyperglycemia and glycosuria will be present, but effective, although clinical improvement may be
ketosis is rare. slow to develop. The few cats that have been treated
● Affected cats may also show azotemia, hypercho- in this way have shown variable results. Treatment
lesterolemia, hyperphosphatemia, hyperproteine- requires repeated anesthetics and suitable facilities
mia, erythrocytosis and mildly raised liver are limited.
enzymes. ● Although they require frequent administration and
usually cause side-effects, somatostatin analogs
Comparing the cat to a previous photograph of itself (e.g. octreotide) and dopamine agonists (e.g.
can be helpful in confirming the disproportionate bromocriptine) are sometimes used in the treatment
enlargement and thickening of its head. of humans with acromegaly. Unfortunately, limited
A definitive diagnosis can be made by measuring trials with octreotide in acromegalic cats have not
growth hormone levels (where available) or insulin- been promising, and dopamine agonists have not
like growth factor-1 (IGF-1) assay, which gives similar yet been evaluated in this species.
results. Unfortunately, the degree of elevation does not
Temporary management consists of trying to treat
always correlate with the clinical signs, and IGF-1 will
the diabetes and any other concurrent or related dis-
also be increased in most cats treated long-term with
eases (e.g. hypertension, heart failure, renal disease).
insulin.
● Control of the diabetes can usually be achieved by
The presence of acromegaly can be confirmed by eval- giving extremely high doses of exogenous insulin
uating the growth hormone response to a glucose (20–130 IU/day), sometimes in various combina-
suppression test. tions of short-, intermediate- or long-acting insulin.
Other tests can be used to gain supportive evidence. However, because the severity of the insulin resist-
● Radiography may show organomegaly, increased ance can fluctuate, the dose should not exceed
interdental spaces, hyperostosis of the skull and/or 12–15 IU/injection so the risk of iatrogenic hypo-
degenerative arthritis. glycemia is reduced.
● Very rarely, spontaneous necrosis of the tumor can Clinical signs

result in temporary or permanent remission of clin-
ical signs. Hyperadrenocorticism is typically seen in middle-aged
to older cats. Females may be over represented.
History is often vague, but usually includes polyuria,
Prognosis polydipsia, polyphagia, weight loss and lethargy,
and affected cats may have a history of recurrent infec-
The long-term prognosis is poor. However, because the tions and/or abscesses.
tumors grow very slowly, the short-term prognosis may
be good to guarded with survival times of 4–48 Since cortisol antagonizes insulin, approximately
or more months reported. 80% of cases develop diabetes, which may or may not
be insulin resistant, based on the insulin dose adminis-
tered.
Prevention Cats with hyperadrenocorticism typically have poor

coat condition, spontaneous alopecia, very fragile
Since acromegaly is usually caused by a slow growing thin skin that bruises easily and a pot-bellied
pituitary tumor, its development cannot be prevented. appearance. Hepatomegaly is often palpable.
Diagnosis
Hyperadrenocorticism should be suspected in any cat
Classical signs with the clinical signs described above, particularly if it
has unstable diabetes, and/or a long history of exoge-
● A rare condition of middle-aged and older
nous corticosteroids administration.
cats.
● Poor coat condition and pot-bellied Since hyperadrenocorticism is frequently associated
appearance. with diabetes, serum biochemistry and urinalysis often
● Polyuric, polydipsic, polyphagic and often reveal persistent hyperglycemia, glucosuria ±
diabetic. ketonuria.
Unlike in dogs, a stress leukogram is rarely present,
although lymphopenia may be seen.
Pathogenesis
Increased liver enzymes and hypercholesterolemia
In cats, hyperadrenocorticism, more correctly termed may be seen regardless of whether or not the cat has
hypercortisolism, can be caused by: diabetes.
● Adrenocorticotropin (ACTH)-secreting pitu-
Making a diagnosis of hyperadrenocorticism can be
itary tumors;
very difficult:
– Approximately 80% of cats with hyperadreno-
● Few of the tests have well-established specificity
corticism have a pituitary tumor and most are
and sensitivity in cats.
microadenomas.
● It is usually necessary to use a combination of tests.
● Adrenal tumors that autonomously secretes cor-
tisol; In cats, the most useful screening tests are:
– Represent about 20% of cases, and approxi- ● Adrenocorticotropic hormone (ACTH) stimula-
mately 50% of adrenal tumors are benign ade- tion test – Collect baseline blood sample, give
noma, and 50% are malignant. 0.125 mg of synthetic ACTH IV, collect blood after
● Iatrogenic hyperadrenocorticism can be caused 1 ± 2 hours. Normal basal serum cortisol concen-
by giving long courses of exogenous corticos- tration is 10–110 nmol/L (0.36–3.6 μg/dl); at 1 h
teroids (parenteral, oral or topical) or megestrol and/or 2 h after ACTH is 210–330 nmol/L
actetate. (7.6–11.9 μg/dl); > 330 nmol/L (> 11.9 μg/dl) is
consistent with hyperadrenocorticism. False nega- dependent hyperadrenocorticism, but may be seen
tives and positives occur. in cats with PDH.
● Low-dose dexamethasone suppression test – ● Measurement of endogenous ACTH – Collect
Collect baseline blood sample, give dexamethasone blood sample in EDTA, spin immediately, transfer
0.01 mg/kg IV, collect blood after 4 and 8 hours. In plasma to a plastic tube, ship overnight on ice or
normal cats serum cortisol should be < 30 nmol/L freeze for storage. Plasma ACTH is high normal or
(< 1.0 μg/dl) at 4 h and 8 h after dexamethasone. above (>15 pg/ml) with PDH, and low (<10 pg/ml)
Lack of suppression is seen in most cats (95%) with with adrenal tumors.
hyperadrenocorticism, and some cats with non- ● Radiography, ultrasonography and, where avail-
adrenal illness. able, CT or MRI. Use to determine adrenal size
● Urine cortisol to creatinine ratio (UC/CR) – and shape. The presence of adrenal mineraliza-
Collect urine sample, centrifuge and submit super- tion should not be over-interpreted as it occurs in
natant. A normal ratio almost always rules out ~30% of normal cats. Unilateral adrenal enlarge-
hyperadrenocorticism. Unfortunately, an increased ment is typical of an adrenal tumor. While bilateral
ratio is commonly caused by non-adrenal illness. enlargement usually indicates PDH, it can occa-
The test is more reliable if the sample is collected at sionally result from bilateral adrenal tumors.
home. Hepatomegaly is found in ~75% of all cats with
hyperadrenocorticism. CT and MRI can be used to
Additional tests may be used to try to differentiate
image the pituitary gland as well as the adrenal
pituitary-dependent hyperadrenocorticism (PDH)
glands.
from adrenal neoplasia. These include:
● High-dose dexamethasone suppression test –
Performed as low-dose dexamethasone suppression Differential diagnoses
test but give 0.1 mg/kg. Lack of suppression at 8 h
Differential diagnoses include most of the other causes
is seen in most cats (80%) with hyperadrenocorti-
of weight loss with a good appetite. However, since
cism. Suppression at 4 h but not at 8 h is consistent
most cats with hyperadrenocorticism develop polyuria,
with PDH. False negatives may occur in mild cases
polydipsia and diabetes, other causes of diabetes,
of hyperadrenocorticism.
acromegaly, hyperthyroidism and renal insuffi-
● Ultra-high-dose dexamethasone suppression test –
ciency are the most important differentials.
Performed as low-dose dexamethasone suppression
test but give 1.0 mg/kg. Suppression at 4 h or 8 h to
< 30 nmol/l (< 1.0 μg/dl) or <50% of baseline is Treatment
consistent with PDH, but lack of suppression may
While there are a number of different treatment
be seen with PDH and adrenal tumors.
options, there have been few good studies into their use
● Combination test – Collect blood sample, give 1.0
in cats.
mg/kg dexamethasone IV, collect blood after 4 h,
then immediately perform ACTH stimulation test Medical therapies have generally given poor results,
as above. Interpretation is as for ACTH stimulation and safe dosages have not been established. They
test and ultra-high-dose dexamethasone suppres- may be given pre-surgically to reduce the operative
sion test (taking ultra-high-dose dexamethasone risks.
suppression test result as result at 4 h). ● Trilostane has produced promising results in a very
● ‘At home’ protocol – Collect urine on the morn- small number of cases and warrants further investi-
ing of Days 1 and 2; give two oral doses of dexam- gation, particularly given that side effects have not
ethasone at 8 hour intervals at 4 pm and 12 pm; been significant.
then collect a third urine sample on the morning of ● Mitotane gave poor results in early trials, and it has
Day 3. All three samples are assessed for UC/CR. been suggested that higher doses and/or longer
The mean of the first two UC/CR = basal value courses may be needed.
and acts as a screening test. Suppression < 50% ● Ketoconazole has given mixed results and consid-
basal on Day 3 is not seen in cats with adrenal- erable toxicity.
● Metyrapone has given mixed results and is diffi- prevented by not giving long courses of exogenous cor-
cult to obtain. ticosteroids.
● L-depronyl has little information available on use
in cats, and no proven efficacy.
GLOMERULONEPHRITIS (PROTEIN-
Radiation therapy with ablation of the pituitary tumor LOSING NEPHROPATHY)
has given mixed results.
Classical signs
Adrenalectomy. Because of the difficulties of med-
ical therapy, surgery has been considered the treat- ● Rare disease seen most frequently in
ment of choice. However, this is changing with the young male cats.
success of trilostane treatment. Where a single adrenal ● Weight loss with a good appetite early in
tumor is present, the removal of the affected adrenal disease.
gland is recommended. With PDH or bilateral adrenal ● Often marked subcutaneous edema and
tumors, bilateral adrenalectomy is recommended. ascites.
While surgery can provide successful treatment, the ● ± polydipsia and polyuria.
risk of a fatal peri-operative hypoadrenal crisis, ● ± vomiting and/or diarrhea.
renal failure or surgical complications are great.
The procedure should only be performed by an expe-
Pathogenesis
rienced surgeon. Consideration of the diabetic state
must be given, and peri-operative and post-operative Glomerulonephropathy can arise from one of two
treatment with glucocorticoids is essential. Gluco- mechanisms:
corticoids are needed in all cases. Short-term treat- ● Primary glomerulonephritis has antibodies tar-
ment will be needed after unilateral adrenalectomy, geted directly against the glomerular basement
because the contralateral gland will be temporarily membrane.
atrophied. Long-term treatment will be needed after ● Secondary glomerulonephritis has deposition of
bilateral adrenalectomy, and should also include min- immune complexes within the glomeruli that have
eralocorticoids. arisen elsewhere in the body.
– This is the most common form in cats.
– It tends to be membranous or membrano-pro-
Prognosis
liferative in nature.
Without successful treatment, the prognosis is poor. – It may be associated with many different condi-
Where PDH is present, successful bilateral adrenalec- tions (see below), but in most cases the underly-
tomy will reduce the signs of hyperadrenocorticism, ing cause cannot be found.
but the risk of a hypoadrenal crisis is high and tumor ● Diseases that may be associated with secondary
expansion will eventually lead to neurological signs. glomerulonephritis in cats include infection
If adrenal tumors are successfully removed the hyper- with FeLV, FIV, FIP, Mycoplasma spp., or
adrenocorticism should resolve, and the diabetic state Ehrlichia spp., chronic pyoderma, chronic gin-
may become less insulin resistant or even resolve. givitis, dirofilariasis, endocarditis, pancreatitis,
Early studies with trilostane appear to show that while pyometra, neoplasia or other immune-mediated
it may ameliorate signs of hyperadrenocorticism, it diseases.
may not alter the need for exogenous insulin in cats
Deposition of immune complexes within the glomeru-
that are also diabetic.
lus leads to the initiation of inflammation and this
results in proteinuria (protein-losing nephropathy).
Prevention
Clinical signs
Since hyperadrenocorticism is usually caused by pitu-
itary or adrenal tumors, its development cannot be pre- Rare condition seen most typically in young male
vented. Iatrogenic hyperadrenocorticism can be cats.
Clinical signs may be non-specific. Typically in the Urinalysis may reveal an inactive sediment, with or
later stages there is anorexia, depression, weight loss, without hyaline and/or granular casts.
lethargy and poor coat condition. More specific signs
It is important to try to determine an underlying
include subcutaneous edema, ascites, and polyuria
cause. This may involve screening radiography and
and polydipsia.
ultrasonography, tests for immune-mediated disease,
It tends to takes one of two clinical forms: and numerous tests for infectious disease (see above for
● Nephrotic syndrome with ascites and subcuta- the list of possible diseases).
neous edema, usually affecting the hind legs, ven-
Systemic blood pressure should be assessed.
tral body wall and neck. This form may or may not
be associated with signs of renal failure (polyuria, Abdominal radiographs and ultrasound examination
polydipsia). rarely reveal obvious renal changes.
● Renal failure with no signs of nephrotic syn-
Renal biopsy is necessary to confirm the diagnosis
drome.
and find which type of glomerular disease is present.
Cats with early nephrotic syndrome may present ● Blood clotting times, platelet number, and systemic
with weight loss with a good appetite. blood pressure should be assessed prior to biopsy.
● Ultrasound-guided percutaneous biopsy is rela-
Edema affecting the intestines can exacerbate the pro-
tively safe but laparotomy or laparoscopy reduces
tein loss and result in malabsorption, diarrhea, vom-
the risk of post-operative bleeding. Renal hemor-
iting and weight loss.
rhage is a risk, especially if hypertensive.
Systemic hypertension may arise secondary to the ● Sample must contain >5 glomeruli to make a diag-
renal dysfunction and result in acute blindness, ocular nosis; this usually means multiple needle biopsies
hemorrhages or signs of CNS dysfunction. or a wedge biopsy are required.
● Routine histopathology (fix sample in buffered
Other clinical signs may result from any primary dis-
normal formalin), electromicroscopy (fix sample
ease conditions.
in paraformaldehyde-glutaraldehyde), ± immuno-
On abdominal palpation, the kidneys may appear histochemistry (keep fresh and paraffin embed) are
small and/or irregular or, occasionally, enlarged. needed to confirm a diagnosis.
● On gross inspection kidneys may appear normal,
be slightly small, firm and pale, or show irregular
Diagnosis
pitting and fibrosis.
Cats with nephrotic syndrome have marked pro- ● Light microscopy typically shows diffuse thicken-
teinuria, hypoalbuminemia and hypercholes- ing of the glomerular basement membrane, with
terolemia. variable degrees of cellular proliferation in the
affected glomeruli. Special stains can help to define
Other findings may include hypertriglyceridemia,
the changes, but electromicroscopy and immunohis-
hypocalcemia, non-regenerative anemia and neu-
tochemistry are needed to define the exact nature and
trophilia.
extent of the disease.
Increased concentrations of blood urea and creatinine
(azotemia) and a low urine specific gravity (<1.035) will
indicate whether or not renal insufficiency is present. Differential diagnosis
Persistent proteinuria is the hallmark of glomeru- Chronic renal failure, diabetes, acromegaly, hyper-
lonephritis. adrenocorticism and hyperthyroidism are impor-
● This should be quantified by determining the urine tant differentials in those cats that develop polyuria
protein to creatinine ratio (UPC ratio). and polydipsia. However, the presence of ascites
● UPC ratio: < 0.4 = normal, > 0.4–2 suggestive of in combination with polyphagia is suggestive of lym-
glomerulonephropathy or tubular disease, > 2 con- phocytic cholangitis/cholangiohepatitis complex.
sistent with glomerulonephropathy. Once hypoalbuminemia is detected, then a protein-
losing enteropathy or severe liver failure should be Very careful use of diuretics can help to reduce fluid
considered. retention and improve the patient’s well-being (e.g.
frusemide 1–2 mg/kg q 8–12 hours PO, reducing to as
low dose as possible and monitoring closely for side-
Treatment
effects).
Treatment for nephrotic syndrome is controversial
Thromboembolic disorder is rare in cats, but if present
and usually empirical.
consider giving low doses of aspirin (10–25 mg/kg
Monitor response to treatment by assessing changes every 3 days PO).
in body weight, serum and urinary protein levels.
Where an underlying cause can be found it should be Prognosis
treated.
Very variable and often unpredictable. Some
Alter the level of dietary protein: undergo spontaneous complete or partial remissions
● High protein diets may help to correct hypoalbu- (~30%), others need temporary or continuous therapy,
minemia and reduce protein malnutrition. while others progress relatively rapidly to require
● However, they may exacerbate proteinuria, glomeru- euthanasia.
lar hypertension and glomerular damage.
● High-protein diets should not be fed if serum urea Approximately 50% survive for 2.5–6 years.
is elevated. Cats with nephrotic syndrome that do not originally
● Some cats benefit from mild protein addition while have renal insufficiency, may or may not progress to
others benefit from mild protein restriction. Feed develop renal insufficiency.
the chosen diet for ~ 2 weeks then reassess.
Prognosis is poor with worsening clinical signs or pro-
Angiotensin-converting enzyme (ACE) inhibitors gression to renal failure.
help to reduce proteinuria and any associated systemic
hypertension (e.g. benazepril 0.25–0.5 mg/kg/day PO).
Prevention
If systemic hypertension is significant, the calcium
channel antagonist amlodipine (0.625 mg/cat/day
Prompt recognition and treatment of underlying dis-
PO) should be given.
ease may prevent the development of secondary
Use of corticosteroids and immunosuppressive drugs glomerulonephritis. However, since it is not usually
is controversial. They may or may not help to reduce possible to detect the underlying cause, it is not usu-
immune complex formation, will worsen any azotemia, ally possible to prevent the onset of glomeru-
and are contraindicated once renal failure is evident. lonephritis.
RECOMMENDED READING
Arthur JE, Lucke VM, Newby TJ, Bourne FJ. The long-term prognosis of feline idiopathic membranous glomeru-
lonephropathy. J Am Anim Hosp Assoc 1986; 22: 731–737.
Fondacaro JV, Richter KP, Carpenter JL, et al. Feline gastrointestinal lymphoma: 67 cases (1988–1996). Eur J Comp
Gastroenterol 1999; 4: 5–11.
Foster DM, Gookin JL, Poore MF, Stebbins ME, Levy MG. Outcome of cats with diarrhea and Tritrichomonas foe-
tus infection. J Am Vet Med Assoc 2004; 225: 888–892.
Gookin JL, Breitschwerdt EB, Levy MG, Gager RB, Benrud JG. Diarrhea associated with tritrichomonas in cats.
J Am Vet Med Assoc 1999; 215: 1450–1454.
Gookin J, Copple C, Papich M, Poore M, Levy M. Efficacy of ronidazole in vitro and in vivo for treatment of feline
Tritrichomonas foetus infection. Proceedings of the ACVIM, 2005, Abstract 131.
Gookin J, Stebbins ME, Hunt E, et al. Prevalence of and risk factors for feline Tritrichomonas foetus and Giardia
infection. J Clin Micro 2004; 42: 2707–2710.
Goossens M, Nelson RW, Feldman EC, Griffey SM. Response to insulin treatment and survival in 104 cats with dia-
betes mellitus (1985–1995). J Vet Intern Med 1998; 12: 1–6.
Lees GE, Brown SA, Elliot J, et al. Assessment and management of proteinuria in dogs and cats. 2004 ACVIM
Forum Consensus Statement (small animal). J Vet Intern Med 2005; 19: 377–385.
Lucke VM. Glomerulonephritis in the cat. Vet Ann 1982; 22: 270–278.
Lutz TA, Rand JS. Pathogenesis of feline diabetes mellitus. Vet Clin North Am Small Anim Pract 1995;
25(3):527–552.
Neiger R, Witt AL, Noble A, German AJ. Trilostane therapy for treatment of pituitary-dependent hyperadrenocorti-
cism in 5 cats. J Vet Intern Med 2004; 18: 160–164.
Peterson ME, Taylor RS, Greco DS, et al. Acromegaly in 14 cats. J Vet Intern Med 1990; 4: 192–201.
Rand JS, Bobbermien LM, Hendrikz JK, Copland M. Over representation of Burmese cats with diabetes mellitus.
Aust Vet J 1997; 75: 402–405.
Vail DM, Moore AS, Ogilvie GK, Volk LM. Feline lymphoma (145 cases): Proliferation indices, cluster of differen-
tiation 3 immunoreactivity, and their association with prognosis in 90 cats. J Vet Intern Med 1998; 12: 349–354.
Zwahlen CH, Lucroy MD, Kraegel SA, Madewell BR. Results of chemotherapy for cats with alimentary malignant
lymphoma: 21 case (1993–1997). J Am Vet Med Assoc 1998; 213: 1144–1149.
18. The thin, inappetent cat
Penny Barber†, James B Miller and Jacquie Rand
KEY SIGNS
● Thin cat or cat with weight loss and a poor appetite.
MECHANISM?
● Weight loss occurs when nutrient loss or metabolic utilization exceeds intake. Weight loss
results from one or more of the following mechanisms: inadequate intake; impaired ability to
digest or absorb; inability to utilize; increased utilization or the increased loss of nutrients.
A lack of appetite is associated with suppression of the appetite center in the hypothalamus.
WHERE?
● Diseases involving most body systems can cause weight loss and affect appetite.
WHAT?
● The most common causes of a thin, inappetent cat are chronic renal failure, neoplasia
and several of the viral diseases (FIV, FeLV, FIP). Many other diseases will cause weight
loss, but inappetence will frequently occur late in the disease process.

Diseases causing signs of a thin, inappetent cat
ANOMALY
● Portosystemic shunts (p 361)
May be congenital or acquired. In congenital portosystemic shunts, growth may be stunted.
Neurological signs of hepatic encephalopathy (behavioral, seizures, blindness) may occur and
hypersalivation is a frequent sign.
METABOLIC
● Chronic renal failure*** (p 333)
Chronic history of gradual weight loss, polyuria and polydipsia. Systemic signs such as inappe-
tence and vomiting are common.
330
18 – THE THIN, INAPPETENT CAT 331
● Septic focus/persistent fever ** (p 344)

Anorexia is associated with the pyrexia. Anorexia and a hypermetabolic state lead to weight loss.
Fluctuating pyrexia, poor appetite and weight loss are present, along with other clinical signs
dependent on the etiology of the pyrexia. Common sites of bacterial infection include pyothorax,
upper urinary tract infections and bite wounds, with peritonitis, osteomyelitis, endocarditis
and pneumonia occurring less commonly.
●Apathetic hyperthyroidism* (p 346)
Weight loss, poor appetite, tachycardia and intermittent vomiting and diarrhea are common.
Usually affects cats greater than 6 years of age.
●Cholangiohepatitis complex* (p 348)
Anorexia or poor appetite, weight loss and depression. Icterus and hepatomegaly are common.
Ascites occasionally occurs.
● Cardiac cachexia (p 356)
Clinical signs relating to the cardiac disease including murmurs, gallop rhythm and arrhythmias.
Dyspnea caused by pleural effusion or pulmonary edema may also be present.
● Diabetes mellitus (p 355)
Polyuria and polydypsia. Frequently history of good appetite with weight loss prior to inappetence.
NEOPLASTIC
● Cancer cachexia** (p 342)
Paraneoplastic syndrome characterized by anorexia, wasting and weight loss. Occurs with a variety
of malignancies, and more specific signs will relate to the site of the neoplasm.
INFECTIOUS
● Feline immunodeficiency virus (FIV)*** (p 339)
Chronic weight loss, stomatitis, lymph node enlargement and neurologic signs. Signs may be
vague and variable. Immunosuppression resulting in secondary, opportunistic infections is com-
mon.
● Feline leukemia virus (FeLV)* (p 350)
A variety of clinical signs depending on the system(s) of the body affected. Neoplasia, particularly
lymphoma, and chronic anemia or pancytopenia occur. Immunosuppression resulting in secondary,
opportunistic infections is common.
● Feline infectious peritonitis (FIP)* (p 352)
Chronic, fluctuating pyrexia with anorexia and weight loss. The non-effusive (“dry”) form fre-
quently leads to clinical signs associated with the organs involved (liver, kidney, ocular or central
nervous system). The effusive (“wet”) form of the disease causes ascites, pleural or occasionally
pericardial effusions.
●Chronic bacterial rhinitis and sinusitis (p 356)
Chronic sneezing, and mucopurulent nasal discharge may be associated with a poor appetite and
weight loss.
● Toxoplasmosis (p 359)
Muscle hyperesthesia, respiratory distress, fever, uveitis and neurological signs including seizures
occur variably.
continued
continued
● Cryptococcosis (p 360)
Chronic mucopurulent or hemorrhagic nasal discharge, sneezing and distortion of the dorsum of
the nose are typical. Central nervous system signs including seizures are less common.
● Systemic mycoses (p 361)
Blastomycosis and histoplasmosis may cause depression, anorexia and weight loss in endemic
areas. The most common clinical sign is dyspnea, but signs vary with the organ systems affected.
INFLAMMATION
● Oral inflammatory disease* (p 353)
Usually lymphocytic-plasmacytic in nature. Causes reluctance to eat, dysphagia and drooling of
saliva with associated weight loss.
● Inflammatory bowel disease* (p 349)
Chronic weight loss, intermittent vomiting and/or diarrhea. Cats may have minimal clinical signs
other than weight loss.
● Protein-losing nephropathy (p 358)
Results from glomerulonephritis (rare) and amyloidosis (familial disease in Abyssinian). Marked
weight loss occurs initially, followed by decreased appetite, polyuria and polydipsia associated
with the development of renal failure. Ascites and peripheral edema occur if protein loss is severe.
IDIOPATHIC
● Chylothorax (p 357)
Respiratory distress. Decreased appetite may occur late in the disease.
● Increased loss of nutrients (e.g. protein-losing

INTRODUCTION enteropathy or nephropathy).
Maintenance energy requirements in the adult cat are
MECHANISM? approximately 50–70 kcal/kg body weight/day. Intakes
below maintenance will result in weight loss.
Weight loss of greater than 10% of body weight is
significant and should be investigated. Anorexia has a diverse etiology including stress,
pain, fear, trauma, disease or neoplasia.
Any cause of weight loss may present as failure to
grow or stunting if affecting an immature cat. Causes of anorexia may broadly be categorized as:
● Pseudoanorexia (e.g. oral cavity disease, dental pain).
Weight loss occurs when there are one or more of the ● Primary anorexia (e.g. central nervous system dis-
following:
orders affecting appetite center).
● Inappetence (inadequate caloric intake).
● Secondary anorexia (e.g. metabolic diseases such as
● Inability to digest or absorb nutrients (e.g. pancre-
renal failure).
atic exocrine insufficiency, inflammatory bowel
disease). It is important to note that many diseases leading to
● Inability to utilize absorbed nutrients (e.g. diabetes a thin inappetent cat involve more that just loss of
mellitus). appetite. When weight loss appears to exceed that which
● Increased utilization of absorbed nutrients (e.g. can be accounted for by decreased intake, other mecha-
hyperthyroidism, fever). nisms need to be considered.
WHERE? PATHOGENESIS
Signs of a thin inappetent cat may be the result of any Chronic renal failure is defined as primary renal
disease process that can cause decreased body weight failure that has persisted for an extended period
and/or suppression of appetite. (usually greater than 2 weeks).
The appetite center is in the hypothalamus. Chronic renal failure is associated with irreversible
Diseases affecting the oral cavity and pharynx may structural lesions in the kidney.
cause pain or dysphagia and so decrease nutrient Chronic renal failure is the end result of many dis-
intake. Such animals will often show interest in food ease processes affecting the kidney:
but cannot eat. Inability to smell food (anosmia) will ● Anomaly: Familial renal disease, polycystic kidney
frequently cause anorexia (e.g. chronic nasal disease). disease.
Diseases of the gastrointestinal tract, liver and pancreas ● Metabolic: Hypercalcemia (from cholecalciferol
may cause anorexia, maldigestion or malabsorption of rodenticide, granulomatous disease or neoplasia),

nutrients, and therefore weight loss. ischemic injury.
● Mechanical: Chronic urinary tract obstruction (e.g.
Careful history taking regarding the animal’s environ- urolith) resulting in hydronephrosis.
ment (inside, outside; single-, multiple-cat household) ● Neoplastic: Lymphoma, primary neoplasia.
may aid in deciding a diagnostic approach. ● Infectious: Feline infectious peritonitis, upper uri-
Good history taking and complete physical exami- nary tract infection (pyelonephritis).
nation are essential, due to the lack of specificity of ● Immune: Secondary to glomerulonephritits, amy-
these clinical signs. loidosis.

● Toxic: Therapeutic agents (e.g. gentamicin, ampho-
tericin B, NSAIDs), intravenous contrast agents,
WHAT? heavy metals (e.g. lead), hemaglobin, ethylene gly-
The most common causes of the thin innappetent col and plants (lilies).
cat with few other clinical signs are chronic renal The initiating cause of chronic renal failure is often
failure, neoplasia and, depending on geographical not identified.
location, several viral diseases (FIV, FeLV and FIP).
At the time of diagnosis there is usually diffuse
Weight loss followed by inappetence tends to be a pathology of the renal parenchyma termed chronic
terminal event in many disease processes. generalized nephropathy.
Many other causes will usually have other significant Polycystic kidney disease is a common cause of renal
clinical problems that will aid the clinician in formulat- failure in some breeds of cats and has the following
ing a diagnostic plan. characteristics:
● Renal cysts may be congenital or acquired and may
affect one or both kidneys.
DISEASES CAUSING SIGNS OF A THIN ● Polycystic kidney disease is characterized by multi-
INAPPETENT CAT ple cysts occurring in both kidneys.
● Polycystic kidney disease occurs as an autosomal
dominant inherited renal disease of Persian and
CHRONIC RENAL FAILURE*** Persian-related cats, with a prevalence of at least
45% in some Persian populations.
Classical signs ● Renal cysts are fluid-filled sacs lined with epithelium,
● Polyuria, polydipsia. that generally originate in existing nephrons and may
● Weight loss, inappetence. therefore occur in the renal cortex or medulla. Cystic
● Vomiting. structures have also been noted in other organs, such
as the liver, in cats with polycystic kidney disease.
● Cysts vary in size and tend to increase in number Early cases may be asymptomatic.
and size with time. Eventually progressive cyst
Signs associated with chronic renal failure result
enlargement compresses the adjacent renal
from failure of excretory, regulatory and synthetic
parenchyma and if sufficient renal mass is affected
functions of the kidney.
renal failure will develop. Renal failure may occur
at any age, however affected Persian cats typically Polydipsia is the most commonly reported clinical
present at approximately 7 years. sign. The polydipsia is compensatory to an obliga-
● Renomegaly may be obvious with the kidneys tory polyuria. If fluid intake is insufficient, dehydra-
being irregular in outline. Laboratory evaluation is tion will result. Polyuria results from:
necessary to determine the extent of the renal dys- ● Increased solute load in surviving functional
function. Ultrasonographic examination is non- nephrons (solute diuresis).
invasive and a very sensitive diagnostic technique ● Disruption of medullary anatomy.
for this condition. Cysts are seen as multiple, round ● Impaired response to antidiuretic hormone.
anechoic regions.
Inappetence or anorexia, weight loss and poor body
In chronic renal failure resulting from many of the dis- condition are common clinical signs as the disease
ease processes, renal function often slowly deterio- progresses.
rates over months or years, but the rate of deterioration
Lethargy, weakness and depression.
is very variable between cats. Deterioration is not neces-
sarily linear and many cats are stable for long periods of Vomiting (with possible hematemesis) is usually inter-
time with intermittent acute decrements. The postulated mittent and often low grade. Vomiting and nausea
causes of progression include: may be associated with:
● Primary disease process; the inciting cause may ● The action of uremic toxins on the medullary
lead to ongoing renal damage. emetic chemoreceptor trigger zone.
● Systemic and metabolic derangements of chronic ● Uremic gastritis and gastrointestinal ulceration.
renal failure.
Constipation is common and results from dehydration.
● Renal compensatory mechanisms (increase in sin-
gle nephron glomerular filtration rate). Severe uremia associated with an acute exacerbation
of chronic renal failure (acute on chronic) or end-stage
In chronic renal failure, surviving functional nephrons
chronic renal failure may be associated with extreme
undergo compensatory changes including glomerular
clinical signs including:
hypertension, hypertrophy and hyperfiltration (leading to
● Halitosis, ulceration of oral mucosa or tongue
an increase in single nephron glomerular filtration rate).
and brownish discoloration of dorsal surface and
● These adaptive mechanisms compensate for the
sloughing of anterior tip of tongue (due to fibinoid
loss of nephrons and so minimize the overall
necrosis, arteritis and bacterial degradation of urea
decrease in glomerular filtration rate.
to ammonia).
● However, it is postulated, based on extrapolation
● Occasionally diarrhea, which may be hemorrhagic
from other species, that these compensatory
from uremic enterocolitis.
changes are maladaptive and represent a final com-
● Terminally, seizures, stupor or coma may occur.
mon pathway for the progression to eventual
glomerular sclerosis and end stage renal failure. Clinical signs relating to systemic arterial hypertension
are common. Hypertension is reported in 29–61% of
cats with chronic renal failure. Clinical signs which
may be associated with hypertension include:
Clinical signs
● Ocular signs include sudden blindness with dilated
Chronic renal failure is mainly a disease of older pupils, hyphema or retinal hemorrhage, retinal
cats, with Persian, Abyssinian, Maine coon, Siamese edema, retinal vessel tortuosity, retinal detachment.
and Burmese breeds of cat being identified to be at ● Systolic heart murmurs and a gallop rhythm.
increased risk. ● Neurological signs including seizures and stupor.
Small and/or irregular kidneys may be palpable, Renal secondary hyperparathyroidism is character-
occasionally kidneys are enlarged (for example in neo- ized by excess circulating concentrations of parathy-
plastic or cystic kidney disease). roid hormone (PTH) resulting from altered mineral
homeostasis in renal failure, and is present
in approximately 80% of cats with chronic renal
Diagnosis
failure.
Diagnosis is based on demonstration of persistently ● Chronically increased PTH concentrations are toxic
decreased renal excretory function. to the kidney and contribute to ongoing loss of renal
● Persistently elevated blood urea and creatinine function.
concentrations (azotemia) are indicative. ● Factors involved in the pathogenesis of renal hyper-
● Chronicity and stability is based on two assess- parathyroidism leading to increased PTH concen-
ments, ideally at a 2–4 week interval. trations include phosphate retention with declining
glomerular filtration rate, hypocalcemia and
Diagnosis is further supported by demonstration of
decreased synthesis of 1,25-dihydroxycholecalci-
tubular dysfunction:
ferol (calcitriol) by proximal tubular cells.
● Urine specific gravity of less than 1.030 (typi-
● Diagnosis is based on elevated PTH concentrations
cally less than 1.020).
in a cat with chronic renal failure, and normal or
Any factors contributing to the progression of the slightly low serum calcium concentrations.
renal failure, including the initiating disease, and Measurement of ionized calcium is a better indica-
any systemic complications of renal failure should tor of calcium levels than total calcium. Cats with
be identified by diagnostic tests. chronic renal failure and hyperphosphatemia will
be hyperparathyroid.
Attempt to identify the renal disease initiating the fail-
– Samples for PTH assay require special handling,
ure using all or any of the following tests:
therefore contact the diagnostic laboratory.
● Routine hematology and biochemistry.
● Hypokalemia occurs in many cats (20–30%)
● Routine urinalysis (including microscopic sediment
with polyuric renal failure.
examination).
● Hypokalemia may be a consequence or cause of
● Assessment of proteinuria by urine protein:creati-
chronic renal failure in the cat.
nine ratio. Proteinuria is typically very low (1.5–2
● The mechanism is unknown but increased renal
times increase in protein excretion), unless there is
losses of potassium, decreased dietary intake and
significant glomerular disease.
decreased gastrointestinal absorption are implicated.
● Quantitative urine bacterial culture.
● Clinical signs of inappetence and generalized mus-
● Imaging, either radiography to assess renal size and
cle weakness (such as ataxia, inability to jump,
shape, and/or ultrasound examination to assess
stiff, stilted gait and ventroflexion of the neck) may
renal architecture.
occur.
● Renal cytology (fine needle aspiration biopsy) and
biopsy. Normochromic, normocytic, nonregenerative anemia
– However, due to the high risk and low diagnosis common when chronic renal failure is advanced.
tic yield of histopathology in CRF, biopsy is ● Occurs mainly from relative erythropoietin defi-
rarely indicated unless atypical features such as ciency, but other factors contribute, such as
renomegaly, proteinuria or hematuria are pres- decreased red cell life span, uremic suppression of
ent. Biopsy is only indicated in cases where erythropoiesis and gastrointestinal blood loss.
the result of histopathology will influence the ● Routine hematology should be used to monitor ane-
treatment options and therefore, outcome of mia and rule out other causes.
the case.
Systemic hypertension is present in many cats with
Secondary hyperperathyroidism, hypokalemia, anemia chronic renal failure.
and systemic hypertension are all possible complica- ● Diagnosis is based on serial blood pressure meas-
tions of chronic renal failure. urements.
● Systemic hypertension is usually measured using ● Ameliorating the clinical signs and systemic
a Doppler technique (Doppler ultrasonic sphyg- complications associated with renal dysfunction.
momanometry) to assess systolic blood pressure. ● Prevention of further deterioration of renal
● Normal range is technique dependent, however sys- function (progression).
tolic pressures > 200 mmHg indicate severe hyper- – Management of end-stage renal failure by renal
tension. replacement therapy (dialysis or transplant) is
● Retinal examination to detect end organ damage generally prohibitive because of cost, technical
should also be carried out. and ethical considerations.
Proteinuria is a risk factor for progression of chronic Although chronic renal failure is irreversible, many
renal insufficiency in cats, and may be a marker of cats presented in a uremic crisis have superimposed
glomerular hypertension. Median survival times are prerenal azotemia or acute renal failure (so called
significantly reduced if the urine protein/creatinine acute on chronic).
ratio is > 0.43. ● It is very important that appropriate therapy be used
to correct reversible azotemia.
All chronic renal failure cases should receive regu-
● Once reversible azotemia is corrected, more accu-
lar monitoring, involving full clinical examination
rate assessment of the severity of the underlying
(including assessment of body weight), measure-
irreversible chronic renal failure can be made.
ment of systemic arterial blood pressure and analy-
sis of blood and urine samples. This allows early Treatment of progression of chronic renal failure
detection of problems, and assessment of efficacy of involves:
therapy and tailoring of treatment to the individual. ● Identifying and eliminating the inciting cause of
the renal damage.
● Correcting the systemic and metabolic derange-
ments of chronic renal failure.
Pre-renal azotemia occurs secondary to dehydration ● Preventing the intrinsic progression of renal fail-
or circulatory collapse, and the azotemia results from ure (if such progression occurs in the cat).
reduced renal perfusion. – A number of therapeutic maneuvers may be
● Typically urine specific gravity is greater than 1.035. effective slowing intrinsic progression. These
● Pre-renal azotemia concurrent with primary disease include dietary protein restriction, angiotensin-
affecting renal concentrating ability can mimic converting enzyme (ACE) inhibitors, modifica-
renal failure, for example a dehydrated cat with diation of dietary lipid intake and phosphate
betes inspidus. restriction. Evidence for a beneficial effect on
survival for each of these treatments is limited
Acute renal failure.
and therefore currently each case should be
● Therapeutically and prognostically it is important
assessed on an individual basis.
to distinguish between chronic and acute renal
failure. Maintenance of hydration.
● Evidence of chronicity is usually obvious from ● Unrestricted access to water is essential in any cat
the history (polydipsia, weight loss), physical with chronic renal failure to allow thirst to compen-
examination (small kidneys), and diagnostic tests sate for the obligatory polyuria. Additional fluids
(non-regenerative anemia). (oral, subcutaneous or intravenous) may be required
● Due to the gradual decline in glomerular filtration when intake fails to keep pace with diuresis. Home
rate in chronic compared to acute renal failure, administration of subcutaneous fluids are indicated
clinical signs in chronic renal failure tend to be less when the cat is unable to maintain hydration.
dramatic relative to the metabolic derangements. Typically, cats require 75–150 ml SQ q 12–72 h.
Begin a 4–5 kg cat on 150 ml twice weekly, and use
normal saline with 35 mmol (mEq)/L of KCl added.
Treatment
Education of the owner on proper administration
Treatment of chronic renal failure is aimed at: and sterile technique is vital.
Dietary management of chronic renal failure. ● The mechanisms of these effects are unclear, but
● Treatment of cats with chronic renal failure by may be hemodynamically mediated by causing
dietary modification has been proven to significantly renal vasodilation especially of the efferent arteri-
increase survival. Generally, commercially available ole, and reducing glomerular capillary pressure.
“renal diets” are recommended. These diets have ● Preliminary studies of ACE inhibitor use in natu-
restricted protein, calcium, sodium, phosphorus and rally occurring chronic renal failure in cats have
acid-load, and added potassium. shown significantly increased survival times for the
subgroup of renal-failure cats with urine protein/cre-
Dietary protein restriction is frequently advocated.
atinine ratios > 1.
● In moderate to severe chronic renal failure, con-
● By reducing glomerular pressure, ACE inhibition
trolled restriction of non-essential protein will
would be expected to cause a decrease in glomeru-
reduce the accumulation of nitrogenous waste prod-
lar filtration rate and so may increase azotemia.
ucts that are believed to contribute to the uremic
A rise in creatinine of > 50% warrants withdrawal
syndrome.
of the drug.
● More controversially, the use of a restricted protein
diet in early CRF may slow the rate of progression Treatment of renal secondary hyperparathyroidism
to end-stage renal failure by preventing maladaptive should be instituted in a staged manner.
changes in surviving nephrons. However, evidence
The cornerstone of therapy is dietary phosphate
for a beneficial effect of protein restriction on renal
restriction.
function in cats with early renal failure is not avail-
● After initiation of phosphate restriction, plasma
able.
phosphate levels usually stabilize at a lower level by
● Poor appetite and the decreased palatability of
2–8 weeks, however PTH concentrations may con-
restricted protein diets make mal-nutrition a seri-
tinue to decline without additional intervention.
ous problem in renal-failure patients. Monitor
● Proteinaceous foods are the main source of phos-
carefully for weight loss and decreasing muscle
phate in the diet, so phosphate restriction is gener-
mass.
ally combined with protein restriction.
● Dietary protein intake should be tailored to the
● The aim of dietary phosphate restriction is to
metabolic needs of the individual cat. Usually a diet
reduce plasma phosphorus to the lower limit of
containing at least 21% of gross energy as protein is
the reference range, the point at which the most
required (usual maintenance diets contain 35–55%
effective control of PTH secretion is usually
gross energy as protein). The goal is to maintain a
attained.
BUN of ≤ 29 mmol/L (80 mg/dl). In general, the
more severe the renal dysfunction, the greater the If after 4 weeks dietary management alone is not
protein restriction required, but protein should not achieving this, or if PTH concentrations are not
be decreased below 19–20% of gross energy decreasing, then intestinal phosphate-binding agents
(metabolizable energy). should be introduced to further restrict phosphate
intake.
A number of other dietary components have been stud-
● Intestinal phosphate-binding agents form non-
ied for their effect to modify the rate of progression
absorbable salts of phosphate, binding phosphate in
including calorie intake and fatty acid composition.
both the diet and intestinal secretions. To achieve
Dietary phosphate restriction is discussed under the sec-
efficient phosphate binding, the medication should
tion on renal secondary hyperparathyroidism.
be given, ideally mixed through the food or imme-
Angiotensin-converting enzyme (ACE) inhibitors diately before feeding.
may have a renoprotective effect, which is inde- ● Aluminum hydroxide should be dosed at 30–100
pendent of any effect on systemic blood pressure. mg/kg/day PO in divided doses with each meal,
ACE inhibitor therapy may also be useful in titrated to effect based on plasma phosphate concen-
reducing the degree of proteinuria in cats with trations. Dose can be increased to 200–300 mg/kg if
chronic renal failure. benazepril 0.25–0.5 mg/kg necessary to control phosphate. If the cat refuses to eat
PO q 24 h. it with food, a compounding pharmacy can formulate
it in capsules to administer immediately after a meal. ● The long-term advantages of this form of therapy
Calcium-containing phosphate binders such as cal- are as yet unproven. The aim is to decrease pro-
cium acetate (60–90 mg/kg/day divided with meals) gression of renal failure through a reduction in PTH
or calcium carbonate (90–150 mg/kg/day divided with concentrations. If there is marked hypercalcemia
meals) can be used, but serum calcium must be moni- based on measurement of ionized calcium, care
tored carefully. Do not use if there is hypercalcemia. should be taken to rule out other causes of hypercal-
● High dietary phosphate limits the effectiveness of cemia, because the hypercalcemia of renal failure is
phosphate-binding agents, so preferably these usually only mild to moderate in severity (total
should be used in combination with a low- calcium <3.4 mmol/L or 13.5 mg/dl).
phosphate diet.
Treatment of hypokalemia.
Treatment with an active form of vitamin D directly
Hypokalemia may be treated with oral potassium glu-
inhibits PTH secretion. This group of drugs has a
conate (2–6 mmol/cat/day PO). The exact dose is
very narrow therapeutic index.
dependent on the response to therapy, determined by
● Calcitriol or alphacalcidol 1.5–3.5 ng/kg/day PO
monitoring plasma potassium concentrations.
on an empty stomach (maximum 10 ng/kg/day).
Because of the very low dose, the human prepara- Treatment of the anemia.
tions must be re-formulated by a compounding
Management of the anemia of CRF should include an
pharmacy for use in cats.
initial assessment of the cat to rule out and treat other
● All active vitamin D preparations enhance intestinal
potential causes of anemia, such as flea infestation and
absorption of calcium and phosphorus, and so are
gastrointestinal ulceration.
contraindicated unless plasma concentrations of
calcium and phosphate are normal. In addition, they Nutritional and iron deficiencies will impair the ery-
are ineffective in decreasing PTH concentrations if thropoietic potential, and should be corrected prior to
phosphorus is elevated. Phosphorus concentration initiating other treatment.
must be below 2 mmol/L (6 mg/dl) before calcitriol
Blood transfusions (limited availability), androgen
use is optimal. Between serum phosphorus
(poor efficacy) and recombinant erythropoietin therapy
of 2–2.25 mmol/L (6–7 mg/dl), the effectiveness of
have all been used to treat the anemia of CRF.
calcitriol is decreased, and above a phosphorus
of 2.5 mmol/L (8 mg/dl) it is ineffective in reducing Recombinant human erythropoietin (rHuEPO) is
PTH concentration. the most effective therapy.
● Plasma calcium must be closely monitored, ini- ● Therapy should be started only if clinical signs
tially weekly. If possible measure ionized calcium relating to the anemia are present, such as weak-
rather than total calcium. The dosage should be ness, inactivity or lethargy, which is usually when
titrated to maintain normocalcemia, not merely to the packed cell volume (PCV) is less than 18%.
decrease PTH concentrations, and therapy should Because of potential side effects of treatment, it is
be discontinued if hypercalcemia occurs. If hyper- usually only commenced once PCV is <15%.
calcemia does not resolve within 7–10 days of ● Initial dosage is 50–100 U/kg injected subcuta-
stopping calcitriol, begin intermittent dosing of neously three times weekly, with PCV monitored at
calcitriol. For cats with mild hypercalcemia based least twice weekly. Once the PCV has increased to
on the ionized calcium concentration, give cal- the lower end of the reference range, the dosage is
citriol every other day at twice the daily dose, so usually reduced to once or twice weekly.
the total amount per week is the same. If calcium ● Adverse effects of rHuEPO include polycythemia,
levels do not decrease, try twice weekly dosing at seizures, hypersensitivity reactions and systemic
3.5 times the daily dose (8 pm one day and 8 am hypertension. Absolute failure to respond to
4 days later). Do not use less than twice weekly. rHuEPO is usually due to iron deficiency.
PTH concentrations should be measured to docu- ● After an initial response, many treated cats develop
ment successful control of renal secondary hyper- antibodies to rHuEPO, which leads to a severe
para-thyroidism. refractory anemia greater than that present prior to
treatment. This anemia is usually reversible when Prevention

therapy is discontinued. For this reason rHuEPO
should not be initiated too early in the course of Since the majority of cases of chronic renal failure are
progressive CRF. of unknown primary cause, there are currently no pre-
ventative recommendations.
Treatment of systemic hypertension.
● Treatment is usually carried out on a trial basis,
Avoid any potential renal insults, particularly in cats
monitoring for a decrease in blood pressure without with pre-existing comprise of renal function or renal
adverse effects or the development of hypotension. perfusion. For example, avoid using NSAIDs in dehy-
Generally a period of about 2 weeks is sufficient to drated cats, and use intravenous fluids prior to induc-
document a response. If severe clinical signs are tion of anesthesia and during surgery, to maintain renal
present, therapy may need to be more aggressive. perfusion in elderly cats and cats with compromised
● Classically, a staged therapeutic response is recom-
renal function. Remember that minor renal insults may
mended, starting with dietary sodium restriction, summate to cause clinically significant renal damage.
● Promptly and appropriately treat conditions causing
followed by the use of various pharmacological
agents. decreased renal perfusion including dehydration,
shock and hypotension associated with anesthesia
The current treatment of choice for the cat is and surgery.
amlodipine besylate. An initial dose of 0.625 mg/cat
PO q 24 h is recommended and may be increased cau- Pre-renal and post-renal azotaemia, if not corrected,
tiously if the response is poor, to 1.25 mg daily. may lead to renal damage and renal failure.
Combination therapy is required in some cases, with

the addition of an ACE inhibitor or beta blocker. FELINE IMMUNODEFICIENCY VIRUS
Treatment of proteinuria involves protein restriction (FIV)***
to maintain a BUN of ≤ 29 mmol/L (80 mg/dl) and use
of an ACE inhibitor to reduce glomerular pressure. Classical signs
Treatment of anorexia associated with chronic renal ● Middle-aged to older cats, particularly
failure. entire males and feral cats.
● Anorexia is usually associated with moderate to ● Clinical signs variable, often vague.
severe uremia, and contributes to further uremia by ● Weight loss, inappetence.
resulting in catabolism of tissue protein for energy. ● Pyrexia, lymphadenopathy.
● Change food gradually over 1–2 weeks in a renal ● Immunosuppression (cat flu, diarrhea,
diet, and increase palatability by warming to just neoplasia).
below body temperature. ● Gingivitis/stomatitis.
Reduce gastric hyperacidity from hypergastrinemia.
● H2-receptor antagonists such as famotidine (0.5–1 Pathogenesis
mg/kg PO q 24 hours). Feline immunodeficiency virus (FIV) is a lym-
● Gastric mucosal protectant, sucralfate (250 mg/cat
photrophic lentivirus, which causes an acquired
q 8–12 hours, on an empty stomach). immunodeficiency syndrome (AIDS) in cats.
Modify doses of drugs if excreted by kidneys. ● FIV is morphologically and biochemically similar
to human immunodeficiency virus (HIV), however
it is antigenically distinct and the viruses are
Prognosis species specific.
Chronic renal failure tends to be progressive and the Infectious virus is found in the saliva of FIV-positive
long-term prognosis is poor, although with careful cats and transmission occurs primarily though inocula-
management some cats will live for years. tion of the virus through saliva or blood.
● Bite wounds are considered a primary source of adenopathy, AIDS-related complex (ARC), and AIDS.
infection. However it may be difficult to distinguish these stages
● Vertical transmission either transplacentally or via clinically.
infected milk occurs experimentally but is of ques- ● The acute phase begins about 4 weeks following
tionable significance in natural settings. infection and may persist for up to 4 months.
● Horizontal transmission in multiple cat households – Mild lymphadenopathy, neutropenia, fever,
via food bowls, mutual grooming appears rare. malaise and diarrhea may occur.
● Sexual transmission is not thought to be a signifi- – These signs may be mild and go completely
cant route of infection. unnoticed by the owner.
– These cats will usually test seronegative for the
The prevalence of FIV infection varies with the popu-
virus.
lation studied:
● The asymptomatic carrier phase may last for
● FIV infection in healthy cats in the United States
months to years.
and United Kingdom ranges from 2–3%, compared
– Despite being asymptomatic, significant immune
to rates approaching 30% in sick cats or cats with a
aberrations may be present
high risk of exposure.
● Persistent generalized lymphadenopathy lasts for
● Male cats are three times more likely to be
less than 2–4 months.
infected than female, especially male entire cats.
– Poor hair coat, fever and leukopenia may be
● Risk of infection is greater in free-roaming and
noted.
feral cats than indoor cats.
● The terminal clinical phase can sometimes be
FIV has a worldwide distribution in domestic cats. divided in to ARC and AIDS.
● ARC is the presence of clinical disease that does
The course of the disease following FIV infection is
not fulfill the criteria for AIDS.
dependent on a number of host- and virus-related fac-
● AIDS is the final stage of the infection.
tors, such as the age and health status of the cat and the
– Profound weight loss (> 20% of body weight)
strain and dose of the virus.
and a variety of opportunistic infections.
Acute infection involves rapid replication of virus in – Frequently there is persistent leukopenia and
lymphoid organs and salivary glands. anemia.
– Additionally, cats may have neurological dis-
Although CD4+ (helper) and CD8+ (cytotoxic) T lym-
ease or malignancy.
phocytes may be infected by FIV, FIV selectively
– Average life expectancy is less than 1 year.
destroys CD4+ cells.
● The ratio of CD4+ to CD8+ becomes “inverted” in Many diseases found in the asymptomatic phase
cats with FIV because of the relative lack of CD4+ may or may not be related to the virus.
cells.
Immunosuppression leads to opportunistic infections
● The lack of CD4+ leads to the immunosuppression
with bacterial, fungal or protozoal agents.
associated with many of the clinical signs of FIV
● Little good statistical evidence is available to show
infection.
that there is a higher incidence of many of these dis-
Many cats remain completely asymptomatic for years, eases in FIV-infected cats.
despite severe lack of CD4+ lymphocytes. ● Some studies indicate that these diseases may be
more severe in the FIV-infected cat.
Clinical signs Certain disease processes have been directly associated
with the terminal clinical phase of the disease.
Clinical signs are very variable from cat to cat, and may
● Chronic ulceroproliferative stomatitis is com-
be a direct effect of the virus or secondary to immuno-
mon, and may be associated with concurrent cali-
suppression.
civirus infection.
The infection can be divided into stages: acute, ● Ocular disease including uveitis, glaucoma, infil-
asymptomatic carrier, persistent generalized lymph- tration of inflammatory cells in the posterior chamber
(pars planitis), focal retinal chorioretinitis and reti- – Small numbers of cats (up to 10–20%) have
nal hemorrhages have been reported. delayed seroconversion or may never seroconvert.
● Neoplasia including lymphoma (often extra-nodal), – The cat is in the terminal stages of the disease,
leukemia, and several others have been associated when antibody production declines.
with the terminal stage of the disease. However, the
Detection of FIV infection does not prove that
exact role of FIV in the neoplastic process is
the clinical signs are necessarily related to the
unclear.
infection.
● Central and peripheral nervous system disease
● Since cats can live for years in the “asymptomatic”
has been associated with FIV infections. These
stage of the disease, the clinician should try to
signs may be transient. Clinical signs include
decide if the virus is a cause, contributing factor, or
behavior changes, seizures, paresis and anisocoria.
just incidental to the cat’s problem.
Concomitant infections (cryptococcosis, toxoplas-
mosis or FIP) may contribute to neurologic signs. Immunoflourescent antibody or western blot tech-
● Renal disease and failure may have an association niques may be used to confirm the presence of FIV
with the FIV virus. Since many older cats suffer antibody, particularly in ELISA-positive cats from
from chronic renal failure, the exact association low-risk populations, or if initial test results were
between the virus and renal failure has yet to be equivocal.
determined.
Non-specific findings on routine hematology and bio-
chemistry include:
Diagnosis ● Various cytopenias including neutropenia, throm-
bocytopenia, lymphopenia, and anemia.
Diagnosis of FIV infection is based on serological
● Mild non-regenerative anemia.
evidence of the presence of FIV specific antibodies.
● A polyclonal hyperglobulinemia.
● In practice, diagnostic kits are available to detect
antibody to either p24 core protein or gp41 enve-
lope protein using enzyme-linked immunosor-
bent assay (ELISA) or rapid immunomigration Differential diagnosis
(RIM).
Feline leukemia virus infection (FeLV) may be clini-
Interpretation of a positive antibody result: cally very similar to FIV infection, as many signs are
● Vaccinated cats will test positive with all current associated with the immunosuppression which is common
testing methods. to both conditions.
● In unvaccinated cats, FIV antibodies are associated ● Most cats that are tested for FeLV probably should
with lifelong viral infection. A positive test implies be tested for FIV.
a persistently infected cat.
The dry form of feline infectious peritonitis (FIP)
● Passive transfer of antibody via milk will result in
may lead to signs of wasting, neurologic signs, renal
a positive test in kittens nursed by an infected
failure and ocular disease. The “dry” form of FIP is
queen. Such kittens should not be tested until at
extremely difficult to diagnose without histologic
least 6 months of age.
examination of tissue.
● False-positive results occur with ELISA or RIM
tests, but at a low frequency. A positive test should be Toxoplasmosis causes neurologic and ocular signs as
confirmed using a western blot if it will influence well as wasting. FIV and toxoplasmosis may also occur
management of the cat. concurrently.
Interpretation of a negative antibody result:
● The cat is not infected with FIV.
Treatment
● The cat is infected but no antibodies are present.
– This occurs in early stages of infection, usually The FIV status of the cat should not necessarily pre-
2–4 weeks after infection. clude treatment for other diseases.
No specific therapy has proven effective against the Prognosis

virus in the long term, but reverse transcriptase In the acute or asymptomatic phases of the disease, it is
inhibitors and immunomodulating drugs may provide not possible to predict the short- or long-term prognosis.
some benefit in rescuing severely ill cats in the short-
term. Although some drugs can reduce viral load Many cats appear to live for years with no or minimal
(AZT and PMEA), there are no studies showing a problems.
proven clinical benefit long term, or resolution of In the terminal clinical phase, the prognosis is poor
infection, and long-term use is hindered by side to grave with average life expectancy of less than
effects. 1 year.
Reverse transcriptase inhibitors may suppress viral
replication. Prevention
● Zidovudine (3′-azido-3′-deoxythymidine, AZT)
(5–15 mg/kg PO or 5 mg/kg subcutaneously q 12 One vaccine has been approved for the prevention of
hours) has been shown to improve clinical signs, FIV. There are still questions on its efficacy and the
but does not eliminate the virus. American Association of Feline Practitioners (AAFP)
– Increased numbers of CD4+ cells and improve- has yet to recommend its use.
ment in CD4+:CD8+ ratios have occurred in nat- Until a proven effective vaccine is developed and the
urally infected FIV cats. ability to differentiate a false positive vaccine titer
– Remission in stomatitis has been reported. from infection, prevention is achieved by avoiding
– The virus may become resistant to AZT exposure to infected cats.
– Anemia and hepatotoxicity are potential side ● FIV-positive cats should be neutered to reduce the
effects. tendency to fight.
● Confinement of FIV-positive cats to indoors will
Immunomodulating drugs to potentiate the immune
response against the virus include: reduce the spread of the virus, and will also reduce
● Evening primrose oil (550 mg PO q 24 hours).
the exposure of the affected cat to secondary infec-
● Low-dose oral human recombinant alpha inter-
tious diseases.
● In single-cat households or multiple-cat households
feron (30 IU/cat PO q 24 hours, 7 days on, 7 days
off). where all cats are seronegative for the virus, the ani-
● Acemannan, Propionibacterium acnes and
mals are at negligible risk if they are kept as indoor
staphylococcal protein A have been suggested as cats.
● FIV is readily killed by disinfectants and survives
immunomodulating agents in FIV infection.
only a few hours in the environment, so risk of
Aggressive supportive care and management of fomite transmission is low.
secondary infections are essential in FIV-positive
cats. All infections should be fully assessed in terms The FIV status of new cats should be determined prior
of extent and appropriate treatment administered, ide- to introduction to a group. Ideally these cats should be
ally based on culture and sensitivity results. Response rechecked in 4–6 weeks because of the latency period
to treatment may be slower in FIV-infected cats, and between exposure and production of antibody.
so sufficient duration of antibiotic must be adminis-
tered. CANCER CACHEXIA**
Appropriate preventative medicine is important in
immunosuppressed cats. Classical signs
● Inactivated vaccines should be used against respira- ● Anorexia, muscle wasting and weight loss.
tory or enteric pathogens. ● Weakness, lethargy.
● However the ability of an FIV-infected cat to pro- ● Clinical signs associated with the
duce an adequate immune response to a vaccine is neoplastic lesion.
unknown.
Pathogenesis ● Diagnostic imaging (radiography, ultrasound

examinations and computed tomography) of the
Cancer cachexia is probably the most common thorax and abdomen.
paraneoplastic syndrome. – Evaluation of pulmonary neoplasia should
It is associated with a variety of malignancies. include two lateral and ventrodorsal radi-
ographic views.
Although many cats with neoplasia are cachexic, little ● Cytological or histopathological evaluation of tissue
information is available on the metabolic derangements is required to confirm the diagnosis.
present. Care must be taken extrapolating data from the
dog and man, given the differing nutritional require- Cats with neoplastic lesions should be monitored
ments of these species. closely for evidence of malnutrition. A detailed dietary
history and physical examination are important for
Weight loss occurs in patients with neoplasia because: monitoring. Regularly assess body weight and use a
● Nutrient intake is reduced.
body condition scoring system.
– This is related to tumor size and location. For
example, intraoral masses cause dysphagia, and Hematological and biochemical parameters are rela-
infiltrative intestinal neoplasia may reduce nutri- tively insensitive markers of nutritional status, but may
ent assimilation. provide additional information. However these markers
– Decreased appetite may be a consequence of may be affected by the neoplasia itself.
therapy. ● Creatine kinase concentrations may increase rap-
● Metabolic and hormonal changes secondary to idly in response to anorexia.
neoplasia lead to inefficient energy utilization. ● Protein malnutrition may lead to hypoalbuminemia.
● Malnutrition may also cause anemia and lym-
phopenia.
Clinical signs
Inappetence and weight loss are common clinical Differential diagnosis
findings in many cats with varying malignancies.
Differential diagnoses include most causes of inappe-
Weight loss is frequently associated with muscle wast- tence and weight loss.
ing, and consequent lethargy and weakness.
Other differentials to be considered depend on the site,
Poor hair coat, delayed wound healing and impaired location and nature of the tumor.
immune function are associated with cachexia.
Other clinical signs will vary with the nature and loca- Treatment
tion of the neoplasia.
Treatment specific to the neoplastic lesion will depend on
the nature, extent and location of the tumor, but may
Diagnosis include excisional surgery, radiotherapy or chemotherapy.
Neoplasia should be suspected in any cat showing Dietary recommendations postulated to prevent or ame-
inappetence and weight loss, with no obvious other liorate cancer cachexia include:
cause. ● Palatable, highly digestible, complete and bal-
A thorough clinical examination, including palpation of anced diets.

all lymph nodes, may provide an indication of the site ● Tumor cells have an obligate requirement for glucose
of the lesion and direct further investigation. and are unable to utilize significant amounts of lipid
for energy. Therefore, energy-dense diets, which are
Principal diagnostic efforts are aimed at establishing relatively high in fat and restricted in carbohydrate,
the nature and extent of the neoplastic lesion. The may theoretically have beneficial effects.
exact diagnostic investigation will depend on the loca-
tion and type of lesion being investigated but may Appropriate treatment of associated symptoms such as
include: nausea, diarrhea or vomiting.
Pharmacological appetite stimulation may be consid- Hyperthermia describes a core body temperature
ered but objective evidence of their efficacy is not avail- above that considered normal in the cat. In fever, the
able. set point of the thermoregulatory center is
increased.
In cats which are unable or unwilling to eat, enteral or
parenteral feeding may be considered. Fever may be caused by exogenous pyrogens such as
● Enteral nutrition should be used wherever possi- infectious agents, immune complexes and tissue
ble, as this prevents intestinal mucosal atrophy inflammation or necrosis.
– Nasoesophageal, esophageal, gastrostomy and ● Exogenous pyrogens principally act by causing the
jejunostomy tubes may be used host to release endogenous pyrogens.
– Esophagostomy and gastrostomy tubes are ● Endogenous pyrogens act on the thermoregulatory
preferable in cats requiring more long-term center, alter the set point and induce a febrile response.
nutrition.
Weight loss frequently occurs in cats with prolonged
● Parenteral feeding is more technically complex and
fever because:
expensive, and should only be used when feeding
● Febrile cats are frequently inappetent.
via the gastrointestinal tract is impossible.
● A febrile cat is in a hypermetabolic state.
● Weight loss may be associated with the fever per se,
or more often with the disease causing the fever.
Prognosis
The differential diagnosis list for causes of fever is
The prognosis for each individual case will be depend-
extensive but may be broadly categorized:
ent on the nature of the neoplasm and the response to
● Localized infection.
therapy.
– Including urinary tract infection, pyometra,
Cachexia and hypoalbuminemia tend to be poor prog- pyothorax, peritonitis, abscess, bronchopneumo-
nostic indicators. nia, endocarditis, suppurative cholangitis/ cholan-
giohepatitis, dental disease, retrobulbar or
pulmonary abscess and osteomyelitis.
Prevention ● Systemic infection.
– Including FeLV, FIV, feline infectious peritoni-
Cats with neoplastic lesions should be monitored
tis (FIP), feline panleukopenia, respiratory tract
closely for evidence of malnutrition.
virus infection, bacteremias, toxoplasmosis,
mycobacterial infection and systemic mycoses.
● Immune-mediated disorders.
SEPTIC FOCUS/PERSISTENT FEVER**
– Including primary immunodeficiencies, sys-
temic lupus erythematosus, polyarteritis nodosa,
Classical signs
chronic progressive polyarthritis, immune-
● Fluctuating pyrexia and associated mediated hemolytic anemia and immune-medi-
inappetence. ated thrombocytpenia.
● Weight loss. ● Neoplasia.
● Clinical signs associated with the etiology – Including lympho- and myeloproliferative dis-
of the fever. eases and large neoplastic lesions with central
necrosis.
See main references on page 364 for details (The ● Miscellaneous conditions.
Pyrexic Cat). – Including drug reactions.
Pathogenesis Clinical signs

The thermoregulatory center is located in the preoptic Principal clinical signs will be fever, weight loss and
region of the anterior hypothalamus. inappetence.
Fever may be sustained or fluctuating. Other differentials to be considered depend on the site,
location and nature of the disease causing fever.
Other clinical signs will vary with the nature of the dis-
ease causing the fever.
Treatment
Effective treatment is based on accurate assessment of
Diagnosis
the cause of the fever, followed by appropriate man-
A thorough history and clinical examination is vital to agement.
identify any localizing signs that would narrow the dif-
Use of antibiotics, corticosteroids and NSAIDs prior to
ferential diagnosis list.
diagnosis should be avoided where possible, as it will
Monitoring the cat’s temperature three or four mask the clinical signs and interfere with diagnostic
times daily over a period of 48–72 hours confirms testing.
the presence and nature of the fever.
If a septic focus is identified, treatment involves
Routine hematology often reveals a neutrophilia with drainage where appropriate (e.g. placement of tho-
or without a regenerative left shift. racic drains in pyothorax) and use of antibiotic ther-
● Occasionally a degenerative left shift occurs when apy based on the results of culture and sensitivity
the bone marrow is unable to make an adequate testing.
response, and neutropenia develops in the face of a
Mild fever is unlikely to be fatal and may be beneficial
left shift. This has a poor prognosis.
in inhibiting viral and bacterial replication and increas-
In the absence of localizing signs a series of initial ing leukocyte function.
screening tests are carried out to identify the septic focus:
Fever in excess of 41.0˚C often results in significant
● Routine hematology and biochemistry.
organ damage and may initiate disseminated
● Routine urinalysis including bacterial culture and
intravascular coagulation.
sensitivity.
● Thoracic and abdominal radiographs. Symptomatic therapy for fever includes:
● Fecal analysis and culture for enteric pathogens. ● Oxygen.
● Crystalloid fluid therapy.
Further diagnostic investigation may be required
● Antipyretic drugs (NSAIDs) – these act directly
depending on the cause of the fever, this may include:
on the thermoregulatory center and should be tried
● Blood culture.
before surface cooling, unless the fever is life-
● Synovial fluid aspirates.
threatening, when they may be instituted together.
● Echocardiography.
● Surface cooling. Core temperature will continue to
● Bone marrow aspirates.
decrease after surface cooling has ceased, so to
● Immunological tests such as Coomb’s, antiplatelet
avoid large oscillations in temperature, aggressive
antibody and antinuclear antibody tests.
cooling should stop just prior to reaching the
● Serum protein electrophoresis.
desired temperature.
● Serology.
– With cool, not cold, water (avoid inducing shiv-
If a bacterial cause is suspected, strenuous attempts ering).
should be made to obtain a sample of infected mate- – Fans.
rial for bacterial culture and sensitivity testing – Ice packs over large blood vessels.
prior to administering antibiotics.
Prognosis
The prognosis for each individual case will be depend-
Differential diagnoses include most causes of inappe- ent on the etiology of the fever and the response to
tence and weight loss. therapy.
Serum biochemistry frequently shows elevations of

APATHETIC HYPERTHYROIDISM*
hepatic enzymes (alanine amino transferase and alka-
line phosphatase).
Classical signs
A definitive diagnosis of hyperthyroidism is made on
● Older cats (usually > 8 years).
the basis of high serum basal total thyroxine (T4)
● Weight loss and inappetence.
concentrations.
● Weakness and depression.
● Palpable goiter. Normal serum thyroid hormone concentrations are
● Tachycardia ± gallop rhythm. occasionally found in hyperthyroid cats due to:
● Day-to-day fluctuation in hormone levels.
See main references on page 304 for details (The Cat ● Early or mild hyperthyroidism.
With Weight Loss and a Good Appetite). ● The presence of concurrent non-thyroidal disease
that suppresses serum thyroid levels.
Clinical signs Given that concurrent disease is common in cats with
Hyperthyroidism is a disease of older cats, with only apathetic hyperthyroidism, suspect hyperthyroidism
5% being under 10 years of age at first diagnosis. despite normal Total T4 concentrations if the cat is
older than 8 years and has signs consistent with hyper-
The majority of cats with hyperthyroidism present with thyroidism. e.g. tachycardia or thyroid goitre.
weight loss and polyphagia.
If hyperthyroidism is suspected despite normal total
In approximately 5% of cases, apathetic or masked T4 concentrations, diagnostic possibilities include:
hyperthyroidism occurs. ● Repeat basal total T measurement in 1–2 weeks.
4
● Weight loss is accompanied by a decreased appetite. ● Identify and treat concurrent disease, then
● Cats tend to be depressed. repeat basal total T4 measurement.
● Muscle weakness may be evident as ventroflexion ● Measure basal free T concentrations, although
4
of the neck. euthyriod cats with non-thyroidal illness may have
● Cats with apathetic hyperthyroidism may show an elevated concentration.
signs of concurrent disease including congestive ● Dynamic thyroid testing may also be used:
cardiac failure, renal failure or neoplasia. – Triiodothyronine (T3) suppression test.
Other clinical signs are those typical for hyperthyroidism. – Thyrotropin (TRH) stimulation test, although the
● Unilateral or bilateral palpably enlarged thyroid usefulness of this test in cats with non-thyroidal
(goiter). illness to distinguish those with and without
● Polyuria and polydipsia. hyperthyroidism has recently been questioned.
● Vomiting and diarrhea (bulky feces). ● Radionucleotide uptake and imaging.
● Tachycardia, gallop rhythm, murmur and arrhyth- Concurrent disease may be present and should be
mia may be noted. investigated, in particular:
● Poor coat condition with decreased grooming. ● Evidence of concurrent renal failure with increased
creatinine and urea concentration may also be pres-
Diagnosis ent. Urine specific gravity will also provide further
information regarding renal function.
Although clinical signs of inappetence and depression
● Hypertrophic cardiomyopathy secondary to hyper-
are atypical for hyperthyroidism, the presence of a
thyroidism (thyrotoxic cardiac disease) is frequently
thyroid goiter or tachycardia should alert the clini-
seen on echocardiography. This may be reversible
cian to the possibility of hyperthyroidism.
with resolution of the hyperthyroid state but may
As apathetic hyperthyroidism typically occurs in progress to congestive cardiac failure.
hyperthyroid cats with significant concurrent
disease, a thorough investigation is required to estab- Differential diagnosis
lish the presence of such disease.
These include most other causes of inappetence and
Routine hematology may reveal a mild erythrocytosis. weight loss.
As tachycardia (with or without cardiac failure) is often roidism) and methimazole (10–15 mg/day PO
present, cardiac disease should be placed high on the divided q 8–12 hours for 2–3 weeks, then 7.5–10
differential diagnosis list. mg/day PO divided q 12 hours to maintain euthy-
roidism) are the drugs of choice for both short-
For cats with polydipsia and polyuria in addition to
and long-term medical management of hyperthy-
inappetence and weight loss, the main differential diag-
roidism. Transdermally absorbed methimazole
noses would include chronic renal failure and diabetes
may be obtained from a compounding pharmacist,
mellitus.
and may be useful if the owners are unable to give
oral medication.
Treatment – Exact dosage should be adjusted on the basis of
basal total T4 concentrations.
Hyperthyroid cats may be treated by surgical thy-
– Failure of efficacy is usually due to poor com-
roidectomy or radioactive iodine (131I), which are
pliance.
curative, or alternatively the condition may be con-
– Adverse effects appear to be less common with
trolled using antithyroid therapy.
carbimazole than methimazole and usually occur
The ideal form of treatment for each case will depend in the first 3 months of therapy.
on a number of factors: – Transient vomiting, anorexia and lethargy have
● Age of the cat. been reported, and usually resolve without with-
● Presence of concurrent disease, particularly chronic drawal of the drug.
renal failure or cardiovascular disease. – Serious hematological adverse effects may
● Availability of appropriate nuclear medicine facilities. occur, and so routine monitoring is required.
● Owner’s wishes, including ability to medicate cat – Hepatopathy and self-induced facial excoriation
and cost. may rarely occur.
● Other medical therapies may be considered includ-
Cats with apathetic hyperthyroidism frequently
ing atenolol (to reduce the cardiac effects of hyper-
have concurrent disease, and it is essential that this
thyroidism), stable iodine (preoperatively to
is thoroughly investigated and considered prior to
reduce gland vascularity) and ipodate.
embarking on therapy.
● Cardiac disease may preclude safe anesthesia and Surgical thyroidectomy is curative when it is possi-
surgical thyroidectomy. ble to remove all abnormal thyroid tissue.
● Glomerular filtration rate declines with resolution ● Medical stabilization, ideally for 3 weeks pre-
of the hyperthyroid state. Therefore, any cat sus- operatively significantly reduces the anesthetic
pected of having underlying renal disease (azotemia, and surgical complications.
creatinine and urea concentrations in the upper part of ● The most common complication is post-operative
the reference range, or lack of urine-concentrating hypoparathyroidism, although Horner’s syndrome
ability) should be treated with antithyroid medication and laryngeal paralysis may also occur.
until it can be determined if induction of euthy-
Radioactive iodine therapy is the treatment of
roidism would have detrimental effects.
choice for most hyperthyroid cats when suitable
Medical therapy for hyperthyroidism is used in the facilities for treatment are available.
short term to stabilize a hyperthyroid cat prior to ● This is the treatment of choice for cats with hyper-
surgical thyroidectomy, as trial therapy assesses the thyroidism induced by thyroid carcinoma.
effect on renal function prior to curative treatment, ● Complications include the induction of permanent
or for long-term management if surgery or radioio- hypothyroidism and incomplete ablation requiring
dine therapy are not suitable. an additional treatment.
● Medical management merely blocks thyroid hor- ● The principal disadvantage is a period of isola-
mone synthesis and so requires continuous life-long tion is required to comply with local radiation
treatment. safety regulations. This makes treatment of inter-
● Carbimazole (5 mg PO q 8 hours for 2–3 weeks, current disease difficult or impossible during this
then 5 mg PO q 12 hours to maintain euthy- time.
If there is significant biliary stasis, intestinal absorption

CHOLANGIOHEPATITIS COMPLEX*
of vitamin K may be impaired leading to impaired sec-
ondary hemostasis and a coagulopathy.
Classical signs
Abdominal radiography may be normal or reveal:
● Inappetence and weight loss.
● Hepatomegaly.
● Lethargy.
● Loss of abdominal contrast due to the presence of
● Jaundice.
ascites, or if more localized, due to pancreatitis.
● Hepatomegaly and/or ascites.
● Occasionally, choleliths may be noted.
See main references on page 427 for details (The Hepatic parenchymal changes on abdominal ultra-
Yellow Cat or Cat With Elevated Liver Enzymes). sound are not specific to cholangiohepatitis, varying
from normal parenchymal architecture, to diffuse
increases (particularly if cirrhosis is present), or
Clinical signs decreases (especially in acute or suppurative inflamma-
tory disease) in echogenicity. Ultrasonography is help-
The most consistent clinical signs in these cases
ful to demonstrate:
are weight loss, variable anorexia, lethargy and
● Abnormalities of the biliary tract including biliary
depression.
stasis or sludging, cholecystitis, biliary tract disten-
Fever may occur, particularly in the acute or suppura- tion and obstruction.
tive form of the disease. ● Concurrent pancreatic or intestinal disease.
Vomiting, diarrhea and abdominal pain may also A definitive diagnosis requires histopathological
occur. examination of hepatic tissue. Although as a diffuse
disease, cholangiohepatitis should be amenable to diag-
Clinical signs more specific to hepatic disease such as
nosis by percutaneous fine-needle aspiration techniques,
hepatomegaly and jaundice are common, particularly
blood contamination and the inability to assess hepatic
in the early stages of the condition.
architecture make definitive diagnosis of inflammatory
Occasionally polyphagia or a normal appetite may disease difficult. Tissue core biopsy or surgical wedge
be seen, particularly associated with lymphocytic biopsy yield improved diagnostic accuracy.
cholangiohepatits. ● Surgical exploration and wedge biopsy are required if
there is evidence of extra-hepatic biliary stasis, severe
Ascites, hepatic encephalopathy and a generalized
biliary sludging or clinically significant choleliths.
lymphadenopathy are uncommon clinical signs.
● In addition, surgical exploration permits a complete
In some cats, cholangiohepatitis is associated with evaluation of the biliary tree and pancreas, aspira-
inflammatory bowel disease and pancreatitis. tion of bile for culture (although this may be carried
out percutaneously by ultrasound guidance), biopsy
of pancreas, and intestine and placement of feeding
Diagnosis tubes.
Routine serum biochemistry findings include mild to
severe elevations in hepatic enzymes (especially ala- Differential diagnosis
nine amino transferase (ALT)). Hyperbilirubinemia
Differential diagnoses for inappetence and weight loss
and elevated bile acids are often also present.
associated with suspicion of hepatic pathology includes
Elevated serum globulin concentrations are common hepatic lipidosis, hepatic neoplasia, feline infectious
in the chronic stage of the disease. peritonitis affecting the liver and hyperthyroidism.
A neutrophilia, often with left shift may be present in Feline infectious peritonitis is an important differen-
acute cases on routine hematology. More chronic cases tial diagnosis for cholangiohepatitis, as both may pres-
often have a lymphocytosis. ent with hyperglobulinemia or ascites.

Acute or suppurative cholangiohepatitis is treated Clinical signs vary with the type and severity of the
primarily with antibiotics, ideally based on the inflammation, and with the anatomical extent of the
results of culture and sensitivity testing. disease, although the correlation is poor.
● Ampicillin (10–40 mg/kg PO q 8 hours), amoxy-
Characteristically, any combination of weight loss,
cillin (11–22 mg/kg PO q 8–12 hours), amoxycillin
vomiting or diarrhea may be seen.
clavulanate (12.5–25 mg/kg PO q 12 hours), or
cephalexin (10–30 mg/kg PO q 8–12 hours) are Vomiting is particularly evident if the pathology
good empirical choices. involves the stomach or proximal small intestine and
● Metronidazole in combination with the above antibi- may occur every few days to weeks. Vomiting is usu-
otics, provides broader anaerobic cover. Use at a lower ally unrelated to feeding, and is more frequently com-
dose (7.5–10 mg/kg PO q 12 hours) because of hepa- posed of fluid rather than food.
totoxicity and the increased potential for neurological
Diarrhea may be soft and semi-formed to watery in
signs in animals with pre-existing hepatic disease. In
consistency, with or without steatorrhea. Occasionally
addition it may have immunomodulating properties.
large bowel diarrhea with tenesmus, mucus and hema-
Immunosuppressive therapy is used if there is a lym- tochezia may be present.
phocytic component to the pathology, and in more
Clinical signs are usually chronic and may initially be
chronic cases, although definitive evidence of efficacy
intermittent.
is lacking.
● Prednisolone (2–4 mg/kg q 12–24 hours), gradually Weight loss initially results from malabsorption and
tapering the dose. later from inappetence. In some cases, progressive
● Other immunosuppressive agents may be consid- weight loss is the only clinical sign.
ered in non-responsive cases.
Flatus and borborygmi may be reported.
Fluid therapy and nutritional support will be required if
Initially, polyphagia or a normal appetite may be
anorexia is present.
seen, but this frequently progresses to inappetence as
Supportive and adjunctive therapy is often recom- the disease increases in severity.
mended on an empirical basis.
Intestinal thickening, mesenteric lymphadenopathy
● Ursodeoxycholic acid (10–15 mg/kg PO q
or abdominal pain may be revealed by abdominal
24 hours) is a hydrophilic bile acid which has cyto-
palpation.
protective properties.
● Parenteral vitamin K1 (0.5 mg/kg SC q 12 hours Occasionally, severe small intestinal disease leading to
for 3 days) may be provided for those cases show- protein leakage into the gut lumen (protein-losing
ing evidence of a coagulopathy. enteropathy) leads to extreme weight loss and
● S-adenosylmethionine (18 mg/kg PO q 24 hours) hypoproteinemia. Although usually polyphagic, if the
and vitamin E have antioxidant properties and may condition is associated with severe inflammatory or
be useful supplements. malignant disease, anorexia may occur. Vomiting and
diarrhea may rarely be accompanied by ascites and
peripheral edema.
INFLAMMATORY BOWEL DISEASE*

● Weight loss. The diagnosis of inflammatory bowel disease is
● Chronic vomiting and/or diarrhea. made based on exclusion of all other causes of the
● Variable appetite. clinical signs in association with appropriate
histopathology.
See main references on page 307 for details (The Cat ● Intestinal infiltration with inflammatory cells is
With Weight Loss and a Good appetite). non-specific.
● Inflammatory bowel disease is an idiopathic treatment involves immunosuppressive therapy in

condition. combination with dietary management.
Initial diagnostic investigation should aim to exclude A therapeutic dietary trial may be undertaken as part
other causes of gastrointestinal signs and may include: of the diagnostic evaluation (to eliminate dietary sensi-
● Routine hematology and biochemistry and serum tivity), as the initial stage of treatment, or in combina-
basal total T4 concentrations. tion with immunosuppressive therapy, depending on
– Stress leukogram and occasionally eosinophilia. the severity of the clinical signs.
– Serum globulins may be increased as part of the ● A nutritionally balanced, highly digestible diet
chronic immune stimulation. In severe cases should be used.
hypoproteinemia may result from protein-losing ● Usually a single protein, single carbohydrate source
enteropathy. diet is used (hypoallergenic), preferably one to
● Fecal analysis and culture to exclude fecal parasites which the cat has not previously been exposed.
and enteric pathogens. ● Use of diets with hydrolized protein (e.g. Hill’s z/d
● Radiography and ultrasonography should be per- or Royal Canin HA) may be efficacious in some
formed. cats. Hydrolization reduces the molecular weight of
– Radiography is frequently unremarkable, dietary proteins to < 10 000 so they are not detected
although increased gas may be present in intes- by the immune system.
tinal loops. ● A high-fiber diet has proven beneficial in cases with
– Ultrasonography may show evidence of thick- large intestinal involvement.
ened or abnormal intestinal walls. Abdominal ● Minimum duration of the trial should be 3 weeks,
lymph node enlargement may be present. but may be longer. If an improvement is seen, the
● A dietary trial is a valuable tool to determine if cat should then be challenged with the original diet
signs resolve when the cat is fed a novel single pro- to confirm sensitivity.
tein and carbohydrate diet.
Immunosuppressive therapy is required in the major-
Assessment of serum cobalamin and folate concentra- ity of cases:
tions, breath hydrogen analysis and sugar permeability ● Prednisolone (2–4 mg/kg PO q 12–24 hours) is
studies may be supportive of inflammatory bowel disease. used at higher initial doses, which are gradually
reduced to the lowest maintenance dose.
Definitive diagnosis requires multiple intestinal biop-
● Metronidazole (7.5–15 mg/kg PO q 12 hours) is used
sies either by endoscopy, laparoscopy or laparotomy:
either as sole therapy in mild cases, or in addition to
● Gastrointestinal endoscopy permits visual evalua-
prednisolone for those cats in which the response to
tion of the mucosa, but the superficial nature of the
prednisolone is inadequate. Metronidazole has activity
mucosal biopsies obtained by this technique limits
against anaerobic bacteria, protozoa and may be anti-
their diagnostic value.
inflammatory and influence cell-mediated immunity.
● Laparotomy allows the collection of full-thickness
● Other more potent immunosuppressive therapy may
biopsies, and gross evaluation and biopsy of other
be required in some cases.
abdominal organs if required.
FELINE LEUKEMIA VIRUS (FELV)*

The principal differential diagnoses are those conditions Classical signs
causing inappetence and weight loss in conjunction with
● Younger cats, often less than 6 years of
gastrointestinal signs, namely other causes of enteropa-
age, clinical signs variable.
thy, chronic pancreatitis, cholangiohepatitis, gastroin-
● Inappetence, weight loss and lethargy.
testinal neoplasia and apathetic hyperthyroidism.
● ± Neoplasia (lymphoma) – lymph node
enlargement, organomegaly, solid masses.
Treatment
● ± Anemia – pica, lethargy, pale mucous
As the etiology of the immune response in inflamma- membranes, tachycardia.
tory bowel disease is unknown, the principal form of
Classical signs—Cont’d Many of the clinical signs relate to the presence of con-
current disease such as toxoplasmosis or hemobar-
● Immunosuppression – abscesses, cat flu, tonellosis.
vomiting, diarrhea, neoplasia.
● Ocular signs – uveitis.
● Neurological signs – ataxia, behavioral
changes. Diagnosis
When clinical disease warrants evaluation for FeLV,
See main references on page 540 for details (The testing should be performed.
Anemic Cat). ● However a positive test does not prove that the
disease process is caused by the virus.
Clinical signs Diagnosis is usually based on the detection of viral
There are no “classical signs” in a FeLV infection. antigen (usually the p27 core protein) by immuno-
A variety of clinical signs may be noted dependent assay. The ELISA test is recommended by the
on the body system affected. No one clinical sign is American Association of Feline Practitioners.
● Serum or plasma is preferred over whole blood
found in all cats with persistent viral infection.
when ELISA testing because there are reported to
The most consistent clinical signs are weight loss, be fewer false positives.
variable anorexia, lethargy and depression.
A positive result may indicate:
Early infection with the virus is usually characterized ● Transient viremia in the early viremic state; the
by submandibular lymph-adenopathy and fever. cat may become negative later if a successful
This usually resolves in several days to weeks. immune response is mounted.
● Persistent viremia; such cats are likely to develop
Pale mucous membranes, weakness and anorexia are
seen if the virus causes anemia or bone marrow sup- FeLV-related disease.
● Discordant results (positive antigen test and nega-
pression. Hematological disease may be a primary viral
effect on the bone marrow or secondary (e.g. neoplastic tive on virus isolation) may occur early in the
infiltration, hemobartonellosis) course of the infection or may indicate focal infec-
tion with no virus present in the circulation.
Respiratory distress occurs if the virus leads to devel- ● False-positive result.
opment of an anterior mediastinal lymphoma with or
without pleural effusion. Confirmatory tests should be considered in cats
with a positive ELISA result, especially if the cat is
Signs of vomiting, diarrhea, and weight loss may be asymptomatic.
evident if there is gastro-intestinal infiltration with ● Immunoflorescent antibody test (IFA) detects
malignant lymphocytes. p27 antigen within neutrophils and platelets.
Signs of liver or renal failure occur if these organs are – A positive result indicates that the bone marrow
involved in lymphoma. is infected and such cats are likely to be persist-
ently infected. The IFA test is considered more
Gingivitis/stomatitis. specific, although slightly less sensitive, than the
Ocular signs are relatively common, primarily uveitis, ELISA.
● Virus isolation is considered the gold standard
although neuro-ophthalmic signs, such as anisocoria
may occur. test for confirmation of FeLV infection.
● Polymerase chain reaction (PCR) assays have been
Various neurological signs may also be noted including recently developed, however testing protocols
ataxia and behavioral changes. require further validation.
Immunosuppression may cause recurrent bacterial Certain forms of diseases (abdominal visceral lym-
infections, especially subcutaneous abscesses, which phoma) may be negative for the virus, although FeLV
recur or fail to respond to appropriate therapy. may have played a role in their development.
Other diagnostic tests should be carried out as required Classical signs—Cont’d

to investigate the presenting signs.
● Fever.
● Pleural and/or peritoneal effusions
Differential diagnosis (abdominal enlargement and respiratory
The differential diagnoses will vary depending on the difficulties).
clinical manifestation(s) of the FeLV-related disease. ● Uveitis and neurological signs.
Because the clinical signs in a cat having disease See main references on page 372 for details (The
caused by this virus are so extremely diverse, FeLV- Pyrexic Cat).
associated disease must be considered in any chroni-
cally ill cat.
FIV infection is a principal differential diagnosis, as Clinical signs
this may also be a cause of immunosuppression and Most common in pure-bred cats from multi-cat house-
neoplasia. holds.
FIP is primarily seen in cats from 3 months to 3 years
Treatment of age, although a second peak in incidence may occur
The FeLV status of the cat should not necessarily in geriatric cats.
preclude treatment for other diseases. FIP occurs in two main forms, wet (or effusive) and
Chemotherapy has been used to treat a variety of lym- dry (non-effusive). Weight loss, variable appetite,
phomas caused by the FeLV virus. Certain forms fever, lethargy and depression occur in both forms
(mediastinal) seem to be more chemoresponsive than and may be the only clinical signs in early disease.
others (abdominal visceral). The wet form tends to progress more rapidly, and is
Blood transfusions can give temporary help for the ane- characterized by combinations of abdominal, pleural
mic patient. or pericardial effusions.
● Non-painful abdominal enlargement is the main
Aggressive supportive care and management of sec- clinical sign if ascites is present. Vomiting and diar-
ondary infections are essential in FeLV-positive cats. rhea may occur as the disease advances.
All infections should be fully assessed in terms of ● Dyspnea is characteristic of pleural effusions.
extent, and appropriate treatment administered, ideally
based on culture and sensitivity results. Response to The dry form leads to clinical signs associated with
treatment may be slower in FeLV-infected cats, and so pyogranulomatous perivascular disease in multiple
sufficient duration of antibiotic must be administered. organs and clinical signs vary with the affected body
system.
A variety of immunomodulator and antiviral therapies ● This form of the disease tends to be more chronic
have been tried. As with FIV, the efficacy of these (months) and progressive.
agents to clear the virus completely is questionable, ● Neurological (seizures, nystagmus, behavioral
although there is evidence that they may decrease total changes, peripheral neuropathies) and ocular (pos-
viral load. terior and anterior uveitis) involvement is common.
● The liver, kidney and abdominal lymph nodes may
FELINE INFECTIOUS PERITONITIS (FIP)* also be involved.
Classical signs
Diagnosis
● Younger cats, pedigree cats with variable
clinical signs. Definitive diagnosis is difficult, if not impossible,
● Inappetence, weight loss and depression. without histopathological examination of affected
tissues.
● Histologic evaluation revealing typical pyogranulo- Heart failure, diaphragmatic hernias, neoplasia and
matous is diagnostic. chylothorax may all present signs similar to effusive
FIP in the thorax. Fluid analysis and thoracic radi-
By combining clinical signs with other testing, a high
ographs will help in differentiating the cause of fluid
suspicion of FIP may be obtained.
accumulation.
In the wet form, evaluation of the fluid is helpful.
● Fluid is typically yellow, viscous, and may have
Treatment
fibrin clots.
● Fluid is high in protein (> 35g/L or 3.5 g/dl and usu- Clinical FIP is invariably fatal, and no effective treat-
ally 50–120g/L or 5–12 g/dl) with moderate numbers ment has been found in cats.
of non-degenerate neutrophils and macrophages,
Anti-inflammatory and immunosuppressive ther-
although lower than usual for an exudate.
apy may increase life span by controlling the comple-
● If the albumin:globulin ratio of the fluid is > 0.81,
ment mediated vasculitis, but will not cure the
FIP is an extremely unlikely diagnosis.
condition.
Aspiration of affected organs (liver, lymph nodes, ● Prednisolone (2–4 mg/kg PO daily).
kidney) will often reveal a pyogranulomatous response. ● Cyclophosphamide and chlorambucil may be
used for more potent immunosuppression, but
Increased serum globulin concentration (polyclonal
cytotoxic agents should be avoided in debilitated
gammopathy) is present in the majority of cats with
cats.
FIP.
– Broad-spectrum antibiotic cover should be given
● Other biochemical findings will vary, dependent on
if immunosuppressive drugs are used to prevent
the organ system involved.
secondary infections.
Complete blood count usually often reveals a normo- – Therapy should be re-evaluated regularly,
cytic, normochromic, nonregenerative anemia, a neu- including monitoring for myelosuppression.
trophilic leukocytosis and lymphopenia.
Other immunomodulating drugs (recombinant human
“FIP titers” reported by laboratories are either corona- interferon-α) and anti-viral agents have been promis-
virus titers or titers to the 7B protein in coronavirus. ing in vitro but have limited efficacy in in vivo studies.
Neither are specific for the mutated FIP-coronavirus
Supportive care should be provided if the cat is not
virus. Although claimed that 7B protein was specific
euthanized.
for FIP strains, subsequent studies have shown that it is
not present in some FIP strains, and that non-FIP coro-
navirus may have an active 7B component. Currently
ORAL INFLAMMATORY DISEASE*
there is no serological test that is specific for FIP-coro-
navirus.
Classical signs
● Inappetence associated with dysphagia.
● Weight loss.
FIV, FeLV and toxoplasmosis are the three most com- ● Ptyalism, halitosis and oral pain.
mon differentials for the non-effusive form of FIP. All ● Oral inflammatory, ulcerative and
three can lead to fever, inappetence and weight loss. proliferative lesions.
Toxoplasmosis and FeLV can both present with ocular
and neurological signs. See main references on page 585 for details (The Cat
With Salivation).
Abdominal neoplasia, liver disease (especially cholan-
giohepatitis), pancreatitis, peritonitis and diseases
causing hypoproteinemia can lead to abdominal effu-
Clinical signs
sion. Fluid analysis and cytology of the fluid can fre-
quently distinguish between these diseases. Pure-bred cats may be predisposed.
Continuum of disease from mild gingivitis to ● Perform a full oral examination under general anes-
chronic, severe, intractable oral inflammation. thesia to assess for periodontal disease and feline
● Most cases are due to lymphoplasmacytic gin- odontoclastic resorptive lesions, including a full
givitis/stomatitis. mouth radiographic dental survey.
The condition may be waxing and waning in nature but Biopsy and histopathological examination of
in some cases is progressive. affected areas is required for definitive diagnosis of the
lymphoplasmacytic nature of the lesions.
Oral examination reveals erythema, swelling, ulcera-
tion and proliferative lesions (giving a cobblestone
appearance) of varying severity. The tissue is friable
and therefore tends to bleed easily.
● These lesions may involve the gingiva, glos- Other diseases that may appear clinically similar on
sopalatine arches (fauces), pharynx, buccal examination include neoplasia (squamous cell carci-
mucosa and less commonly the tongue, hard palate noma and fibrosarcoma), eosinophilic granuloma com-
and lips. plex and autoimmune disease (pemphigus vulgaris and
● Many cats have significant dental disease but it is systemic lupus erythematosus).
not clear whether the inflammation precedes, con-
FIV, FeLV and the respiratory tract viruses, particularly
tributes to, or results from this.
feline calicivirus, may be associated with oral ulcera-
Submandibular lymphadenopathy is also common. tion or stomatitis.
A poor hair coat may be noted due to decreased groom- Stomatitis may be found in association with severe
ing. It is usually accompanied by varying degrees of uremia.
dental disease.
Dental disease may be associated with oral inflamma-
A particular form of oral inflammatory disease is feline tory lesions. If the oral inflammation does not resolve
juvenile hyperplastic gingivitis. with treatment of the dental disease, lymphoplasma-
● This condition affects young cats at the time of cytic gingivitis/stomatitis should be considered.
eruption of adult teeth. Abyssinian and Persian cats
may be predisposed.
● There is a tendency for spontaneous remission with Treatment
maturity.
Initial management involves removing or treating
● Lesions consist of a very proliferative, hyperemic
any underlying etiology identified.
gingivitis.
Attention should be given to the nutritional status of the
cat, including other forms of feeding, if the severity of
Diagnosis
the lesions is preventing the oral intake of food.
The identification of this condition is usually obvious ● A dietary trial of a novel protein source should also
on oral examination. be considered to exclude hypersensitivity as a
● A complete history and clinical examination is cause.
essential to ensure evidence of concurrent disease
Pivotal to management is thorough dental manage-
or additional lesions are not overlooked.
ment. The aim is to improve the overall oral hygiene
The investigation should aim to identify any possible by scaling and polishing, followed by extraction of
predisposing causes of oral inflammation. any anatomically compromised teeth which may be
● Perform routine hematology, biochemistry and uri- acting as foci of inflammation.
nalysis to assess for systemic predisposing disease. ● Repeated dental prophylaxis may be required to
– Approximately half the cats have a polyclonal maintain oral hygiene.
gammopathy. ● In a number of cases the condition resolves or can
● Test for FeLV, FIV and respiratory tract viruses. be more effectively managed after extraction of all
the teeth caudal to the canines. Occasionally Body condition varies from obese to thin.
removal of the canines and incisors is also required.
Coat condition is often poor, with seborrhea and scales.
Systemic antibiotics frequently produce only a tran-
Hepatomegaly is common. If diabetes mellitus is asso-
sient improvement.
ciated with pancreatitis, abdominal discomfort may be
● Effective antibiotics include clindamycin, clavu-
present.
lanate potentiated amoxycillin, metro-nidazole and
spiramycin (which is concentrated in saliva). A plantigrade stance may be noted due to diabetic
neuropathy.
Immunosuppressive therapy appears to produce the
most reliable responses in chronic cases. If the diabetic cat is ketoacidotic, dehydration, depres-
● Prednisolone (2–4 mg/kg PO once daily) on a taper- sion and weakness may also be present.
ing regime to the lowest maintenance dose.
● In cases failing to respond to corticosteroid therapy,
Diagnosis
alternative immunosuppressive or immunomodulat-
ing therapies should be considered. Documenting a persistent fasting hyperglycemia
– Including chlorambucil, cyclosporin A, gold (blood glucose > 12 mmol/L, 217 mg/dl) and gluco-
salts, human recombinant interferon alpha and suria in a cat with appropriate clinical signs is
topical application of bovine lactoferrin. There required to establish a diagnosis of diabetes mellitus.
have been few studies evaluating these drugs and ● It is important to distinguish diabetes mellitus from
most have more potential side effects, requiring stress hyperglycemia.
closer monitoring. – Glucosuria rarely results from stress hyper-
glycemia because the hyperglycemia is usually
below the renal threshold or only transient, how-
DIABETES MELLITUS ever glucosuria does not exclude this possibility.
– Monitoring for glucosuria at home may aid dif-
Classical signs ferentiation.
● More common in older cats, especially Blood glycosylated hemoglobin and serum fruc-
neutered males. tosamine concentrations represent the average
● Polyuria and polydipsia. blood glucose concentrations over the preceding 4–6
● Usually polyphagia and weight loss. weeks and 2–3 weeks respectively.
● May progress to decreased appetite. ● They may be helpful to distinguish diabetes melli-
tus from stress hyperglycemia.
See main references on page 236 for details (The Cat ● They also provide further information regarding
With Polydipsia and Polyuria). glycemic control when monitoring patients under
treatment.
Clinical signs Further investigation is required to assess for concurrent
disease or systemic complications of diabetes mellitus.
Although diabetes mellitus may occur in any cat, it is
● Routine hematology and biochemistry, including
more frequent in older cats, especially neutered males.
assessment of electrolytes.
● In some regions Burmese cats may be predisposed.
– Diabetic cats frequently have mild to moderate
The classic clinical signs are those of polydipsia, increases in hepatic enzymes and cholesterol.
polyuria, polyphagia and weight loss. – Concurrent renal failure or pre-renal azotemia
● These signs are frequently unnoticed by cat owners. may be present.
● Therefore many cats do not present until the cat ● Complete urinalysis should be carried out.
develops more severe clinical signs such as inappe- – The presence of ketones in the urine confirms
tence, vomiting and depression. the diagnosis of diabetes mellitus. Sick ketoaci-
– These clinical signs may be associated with the dotic cats require aggressive monitoring and
development of ketoacidosis. management.
– Symptomatic or asymptomatic urinary tract ● Thoracic radiography may show cardiomegaly, vas-
infections are frequently present in diabetes cular congestion and possibly pleural effusion or
mellitus. pulmonary edema.
● Echocardiographic examination is usually
required to make a definitive diagnosis of the
CARDIAC CACHEXIA
type of cardiac disease.
Classical signs
● Decreased appetite and weight loss. CHRONIC BACTERIAL RHINITIS AND
● Lethargy. SINUSITIS
● Signs relating to cardiac disease –
tachycardia, cardiac murmurs and Classical signs
arrhythmias.
● Chronic sneezing and snuffling.
● Dyspnea if pleural effusion or pulmonary
● Chronic, persistent or intermittent,
edema present.
mucopurulent nasal discharge.
● Stertorous respiration.
Clinical signs
Inappetence and weight loss may occur, associated with Clinical signs
cardiac disease.
Usually there is a history of chronic upper respiratory
● The remaining clinical signs will vary with the nature
tract disease following an acute episode of signs.
of the cardiac disease, although cardiac cachexia
● Typically there is serous to mucopurulent, unilat-
usually only occurs in cats with cardiac disease suf-
eral or bilateral oculonasal discharge, often associ-
ficient to cause failure.
ated with sneezing.
● Generally it is seen in cats with chronic, severe
– Signs may be persistent or intermittent, but are
right-sided congestive cardiac failure.
usually gradually progressive.
Lethargy and exercise intolerance are present. – Rarely epistaxis may be noted, but this is more
frequently associated with neoplasia.
Dyspnea due to the presence of pleural effusion or pul-
● Stertorous respiration may be audible.
monary edema may be present.
If chronic and severe, in rare cases, bone destruction
Rarely ascites may be present.
may lead to nasal distortion.
Physical examination may reveal poor peripheral
Inappetence, which is often associated with inability to
pulses or evidence of venous congestion (jugular dis-
smell food, and weight loss may occur.
tention and pulses, hepatojugular reflux).
Systemic signs such as depression and anorexia are
Cardiac auscultation may reveal tachycardia, arrhyth-
often associated with intermittent exacerbation of
mias or cardiac murmurs.
disease.
Diagnosis
Diagnosis
Diagnosis is based on documenting the presence of
Appropriate clinical signs and a history of previous
severe cardiac disease in a cat with weight loss.
acute upper respiratory tract disease are supportive
Evidence of cardiac disease may be provided by tho- of the diagnosis, however a full investigation is
racic radiography, electrocardiography, measurement required to exclude other causes of nasal discharge
of systemic blood pressure and echocardiography. including neoplasia and fungal disease.
● Neoplasia and fungal causes are unlikely if the clin- Clinical signs
ical signs have been constant for a protracted period
(1–2 years). Although signs of respiratory distress may appear
acute, the disease process is often more chronic.
A thorough examination of the oral cavity and phar-
ynx should be made whilst the cat is anesthetized to Clinical signs will vary with the quantity of fluid present.
● Cats adjust to the decreased lung volume, and
exclude congenital and traumatic palate defects, dental
disease, nasopharyngeal polyps and neoplasia as a distress is not usually apparent until late in the
cause. disease.
● Tachypnea and dyspnea are often present.
Radiographic evidence of bilateral fluid density in ● If ventilation is severely impaired, cyanosis may be
nasal passages often extending into the frontal sinuses noted.
is typical.
● Occasionally bone destruction is seen on radi-
Auscultation usually reveals decreased breath sounds
ographs. (muffled and dull) ventrally.
● Occasionally fluid may accumulate in focal areas,
Cytology of the nasal discharge reveals neutrophils, and unilaterally rather than bilaterally.
bacteria, and the absence of neoplastic or fungal ● Heart sounds may be muffled.
elements.
The thorax may be dull on percussion.
Rhinoscopy (anterior and posterior) will permit visual
examination and flushing of the nasal cavity, and facil- Weight loss in usually present, accompanied by inap-
itate nasal biopsy. petence as the respiratory difficulty increases.
● Blind biopsy or traumatic flushing may be used to Clinical signs to a certain degree will depend on the
obtain biopsy material from the nasal cavity. underlying cause of the pleural effusion.
● It is extremely difficult to definitively exclude ● Possible causes of chylothorax include neoplasia,
neoplasia in these cases. heart failure, trauma and hyperthyroidism, although
– A diagnosis should not be made on cytology in many cases the underlying etiology is not deter-
alone, because both neoplasia and fungal disease mined despite extensive investigation (termed idio-
frequently reveal only neutrophils and bacteria pathic chylothorax).
on cytologic examination.
– Rhinotomy and biopsy may be necessary to
definitively exclude neoplasia, particularly in Diagnosis
cases with suggestive clinical signs. The presence of a pleural effusion may be confirmed
Respiratory virus status may be evaluated by virus iso- radiographically or ultrasonographically.
lation from oropharyngeal and nasal swabs. ● Care should be taken in handling and position-
ing cats with respiratory distress, and thoraco-
FeLV and FIV status should be assessed and other centesis may be required to stabilize the cat
causes of immunosuppression should be excluded. prior to these procedures.
● Radiographic evidence of a pleural effusion
CHYLOTHORAX includes:
– Presence of pleural fissure lines.
Classical signs – Separation of lung borders from the thoracic
wall and rounding of edges of the lung lobes.
● Respiratory distress – tachypnea, dyspnea – Loss of cardiac silhouette.
and open mouth breathing.
● Weight loss. Thoracocentesis with biochemical and cytological
● Inappetence. analysis of thoracic fluid is required for definitive
diagnosis:
See main references on page 77 for details (The Cat ● Chylous fluid is usually a white “milky” fluid.
With Hydrothorax). – It may be slightly pink on repeated aspirations.
– If the cat has not eaten recently, the fluid may ● Initially the glomerular injury is characterized by
appear only slightly opaque. proteinuria, but as the condition progresses, the
● Lymphocytes are usually the predominant cell type, entire nephron may become non-functional, with
with some non-degenerate neutrophils. decreased glomerular filtration rate and azotemia.
● The concentration of triglycerides in the fluid ● Glomerulonephritis may be found in association
exceeds that of the serum in a true chylous with any chronic antigenic stimulus, including
effusion. infectious, inflammatory and neoplastic diseases.
– In the cat, glomerulonephritis has been particu-
It is important that, where possible, the underlying
larly associated with infectious diseases including
cause is investigated, as this will influence the treat-
FeLV, FIV and FIP, and hemolymphatic neoplasia.
ment and prognosis.
– In the majority of cases an underlying antigen
source is not identified and the disease is classed
PROTEIN-LOSING NEPHROPATHY as idiopathic.
Glomerular proteinuria is characteristically mas-
Classical signs
sive, and in many cases may lead to clinical signs
● Marked weight loss. related to protein loss and eventually the nephrotic
● Initially polyphagia may be present but syndrome.
progresses to inappetence.
The nephrotic syndrome is characterized by mas-
● Polydipsia and polyuria.
sive proteinuria, hypoalbuminemia, hyperlipidemia
● Subcutaneous edema and/or ascites.
and subcutaneous edema and/or ascites.
● The proteinuria leads to hypoalbuminemia and sub-
sequent development of edema.
Pathogenesis
The most common causes of protein-losing
nephropathy are glomerulo-nephritis and renal
Clinical signs
amyloidosis.
Protein-losing nephropathies are uncommon conditions
Renal amyloidosis is characterized by the extra-
in the cat.
cellular deposition of fibrillar proteins arranged in a
● Glomerulonephritis usually affects young adult
beta-pleated sheet configuration.
cats (average age 3–4 years), with males being pre-
● Reactive (secondary) systemic amyloidosis is the
disposed. The condition is rare.
form of amyloidosis occurring in cats.
● Most cats with amyloidosis are over 5 years of age
– It is considered to be secondary to inflamma-
at diagnosis. Systemic reactive amyloidosis occurs
tory, neoplastic and chronic infectious disease,
as a familial disease in Abyssinian cats.
although in many cases the predisposing disease
is not found. Clinical signs in early disease are principally weight
● Severe proteinuria occurs when amyloid deposits in loss with a good appetite and even polyphagia.
the glomerulus cause glomerular damage. ● Signs frequently progress to inappetence and
– Most domestic cats with amyloidosis and at least depression.
25% of Abyssinian cats with familial amyloi- ● Continued protein loss eventually leads to the
dosis have medullary amyloid deposits, without nephrotic syndrome with subcutaneous edema
significant glomerular deposits. and/or ascites.
– In cases of medullary amyloidosis, proteinuria
Polyuria and polydipsia are common if the condition
may be mild or absent, although the deposits will
progresses to renal failure and uremia.
interfere with renal concentrating ability.
● Polyuria and polydipsia are also common if there
Glomerulonephritis is caused by antibody–antigen are medullary amyloid deposits.
complexes present in the glomerulus that lead to ● Clinical signs of uremia may also be noted (see
immune-mediated glomerular damage. page 334, chronic renal failure).
The kidneys are usually small, firm and irregular on Routine biochemistry should be evaluated.
palpation. ● Plasma protein concentrations may be variable,
with hypoalbuminemia occurring if the protein loss
Both conditions are associated with an underlying
is severe. Conversely, hyperglobulinemia may
chronic antigenic stimulus, including infectious,
occur associated with the chronic inflammatory
inflammatory and neoplastic diseases. Clinical signs
focus initiating the lesion.
may also relate to the underlying disease.
● Hypercholesterolemia is reported as a characteris-
Systemic hypertension may occur and result in hyper- tic feature of the nephrotic syndrome, however it is
tensive retinopathy, acute-onset blindness or neurolog- a common non-specific finding in cats with any
ical signs. form of renal disease.
● Azotemia and a low urine specific gravity will indi-
The prognosis is variable depending on the cause of the
cate the presence of renal failure.
protein-losing nephropathy, although is generally con-
sidered poor if actual renal failure is present. Abdominal radiography and ultrasound may provide
● Clinical signs in glomerulonephritis may wax and information on renal architecture and size.
wane, and occasionally undergo complete or pro-
Renal biopsy is the only definitive method of dis-
longed periods of remission.
tinguishing between glomerulonephritis and amy-
● Amyloidosis tends to be slowly progressive, and is
loidosis.
generally fatal.
● Complete morphological classification of glomeru-
lar lesions may require light, electron and immuno-
fluorescence microscopy.
Diagnosis
● Amyloid deposits demonstrate characteristic green
Diagnosis of protein-losing nephropathy is made on birefringence after Congo red staining when viewed
the documentation of proteinuria, in the absence of under polarized light.
pre- and post-renal causes. A complete urinalysis – The diagnosis is frequently difficult to achieve if
should therefore be carried out. glomerular involvement is minimal or absent,
● Urinalysis typically reveals proteinuria with requiring medullary biopsies.
a benign sediment. A benign sediment excludes
A thorough investigation for an underlying inflam-
lower urinary tract disease as a cause of the
matory focus should be made, including assessment
proteinuria.
of FeLV and FIV status.
● Hyaline casts may be noted on sediment examina-
tion.
● In the early stages of disease, urine-concentrating TOXOPLASMOSIS
ability may be retained.
● Proteinuria is usually detected on qualitative Classical signs
screening tests, such as urine dipstick reagent
● Especially in immuno-compromised
strips.
individuals, particularly free-roaming cats.
The protein:creatinine ratio should be evaluated to ● Weight loss, lethargy and inappetence.
further quantify the urinary protein loss. ● Fever.
● Although the magnitude of the proteinuria can be ● Respiratory distress.
used to predict the site of protein loss, there is great ● Icterus.
variability in ratios with different diseases. ● Uveitis.
● The quantity of protein loss in glomerular disease is ● Neurological signs including ataxia and
massive compared with that in pre-renal and post- seizures.
renal proteinuria. Protein:creatinine ratios of ● Muscle hyperesthesia.
greater than 13 commonly occur in glomerular pro-
teinuria, although ratios generally range from mild See main references on page 376 for details (The
to severe (ratio of 5–13). Pyrexic Cat).
Clinical signs – A positive response to appropriate treatment pro-

vides a presumptive diagnosis.
Self-limiting small bowel diarrhea is common after
primary exposure, although it is often unrecognized. Routine hematology and biochemistry findings are
variable dependent on the tissues affected.
Acute fatal toxoplasmosis is recognized in kittens and
immuno-compromised cats. Thoracic radiography may reveal a pleural effusion and
diffuse interstitial or alveolar patterns.
Chronic toxoplasmosis is characterized by diverse
clinical signs depending on the tissue affected.
Respiratory distress due to pneumonia is common in CRYPTOCOCCOSIS
kittens and cats with acute infection.
Central nervous system disease, including ataxia Classical signs
and seizures, may occur either with acute or chronic ● Progressive chronic nasal discharge and
infection. sneezing.
Icterus is common due to infection involving the liver. ● Soft tissue swelling over the nose,
polypoid masses in the nasal cavity.
Anterior or posterior uveitis may be the only obvious ● Neurological and ocular signs.
sign present in some cats.
Muscle stiffness or hyperesthesia. See main references on page 25 for details (The Cat
The disease may be chronic with weight loss and lack
of appetite. Occasionally, toxoplasma granulomas
(tissue cysts) form in the gastrointestinal tract or pan- Clinical signs
creas causing chronic vomiting.
Cryptococcosis is the most common systemic fungal
Diagnosis disease of the cat, and has a worldwide distribution.
Routine laboratory testing is not specific for toxo- It is most commonly acquired by inhalation, and so
plasmosis. clinical signs are often localized to the respiratory tract.
● Immune response leads to granuloma formation,
Diagnosis of toxoplasmosis may be made on: leading to facial swellings and polypoid mass
● Rarely tachyzoites or bradyzoites may be identi-
lesions within the nasal cavity.
fied in tissues, broncho-alveolar lavage fluid, ● Stertor and inspiratory dyspnea may occur.
cerebrospinal fluid and effusions. ● Typically there is sneezing and mucopurulent
● Oocysts in the feces do not provide definitive diagno-
nasal discharge (unilateral and bilateral), which is
sis due to difficulties of identification. commonly blood tinged.
– Shedding only occurs for 1 or 2 weeks follow-
ing initial infection, usually prior to illness. The central nervous system and eyes may be affected
● Serologic testing for antibodies is helpful, but not by direct extension from the nose.
definitive because clinically normal cats frequently ● Signs include depression, behavior changes, ataxia
have significant titers. The magnitude of the titers is and seizures.

not proportional to severity of the disease. ● Ocular signs include granulomatous chorioretinitis
– IgG titers may last for years and are common and uveitis.
in normal cats indicating previous infection. Depression, inappetence (which occurs as a result of
A four-fold rise in IgG titer over 2–4 weeks sug- the inability to smell the food) and weight loss are
gests active infection. common.
– A positive IgM titer persists for approximately
3 months, so tends to indicate recent infection Skin involvement (papules and draining nodules) with
but may persist for much longer. peripheral lymphadenopathy may occur.
Diagnosis ● Dyspnea and occasionally coughing may occur,

with increased respiratory noise on auscultation.
Diagnosis based on cytological identification of ● Absence of respiratory signs does not exclude sig-
cryptococcal organisms in nasal discharge, exu- nificant lung involvement.
dates, fine-needle aspiration of masses and lymph
nodes and cerebrospinal fluid. Involvement of the gastrointestinal tract causes diar-
rhea and weight loss.
Histopathology may be required if cytology is not diag-
nostic. Peripheral lymphadenopathy and granulomatous,
ulcerating skin lesions may be noted.
Using a latex agglutination test to identify cryptococcal
capsular antigen (on serum, urine or cerebrospinal Ocular involvement is common, and may cause a
fluid) provides a non-invasive, sensitive and specific granulomatous retinitis, uveitis and panophthalmitis.
diagnostic test. Hepatomegaly, splenomegaly and neurological signs
Nasal radiography may reveal increased soft tissue den- may also be seen.
sity and bone destruction. Cats with disseminated disease are generally extremely ill.
PCR (polymerase chain reaction) assays are now avail-
able to detect cryptoccal antigens in biopsy material. Diagnosis
Diagnosis is based on cytological identification of
SYSTEMIC MYCOSES the organisms in exudates, fine-needle aspiration of
lesions and lymph nodes, cerebrospinal fluid and
Classical signs bronchoalveolar lavage fluid.
● Vague, non-specific signs of weight loss, ● Fungal culture may assist, but is not required for
inappetence and depression. identification of the organism.

● Dyspnea. Histopathology may be required if cytology is not diag-
nostic, and shows pyogranulomatous lesions.
See main references on pages 371, 388 for details (The
Pyrexic Cat). Serology may be useful in the diagnosis of blastomy-
cosis, but false-negative results may occur both early
and late in the infection. It should be used in cases
Clinical signs where there is a high level of suspicion of the disease,
The most common systemic mycoses (excluding cryp- but organisms can not be demonstrated.
tococcosis) are histoplasmosis and blastomycosis. Thoracic radiography may show varying changes,
● Both are geographically restricted infections.
however a diffuse interstitial or nodular interstitial
– Histoplasma capsulatum, the agent causing pattern is most commonly seen.
histoplasmosis, is endemic throughout large
areas of the temperate and subtropical regions of Hematological changes tend to be non-specific, and
the world. include the presence of a mild non-regenerative anemia
– Blastomycosis (caused by Blastomyces dermati- in some cases.
tidis) is principally a disease of North America,
but has occurred in Africa and Central America. PORTOSYSTEMIC SHUNTS
History tends to be vague and chronic, including
weight loss, inappetence and weakness. Classical signs
Mild to moderate fever. ● Congenital shunts usually show clinical
signs by 6 months of age.
Infection is commonly acquired by inhalation, and so ● Weight loss or stunting (congenital shunts).
clinical signs are often localized to respiratory tract.
continued
Classical signs—Cont’d Copper- or golden-colored irises have been noted in

some cats with portosystemic shunts.
● Neurological signs – hypersalivation,
seizures, ataxia, blindness and behavioral Heart murmurs have also been noted in some affected cats.
changes. Ascites and signs of primary hepatic disease may be
● Inappetence, vomiting or diarrhea. seen in cats with acquired portosystemic shunts.

With Salivation).
Diagnosis
Clinical signs Routine hematology and biochemistry may be unre-

markable in cats with congenital portosystemic shunts
Portosystemic shunts are vascular communications however:
between the portal and systemic venous circulation, ● Routine hematology may reveal a mild non-regener-
and may be a congenital anomaly or acquired. ative, microcytic anemia often with poikilocytosis.
● Congenital portosystemic shunts in cats are usu- ● Hypoglycemia, hypoalbuminemia, hypocholes-
ally single extrahepatic shunts resulting from terolemia and decreased blood urea concentra-
developmental anomalies of the vitelline system. tions may indicate hepatic dysfunction.
– Persian and Himalayan cats are predisposed.
– A predilection for male cats has been suggested, Pre- and post-prandial serum bile acids should be
and such cats are often crypt-orchid. assessed.
● Pre-prandial bile acid concentrations may be nor-
– Cats with congenital shunts will usually show
clinical signs by 6 months of age, however a mal or elevated.
● Post-prandial bile acids are typically elevated,
congenital portosytemic shunt should not be
excluded on the basis of age alone. frequently exceeding 100 μmol/L (39.2 mg/L).
● Multiple extrahepatic acquired portosystemic Hyperammonemia, particularly post prandial is com-
shunts are formed secondary to portal hyperten- monly present.
sion, and are extremely uncommon in the cat.
– Acquired shunts usually occur in cats with Abdominal radiographs may demonstrate microhep-
chronic, severe, diffuse hepatic disease. atica, but in many cats hepatic size is normal.
Signs are often vague or non-specific and episodic. Ammonium biurate crystals may be present on urine
sediment examination.
Cats with congenital shunts may show stunting ● Ammonium urate calculi are often radiolucent.
(smaller than littermates) or weight loss.
Portosystemic shunts may be identified and local-
Clinical signs of hepatic encephalopathy predomi- ized on abdominal ultrasound.
nate in cats with portosystemic shunts.
● Vague anorexia, depression and weakness.
Other techniques may be required to definitively
● Ataxia, behavioral changes (bizarre and aggressive
demonstrate the presence of shunting vessels.
● Transcolonic portal scintigraphy is a non-invasive
behavior), aimless pacing, blindness and seizures
may occur. technique but requires specialist equipment.
● Hypersalivation, often profuse, is also common.
– It may produce false-negative results when the
shunt connects the gastric vein to the caudal vena
There are often intermittent episodes of vomiting, diar- cava, a common type of shunt in the cat.
rhea and inappetence with normal periods between. ● Venous portography, although requiring sur-
Lower urinary tract signs are present in cats with con- gery, is the definitive method for identifying
current urate urolithiasis. shunts.
RECOMMENDED READING
Elliott J, Rawlings JM, Markwell PJ, Barber PJ. Survival of cats with naturally occurring chronic renal failure: Effect
of dietary management. J Small Anim Pract 2000: 41: 235–242.
Levy JK CVT Update: Feline immunodeficiency virus. In: Bonagura (ed) Kirk’s Current Veterinary Therapy XIII.
W.B. Saunders, Philadelphia, 2000, pp 284–288.
Nagode LA, Dennis JC. Frequently Asked Questions RE: Use of Calcitriol Versus Renal Secondary
Hyperparathyroidism. Veterinary Information Network, June 8, 2001. Retrieved June 20, 2003 from
www.vin.com/Members/SearchDB/misc/m05000/m01284.htm
Polzin DJ, Osborne CA, Jacob F, Ross S. Chronic renal failure. In: Ettinger, Feldman (eds) Textbook of Veterinary
Internal Medicine, 5th Edition. W.B. Saunders, Philadelphia, 2000, pp 1634–1662.
PART 7
Sick cat with specific signs
19. The pyrexic cat

Kristy L Dowers and Michael R Lappin
KEY SIGNS
● Temperature > 39.2˚C (102.5˚F).
MECHANISM?
● True fever results from a cascade of events, which starts with activation of leukocytes.
Pyrogenic factors released from the leukocytes increase the thermoregulatory set point in the
hypothalamus.
Signs that may be associated with fever include:
● Elevated body temperature.
● Reluctance to move.
● Anorexia.
● Depression.
● Hyperpnea.
● Muscle or joint stiffness/discomfort.
● Shivering.
WHERE?
● Inflammation anywhere in the body can result in elevation of core body temperature above
39.2˚C (102.5˚F).
WHAT?
● The most common etiology for fever in the cat is percutaneous cellulitis or abscess.
Viral diseases such as FIV, FeLV and FIP are important diseases to consider.
364
19 – THE PYREXIC CAT 365

Diseases causing a pyrexic cat
METABOLIC
● Hyperthyroidism (p 389)
Occasionally mild fever occurs from the increased metabolic rate. Typical signs are history
of weight loss despite good appetite, unkempt hair coat, change in temperament and vomiting/diar-
rhea.
NEOPLASTIC
● Neoplasia (p 385)
Fever associated with antibody stimulation from tumor antigens, tissue necrosis or destruction of
bone marrow. Lymphoma is the most common neoplasia in cats.
INFLAMMATION
INFECTIOUS
Viral:
● Feline leukemia virus (FeLV)***** (p 374)
Fever may occur in any age cat but is primarily seen initially in the viremic stage or later in
response to neoplastic, inflammatory or immunosuppressive effects. Signs include chronic infec-
tions, anemia, thrombocytopenia, elevated MCV and lymphoma.
● Feline immunodeficiency virus (FIV)** (p 378)
Fever in adult cats is associated with the acute stage and in older cats with the chronic terminal
stage. Signs include chronic infections, especially upper respiratory and skin infections, gingivi-
tis, weight loss and diarrhea.
● Feline infectious peritonitis (FIP)***** (p 372)
Tends to occur in very young or very old cats. Signs include fever, anorexia, lethargy, weight loss,
pleural effusion and dyspnea, peritoneal effusion, vomiting/diarrhea, ocular changes (uveitis, in
particular), neurologic signs, hyperglobulinemia, leukopenia.
● Panleukopenia* (p 382)
Acute onset of fever in young cats with vomiting, anorexia, depression, dehydration and profound
leukopenia. Diarrhea usually follows 1–2 days later.
● Feline viral rhinotracheitis (herpesvirus-1)*** (p 370)
Paroxysms of sneezing followed by severe conjunctivitis with serous to mucopurulent nasal dis-
charge, fever, anorexia and lethargy. Ocular signs (corneal ulcerations) may follow 1–2 weeks later.
● Calicivirus*** (p 370)
Inconsistent fever, anorexia, lethargy, mild upper respiratory signs with a serous to mucopurulent
oculonasal discharge, oral ulcers predominately on the anterior or lateral margins of the tongue
and salivation.
Bacterial/rickettsial:
● Percutaneous cellulitis/abscess*** (p 368)
Fever, anorexia, depression, localized swelling/pain in area of abscess.
continued
366 PART 7 SICK CAT WITH SPECIFIC SIGNS
continued
● Chlamydophila felis* (p 381)

Conjunctivitis is the predominant sign and is often initially unilateral and becomes bilateral.
Ocular discharge is serous initially then mucopurulent, but is usually mild. Fever, anorexia and
lethargy may occur.
● Yersinia pestis (feline plague)* (p 383)
Acute onset of a high fever, anorexia and depression. Lymphadenopathy, with marked swelling over
submandibular or cervical lymph nodes, which may abscess. Pneumonic form is less common and
may have upper and lower respiratory signs with sneezing, nasal discharge, dyspnea or cough.
● Salmonella spp. (songbird fever)
Signs occur in outdoor cats which hunt. Acute onset of fever, anorexia and depression, and 50%
of cats have GI signs with vomiting and diarrhea.
● Francisella tularensis (tularemia)* (p 382)
Occurs in outdoor cats which hunt and have recent exposure to rabbits. Signs include fever,
depression, anorexia, peripheral lymphadenopathy, oral ulcerations and hepatomegaly.
● Ehrlichia spp. and Anaplasma phagocytophilum* (p 385)
Chronic intermittent fever, weight loss and anorexia occur. Hyperesthesia, joint pain or irritable
disposition is common. Exposure to ticks may or may not be documented.
● Mycoplasma haemofelis and Candidatus ‘M. haemominutum’ (Haemobartonella
felis)** (p 374)
Pale mucous membranes, anorexia and depression. Fever occurs in approximately 50% of cats and
icterus may be evident.
● Bartonella henselae (cat-scratch fever)
Mild, self-limiting fever occurs in experimentally infected cats. Naturally infected cats are usually
subclinical and fever is not well documented.
Parasitic/protozoal:
● Toxoplasma gondii** (p 375)
Fever, anorexia and depression are often present. Dyspnea is common. Kittens and cats may also
have icterus, abdominal distension or pain/discomfort, ocular signs (uveitis, retinochoroiditis) or
neurologic signs.
● Cytauxzoon felis
Rapid onset of fever with lethargy, anorexia, pale mucous membranes, dehydration, icterus and
splenomegaly.
Fungal:
● Blastomyces dermatiditis (blastomycosis)
Fever, anorexia, depression and lymph-adenopathy occur together with respiratory signs (dyspnea,
coughing). Ocular signs are frequent. Signs are more common in dogs than cats.
● Coccidioides immitis
Clinical disease is uncommon in cats. Fever, anorexia and depression are common. Skin lesions
occur in 50% of cats with nodules progressing to abscesses. Respiratory, musculoskeletal and ocular
signs are less common.
● Cryptococcus neoformans (cryptococcosis)** (p 379)

Low-grade fever, malaise, anorexia and weight loss are typical. Most common form presents with
chronic mucopurulent or hemorrhagic nasal discharge, sneezing, stertorous respiration, distortion
over bridge of nose (Roman nose) or polyp-like mass in nasal opening.
● Histoplasma capsulatum (histoplasmosis)** (p 371)
Signs are often non-specific with fever, depression, and weight loss. Dyspnea, lymphadenopathy,
pale mucous membranes, gastrointestinal signs or ocular signs may be present.
Non-infectious:
● Pancreatitis** (p 377)
Signs are often vague and non-specific with anorexia and depression predominating. Fever is
inconsistent and may be accompanied by abdominal pain, vomiting and dehydration.
● Cholangiohepatitis** (p 378)
Typically anorexia and depression are present together with icterus or increased liver enzymes.
Vomiting may be evident and fever is present in about 1/3 of cats.
● Non-suppurative meningoencephalitis** (p 379)
Signs are chronic, of 1–4 weeks duration and include fever in some cats and variable CNS signs,
especially seizures and focal or multifocal neurologic signs.
● Myocarditis/diaphragmitis** (p 380)
Uniphasic or biphasic fever together with depression and lethargy are typical. Mild generalized
lymphadenopathy may be present and in a few cats overt cardiac failure occurred.
● Immune-mediated disease
Primary immune-mediated disease, such as systemic lupus erythematosus, is extremely rare in cats.
Secondary immune-mediated disease can occur due to primary infection, vaccination or neoplasia.
Anorexia, weight loss, fever and signs specific for the disease occur, such as bleeding, pale mucous
membranes, skin lesion or lameness.
Toxins/drugs:
● Drug-induced fever* (p 381)
Tetracyclines, amphotericin B and other drugs may cause a fever. The severity of fever is out of
proportion with the mild clinical signs. There is a history of antibiotic or antifungal therapy.
Trauma:
● Trauma** (p 380)
Mild fever associated with pain and inflammation often occurs 10–14 h after injury. There is evidence of
external or internal trauma. Sterile surgical trauma causes fever in some cats for 24 hours post-surgery.
INTRODUCTION
True fever results from activation of leukocytes that
MECHANISM? release factors (pyrogens) such as interleukin-1 and
tumor necrosis factor.
True fever must be differentiated from hyperthermia, ● These factors cross the blood–brain barrier and
which can be caused by increased muscle activity,
increase the thermoregulatory set point in the
increased environmental temperature and stress.
hypothalamus.
● Leukocytes are activated by a multitude of infec- scratches, but can be from other animal bite wounds,
tious agents, neoplasia, tissue necrosis and or foreign bodies such as grass awns.
immune-mediated diseases.
Tissue trauma results in decreased blood flow to the
area, and therefore selects for those bacteria which are
WHERE? facultative or obligate anaerobes.
Fever is defined as systemic elevation of core body Common bacteria isolated from cat abscesses
temperature above 39.2˚C (102.5˚F). are obligate anaerobes (Fusobacterium, anaerobic
cocci, Bacteroides, Eubacterium, Peptococcus and
The most accurate measurement of core body tempera-
Peptostreptococcus) and/or microaerophilic or facul-
ture is obtained rectally.
tative organisms (Pasteurella, Corynebacterium,
Aural temperature is approximately −17.2˚C (0.5˚F) Actinomyces and Micrococcus); abscesses commonly
lower than the rectal temperature. contain more than one isolate.
Abscesses resulting from cat bites are often infected
WHAT? with Pasteurella spp.; L-forms and Mycoplasma spp.
are occasionally involved.
Fever is a general clinical sign that can be associated
with many different diseases. Proliferation of injected organism results in infiltration
of tissue by neutrophils and other phagocytes and even-
The most common disease causing fever in the cat is
tual pus production.
percutaneous cellulites or abscess.
The body generally walls off infection, and purulent
Many viral and bacterial diseases cause fever because
products build up to form a soft, fluccuant swelling,
leukocytes are recruited and activated as part of the
usually associated with hair loss over the area.
general immune response.
The abscess may rupture spontaneously.
Organ inflammation, such as pancreatitis, cholangio-
hepatitis and myocarditis, can be associated with an ele- Persistent cellulitis can be a consequence of long-
vated temperature even when an infectious agent is not standing abscess.
present.
Bone involvement may also occur with long-standing
abscesses. Osteomyelitis should be suspected if the
DISEASES CAUSING AN ELEVATED abscess heals but repeatedly breaks as a draining tract.
TEMPERATURE
Clinical signs
PERCUTANEOUS
CELLULITIS/ABSCESS*** Owners will report that cats are indoor/outdoor or
recently escaped up to a week prior to appearance of
Classical signs the clinical signs.
● Fever. Pyrexia may occur within 12 hours of a fight. Cats

● Anorexia (partial or complete). may be quite depressed following a fight, even prior to
● Reluctance to move, lethargy and the onset of fever.
depression. Some cats present without systemic signs and only a
● Pain, heat or swelling at site of abscess or mild swelling in the fore- or hindlimbs, neck, face or
cellulitis. head.
If limbs are involved, the only complaint may be pro-
Pathogenesis gressive lameness.
Percutaneous abscesses and cellulitis are caused by Reluctance to move and anorexia may be a conse-
puncture wounds, most typically from cat bites or quence of pain, fever or systemic response to infection.
Cellulitis usually precedes an abscess, and if treated mycobacteria, and tumors. See page 1081, The Cat
appropriately, the abscess may not even form. With Non-Healing Wounds.
Cellulitis may be the only evidence of a previous
abscess.
An abscess may rupture spontaneously, and the owner
In plague-endemic regions, Yersinia pestis (plague)
may notice foul-smelling, purulent discharge on the
must be considered, if the swelling is predominately
fur.
in the neck region and the cat’s fever is in the region of
● Some abscesses resolve on their own with or with-
40.5˚C (105˚F). Cautionary measures such as gloves,
out rupture, if they have been present long enough.
masks and isolation of the suspect cat should be taken
Regional lymphadenopathy may occur near the until diagnosis established. (See below for discussion
affected site. of Y. pestis infections).
L forms produce cellulitis 4–5 days after injury. Fracture.
Cellulitis spreads rapidly with the development of mul-
Ligament/tendon injury.
tiple fistulae and a febrile response.
● Lameness from septic arthritis is a common seque- Cellulitis.
lae to infection with L forms. Joints are affected by
Neoplasia.
the hematogenous route and may be distant to the
initial site. Lower limbs (tarsus and carpus) are
most commonly affected. The joints often ulcerate Treatment
with a grayish mucinous exudate. Infection remains
Clip area looking for evidence of puncture wounds.
confined to subcutaneous tissues and joints without
systemic spread to internal organs. Drainage of the purulent material is the key to treat-
ment. Surgical drainage can be done under sedation or
general anesthesia with a #15 blade. Make a 1/4–1/2"
incision over the dependent area, or the area most likely
Diagnosis
to allow for continued drainage.
History supports access to outdoors or conflict with
Flush the wound thoroughly with sterile saline or a
other cats indoors.
saline/betadine mixture.
Palpation reveals a tender area or fluctuant swelling,
Explore the wound with a sterile cotton swab or hemo-
with or without evidence of puncture wounds.
stats to assess the extent of dead-space and to look for
Microscopic examination of a fine-needle aspirate of a possible foreign body.
the abscess reveals a heterogeneous population of
Leave the wound open to allow drainage of further
bacteria, numerous degenerate neutrophils and intra-
purulent material. Do not suture incision closed, as this
cellular bacteria.
will only allow the abscess to reform. A Penrose drain
A complete blood count will generally show neu- may be placed for 2–3 days to allow maximum
trophilia. drainage for abscesses that close too early.
L forms are not visible in tissue samples even with spe- Antibiotic therapy for 7–10 days directed against
cial stains, nor do they grow on culture. On electromi- anaerobes: penicillins, cephalosporins, clindamycin and
croscopy, organisms are visible intracellularly within metronidazole are reasonable choices. Most abscesses
phagocytes. Diagnosis is often made by response to respond extremely well to drainage and amoxicillin at
tetracyclines in a therapeutic trial (doxycycline 10 10–20 mg/kg PO q 12 hours for 7 days or amoxi-
mg/kg PO, q 24 h). Response is rapid and evident cillin/clavulonic acid (12.5 mg/kg PO q 12 hours).
within 48 h.
L-forms and Mycoplasma spp. respond to doxycycline
Non-healing abscesses should have histopathology or tetracycline within 48 hours, but not other anti-
and culture of tissue. Causes include nocardia, fungi, biotics.
If the wound is not healing well, or the cat has had Severe conjunctivitis with tearing, photophobia and
recurrent abscesses, FeLV/FIV testing is recommended chemosis.
to rule out an underlying immunodeficiency. Further
Hypersalivation may occur as an initial sign before the
considerations are inappropriate antibiotics (consider
classic signs of upper respiratory tract appear.
culture and sensitivity testing) or the presence of an
undetected foreign body (consider surgical exploration Punctate corneal ulcers that may coalesce to larger
of the area) or involvement of underlying bone ulcers or perforation.
(osteomyelitis).
Fever of 1–2 days duration, anorexia and depression.
Retching or coughing may occur.
Prognosis
Cats with anterior uveitis have occasionally have herpes-
Prognosis is good unless there is an underlying immuno-
virus 1 in the aqueous humor.
deficiency.
Prevention
Diagnosis
Restrict the cat to an indoor environment only;
Presumptive diagnosis can be made on the basis of
although less effective, confine cat indoors at least from
history and clinical signs because treatment for feline
dusk to dawn.
herpes virus-1 and calicivirus are similar.
Neuter male intact animals to decrease territorial
Ocular ulcerations and chemosis are more suggestive
behavior.
of FHV-1.
FeLV and FIV serology should be repeated 2–4 months
Definitive diagnosis is by direct IFA of cells obtained
following bite wounds.
from conjunctival or nasal scrapings, or by viral isola-
tion or polymerase chain reaction assays from
oropharyngeal or nasal swabs.
FELINE VIRAL RHINOTRACHEITIS
(FVR)*** (FELINE HERPESVIRUS
INFECTION (FVH-1))
CALICIVIRUS***
Classical signs
Classical signs
● Sneezing.
● Conjunctivitis. ● Mild conjunctivitis and ocular discharge.
● Punctate corneal ulceration. ● Serous to mucoid nasal discharge.
● Ocular discharge. ● Stomatitis, oral ulcerations.
● Anterior uveitis. ● Fever.
● Nasal discharge. ● Signs associated with pneumonia.
● Fever, anorexia and depression. ● Rarely, facial and paw edema, hemorrhage,
icterus and rapid death.
See main reference on page 7 for details (The Cat With
Acute Sneezing or Nasal Discharge). See main reference on page 11 for details (The Cat
With Acute Sneezing or Nasal Discharge).
Clinical signs
Acute onset of sneezing followed by oculonasal dis- Clinical signs
charge.
Sudden onset of serous ocular discharge and mild
Discharge progresses from serous to mucoid to conjunctivitis; these signs may begin unilaterally, but
mucopurulent. often progress bilaterally.
Initial signs are rapidly followed by sneezing, which

HISTOPLASMA CAPSULATUM
are not paroxysmal and are less prominent than in
(HISTOPLASMOSIS)*–***
herpesvirus.
Nasal discharge is primarily serous to mucoid and Classical signs
rarely progresses to purulent.
● Fever.
Oral ulcerations are common, especially on the ● Weight loss.
tongue, and may be associated with drooling or hyper- ● Anorexia.
salivation. Ulcers may also occur at the mucocutaneous ● Pale mucous membranes.
junction, hard palate and nose. ● Dyspnea.
Fever generally spikes initially after infection prior
to onset of signs, and returns with onset of clinical
signs.
With Signs of Chronic Small Bowel Diarrhea).
Viral pneumonia occurs occasionally with certain
strains, and may produce significant mortality. Death is
often sudden and preceded by laboured respiration.
Clinical signs
A rare variant strain (FCV-Ari) reported from the
Clinical signs are often non-specific and include
United States, produces a high fever, facial and paw
fever, anorexia and weight loss.
edema (50% of cats), ocular and nasal discharge, con-
junctivitis and ulcerative stomatitis (50% of cats), hem- Dyspnea and harsh lung sounds without coughing is
orrhage from the nose, GIT, etc. (30–40% of cats), common.
icterus (20% of cats) and rapid death. Mortality is high
Peripheral and visceral lymphadenopathies are fre-
(30–50%).
quently present.
Pale mucous membranes, icterus, hepatomegaly or
splenomegaly may be evident.
Diagnosis
Ocular signs are uncommon, but can occur.
Presumptive diagnosis can be made on basis of history
and clinical signs because treatment for feline herpes Gastrointestinal signs are uncommon in cats com-
virus-1 and calicivirus are similar. pared to dogs, and include chronic diarrhea, mesenteric
lymphadenopathy and anorexia.
Oral ulcerations or clinical signs of pneumonia are
more suggestive of calicivirus. Osseous lesions produce soft tissue swelling and
lameness.
Definitive diagnosis is by viral isolation or reverse
transcriptase polymerase chain reaction assays from
swabs taken from the oropharynx, ideally in the first
week of illness.
Diagnosis
Demonstration of increasing serum antibody titers to
Diagnosis is by demonstration of the organism in
feline calicivirus in paired samples is also useful,
lymph nodes, draining tracts, bone lesions or vitreous
whereas measurement of a single titer is not useful
humor.
because many cats have titers from vaccination.
The organism has a thin capsule and is intracellular
Identification of FCV-Ari is based on the clinical
within macrophages.
syndrome, pathology and culture of virus from blood,
nasal or ocular discharge, spleen or lungs. No reliable serologic test available.
Genetic predisposition appears to play a role.

FELINE INFECTIOUS PERITONITIS
(FIP)*–*** FIP is most common in catteries and multi-cat house-
holds.
Classical signs
● Fever.
Clinical signs
● Weight loss, anorexia.
● Lethargy. There are two clinical forms of FIP, effusive or wet
● Abdominal effusion. form and non-effusive or dry form. Both are charac-
● Dyspnea from pleural effusion. terized by a fluctuating fever unresponsive to anti-
● Ocular and/or neurologic signs. biotics, anorexia, lethargy and weight loss.
● Hepatic, intestinal and/or renal signs.
Typical age of onset is 6 months to 2 years, but any
age can be affected.
Pathogenesis The effusive form may have any of the following signs:
● Abdominal effusion that is non-painful but pro-
Feline coronaviruses (FCoV) are divided into:
gressive. The amount of effusion varies from vol-
● FIP-inducing strains, which are mutated strains
umes causing abdominal enlargement, to amounts
that infect macrophages and can be distributed to
only detectable by abdominocentesis. Fluid is
many organ systems.
straw-colored and highly viscous, like egg white.
● Feline enteric coronavirus (FECV) which are
● Pleural effusion resulting in dyspnea occurs in
mildly pathogenic strains producing signs limited
30% of cats with the effusive form. Pericardial
to the intestinal lumen.
fluid may be evident on ultrasound. Usually it not
Mutations of FECV that lead to FIP can occur in the associated with clinical signs, but occasionally can
host within about 18 months of contracting the virus. produce cardiac tamponade.
● Male cats may present with scrotal swelling.
The chance of developing FIP decreases the longer the
cat has high coronavirus titers. The non-effusive form may have any of the following
signs:
Immune responses play a large role in the develop-
● Ocular signs result from pyogranulomatous
ment of this disease:
inflammation of the iris and ciliary body. They
● If a cell-mediated response is not mounted
include bilateral uveitis, perivascular exudates
to mutated FCoV, effusive FIP generally results,
(cuffing), retinal hemorrhage, retinal detachment.
producing abdominal, thoracic, pericardial and/or
● Neurologic signs include cerebral and cerebellar-
scrotal effusions.
vestibular signs such as seizures, personality
● A partial cell-mediated response to mutated
changes, nystagmus, head tilt, circling, head tremor
FCoV generally results in non-effusive FIP, and
and hyperesthesia.
clinical signs are due to formation of granulomas,
● Dysfunction of any organ system may result from
with signs depending on the organ affected.
granuloma formation within the tissue of that
● A strong cell-mediated response results in clear-
organ, e.g., liver, kidney, spleen, intestines, lungs,
ance of the virus.
etc., however, organ failure producing clinical signs
Stress may contribute to development of disease, as only rarely occurs, and most dysfunction is only
stress can interfere with the immune response. detected on biochemical tests.
Multiple-cat households, surgery, illness and pregnancy ● Granulomatous masses may be palpable in abdom-
may be part of the history in a cat with clinical signs of inal viscera especially mesentery, mesenteric lymph
FIP. nodes and omentum as tender, irregular masses.
Occasionally vomiting or diarrhea results from
Typically, cats have been in multi-cat environments
extensive lesions on the bowel wall.
(cat breeders or rescue facilities) within the previous
year. Jaundice may occur with either form of the disease.
Diagnosis from an effusion is used for analysis. Note that when

whole blood is used for analysis, positive results do not
Histopathology of affected tissues provides the only correlate to FIP.
definitive antemortem diagnosis. The classic FIP lesion ● To date, no nucleoprotein sequences specific for
is pyogranulomatous infiltration around venules. FIP-coronavirus have been identified. Some non-
The following are typical abnormalities associated pathogenic coronaviruses have systemic spread,
with FIP. All asterisked items must be present for a therefore finding coronavirus nucleoprotein by
high likelihood of FIP; if any one parameter is not PCR in the systemic circulation or tissue is not
present, FIP is unlikely. A negative coronavirus (“FIP”) indicative of FIP-coronavirus infection.
titer suggests FIP is not the cause of the fever, Except where the classical effusive fluid is present,
although a few cats with the effusive form of the dis- definitive diagnosis of FIP requires organ biopsy and
ease are titer negative. demonstration of classical histopathological lesions.
Lymphopenia (< 1.5 × 103 cells/μl).* Occurs in many Various non-specific abnormalities may be evident on
cats with FIP, and many cats without FIP. laboratory tests, including increased total white cell
Hyperglobulinemia > 51 g/L [> 5.1 g/dl].* Present in 50% count, mild to moderate anemia, and increased concen-
of cats with effusive FIP and 70% with non-effusive FIP. trations of bilirubin, liver enzymes, BUN, creatinine,
fibrinogen, globulin and mild proteinuria.
High coronavirus/FIP titers (>= 1:160).* Present in
most cats with FIP and many healthy cats without FIP. Disseminated intravascular coagulopathy (DIC) is
evident in some cats.
The effusive or wet form of FIP has pleural and/or
abdominal effusion with: CSF typically has increased protein (> 2 g/L) and cell
● Protein 35 g/L [> 3.5 g/dl]. counts (>100 cells/ml) which are predominantly non-
● Albumin:globulin ratio < 0.8. lytic neutrophils.
● Protein electrophoresis should demonstrate a poly-
clonal gammopathy with gamma globulins repre- Differential diagnosis
senting > 32%.
● Cell count varies from low to moderate (1500 to Ocular signs: toxoplasmosis, fungal agents.
more than 25 000 cells/μl) and mainly non-lytic Neurologic signs: toxoplasmosis, neoplasia (e.g., lym-
neutrophils, lymphocytes and macrophages. phoma), trauma, congenital abnormalities in young cats.
“FIP titers” reported by laboratories are either corona- Other clinical signs: rule out other diseases associated
virus titers or titers to the 7B protein in coronavirus. with the apparent organ dysfunction.
Neither are specific for the mutated FIP-coronavirus.
Although it had been claimed that 7B protein was Lymphocytic, plasmocytic cholangiohepatitis occa-
specific for FIP strains, subsequent studies have shown sionally produces a high protein abdominal fluid simi-
that it is not present in some FIP strains, and that non- lar to that of effusive FIP.
FIP coronavirus may have an active 7B component.
Currently there is no serological test that is specific for
FIP-coronavirus. Treatment
● 30% of household pet cats and 80–90% of cat-
FIP is a fatal disease with no known treatments. The
tery cats carry coronavirus and have positive therapies listed below have been used in an attempt to
coronavirus titers. slow progression and/or to improve quality of life.
● Although a few cats with effusive FIP have a nega-
tive coronavirus titer, cats with a negative coron- Glucocorticoids at immunosuppressive doses (pred-
avirus titer are unlikely to have FIP. nisolone 4 mg/kg/day).
Reverse transcriptase, polymerase chain reaction Cyclophosphamide (200–300 mg/m2 q 2–3 weeks or
(PCR) is available for detection of viral RNA. Positive 2.2 mg/kg daily for 4 days each week) or chlorambucil
results correlate with a diagnosis of FIP when fluid (20 mg/m2 q 2–3 weeks).
+/− Broad-spectrum antibiotics to control secondary

FELINE LEUKEMIA VIRUS (FELV)*–***
bacterial infections while the cat is immunosup-
pressed.
Classical signs
+/− Interferon-alpha (see FeLV/FIV section for rec-
● Opportunistic infections.
ommended dosages).
● Weight loss/cachexia.
● Chronic fever.
● Neoplasia.
Prognosis
Prognosis is poor. The mortality is > 95%. See main reference on page 540 for details (The Anemic
Cat).
Transmission Clinical signs

Fecal–oral transmission is most likely; transplacental Onset of illnesses occurs over an extended period of
transmission is rare. time (months to years), although young kittens can
Fomites, e.g., food bowls and litter trays, may be an become acutely ill.
important mode of transmission, as some strains of Chronic, opportunistic infections occur that do not
FCoV survive in dried secretions for several weeks. respond to appropriate antibiotic therapy and are
About 1/3 of cats seropositive for coronavirus shed primarily due to immunosuppression.
virus for up to 10 months; 40–75% of cats with FIP Fever may occur in any age cat but is primarily seen
shed virus. initially in the viremic stage or later in response to
A seronegative cat introduced into a household where neoplastic, inflammatory or immunosuppressive
coronavirus is endemic has a 1 in 6 chance of devel- effects. Chronic fever occurs in later stages of disease.
oping FIP; a seropositive cat under the same condi- Weight-loss/cachexia.
tions has a 1 in 12 chance.
Non-regenerative anemia.
Both young and old animals seem to be most suscepti-
ble due to vulnerable immune systems. Thrombocytopenia.
Maternal antibodies that protect kittens wane at approx- Lymphoma is associated with FeLV-positive cats, espe-
imately 5–6 weeks of age. cially thymic and multicentric forms.
Diagnosis
Prevention
History and clinical signs may be suggestive.
Reduce fecal–oral contamination by providing one
Complete blood count showing anemia, thrombocy-
litterbox for every 1–2 cats, cleaning litterboxes daily,
topenia, leukemias, increased MCV and leukopenia are
and placing litterboxes away from feeding areas.
supportive.
Minimize stress, especially crowding in catteries.
Bone marrow aspirate may show myeloproliferation
Do not introduce FcoV-positive cats into a multi-cat and arrested erythroid differentiation.
household.
A positive FeLV antigen test (viral core antigen p27)
Wean kittens at 5 weeks and remove from the on whole blood using an IFA (can also be done on bone
queen’s environment if she is seropositive. marrow sample) or an ELISA test (also on serum,
plasma, saliva, tears). See page 543 for interpretation.
An intranasal vaccine is available for use in seronega-
tive cats. However, efficacy has not yet been demon- Polymerase chain reaction is available from some labo-
strated against wild strains. ratories.
MYCOPLASMA HAEMOFELIS AND Classical signs—Cont’d

CANDIDATUS ‘M. HAEMOMINUTUM’ ● Anterior uveitis, retinochoroiditis.
(HAEMOBARTONELLA FELIS)** ● Seizures, ataxia.
● Dyspnea/polypnea.
Classical signs ● Icterus.
● Pale mucous membranes. ● Abdominal discomfort.
● Depression. ● Small bowel diarrhea.
● Anorexia.
● Icterus.
● Splenomegaly. Pathogenesis
● Fever. Gastrointestinal signs, primarily abdominal discom-
fort and small bowel diarrhea, are due most likely to
See main reference on page 530 for details (The Anemic replication of the organism (tachyzoites) in entero-
Cat). epithelial cells resulting in necrosis.
Clinical signs Clinical signs in the acute, fatal form of extraintestinal

disease are caused primarily by tissue damage from the
Classical signs are pale mucous membranes and/or rapidly dividing tachyzoites.
icterus primarily from extravascular hemolysis due to
complement binding of infected erythrocytes. Tachyzoites begin to disappear from tissues approxi-
mately 3 weeks after infection. The organism may per-
Severe, regenerative hemolytic anemia may ensue. sist in tissues as tissue cysts containing bradyzoites.
Anorexia and depression are typical. Chronic disease may be a result of delayed hypersen-
Fever occurs in 50% of cats in the acute phase, and sitivity reactions and tissue reaction to antibody–-
may occur intermittently in chronic infections. antigen complex deposition.
Concomitant illness, such as FeLV, FIV and immuno-
Diagnosis suppression with glucocorticoids, has been reported in
History and clinical signs are suggestive, especially if some cases.
an immunosuppressive disorder is present concurrently.
Diagnosis is via demonstration of the organism on Clinical signs
the surface of erythrocytes. Use a marginated blood Gastrointestinal disease.
sample for diagnosis, e.g., ear vein. Multiple blood ● Mild, self-limiting small bowel diarrhea may
smears over a number of days may be required as most occur in the definitive host (cats), but only after
of the organisms are removed from circulation by the ingestion of tissue cysts, oocysts or sporulated
time clinical signs are apparent. oocysts.
● Young kittens are more likely to have gastroin-
Infected cats may be Coomb’s positive.
testinal signs, although mild clinical disease has
A polymerase chain reaction test is available in some been reported in adult cats as well. All newborn
laboratories for diagnosis. kittens experimentally infected developed severe
diarrhea 5–6 days later.
TOXOPLASMA GONDII** Fatal extraintestinal disease (acute course).
● Fatal extraintestinal disease is most likely to occur
Classical signs in transplacentally infected kittens.
● Kittens may be stillborn or exhibit signs that are
● Fever.
● Anorexia/weight loss. severe and rapidly progressive and reflect
involvement of the lungs, liver and CNS tissues.
These signs may also be observed in postnatally Differential diagnosis

infected kittens and include:
– A distended abdomen from an enlarged liver Rule out diseases associated with affected organs, e.g.,
and/or ascites. FIP for neurologic and ocular signs.
– Icterus from hepatitis or cholangiohepatitis.
– Dyspnea is present in most kittens and cats with Treatment
signs of acute infection.
– Neurologic deficits; continuous vocalization; Clindamycin at 10–12 mg/kg orally q 12 hours for
excessive sleeping. 4 weeks is usually effective.
● Cats should respond within several days of treat-
– Fever, anorexia, depression often accompanies
the tissue-specific signs. ment.
● If no response is evident after 3 weeks of antibiotic
Non-fatal extraintestinal disease (chronic, intermit- therapy, reconsider the diagnosis.
tent course). ● The chronic form may recur even after successful
● Cats may have a moderate fever, lethargy and treatment, as drugs tend to suppress replication
depression that waxes and wanes. rather than kill the parasite.
● Hyperesthesia and stiff painful joints or shifting
lameness may be evident, presumably due to an Other systemic drugs with potential efficacy include
immune-mediated process. the trimethoprim sulfas combination, doxycycline,
● Unilateral or bilateral anterior or posterior uveitis
minocycline, azithromycin and clarythromycin.
may occur with possible sequelae of lens luxation, Cats with ocular lesions should also be treated with
glaucoma or retinal detachment. corticosteroids, either topically (e.g. topical 0.5%
● Seizures and ataxia may be present if CNS tissues Prednisolone acetate drops applied q 6–12 h) or sys-
are involved. temically to control inflammation and its sequelae
● Rarely, a toxoplasma granuloma (tissue cyst) (glaucoma, lens luxation).
forms in the gastrointestinal tract or pancreas
causing chronic vomiting.
Prognosis
Diagnosis Gastrointestinal disease has a good prognosis,
Clinical signs consistent with toxoplasmosis are sug- although it may lead to inflammatory bowel disease in
gestive, especially when other causes of the signs have rare cases.
been ruled out. Acute extraintestinal disease has a guarded to poor
IgM titers > 1:64 and a four-fold increase in prognosis.
IgG:IgM titers within 2 weeks correlate best with clin- Chronic extraintestinal disease has a fair to good.
ical toxoplasmosis. However, some cats do not develop
detectable IgM titers, and in other cats, positive IgM
titers can persist for months to years after infection. Transmission
Elevated ocular and CSF titers relative to serum Infection in cats can occur via:
● The placenta or milk with tachyzoites.
titers in cats with ocular or neurologic signs, respec-
● Ingestion of meat infected with tissue bradyzoites,
tively, are very suggestive. Coefficient values > 1.0 are
highly suspect and > 8.0 strongly suggest local produc- e.g., rodents.
● Ingestion of sporulated oocysts in food or water.
tion of T. gondii antibodies.
Response to therapy for toxoplasmosis is a useful indi- T. gondii has a zoonotic potential. Infection of
cator of infection. humans can occur via:
● Ingestion of undercooked meat containing tissue
Definitive diagnosis requires demonstration of the bradyzoites (most common mode of transmission).
organism in inflamed tissues by histology, immunohis- ● Ingestion of sporulated oocysts from the environ-
tochemistry or polymerase chain reaction assay. ment.
● Transplacentally, if first-time exposure to the organ- ● Cats tend to have intermittent bouts of chronic
ism occurs during pregnancy. pancreatitis.
● Diagnostic tests for pancreatitis are not as reliable
Only cats host the sexual replication that results in
in cats.
oocysts in the feces.
● There is poor correlation of biochemical parameters
● Oocysts are shed for 1–2 weeks.
with pancreatitis in the cat.
● Most seropositive cats do not shed oocysts on
repeat exposure. Lethargy and anorexia is variable depending on
chronicity.
Oocysts must sporulate to be infectious:
● Sporulation occurs 1–5 days after environmental Vomiting only occurred in 35% of cases in one study.
exposure, thus handling individual cats rarely
Dehydration occurred in 50% of cases in the same
results in infection of humans.
study.
Transplacental transmission occurs in cats and people
Abdominal pain is quite variable.
after primary exposure.
Fever is variably present, and generally mild. In
Prevention severe acute pancreatitis it may progress to hypother-
mia, which is a poor prognostic sign.
Discourage cats from going outdoors and hunting
behavior.
Do not feed cats undercooked meat.
Diagnosis
To prevent human infection:
Diagnosis is unreliable based on a biochemistry panel.
● Cook meat at 80˚C (176˚F) for 15 minutes.
Lipase may be increased or normal in pancreatitis.
● Use gloves when gardening or changing the litter-
● Hyperbilirubinemia and elevated liver enzymes
box, and wash hands well.
may be present.
● Change litterboxes daily. Use litterbox liners or
● Hypocalcemia occurs in 40% (total serum cal-
clean with scalding water.
cium) or 60% (plasma ionized calcium concentra-
tion) of cats due to soponification of fat. Cats with
PANCREATITIS** a plasma ionized calcium concentration < 1.00
mmol/L (< 4.00 mg/dl) have a grave prognosis
Classical signs (77% mortality) and aggressive medical treatment
is indicated.
● Lethargy and anorexia.
● Fever. Pancreatic lipase immunoreactivity is probably a
● Vomiting. more sensitive diagnostic tool for confirming pancre-
● Dehydration. atitis in cats than measurement of plasma lipase
● Tachycardia. concentration or trypsin like immunoreactivity.
● Hypothermia. A feline-specific assay must be used.
● Abdominal pain.
Abdominal ultrasound to visualize an enlarged
pancreas or heterogeneous echogenicity in the area
of the pancreas is considered by many to be most
With Depression, Anorexia or Dehydration).
sensitive.
Demonstration of higher lipase levels in abdominal
Clinical signs
fluid compared to those of the serum is suggestive.
The classical signs are not as well-defined for cats as Diagnostic peritoneal lavage may be necessary to
for dogs for the following reasons: obtain a fluid sample.
Culture and sensitivity of the liver biopsy should be

CHOLANGIOHEPATITIS**
performed if suppurative cholangiohepatitis suspected.
Classical signs Lymphocytic, plasmocytic cholangiohepatitis occa-
sionally produces a high protein abdominal fluid sim-
● Anorexia.
ilar to that of effusive FIP.
● Vomiting.
● Icterus.
● Dehydration.
● Fever. FELINE IMMUNODEFICIENCY VIRUS
● Weight loss. (FIV)**
See main reference on page 427 for details (The Yellow Classical signs
Cat or Cat With Elevated Liver Enzymes).
● Opportunistic infections.
● Gingivitis.
Clinical signs ● Weight-loss/cachexia.
● Diarrhea.
Clinical signs may be acute, chronic or intermittent.
● Chronic fever.
Typically, there is anorexia and depression together
with icterus or increased bilirubin and liver enzymes See main reference on page 339 for details (The Thin,
on a biochemistry panel. Inappetent Cat).
Vomiting and dehydration may be present.
Fever, especially in the suppurative form occurs in Clinical signs
approximately 38% of the cases.
Clinical signs are primarily due to immunosuppres-
Chronic cholangiohepatitis may lead to end-stage liver sion, i.e., chronic recurring infections that do not
disease and the cat may present with ascites and respond to appropriate therapy.
hepatic encephalopathy.
Gingivitis, stomatitis and peridontitis are more com-
Multiple causes include bacterial, protozoal (T. gondii) mon findings in FIV infections than in FeLV, although
and immune-mediated disease. one study suggests that these signs may be to an effect
of age, rather than a consequence of FIV infection.
Diagnosis Fever is chronic and is related to production of tumor
necrosis factor and/or IL-1 in infected cats.
Complete blood count may show neutrophilia with a left
shift, and mild non-regenerative anemia. Weight loss/cachexia are common in the late stages of
FIV, as in human HIV infections.
Biochemistry panel shows hyperbilirubinemia, ele-
vated liver enzyme activities (ALP, ALT, GGT), +/− Diarrhea resembles a panleukopenia-type syndrome
elevated serum bile acids. that may be due to actual enterocyte infection by the
● Signs of late-stage liver disease are occasionally virus or secondary to inflammation.
present, such as decreased BUN, glucose and albu-
Cats are often thin and scruffy with an unkempt hair-
min concentrations.
coat, and may have miliary dermatitis.
Abdominal ultrasound should be performed to evalu-
ate the gall bladder and bile duct for cholelithiasis, bile
sludging and cholecystitis. Diagnosis
Liver aspirates/biopsy allows for differentiation of Diagnosis may be suspected based on history and clin-
suppurative from non-suppurative forms of cholangio- ical signs, but requires antibody or antigen tests for
hepatitis. confirmation.
Diagnosis of FIV infection is by demonstration of Demonstration of Cryptococcus antigen in serum,

FIV-specific antibody titers via ELISA, IFA or urine or CSF is also diagnostic.
Western blot.
Virus isolation and polymerase chain reaction for virus NON-SUPPURATIVE
detection is available at some research facilities. MENINGOENCEPHALITIS**
Cats infected with FIV can be co-infected with FeLV.
Classical signs
● Seizures.
CRYPTOCOCCUS NEOFORMANS
● Focal or multifocal neurologic signs.
(CRYPTOCOCCOSIS)**
● Fever.
● Lethargy.
Classical signs
● Inappetence.
● Sneezing.
● Stertorous breathing. See main reference on page 803 for details (The Cat
● Chronic nasal discharge. With Seizures, Circling and/or Changed Behavior).
● Facial deformity.
● Low-grade fever.
Clinical signs
● Regional lymphadenopathy.
● Neurologic signs: ataxia, seizures, Occurs in cats of all ages, with and without outdoor
blindness. access.
● Skin form: ulcerated lesions.
Progressive clinical signs occur over a period of 1–4
weeks.
With Signs of Chronic Nasal Disease). Recurrent seizures may be the only clinical sign,
while other cats exhibit multifocal neurologic abnor-
Clinical signs malities including:
● Progressive spinal cord signs.
Chronic nasal discharge can be unilateral or bilateral
● Vestibular signs.
and is generally serosanguineous. Sneezing and ster-
● Cerebellar signs.
torous breathing is often present.
● Cranial nerve signs.
Facial deformity may occur due to invasion of the
According to one study, non-supportive meningo-
surrounding bone.
encephalitis may be the most common cause of seizures
Chronic low-grade fever may be present. in cats.
Depression, anorexia and weight-loss are signs of Systemic signs, which are not present in all cats,
disseminated disease. include fever, anorexia, lethargy, vomiting, diarrhea
and lymphadenopathy.
Neurologic signs occur via hematogenous spread or
invasion into the CNS through the cribiform plate but Viral or immune-mediated etiology is suspected.
are uncommon. Signs include seizures, blindness, The condition, however, does not appear to be conta-
depression and ataxia. gious to other cats.
The skin form typically produces nodules which often
ulcerate. Diagnosis
CSF tap can be very useful to rule out other causes
Diagnosis
of CNS signs, specifically toxoplasmosis and FIP;
Diagnosis is by demonstration of narrow-based bud- CSF analysis reveals a normal or mild protein eleva-
ding yeast with a very thick capsule from affected tis- tion (typically < 1 g/L) and/or an increased white cell
sue or by culture of affected tissue or CSF. count (< 50 cells/μl).
Complete blood count findings are non-specific and Diagnosis

may include leukopenia or leuko-cytosis, eosinophilia
and anemia. Myocarditis/diaphragmitis is a diagnosis of exclusion.
Biochemistry and complete blood counts are unre-
MYOCARDITIS/DIAPHRAGMITIS** markable, except for a mild to moderate increase in CK
in less than 50% of experimentally infected cats.
Classical signs Definitive diagnosis can only be made at necropsy.
● Uniphasic or biphasic fever. Histopathology shows a neutrophilic infiltrate with a
● Depression. foci of myonecrosis in myocardium and diaphragm.
● Lethargy.
● Mild generalized lymphadenopathy. Differential diagnosis
● +/- Signs of cardiac failure.
Any other causes of fever should be ruled out includ-
ing infectious, inflammatory, immune-mediated, drugs,
Pathogenesis neoplasia and metabolic.
Several different infectious agents have been impli- Other causes of cardiac failure that should be ruled
cated in cats: out include congenital deformities, hypertrophic car-
● Viral, e.g., FIP has been shown to cause cardiac diomyopathy, restrictive cardiomyopathy and dilatative
infection. cardiomyopathy.
● Trypanosoma cruzi, which causes Chagas’ disease
in humans. Treatment
● Streptococcus and Borrelia (Lyme’s disease) in cer-
tain geographic areas. Supportive therapy is indicated if dehydration or
cardiac disease are present.
No single agent has been identified, and the disease
may be multifactorial. Broad-spectrum antibiotics are indicated if complete
blood count supports an infectious cause.
Clinical signs Prognosis

Fever is biphasic in 50% of the cats; if biphasic: Fever and depression resolve spontaneously in the
● First fever occurs approximately 10 days after
majority of cats.
exposure, lasts 1–3 days and peaks at 39.3–40.7˚C
(102.7–105.2˚F). Prognosis is poor if peracute cardiac failure is present
● Second fever occurs 1–2 weeks after the first fever with systemic signs of fever and depression.
(at 3–4 weeks post-exposure), lasts 5 days and
peaks at 39.9–40.9˚C (103.8–105.6˚F). Prevention
Depression and lethargy lasts 5–10 days. Although an infectious agent is suspected, no single
Appetite is mildly decreased in some cats, but most etiologic agent has been identified, making recommen-
continue to eat and drink. dations for prevention difficult.
Some animals exhibit mild generalized lymph-

adenopathy. TRAUMA**
Irritable disposition and hyperesthesia may occur, Classical signs

and are most likely due to fever and malaise.
● Cardiovascular or respiratory compromise.
In a few case reports, cats have died from peracute ● External signs of injury.
cardiac failure, but this outcome is not common.
Classical signs—Cont’d Onset of fever is idiosyncratic and variable, but the

fever is generally present for the duration of the drug
● Pain on palpation. treatment.
● Moderate fever approx. 39.2˚C–40.0˚C
(102.5–104.0˚F). Tetracycline is the most common antibiotic cause of
drug-induced fever in cats.
See main reference on page 52 for details (The Dyspneic Amphotericin B can cause fever by disrupting cell
or Tachypneic Cat). membranes and releasing pyrogens into circulation.
Be aware that other drugs (griseofulvin, chlorampheni-
Clinical signs col and chemotherapeutic drugs) can cause bone mar-
Cardiovascular compromise may result in tachycardia, row suppression leading to a cat with fever, neutropenia
hypovolemia or hypotension. and secondary bacterial infection. These cats are obvi-
ously sick, whereas the drug-induced fever animals are
Respiratory compromise may produce dyspnea/ bright and alert in comparison.
tachypnea due to pneumothorax, hemothorax or
pyothorax.
Diagnosis
External injuries including abrasions/bruising, de-
gloving injuries, bite wounds and open fractures may Diagnosis is based on history and clinical signs.
● History is of treatment with fever-inducing drugs,
be evident.
especially tetracycline and amphotericin B.
Internal injuries may result in abdominal pain from ● Clinical signs are inappropriate, that is, the cat
organ rupture, bone/joint pain or focal swelling. appears bright and alert although febrile.
Fever from inflammation may occur but often lags Temperature normalizes after drug is discontinued.
behind acute injury by 10–14 hours.
CHLAMYDOPHILA FELIS*
Diagnosis
Diagnosis is based on clinical signs and history. Classical signs
Radiographs of the chest, abdomen and/or limbs may ● Sneezing.
be required to characterize the injury. ● Conjunctivitis and ocular discharge.
● Nasal discharge.
Complete blood count and biochemistry panel is indicated ● Fever.
to rule out specific organ injury and primary infection.
DRUG-INDUCED FEVER* With Acute Sneezing or Nasal Discharge).

● Alert, febrile cat being treated with
Marked conjunctivitis is the predominant sign, which
antibiotics or antifungal agents.
often starts unilaterally, but usually progresses to both
eyes.
Clinical signs Classic triad of upper respiratory infection signs
History of treatment with antibiotics or antifungal including oculonasal discharge and sneezing.
agents.
Serous ocular discharge accompanied by blepharo-
Fever does not correspond to clinical appearance of spasm, chemosis and conjunctival hyperemia are initial
animal. Cats are bright, alert and responsive, despite a signs. Discharge becomes mucopurulent over the
temperature in the range of 39.4–40˚C (103–104˚F). course of the disease.
Mild to moderate fever can be seen in the acute Parvoviral antigen can be detected in feces using the
phase. canine parvoviral antigen tests or electron microscopy.
Pneumonia is rarely associated with this infection. Histopathologic changes include denuded intestinal
crypts and blunted villi (often a post-mortem diagnosis).
Diagnosis
FRANCISELLA TULARENSIS
History and clinical signs are highly suggestive.
(TULAREMIA)*
Cytology of conjunctival scrapings reveal dark blue
inclusion bodies (Giemsa stain). Classical signs
Immunofluorescent antibody staining or polymerase ● Fever.
chain reaction assay to demonstrate the organism ● Anorexia.
in conjunctival scrapings is available from some laborato- ● Lethargy.
ries. ● Lymphadenopathy.
● Oral ulcers.
PANLEUKOPENIA* ● Icterus.
Classical signs
Pathogenesis
● Acute onset of depression.
● Acute onset of vomiting. Francisella tularensis is a Gram-negative coccobacil-
● Diarrhea usually 1–2 days later. lus. Clinical signs are associated with Gram-negative
● Dehydration. endotoxins and bacteremia.
● Fever or hypothermia. There are two main strains of the organism, both of
● In utero infection can result in cerebellar which have been isolated from cats.
signs.
Type A strain is:
See main reference on page 722 for details (The Cat ● Associated with tick–rabbit cycle.
With Signs of Acute Small Bowel Diarrhea). ● Found only in North America.
● Highly virulent for laboratory rabbits.
Clinical signs ● Associated with more severe disease in humans.
Rapid onset of depression, anorexia, and vomiting Type B strain is:

especially in peracute and acute disease. Fetid diarrhea ● Associated with a more complex cycle involving
(may be hemorrhagic) typically follows 1–2 days after rodents, ticks, mosquitoes, mud and water.
initial onset of signs. ● Found throughout the northern hemisphere.
● Avirulent for laboratory rabbits.
Severe dehydration and electrolyte abnormalities.
Initial fever followed by hypothermia as the disease
progresses. Clinical signs
High mortality rate when signs are severe. History of contact with rabbits, especially if the cat is
a hunter.
Diagnosis Any age of cat can be infected, but younger cats are
more susceptible to developing septicemia.
The disease should be suspected in cats less than one
year of age with no history of vaccination and a rapid The spectrum of illness varies from severely affected
clinical course. to asymptomatic.
Panleukopenia evident on hematology. Fever is generally > 40˚C (104˚F).
Marked depression, anorexia and lethargy, with or In humans, the drugs of choice are streptomycin and
without vomiting are typical. gentamycin.
On physical examination, peripheral lymphadenopa-
thy, icterus and palpable splenomegaly and Prognosis
hepatomegaly are reported. Prognosis is poor to fair as mortality rate varies across
Oral, lingual or pharyngeal ulcers may be present. case reports.
Transmission
Diagnosis
F. tularensis has a serious zoonotic potential if there is
Clinical signs together with a history of exposure to contact with infected animal tissue.
wild rabbits is highly suggestive.
Bites from infected ticks, deer flies or mosquitoes
Hematologic and serum biochemical abnormalities are the most common method of transmission.
may include panleukopenia, with severe toxic
Infection can also occur via ingestion of infected meat.
changes in neutrophils, high band neutrophil count,
thrombocyto-penia and hyperbilirubinemia. Transmission may occur via a bite or scratch from an
infected mammal.
Definitive diagnosis is via identification of the bacter-
● This is the most common method of transmission to
ial agent by IFA or bacterial culture, but should only
humans in cat-associated cases.
be performed in a qualified laboratory.
● The infected cat may have no obvious signs of ill-
● Samples can be obtained from affected lymph
ness, but have a history of hunting wild animals,
nodes, bone marrow, urine or blood.
especially rabbits.
Serum antibody titers > 1:120 or a four-fold increase
Inhalation of aerosolized organisms may also transmit
in serum antibodies in samples collected during acute
the disease. Care should be taken by veterinary and
and convalescent phases (10–14 days) are considered
laboratory personnel handling suspected animals or
diagnostic.
samples being prepared for IFA or culture.
Differential diagnosis Prevention

FIP, FIV, panleukopenia. Discourage hunting behavior in cats.
Plague (Yersinia pestis). Ectoparasite control, especially tick control.
Toxoplasmosis.
YERSINIA PESTIS (FELINE PLAGUE)*
Cytauxzoon felis.
Multicentric lymphoma. Classical signs
● Acute onset of signs.
● Moderate to high fever (39.4–41.2˚C;
Treatment
103–106˚F).
Antimicrobial efficacy studies have not been done in ● Submandibular lymphadenopathy.
the cat, therefore therapy is derived from case reports ● Depression.
and/or human therapy regimens. ● Anorexia.
Enrofloxacin (5 mg/kg q 12 hours IV or PO).
Pathogenesis
Tetracycline and chloramphenicol may be effective, but
because they are bacteriostatic for F. tularensis, Onset of illness occurs 24–72 hours after exposure to
relapses can occur. the organism.
Transmission to cats is either via ingestion of infected interpreted carefully, as high titers can persist for up to
rodents or a fleabite from infected fleas. one year after infection.
Rapid multiplication of organism causes tissue damage Chest radiographs may reveal patchy, nodular lesions if
and necrosis. The host immune response contributes to the pneumonic form is present.
pathology.
Be aware that the risk of exposing other staff mem-
Three forms of the plague exist: bubonic (local infec- bers to the disease should be weighed against the
tion), bacteremic/septicemic and pneumonic. benefit of the diagnostic test.
Bacteremia occurs in many cases, resulting in the
septicemic or pneumonic form of plague. Differential diagnosis
Endemic regions of the world include the western Reactive lymph nodes from a percutaneous abscess
USA, South America, Africa, Asia, eastern Europe. or tooth-root abscess.
● Aspirates of cat bite abscesses contain a mixed bac-
Clinical signs terial population compared to Y. pestis, which is

homogeneous.
History of hunting rodents, especially in known
endemic areas. Neoplasia, although it is less common in the US for cats
with lymphoma to have peripheral lymphadenopathy.
Current flea infestation is evident.
Respiratory signs may be due to other upper respiratory
Acute onset of fever, anorexia, depression over a infections (calicivirus, herpesvirus, Chlamydophila)
period of 2–6 days. The clinical course may last 6–20 or lower respiratory disease (parenchymal lung disease,
days. pleural disease).
Submandibular or cervical swelling associated with Other diseases which cause high fever (tularemia,
lymph nodes (can be unilateral or bilateral). The toxoplasmosis, FIP, etc.).
inflamed, swollen lymph node is referred to as a bubo.
Subcutaneous abscessation may occur and appear Treatment
similar to a cat bite abscess.
Absolute caution must be practiced in all suspect
In the pneumonic form (~10% of cases), upper and plague cases. Cautionary measures include gloves,
lower respiratory signs may be present, including sneez- mask, isolation of animal and limited exposure to other
ing, nasal discharge, coughing, dyspnea/tachypnea. staff members.
Doxycycline/tetracycline: (1) Doxycycline at 5 mg/kg
Diagnosis
q 12 hours PO for 14–21 days or (2) tetracycline 25
Initially, microscopic examination of a lymph node mg/kg q 8 hours PO.
aspirate, especially a markedly swollen lymph node ● Begin treatment immediately after samples for
(bubo) should reveal a homogeneous population of diagnosis have been collected.
bipolar-staining coccobacilli. ● Doxycycline is preferred as tetracycline has been
● Blood should be examined in cats with the bac- associated with relapse.
teremic/septicemic form.
Consider aminoglycosides or enrofloxacin (5 mg/kg
Fluorescent antibody testing of sample provides a IM q 8 hours) for the first 3 days to avoid placing
definitive diagnosis. hands into the cat’s mouth (see Transmission section
below).
Culture of organism should be performed by a quali-
fied laboratory only.
Prognosis
A four-fold rise in antibody titers (taken 10–14 days
apart) is suggestive of plague. These results must be Prognosis for bubonic plague is fair to good.
Prognosis for the pneumonic form is guarded to fair. Age range of cats with documented disease was 2–10
years of age, with no breed or sex predilection
Prognosis for septicemic form is guarded.
reported.
Persistent fever > 40˚C (104˚F) despite treatment is
Infection has a variable effect on appetite, from mild
associated with a poor prognosis.
inappetence to anorexia and mild to moderate weight
loss.
Transmission
Chronic intermittent fever in the moderate range is
Y. pestis has a serious zoonotic potential, and great
common.
care should be taken in suspect cats to prevent trans-
mission to humans and other cats. Lymphadenopathy was reported in three of 23 cats.
● Infected cats are no longer a zoonotic risk after
Hyperesthesia, joint pain or irritable disposition is
3 days of antibiotic therapy.
common.
Transmission occurs via rodent flea bites or inges-
Complete blood counts may show a non-regenerative
tion of infected animals.
anemia with a leukopenia or a leukocytosis; thrombo-
Infection can also occur via inhalation of aerosolized cytopenia is present in about 25% of the cats.
organism, either from aspirates of infected tissue or
Biochemistry abnormalities are uncommon, except for
nasal discharge/sneezing of cats with pneumonic
hyperglobulinemia in about 33% of documented cases.
form.
Diagnosis
Prevention
A complete blood count and biochemistry panel consis-
Confine cats indoors in endemic areas. tent with chronic Ehrlichia spp. infection is suggestive.
Discourage hunting behavior especially during the peak Diagnosis is by demonstrating E. canis and/or Anaplasma
flea season (April to October). phagocytophilum serum antibody titers or a positive
IFA test.
Provide effective flea control to prevent flea bites.
Demonstration of morulae in mononuclear cells, neu-
trophils or eosinophils (rare) is diagnostic.
EHRLICHIA SPP. AND ANAPLASMA PCR assays can be positive.
PHAGOCYTOPHILUM*
NEOPLASIA
Classical signs
● Anorexia and weight loss. Classical signs
● Fever.
● Anorexia, lethargy, weight loss.
● ± Fever.
● Lameness.
● Signs depend on tumor type and organ
● Non-specific hyperesthesia.
system involved.
See main reference on page 547 for details (The Anemic
Cat). Clinical signs
Anorexia, lethargy and weight loss.
Clinical signs Poorly groomed coat.
This disease is uncommonly reported in cats and is Some cats have a fever associated with neoplasia,
difficult to diagnose because of its vague and variable which is generally a secondary neoplastic syndrome.
clinical signs. Tumors which destroy the bone marrow and result in
neutro-penia are classically associated with fever. Fever

SALMONELLA SPP. (SONGBIRD FEVER)
may occur with other tumors via other mechanisms,
including antibody stimulation from tumor antigens,
Classical signs
and tissue necrosis which activates leukocytes to
release pyrogenic factors. ● Vomiting/diarrhea.
● Fever (40.0–40.6˚C [104.0–105.0˚F]).
Signs are specific to the organ system involved.
● Depression.
Lymphoma (mediastinal, GI, renal), mammary ● Anorexia.
adenocarcinoma, squamous cell carcinoma (nasal, oral)
and mast cell tumor are the most common tumors in cats. See main reference on page 719 for details (The Cat
With Signs of Acute Small Bowel Diarrhea).
Diagnosis
Hematology, biochemistry panel, radiology, ultra-
sound and/or bone marrow aspirates may be necessary Clinical signs
to provide evidence that a tumor is present, especially
Acute onset of fever and malaise are initial clinical
if it involves the hematopoietic system (leukemia) or is
signs.
located internally (splenic mast cell tumor).
Vomiting, diarrhea and abdominal pain may occur,
Identification of the tumor type is via fine-needle
however, approximately 50% do not have gastrointesti-
aspirates and/or biopsies.
nal signs.
Dehydration.
Shock may occur if septicemia/bacteremia develops.
Organ dysfunction due to infectious or degenerative
disease process. Mortality rate approaches 10% and may be higher if
the cat is concurrently immunosuppressed.
FeLV/FIV or other immunosuppressive illness.
Benign masses (granulomas, abscesses, reactive lymph
nodes, benign tumors).
Diagnosis
Treatment Typically, the cat is an outdoor cat with a history of
hunting behavior, especially of birds.
Treatment involves surgical excision of identifiable
masses +/− regional lymph nodes, especially for mam- Complete blood count and biochemistry panel sup-
mary adenocarcinoma, nasal squamous cell carcinoma, ports infectious diarrhea or septicemia, e.g., neutrope-
splenic mast cell tumor, etc. nia with a left shift, bacterial rods in blood leukocytes
if overwhelming sepsis present, hypoglycemia,
Chemotherapy may be effective and needs to be based hypoproteinemia, pre-renal azotemia.
on tumor type, e.g., COP (cyclophosphamide, vin-
cristine, prednisolone) protocol in lymphoma cases. Blood cultures provide the best definitive diagnosis if
positive. Three separate samples over a 4–6 hour
Radiation therapy is used for local disease only, and period should be taken during febrile episodes using
response to radiation therapy is tumor dependent (e.g., aseptic techniques.
squamous cell carcinoma).
● Radiation therapy is most effective after surgical Fecal cultures may isolate Salmonella organisms,
debulking of the primary mass. The effectiveness of but because many animals are subclinical carriers,
radiation therapy may be enhanced with concurrent positive culture does not prove that the organism is
chemotherapy. the cause of the clinical signs.
Respiratory signs such as coughing and wheezing are

COCCIDIODES IMMITIS
less common in cats and occur in approximately 25%
of cases.
Classical signs
Musculoskeletal signs such as lameness, with or with-
● Skin lesions.
out painful bone swelling, were reported in 19% of
● Respiratory signs.
cats.
● Ocular lesions.
● Fever, anorexia, depression. Ocular lesions are seen infrequently and include chori-
oretinitis and anterior uveitis. Ocular or CNS signs
were reported in 19% of cats.
Pathogenesis
Most cats have clinical signs for less than 4 weeks
The geographical distribution includes south-west
prior to diagnosis.
USA, Central America and South America in areas
that have sandy soil with low rainfall and high tem-
peratures. Diagnosis
Soil is the reservoir for infection, and the highest fre- Hyperproteinemia is present in approximately 50% of
quency of cases occur when the soil is dry and dusty, cats.
and organisms are disseminated in the wind.
Definitive diagnosis is by identification of the organism
Most humans and animals in endemic areas become via biopsy of lesions.
infected, but the majority of infections are subclinical
or cause only mild, transient clinical signs. Antibody detection is available using latex agglutina-
tion (IgM), AGID (IgM) or ELISA (IgM or IgG).
Cats are more resistant to infection and signs are less
common than in dogs. Tube precipitin (TP) for IgM and complement fixation
(CP) for IgG were previously thought to be less reliable
Infection is contracted via inhalation, and only a few in cats, but have been subsequently demonstrated to
organisms are required to produce signs, which occur detect feline infections.
after 1–3 weeks.
Initial infection is confined to the respiratory tract,
Treatment
but dissemination may occur resulting in chronic dis-
ease over months or years with signs referable to bones, Itraconazole (10 mg/kg PO if possible, q 24 h or 5
eyes, central nervous system and abdominal organs. mg/kg q 12 h) is the treatment of choice. Treatment is
required for 4–6 months and must be continued for at
Localized infection following a penetrating skin wound
least 2 months after all signs have resolved.
appears to be rare.
● Some cats develop anorexia, and less commonly
vomiting or diarrhea. Stop the drug for a few days
Clinical signs until the cat is eating, and then restart at 1/2 the
dose for 7–10 days, before increasing back to the
Cats appear to be resistant to clinical disease.
full dose, which is usually then tolerated.
Skin lesions are the most frequent types of infection in
Amphoteracin B is also effective (0.25 mg/kg in 30 ml
cats and were reported in 56% of cats in one study.
dextrose 5% IV over 15 minutes q 48 h or given subcuta-
● Lesions begin as small bumps and progress to
neously) – see page 26, for Cyptococcosis in The Cat
abscesses, ulcers or draining tracts.
With Signs of Chronic Nasal Disease. Continue ampho-
● In cats, underlying bone involvement is uncommon.
tericin B therapy until a cumulative dose of 4 mg/kg is
Systemic signs such as fever, anorexia and depres- given or until BUN > 17.9 mmol/L (50 mg/dl).
sion are commonly reported (44% of cats) and can be Amphotericin has the disadvantage of requiring frequent
seen with skin lesions. parenteral or subcutaneous administration and causes sig-
nificant nephrotoxicity.
● Because of its quick onset of action, amphoteracin Fever, anorexia, depression, weight loss and lymph-
B in combination with itraconazole is useful in adenopathy are systemic signs associated with dissem-
cats with severe pulmonary signs that are rapidly inated disease.
deteriorating. If the cat survives, after a few weeks
Draining skin lesions may occur and are usually a man-
treatment can be continued with itraconazole alone.
ifestation of systemic disease rather than local disease.
● Lipid-complexed amphoteracin formulations
allow higher dosages with less toxicity, and Neurological signs are associated with CNS involve-
should be used in cats with severe pulmonary signs, ment of the brain or spine and include circling, disori-
although the cost is higher. Dose at 2–3 mg/kg IV 3 entation, anisocoria, paresis, decreased conscious
days per week for a total of 9–12 treatments (cumu- proprioception, or upper motor neuron signs, hyperes-
lative dose of 24–27 mg). Dilute to a concentration thesia and extensor rigidity.
of 1 mg/ml in dextrose 5% and infuse over 1–2
hours.
Diagnosis
If the titer has decreased four-fold and there is a sim-
Definitive diagnosis is by demonstration of an extra-
ilar improvement in physical and radiographic
cellular, broad-based budding yeast in aspirates or
signs, treatment can be stopped after 4–6 months.
biopsies from lymph nodes, draining tracts, bone
Antibodies may persist for long periods and obtaining
lesions or vitreous humor.
a zero titer is not a useful treatment goal.
An antibody detection test is available, but may be
negative.
BLASTOMYCES DERMATIDITIS
(BLASTOMYCOSIS)
Treatment
Classical signs
Itraconazole (10 mg/kg PO if possible, q 24 h or
● Fever. 5 mg/kg q 12 h) is the treatment of choice. Treatment is
● Respiratory signs. required for 4–6 months and must be continued for at
● Ocular signs. least 2 months after all signs have resolved.
● Lymphadenopathy. ● Some cats develop anorexia, and less commonly
vomiting or diarrhea. Stop the drug for a few days
until the cat is eating, and then restart at 1/2 the
Pathogenesis dose for 7–10 days, before increasing back to the
full dose, which is usually then tolerated.
The geographical distribution includes North
America, Central America and Africa. Amphoteracin B is also effective (0.25 mg/kg in 30 ml
dextrose 5% IV over 15 minutes q 48 h or given subcu-
Soil is believed to be the reservoir for infection, and
taneously) – see page 26, for Cyptococcosis in The Cat
living near a lake or river increases the risk of infection
With Signs of Chronic Nasal Disease. Continue ampho-
in dogs.
tericin B therapy until a cumulative dose of 4 mg/kg is
Signs are more common in dogs than in the cats. given or until BUN > 17.9 mmol/L (50 mg/dl).
Amphotericin has the disadvantages of requiring fre-
Disseminated disease is primarily contracted via
quent parenteral or subcutaneous administration and
inhalation.
causing significant nephrotoxicity.
● Because of its quick onset of action, Amphoteracin
Clinical signs B in combination with itraconazole is useful in
cats with severe pulmonary signs that are rapidly
Respiratory signs include coughing, dyspnea and
deteriorating. If the cat survives, after a few weeks
harsh lung sounds.
treatment can be continued with itraconazole alone.
Ocular disease, such as uveitis, glaucoma and retinal ● Lipid-complexed amphoteracin formulations allow
detachment, is a frequent finding. higher dosages with less toxicity, and should be
used in cats with severe pulmonary signs, although Demonstration of the organism in erythrocytes
the cost is higher. Dose at 2–3 mg/kg IV 3 days per (merozoite stage) is possible only relatively late in
week for a total of 9–12 treatments (cumulative dose the disease, approximately 1–3 days before death.
of 24–27 mg). Dilute to a concentration of 1 mg/ml in Parasitemic cats usually have only 1–2% of RBCs
dextrose 5% and infuse over 1–2 hours. affected, and up to 50% of cats have parasitemias that
are very low or undetectable.
CYTAUXZOON FELIS Demonstration of the organism in macrophages from
bone marrow, spleen, liver or lymph node aspirates
Classical signs may be possible even when organisms are not evident
in blood.
● Fever.
● Anorexia. Serum antibody levels and direct FA test for detec-
● Dyspnea. tion of tissue phase are available through some labs.
● Icterus.
● Collapse. HYPERTHYROIDISM
See main reference on page 534 for details (The Anemic Classical signs
Cat).
● Weight loss.
● Polyphagia.
Clinical signs ● Polyuria/polydipsia.
● Behavioral changes.
Primarily found in the south-central and southeast
● Unkempt appearance.
United States. The North American bobcat is the natu-
● Mild elevations in temperature.
ral host.
There is usually a history of exposure to ticks in the See main reference on page 304 for details (The Cat
previous 5–20 days (incubation period is 5–20 days). With Weight Loss and a Good Appetite).
The clinical course of disease is approximately 1 week
and often ends in death.
Clinical signs
Clinical signs are the result of an overwhelming
Weight loss in spite of normal to increased appetite.
hemolytic crisis.
Polyuria/polydipsia.
Rapid onset of fever, dyspnea, anorexia, pale mucous
membranes, icterus and dark-colored urine are typical. Behavioral changes which often include hyperactivity
and aggression.
Collapse and death occur 2–3 days after the fever
peak. Hypothermia occurs in the terminal stages. Unkempt, rough hair coat and sometimes overgrown
nails.
There appear to be non-pathogenic strains as well.
Tachycardia accompanied by a “gallop” rhythm and/or
a systolic murmur.
Diagnosis
Mild fever which may be intermittent in nature and
A complete blood count reveals regenerative anemia,
reflect the increased metabolic rate in this disease.
hemoglobinemia and neutrophilia or neutropenia.
These cats are easily stressed and may present dyspneic
The biochemistry panel commonly has hyperbiliru- and tachycardic with a mildly elevated temperature,
binemia. usually not greater than 39.4˚C (103.0˚F).
Urinalysis may show evidence of hemoglobin and Enlarged thyroid glands are often evident on palpation
bilirubin. of the neck.

Diagnosis is based on clinical signs and history and Naturally infected cats usually only develop subclin-
confirmed by demonstrating increased thyroid hormone ical infection.
concentrations (total T4, free T4).
Mild, self-limiting fever lasting 48–72 hours has been
Thyroid glands can be palpated in approximately 80% documented in some experimentally infected cats.
of cats with hyperthyroidism, and are unilaterally or
Anterior uveitis and fever were documented in
bilaterally enlarged.
naturally exposed cats.
● Enlarged thyroid glands may not be palpable if the
abnormal thyroid tissue is within the thoracic inlet. Lymphadenopathy.
Complete blood count and a biochemistry panel are Stomatitis and gingivitis have been proposed as
required to rule out diseases such as diabetes mellitus, clinical manifestations.
renal disease, etc.
Atypical seizures occur in some cats.
A TRH stimulation test may be necessary when clin-
ical signs are highly suggestive and total and free T4
Diagnosis
are in the upper region of the reference range for
normal cats. Antibody titers are prevalent in healthy cats, but there
is a poor correlation with blood culture and PCR
Thyroid radionuclide uptake and imaging with pertech-
assay results.
netate (99mTc) is also available at some institutions.
Intermittent bacteremia may occur for longer than
Response to therapy with anti-rickettsial drugs (tetracy-
one year following infection, with 25–41% of healthy
cline or doxycycline) is highly suggestive.
cats bacteremic for up to 22 months.
The organism is present within erythrocytes, therefore,
hemolyzing red blood cells increases the sensitivity of
BARTONELLA HENSELLA (CAT-SCRATCH
the culture.
FEVER)

● Subclinical or mild fever and occasional Other causes of mild transient fever need to be consid-
ocular signs. ered, such as mild cellulitis following a cat fight.
Other infectious causes of anterior uveitis need to be
ruled out, such as toxoplasmosis, fungal diseases,
Pathogenesis
FeLV, FIV, Cuterebra or dirofilaria.
Bartonella henselae is an intracellular bacterium
within erythrocytes.
Treatment
Bacteremia is present in many healthy cats in the pop-
Antimicrobial efficacy has not been clearly demon-
ulation, and cats are reservoirs for infection.
strated.
B. henselae is an important pathogen because of its
Clinical signs of disease have resolved when the cats
zoonotic potential in immunocompromised humans.
are administered doxycycline at 25–50 mg PO q 12 h
● Humans may develop fever, malaise, lymph-
for 28 days.
adenopathy and skin eruptions following cat
scratches or bites. Azithromycin is used in humans and is a safe alterna-
● B. henselae causes bacillary angiomatosis, bacillary tive in cats when administered at 10 mg/kg PO q 24 h
peliosis and encephalitis in human AIDS patients. for 28 days
Fluoroquinolones also may be effective. Clinical signs

While clinical signs resolve, bacteremia is usually only Primary immune-mediated disease is extremely rare
temporarily suppressed. in cats.
Stimulation from primary infectious disease antigens is
Prognosis the most common cause of immune-mediated disease
in cats, and is most often associated with hemobar-
B. henselae has very low pathogenicity in cats. tonella (mycoplasma) and calicivirus.
Once cleared of infection, cats are resistant to re-infection Systemic lupus erythematosus is rare in cats. A mul-
by innoculation, but are still susceptible if transmitted titude of signs may occur including fever, weight loss
via blood transfusion. and cutaneous lesions.
Immune-mediated hemolytic anemia is most com-
Transmission monly associated with hemobartonellosis. Signs
Transmission is via arthropod vectors. In endemic include anemia, icterus, fever and anorexia. Cats with
areas, cats infested with fleas and/or ear mites are immunosuppressive disorders such as FeLV may be
more likely to be seropositive. more susceptible.
The organism survives in flea feces for at least 9 days. Immune-mediated thrombocytopenia is rarely
reported in cats. FeLV-positive cats, however, may have
Because of the frequency of bacteremia in healthy cats, thrombocytopenia that is thought to be the result of an
blood transfusions are a likely route of infection. immune-mediated response.
Immune-mediated polyarthritis is uncommon in
IMMUNE-MEDIATED DISEASE cats, but has been documented in kittens and adult cats
with post-calicivirus vaccination.
Classical signs
● Fever.
● Anemia or thrombocytopenia.
● Cutaneous lesions.
● Polyarthritis.
RECOMMENDED READING
Dobbinson SS, Tannock GW. A bacteriologic investigation of subcutaneous abscesses in cats. NZ Vet J 1985; 33:
27–29.
Eidson M, Thilsted JP, Rollag OJ. Clinical, clinicopathologic, and pathologic features of plague in cats: 119 cases
(1977–1988). JAVMA 1991; 199: 1191–1197.
Greene CE. Bacterial diseases; fungal diseases; and protozoal diseases. In: Greene CE (ed) Infectious Diseases of the
Dog and Cat. 2nd edn. Philadelphia, WB Saunders Co., 1998, pp 179–509.
Lappin MR. Feline toxoplasmosis: interpretation of diagnostic test results. Sem Vet Med Surg Sm An 1996; 11:
154–160.
Lappin MR, Jensen W, Kordick DL, Karem K, Breitschwerdt EB. Bartonella spp. antibodies and DNA in aqueous
humor of cats. Fel Med Surg 2000; 2: 61–68.
Lindsay DS, Blagburn BL, Dubey JP. Feline toxoplasmosis and the importance of the Toxoplasma gondii oocyst.
Compendium 1997; 19: 448–461.
McReynolds C, Macy D. Feline infectious peritonitis. Part I. Etiology and diagnosis. Compendium 1997; 19:
1007–1016.
McReynolds C, Macy D. Feline infectious peritonitis. Part II. Treatment and prevention. Compendium 1997; 19:
1111–1116.
Neer TM, Breitschwerdt EB, Greene RT, Lappin MR. Consensus statement of ehrlichial disease of small animals
from the infectious disease study group of the ACVIM. J Vet Int Med 2002; 16: 309–315.
Pedersen NC. Feline infectious myocarditis/diaphragmitis. In: August JR (ed) Consultations in Feline Internal
Medicine. Philadelphia, WB Saunders Co., 1997, pp 31–33.
Quesnel AD, Parent JM. Diagnostic approach and medical treatment of seizure disorders. In: August JR (ed)
Consultations in Feline Internal Medicine. Philadelphia, WB Saunders Co., 1997, p 393.
Sparks AH. An appraisal of the value of laboratory tests in the diagnosis of feline infectious peritonitis. J AAHA
1994; 30: 345–349.
Woods JP, et al. Tularemia in two cats. JAVMA 1998; 212: 81–83.
20. The cat with enlarged lymph nodes
Anthony Abrams-Ogg
KEY SIGNS
● Hyperplasia, neoplasia, lymphadenitis most common.
● Edema, vascularization, infarction less common.
● Biopsy and culture lymph node.
MECHANISM?
● Reactive lymphoid hyperplasia, neoplasia or lymphadenitis are the most common causes of
lymphadenopathy.
WHERE?
● Peripheral (superficial) lymph nodes – enlargement may be confined to a solitary/local node, or
be regional or generalized.
There may be accompanying internal (deep) lymphadenopathy.
WHAT?
● The most common causes of generalized lymphadenopathy are generalized skin diseases,
retroviral infections and lymphoma. The most common causes of local and regional
lymphadenopathy are bacterial and fungal infections in the area drained by the node(s). All
causes may result in mild to marked lymphadenopathy.

Diseases causing enlarged lymph nodes
MECHANICAL
● Obstructive edema* (p 411)
Local or regional lymphadenopathy occurs due to nodal edema and/or hyperplasia, secondary to
obstructive edema from a tumor or other mass involving the head, neck or a limb.
NEOPLASTIC
● Nodal lymphoma* (p 403)
Regional (head and neck) or generalized (multicentric) lymphadenopathy occurs with predomi-
nance of lymphoblasts on biopsy. Average age of cats with multicentric lymphoma is 4 years. Age
continued
393
continued
of most cats with Hodgkin’s-like lymphoma is > 6 years. Cats may be presented for nodal enlarge-
ment without concurrent signs, with non-specific signs of illness (lethargy, inappetence and weight
loss), and with specific signs due to internal organ involvement (e.g. icterus with hepatic involve-
ment).
●Metastatic neoplastic lymphadenopathy: mast cell tumor, other tumors (carcino-
mas, sarcomas, plasma cell tumors, myeloid leukemias, malignant histiocytosis,
melanoma)* (p 409)
Local to generalized lymphadenopathy occurs with malignant cells and hyperplasia found on
biopsy. Most metastatic neoplasia occurs in older cats. Cats usually have localizing signs of the
primary tumor or non-specific signs of illness.
NUTRITIONAL
● Steatitis (p 412)
Regional to generalized lymphadenopathy results from hyperplasia. Other clinical signs include
fever, anorexia, depression, reluctance to move, pain on handling, ascites and firm subcutaneous
and abdominal fat.
IDIOPATHIC
● Plexiform vascularization of lymph nodes (p 414)
Solitary or regional lymphadenopathy in neck or inguinal area occur due to capillary vasoproliferation.
Tracheal compression may occur causing dyspnea. No other signs are present.
INFLAMMATION
● Parasitic, immunologic and miscellaneous skin disorders** (p 400)
Regional or generalized lymphadenopathy results from hyperplasia. Signs of skin disease are pres-
ent, such as erythema, pruritus, alopecia, excoriations, scales, crusts, papules, nodules, plaques,
vesicles, pustules, erosions and ulcers.
● Idiopathic atypical hyperplasia (p 412)
Generalized lymphadenopathy occurs due to atypical hyperplasia. Cats are ~ 4 years of age. Cats are usu-
ally presented for nodal enlargement without other signs, but variable non-specific and specific signs may
be present.
● Non-cutaneous immunologic/inflammatory disorders (p 416)
Regional or generalized lymphadenopathy results from hyperplasia associated with polyarthritis (lame-
ness), systemic lupus erythematosus (cutaneous signs) or certain forms of lymphocytic cholangitis
(icterus and ascites).
● Hypereosinophilic syndrome (p 416)
Generalized lymphadenopathy results from eosinophilic lymphadenitis. Other clinical signs are usually
present, including lethargy, inappetence, weight loss, vomiting and diarrhea.
● Post-vaccinal lymphadenopathy (p 416)
Local or generalized lymphadenopathy results from hyperplasia, associated with a history of vaccination in
the preceding few weeks.
20 – THE CAT WITH ENLARGED LYMPH NODES 395
● Cutaneous/subcutaneous foreign body reaction* (p 406)

Local lymphadenopathy occurs due to hyperplasia or lymphadenitis, secondary to aseptic or septic
inflammation around the foreign body. Other localizing clinical signs include erythema, warmth and
pain on palpation, swelling or thickening of tissue, and wounds.
● Oral cavity diseases* (p 406)
Mandibular lymphadenopathy results from hyperplasia or lymphadenitis. Signs of oral cavity disease are
present, including halitosis, gingivitis, ulceration and masses.
INFECTIOUS
Viral:
● Feline leukemia virus (FeLV) infection** (p 398)
Generalized lymphadenopathy occurs due to hyperplasia during acute and persistent viremia.
Lymphadenopathy may also result from lymphoma or secondary infection. Cats may otherwise be
normal, or have lethargy, inappetence and fever. Localizing signs of infection or neoplasia may
also be present.
● Feline immunodeficiency virus (FIV) infection** (p 398)
Generalized lymphadenopathy occurs due to hyperplasia during acute and chronic clinical stages of
infection. Lymphadenopathy may also result from lymphoma or secondary infection. Cats may other-
wise be normal, or have lethargy, inappetence and fever. Localizing signs of infection or neoplasia may
also be present.
Bacterial:
● Acute cat-bite wound cellulitis/abscess** (p 401)
Local to regional lymphadenopathy occurs due to hyperplasia. Other localizing clinical signs
include erythema, warmth and pain on palpation, swelling or thickening of tissue, and wounds.
Systemic signs may be present including lethargy, inappetence and fever.
● Juvenile streptococcal lymphadenitis (p 415)
Cervical lymphadenopathy occurs due to lymph node abscessation in kittens. Kittens are depressed,
inappetent and febrile.
● Mycobacterial infections* (p 407)
Generalized lymphadenopathy results from granulomatous lymphadenitis in tuberculosis, and accompa-
nies chronic vomiting, diarrhea and weight loss. Regional lymphadenopathy due to hyperplasia may
accompany cutaneous nodules in leprosy, and occur with chronic ulcerated subcutaneous lesions in
atypical mycobacteriosis.
● (Pyo)granulomatous bacterial infections*, mycoplasma and L-form infections,
miscellaneous bacterial infections* (p 408)
Local to generalized lymphadenopathy results from hyperplasia or lymphadenitis and often accompanies
an acute or chronic wound. Systemic signs may be present including lethargy, inappetence and fever.
● Plague* (p 404)
Fulminant disease with head and neck lymphadenopathy resulting from abscessation and/or necrosis.
Cats are highly susceptible to plague. Cats typically have acute onset of high fever, depression and
anorexia.
continued
continued
● Tularemia* (p 410)
Fulminant disease with peripheral and internal lymphadenopathy. Cats are moderately susceptible to
tularemia, Cats typically have acute onset of high fever, depression and anorexia.
● Anthrax (p 418)
Fulminant disease sometimes presenting as acute death with no promontory signs. Rare in cats because
they are resistant to anthrax. Cervical lymphadenopathy and edema of the tongue and pharynx.
● Ehrlichiosis and bartonellosis (p 417)
Regional to generalized lymphadenopathy occur due to hyperplasia. Cats with ehrlichiosis usually have
non-specific signs of illness, while cats with bartonellosis are asymptomatic.
● Bacteremia (p 416)
Variable lymphadenopathy due to hyperplasia may occur in chronic bacteremia, accompanied by
chronic signs of fever, lethargy and inappetence.
Fungal and algal:

● Dimorphic fungal infections**, protothecosis (p 418)
Local to generalized lymphadenopathy occurs due to hyperplasia or lymphadenitis. Concurrent
localizing signs include nasal discharge, dyspnea, lameness, cutaneous nodules and ulcers, seizures
and uveitis. Concurrent systemic signs include fever, weight loss and inappetence.
● Miscellaneous fungal infections* (p 411)
Local to generalized lymphadenopathy results from hyperplasia or lymphadenitis. Cats typically
have chronic ulcerating cutaneous or subcutaneous lesions.
Protozoal:
● Cytauxzoonosis, American and African trypanosomiasis (p 418, 419)
Fulminant diseases where generalized lymphadenopathy may be present. Cats with cytauxzoonosis and
African trypanosomiasis are febrile. Cats with American trypanosomiasis have signs of acute heart failure.
Acute toxoplasmosis may cause reactive peripheral lymphadenopathy and mesenteric lymph node
necrosis.
INTRODUCTION ● Lymph node biopsy (fine needle, incisional or exci-

sional) for cytology, histology and culture is
required to identify these mechanisms.
MECHANISM?
Hyperplasia is the most common cause of lymph-
Lymphadenopathy refers to enlarged lymph nodes.
adenopathy. It represents the immune response of nor-
Lymphadenopathy may accompany a number of com-
mal lymphoid cells to antigenic stimulation.
mon and uncommon diseases, but it is uncommonly the
● It is characterized cytologically by a predominance
chief complaint.
of small mature lymphocytes with or without
Reactive lymphoid hyperplasia, neoplasia and lymph- increased numbers of immature lymphocytes,
adenitis are the usual causes of lymphadenopathy. plasma cells and macrophages.
Lymphadenopathy is infrequently due to vasculariza- ● Some distinguish between lymph node hyperpla-
tion, edema or infarction. sia and reactive lymphadenopathy. The former is
characterized by a clinically enlarged node but nor- Lymph nodes may be painful, warm and soft with
mal cellular composition on biopsy; the latter is bacterial and fungal lymphadenitis. Lymph nodes are
characterized by a mild to marked increase of painless, firm and at body temperature with most other
plasma cells, with or without a mild increase of diseases.
immature lymphocytes and/or macrophages. These
Lymph nodes may be fixed (instead of mobile) with
two patterns have the same etiologies, will not be
lymphadenitis, metastatic neoplasia and lymphoma
distinguished here, and will be referred to as
with extracapsular invasion.
“hyperplasia”.
● Based on lymph node histology, patterns of lymph Lethargy, inappetence, weight loss and fever may be
node hyperplasia may vary, e.g. as follicular cen- present, especially with generalized lymphadenopathy.
ter expansion (B-cells), paracortical expansion
Local or regional enlargement is usually due to a disorder
(T-cells), combined B- and T-cell hyperplasia, and
in the area drained by the node(s).
sinusoidal cell hyperplasia (macrophages). In
most disorders lymph node architecture is pre-
served.
● Hyperplasia is generally a non-specific finding.
WHERE?
● Some tendencies for specific cytologic and histologic
patterns occur with certain diseases, e.g. increased The focus of this chapter is peripheral lymph-
numbers of eosinophils in parasitic skin diseases. adenopathy (e.g. mandibular, prescapular, axillary,
Communicating with the pathologist may assist the inguinal and popliteal nodes). There may be accompa-
clinician in determining etiology. nying internal lymphadenopathy (e.g. hilar and mesen-
● Hyperplasia may be the initial finding before the teric nodes).
development of detectable neoplasia or lym- ● Inguinal fat should not be mistaken for enlarged
phadenitis. inguinal nodes and contracted muscles of the caudal
● Hyperplastic nodes without a diagnosis should be aspects of the hindlimb should not be mistaken for
cultured for bacteria and fungi. popliteal nodes.
Neoplastic lymphadenopathy is characterized by pro- Diseases causing primarily internal lymphadenopathy
liferation or invasion of malignant cells. are discussed in The Dyspneic or Tachypneic Cat, The
● Lymphoma and lymphoid leukemia are due to pro- Cat With Chronic Diarrhea and The Thin Inappetent
liferation and invasion of malignant lymphocytes. Cat.
● On histology, lymphoid neoplasia typically dis-
rupts lymph node architecture and demonstrates
a uniform cell-type and chromatin pattern.
● Other hematopoietic tumors and solid tumors WHAT?
may metastasize to local, regional or distant nodes.
The most common causes of generalized lymph-
Lymphadenitis is characterized by a cellular infiltrate adenopathy are chronic generalized skin diseases (der-
of neutrophils (suppurative) macrophages (pyogranulo- matopathic lymphadenopathy), FeLV/FIV infections and
matous), or eosinophils (eosinophilic), focal necrosis or lymphoma.
abscessation. It usually results from an extension of an ● The most common causes of marked generalized
inflammatory process into the node. lymphadenopathy are chronic flea allergy dermati-
● Severe, peracute infectious lymphadenitis may tis, lymphoma, idiopathic atypical hyperplasia and
cause hemorrhage and necrosis with destruction of acute FIV infection.
architecture, minimal inflammatory infiltrate, and
The most common causes of local and regional lymph-
nodal and perinodal edema.
adenopathy are bacterial and fungal infections in the
Lymphadenopathy may be mild to marked with any cause. area drained by the node(s).
● Lymphadenopathy tends to be more prominent in ● The most common cause of marked solitary lymph-
younger animals compared to older animals. adenopathy is abscessation.
Mild to marked lymphadenopathy and various asso-

DISEASES CAUSING PERIPHERAL ciated signs may occur with other FeLV-associated
LYMPHADENOPATHY disorders (e.g. neoplasia and fungal infection).
FELINE LEUKEMIA VIRUS (FELV) Diagnosis

INFECTION**
FeLV tests.
● ELISA, FA and rapid immunomigration (RIM)
Classical signs
tests detect p27 protein produced by the virus.
● Lethargy, inappetence, weight loss, – ELISA test may be weakly positive during pri-
unkempt haircoat. mary viremia; FA test is negative. Because pri-
● Fever, gingivitis, recurrent upper mary viremia may be terminated by an effective
respiratory infections, opportunistic immune response, the ELISA test should be
infections. repeated in 4–6 weeks.
● Anemia. – ELISA and FA tests are usually both positive
● Generalized lymphadenopathy may occur during persistent viremia.
in viremic cats. – RIM test results correlate closely to ELISA test
results.
See main reference, page 540 (The Anemic Cat). ● Some PCR tests are available to detect viral DNA.
PCR may be positive during primary viremia. PCR
is positive during persistent viremia, and is more
Pathogenesis
sensitive than either ELISA or FA. It should be
FeLV infection may cause solitary, regional and gen- noted that PCR testing has not been standard-
eralized lymphadenopathy by several mechanisms. ized and is more likely to give false-positive
These include: results than ELISA and FA if the laboratory
● Lymphoid hyperplasia during primary viremia (ini- does not maintain the highest standards of qual-
tial infection). ity control.
● Lymphoid hyperplasia during persistent viremia. ● If FeLV tests on peripheral blood are negative and
● Atypical hyperplasia. another cause of lymphadenopathy has not been
● Lymphoma. determined, obtain a FA or PCR test on a bone mar-
● Metastatic neoplasia. row or lymph node aspirate, or immunohisto-
● Immunosuppression causing bacterial infections chemistry test on a bone marrow core or lymph
(e.g. gingivitis/stomatitis, pyoderma) and fungal node biopsy.
infections (e.g. cryptococcosis), and reactive hyper-
Lymph node biopsy reveals follicular or paracortical
plasia or lymphadenitis.
lymphoid hyperplasia.
● Immune-complex diseases (e.g. polyarthritis) and
reactive hyperplasia.
Clinical signs Lymphoma, metastatic lymphadenopathy, atypical

hyperplasia, and possibly hyperplasia from other
Mild to moderate generalized lymphadenopathy may causes may be distinguished from FeLV-induced hyper-
occur during primary viremia. plasia by lymph node histology.
● Cats may otherwise be normal or have variable
lethargy, inappetence and fever. Lymphoma may be present at other sites – e.g. bone
marrow, liver, spleen.
Mild to moderate generalized lymphadenopathy
may occur during persistent viremia. A primary tumor should be identifiable with metastas-
● Mandibular nodes may be more affected.
tic lymphadenopathy.
● Cats may otherwise be normal or have variable Signs of infections, skin diseases or immune-medi-
lethargy, inappetence and fever. ated disorders should be present if lymphadenopathy
is due to hyperplasia from a cause other than retrovi- Pathogenesis

ral infection.
FIV infection can cause solitary, regional and general-
An FIV antibody test or PCR test for FIV DNA may be ized lymphadenopathy by several mechanisms. These
used to rule out FIV infection. include:
● Hyperplasia during the acute phase (initial infec-
Treatment tion).
● Hyperplasia during the chronic symptomatic phase
Treat neoplasia, infection, skin disease or immune- of infection (encompassing the phases of progres-
mediated disease as discussed elsewhere. sive generalized lymphadenopathy, AIDS [acquired
There is no specific treatment for lymphadenopathy immunodeficiency syndrome]-related complex and
that is not due to these conditions. terminal AIDS). Some of the hyperplastic changes
may be reactions to secondary infections.
Supportive care as needed. ● Increased risk for lymphoma, which may cause
Immunomodulation with agents such as Staphylococcus lymphadenopathy.
protein A or interferon-α may improve subjective ● Increased risk for non-lymphomatous neoplasia,
impression of the cat’s well-being, but will not acceler- which may cause metastatic lymphadenopathy.
ate resolution of lymphadenopathy. ● Immunosuppression causing bacterial infections
(e.g. gingivitis/stomatitis, pyoderma) and fungal
Prognosis infections (e.g. dermatophytosis), and subsequent
reactive lymph node hyperplasia or lymphadenitis.
Lymphadenopathy of primary viremia will resolve with ● Immune-mediated disorders (which may have
resolution of viremia. associated lymphadenopathy) have been described
● Lymphadenopathy usually resolves within 4 months. in FIV-positive cats, but the role of FIV in patho-
● Cats with more pronounced signs during primary genesis is not known.
viremia are more likely to become persistently
viremic.
Clinical signs
In most cases, lymphadenopathy of persistent
viremia not due to neoplasia, infection, skin disease, or Mild to moderate generalized lymphadenopathy is
immune-mediated disease will resolve spontaneously. common during the acute phase.
● Some cases will progress to lymphoma. ● Concurrent signs include variable lethargy, inappe-
tence, fever and signs of gingivitis/stomatitis,
Long-term prognosis is determined by other FeLV- enteritis, conjunctivitis, respiratory tract infections,
associated disorders. dermatitis and neurologic disorders.
● Although other clinical signs are usually only
FELINE IMMUNODEFICIENCY VIRUS (FIV) present for several days to weeks, lymphadenopathy
INFECTION** may persist for over a year.
● Internal lymphadenopathy occurs concurrently.
Classical signs Mild to moderate generalized lymphadenopathy is
● Lethargy, inappetence, weight loss, common during the chronic symptomatic phase.
unkempt haircoat. ● Concurrent signs include variable lethargy, inappe-
● Fever, gingivitis, diarrhea, dermatitis, tence, fever, and signs of gingivitis/stomatitis, enteri-
recurrent upper respiratory infections. tis, conjunctivitis, uveitis, respiratory tract infections,
● Opportunistic infections. dermatitis, neurologic disorders and other signs due
● Neurologic signs, uveitis. to secondary infections.
● Generalized lymphadenopathy usually ● Internal lymphadenopathy occurs concurrently.
occurs during symptomatic phases. ● In the terminal phase of infection, lymphadenopa-
thy may disappear and lymph nodes may become
See main reference, page 378 (The Pyrexic Cat). small due to marked follicular involution.
Mild to marked lymphadenopathy and various associ- to hyperplasia from a cause other than retroviral infec-
ated signs may occur with other FIV-associated dis- tion.
orders (e.g. neoplasia and fungal infection).
A FeLV antigen test may be used to rule-out FeLV
● In the terminal phase of FIV infection, appropri-
infection.
ate lymphadenopathy due to hyperplasia may not
occur in response to secondary infection because of Generalized lymphadenopathy is a more prominent
marked follicular involution. feature of FIV, compared to FeLV, infection.
Diagnosis
Treatment
FIV antibody test (ELISA, RIM, FA, western blot).
Treat neoplasia, infection, skin disease or immune-
● Antibody is usually detectable within 2 months of
mediated disease as discussed elsewhere.
infection, but may take up to 6 months, therefore
a negative test should be repeated. There is no specific treatment for lymphadenopathy
that is not due to these conditions.
PCR test for FIV DNA. The sensitivity of PCR for viral
DNA compared to antibody tests is not known. It Supportive care as needed.
should be noted that PCR testing has not been stan-
dardized and is more likely to give false-positive Prognosis
results than antibody tests if the laboratory does not
maintain the highest standards of quality control. Lymphadenopathy is not a distinct disorder in FIV-
positive cats, but rather a marker of the symptomatic
During the acute phase, lymph node biopsy reveals phases of infection. There is no specific prognosis
marked follicular hyperplasia with or without dys- attached to lymphadenopathy, except that disappear-
plasia, and less intense parafollicular hyperplasia. ance during the chronic symptomatic phase correlates
During the chronic symptomatic phase, lymph node with progression to terminal illness.
biopsy reveals follicular hyperplasia with or without Prognosis is determined by other FIV-associated disor-
follicular involution, follicular plasmacytosis, and vari- ders.
able erythrophagocytosis by macrophages. These
changes are not specific for FIV infection. Lymph node
histology progresses from follicular hyperplasia, PARASITIC, IMMUNOLOGIC AND
through mixed hyperplasia/involution, to follicular MISCELLANEOUS SKIN DISORDERS**
involution, corresponding to generalized lymphadeno-
pathy, AIDS-related complex and terminal AIDS. Classical signs
Neutropenia and lymphopenia are common hemato- ● Skin lesions typical of the primary disease
logic abnormalities in symptomatic cats. (e.g. miliary dermatitis).
● ± Mild to marked lymphadenopathy.
Lymphoma, metastatic lymphadenopathy, atypical See The Cat With Miliary Dermatitis (page 1022), The
hyperplasia and possibly hyperplasia from other Cat With Skin Lumps and Bumps (page 1067) and The
causes may be distinguished from FIV-induced hyper- Cat With Non-healing Wounds (page 1081).
plasia by lymph node histology.
Lymphoma may be present at other sites – e.g. bone Clinical signs
marrow, liver or spleen.
Mild to marked lymphadenopathy may be present
A primary tumor should be identifiable with metas- with disorders of the skin and subcutis, especially
tastic lymphadenopathy. chronic ones, but it is not the salient feature.
Signs of infections, skin diseases or immune-mediated Mandibular lymphadenopathy may be present with
disorders should be present if lymphadenopathy is due acne, mosquito bite hypersensitivity, notoedric mange,
poxvirus infection, discoid lupus erythematosus and Abscesses may spontaneously rupture, at which time
auricular chondritis. systemic signs usually improve.
Regional and generalized lymphadenopathy may be Mild local non-painful lymphadenopathy may occur.
present with flea allergy dermatitis, eosinophilic granu-
loma complex, food hypersensitivity, neoplasia (includ-
Diagnosis
ing cutaneous lymphoma), dermatophytosis, demodicosis,
pemphigus complex, panniculitis, vasculitis, systemic Diagnosis is based on physical examination findings.
lupus erythematosus, drug eruption, erythema multi-
Culture is not routinely performed, but numerous com-
forme/toxic epidermal necrolysis, mechanobullous skin
mon organisms have been isolated.
disease and steatitis.
Lymph node biopsy is rarely warranted but reveals
hyperplasia.
Diagnosis
Wound and lymph node should be examined cytologi-
Work-up of the primary disease will usually identify
cally and cultured if there is painful local lymph-
the reason for the lymphadenopathy. Skin biopsy is
adenopathy.
often required for a definitive diagnosis.
Lymph node biopsy will reveal hyperplasia with or
without metastasis with neoplastic disorders.
Foreign body cellulitis and abscessation.
Differential diagnosis Lymph node abscessation due to juvenile streptococco-
sis or bubonic plague.
Chronic bacterial and other fungal infections.
Differentiation is on the basis of biopsy and culture. Infection with atypical organism that may progress to a
chronic condition.
Treatment Differentiation is on the basis of clinical progression,
cytology and culture.
Treat the primary disease.
Treatment
ACUTE CAT BITE WOUND
Treat the primary disease. See The Pyrexic Cat (page 369).
CELLULITIS/ABSCESS**
Classical signs
DIMORPHIC FUNGAL INFECTIONS**
● Acute onset fever, lethargy, inappetence.
● Puncture wounds or abscess(es) from bite. Classical signs
● ± Mild local lymphadenopathy.
● Fever, weight loss, inappetence and
localizing signs of infection.
See main reference on page 368 (The Pyrexic Cat).
See main references on page 25 for details of cryptococ-
cosis (The Cat With Signs of Chronic Nasal Disease),
Clinical signs
page 1095 for sporothricosis (The Cat With Non-Healing
Acute-onset fever, lethargy and inappetence. Wounds), and page 62 for histoplasmosis and blastomy-
cosis (The Cat With Dyspnea or Tachypnea).
The wound area is usually swollen and/or painful;
bites to limbs cause acute lameness.
Clinical signs
Gentle passage of a finger back and forth through the
fur over a painful area will reveal puncture wounds. Non-specific signs are common.
Common localizing signs of infection include: ● Histoplasma capsulatum appears as numerous

● Respiratory signs, including nasal discharge small round yeasts with a dark center and surround-
(cryptococcosis), and dyspnea due to fungal pneu- ing halo inside macrophages.
monia; hilar lymphadenitis. More than 50% of cats
Serology is useful for identifying cryptococcosis, coc-
with histoplasmosis are dyspneic.
cidioidomycosis, blastomycosis and sporotrichosis.
● Lameness from bone or joint infection, especially
with coccidioidomycosis. Organisms can be cultured, but this requires special
● Skin lesions: nodules, ulcers and abscesses that media and biohazard containment.
have not resolved with typical wound treatment, i.e.
drainage, irrigation and antibiotic therapy. Skin
lesions are the salient feature of sporotrichosis.
● Neurologic signs, including seizures. Differential diagnosis
● Ocular signs, including uveitis and chorioretinitis.
Neoplasia – signs of neoplasia and systemic mycoses
Solitary, regional, generalized peripheral and inter- are similar because both are due to invasion and prolif-
nal lymphadenopathy may be present. Peripheral eration of eukaryotic cells.
lymphadenopathy is common with sporotrichosis.
Tuberculosis, nocardiosis and other chronic bacterial
infections.
Diagnosis
Differentiation is based on cytology, histology and
Exposure history is important for diagnosis. Endemic culture.
areas include: eastern North America (blastomycosis);
southwest North America, northern and south central
South America (coccidioidomycosis). Others are
Treatment
world-wide.
Itraconazole 5 mg/kg q 12 h for weeks to months is
Blastomycosis is uncommon in cats compared to dogs.
effective against most dimorphic fungi. Treat a mini-
Lymph node biopsy reveals hyperplasia or less com- mum of 30 days beyond clinical resolution. Amphotericin
monly lymphadenitis. B and liposomal-encapsulated amphotericin B are
alternate treatments. Ketoconazole may be substituted
Definitive diagnosis is by identification of the organ-
for itraconazole in some cases to reduce cost of therapy,
isms in biopsy specimens of affected tissues by cytol-
but is often less effective.
ogy or histology. Cytologically:
● Cryptococcus neoformans appears as large, encap- Fluconazole is the drug of choice for central nervous
sulated, narrow-based budding yeasts. With the system infections.
capsule most organisms are the same size or larger
Iodides are the older standard treatments for sporotri-
than surrounding inflammatory and epithelial cells.
chosis. Supersaturated solution of potassium iodide or
India ink stain helps identify the capsule.
20% sodium iodide may be used at a dose of 20 mg/kg
● Sporothrix schenkii appears as a cigar-shaped
PO once or twice daily, with food.
yeast inside macrophages.
● Blastomyces dermatitidis appears as broad-based Zoonotic potential:
budding yeasts, slightly larger than surrounding ● Sporothrix schenkii is highly contagious from
neutrophils. With new methylene blue stain the lesions.
organism has an obvious double wall and green ● Coccidioides immitis may revert from tissue yeast
tinge. phase to mycelial phase on bandage surfaces and
● Coccidioides immitis appears as solitary large non- release highly contagious arthrospores. Avoid
budding yeasts three times the size of surrounding bandaging wounds or change dressings fre-
neutrophils, but it is present in low numbers and quently.
hard to find. Other dimorphic fungi are not contagious.
NODAL LYMPHOMA* Clinical signs

Solitary, regional (especially mandibular or cervical)
Classical signs or generalized, moderate to marked painless periph-
● Painless lymphadenopathy. eral lymphadenopathy.
● Non-Hodgkin’s lymphoma may occur at any age.
The average age for cats with multicentric lym-
phoma is 4 years.
● Most cats with Hodgkin’s-like lymphoma are > 6
Pathogenesis
years of age (range 1–14 years).
Based on the histological classification in humans,
lymphoma in cats may be classified as non-Hodgkin’s Cats may not have other historical signs, or may have
lymphoma and Hodgkin’s-like lymphoma. The latter lethargy, inappetence and weight loss.
has been recently recognized. Hepatosplenomegaly may be present.
● Non-Hodgkin’s lymphoma includes the most
commonly recognized forms of lymphoma in cats, Mediastinal lymphoma and alimentary lymphoma are
including mediastinal, alimentary, multicentric, not typically associated with peripheral lymphadenopa-
other extra-nodal lymphomas and lymphocytic thy, although nodal involvement occasionally occurs.
leukemia.
● Primary multicentric nodal lymphoma (initial site Diagnosis
of disease is a lymph node) causes generalized
peripheral lymphadenopathy from malignant lym- Diagnosis requires finding lymph node cytology con-
phoid cell proliferation. sistent with lymphoma, and biopsy-confirmed
● The disease may metastasize to the bone marrow
lymphoma (cytology or histology) at another site, e.g.
(leukemic lymphoma) and liver and spleen. bone marrow, liver, spleen.
● Primary lymphocytic leukemia (initial site of dis- If lymphoma cannot be confirmed at another site, exci-
ease is the bone marrow) may metastasize to sional lymph node biopsy and histology are manda-
peripheral nodes and cause lymphadenopathy. tory to distinguish from atypical hyperplasia and to
● Non-Hodgkin’s nodal lymphoma less commonly characterize the lymphoma.
involves solitary or regional nodes, and occasion-
ally solitary to generalized nodal involvement FeLV and FIV tests should be obtained.
accompanies other forms (e.g. mediastinal lym-
phoma). Differential diagnosis
● Historically, multicentric nodal lymphoma and
lymphocytic leukemia in most cats has been associ- Differential diagnoses for generalized lymph-
ated with FeLV infection. However, as the preva- adenopathy include atypical hyperplasia, hyperplasia
lence of FeLV declines in some regions, the in response to generalized skin diseases, immunologic
incidence of FeLV-negative nodal lymphoma is disorders and systemic infections, widely metastatic
increasing. neoplasia, and generalized bacterial or fungal lym-
● FIV infection increases the risk of non-Hodgkin’s
phadenitis.
lymphoma. Differential diagnoses for solitary or regional lymph-
Hogkin’s-like lymphoma histologically resembles adenopathy include plexiform vascularization of
“lymphocyte-predominance Hodgkin’s disease” in lymph nodes, atypical hyperplasia, hyperplasia in
humans. response to local tumors, oral cavity and skin diseases,
● Most cases involve a solitary mandibular or cer-
and infections, metastatic lymphadenopathy, and bacte-
vical node. Solitary inguinal, regional cervical and rial or fungal lymphadenitis.
generalized lymphadenopathy have also been rec- These are distinguished on the basis of lymph node
ognized. cytology, histology and culture and work-up for an
● Most cats tested are FeLV and FIV negative. underlying disease.
Treatment where the majority of cats were FeLV-negative,

rate of remission was 86% and 1-year survival
Multicentric lymphoma should be treated with was 57%.
chemotherapy as described in Chapter 31. ● For solitary or regional nodal lymphoma: rate
Some cats with solitary nodal lymphomas have been of complete remission is > 80%, 1-year survival is
cured by surgical excision alone. 35%, and 2 and 3 year survival is 20–30%.
● Because of the tendency for lymphoma to be a sys- ● For primary lymphocytic leukemia: rate of com-
temic disease, chemotherapy is usually recom- plete remission is 25%, 1-year survival is 10%, and
mended following excision. 2 and 3 year survival 5%. Cats with acute pancy-
● If work-up fails to identify lymphoma at another topenia have a worse prognosis.
site, then surgery (or radiation therapy) without It appears that many cats with solitary Hodgkin’s-like
subsequent chemotherapy may be considered, espe- lymphoma may be cured with surgical excision alone.
cially for Hodgkin’s-like lymphoma.
Prognosis PLAGUE*
Reported response rates to therapy provide general
information, but it is difficult to give a prognosis for an Classical signs
individual cat. ● Acute high fever.
Providing a prognosis is even more difficult for a cat ● Cranial body regional lymphadenopathy.
with multicentric nodal lymphoma.
● In some studies “multicentric” included extra-nodal See main reference page 383 (The Pyrexic Cat).
lymphomas involving multiple sites.
● Some cats with only peripheral lymph node disease
and long-term remissions may have had atypical Pathogenesis
hyperplasia or Hodgkin’s-like lymphoma. Infection with Yersinia pestis. Cats are uniquely sensi-
Providing a prognosis for leukemic cats may be com- tive among carnivores.
plicated by difficulty in distinguishing nodal leukemic Most cats appear to be infected by ingestion of an
lymphoma and primary leukemia, which carries a infected rodent. The organism spreads rapidly to the
worse prognosis. regional nodes (mandibular and cervical nodes). Cats
The best predictor of response is response itself, i.e. may also be infected by a bite from an infected flea,
the longer a cat is in remission, the more likely it is where the organism spreads rapidly to the local lymph
to remain in remission. node.
● The organism replicates in the local/regional
FeLV and FIV status does not affect initial response to nodes and from there may progress to other nodes,
therapy. It does negatively affect long-term survival, bacteremia and pneumonia.
mostly because of the occurrence of other FeLV- and
FIV-related disorders.
Clinical signs
Cats with a small tumor burden have a better prognosis.
Signs appear within 1–7 days of infection.
With these caveats, using combination chemotherapy
protocols for the treatment of non-Hodgkin’s nodal High fever (> 40˚C), lethargy, inappetence, dehydra-
lymphoma: tion.
● For multicentric nodal lymphoma: rate of com-
Minimal reaction at site of innoculation.
plete remission is 60–80%, 1-year survival is
10%, and 2 and 3 year survival 5%. These figures Bubonic plague is characterized by marked solitary or
are based on older studies where the majority of regional painful mandibular, retropharyngeal and cer-
cats were FeLV positive. In a more recent study vical lymphadenopathy due to severe lymphadenitis.
The lymphadenitis is characterized by hemorrhage, abscesses have been reported in plague, with lymph-
necrosis and perinodal edema, and later by lymph node adenopathy due to hyperplasia.
abscessation. Abscesses may rupture and drain thick, ● Pasteurella multocida, a frequent organism found
creamy pus. The severely swollen, inflamed nodes are in bite wounds, resembles Y. pestis cytologically.
referred to as “bubos”. However, bite wounds usually contain a mixed
● This distribution of lymphadenopathy results from bacterial population while bubos usually contain a
oral exposure during hunting. monomorphic population of bacteria.
● Flea bites may occur elsewhere resulting in a dif-
Anthrax.
ferent distribution, e.g. solitary inguinal bubo for-
● Rare.
mation.
● Lymph node abscessation probably does not occur
Other possible signs include oral ulcers, tonsillar as with plague.
enlargement, ocular and nasal discharges and ● Lingual, pharyngeal and cervical edema may be
abdominal distention. Cats may initially present with more pronounced than with plague.
less severe signs.
Tularemia.
Septicemic plague, characterized by fever and septic ● A papule may be present at the site of innoculation.
shock may occur with or without bubo formation. ● Lymphadenopathy is not as prominent, and absces-
sation does not occur.
Pneumonic plague in cats, characterized by fever,
dyspnea, oral or nasal discharges, and coughing or Other causes of bacterial lymphadenitis.
sneezing occurs occasionally and is usually a sequel to ● Unlike most other causes of bacterial lymph-
bubonic or septicemic plague. adenitis, there is usually minimal reaction at the site
of innoculation with plague organisms.
● Culture of organism is required to definitively dif-
Diagnosis ferentiate.
History of exposure to infected rodents. Acute infection with FeLV or FIV and regional lymph-
adenopathy.
Cytology of lymph node biopsy/exudate reveals neutro-
● Retroviral infections have clinically a more sub-
phils and a monomorphic population of Gram-
acute to chronic course.
negative, bipolar staining, coccobacilli.
● Lymph node biopsy with retroviral infections will
FA test of air-dried smears of tissues or exudate. reveal hyperplasia.
Culture of organism from lymph nodes or other
affected tissues (e.g. tonsils). Treatment
Acute (as early as possible once illness is detected) and Treat early on the basis of tentative diagnosis.
convalescent (14 days later) antibody titers demon-
Antibiotics (optimal treatment is not known).
strating a four-fold rise in titer are diagnostic for
● Recommended antibiotics include tetracycline,
plague. Titers are useful to confirm a zoonotic disease
doxycycline, chloramphenicol, trimethoprim-
when treatment is based on a tentative diagnosis.
sulfonamide, streptomycin, gentamicin, and
All plague suspects should have thoracic radiographs kanamycin at standard recommended doses.
taken to rule-out pneumonia. Fluoroquiniolones have been effective experimen-
tally.
● Recommended duration of therapy is 10–21 days.
Differential diagnosis ● Use parenteral treatment initially to minimize
contact of nursing personnel with oral cavity. Use
Cat bite abscess.
follow-up treatment with oral antibiotics to mini-
● Most cat bite wounds result in cellulitis and
mize hospitalization and aminoglycoside toxicoses.
subcutaneous abscessation rather than lymph
node abscessation. However, subcutaneous/muscle Treat animal and environment for fleas.
Strict isolation and barrier nursing procedures must

ORAL CAVITY DISEASES*
be followed.
● Treat in an isolation area using isolation gowns,
Classical signs
high-density filter masks and gloves.
● Clean and decontaminate all surfaces with usual ● Oral lesions typical of the primary disease.
hospital disinfectants. ● ± Mild to moderate mandibular
● Lance and irrigate abscessed lymph nodes. lymphadenopathy.
● Place all contaminated material in double-layer bio-
hazard bags and incinerate. See The Cat With Bad Breath or Oral Lesions. (page 602)
Notify public health officials; veterinary personnel
Clinical signs
should contact a physician.
Mild to moderate mandibular lymphadenopathy
may be present with lymphocytic-plasmacytic stomati-
tis/gingivitis, periodontal disease, and oral neoplasia,
Prognosis
but it is not the salient feature of the disorders.
Mortality of plague is 50% in untreated cats.
Diagnosis
There are a number of reports of successful treatment
of cats with bubonic plague. Work-up of the primary disease will usually identify
the reason for the lymphadenopathy. Biopsy of lesions
Cats with septicemic and pneumonic plague have the
may be necessary.
worst prognosis.
Lymph node biopsy is recommended if lym-
phadenopathy is present, and bilateral lymph node
biopsy should always be performed in the staging of
Transmission
oral cancer.
Cats become infected by ingesting, or being bitten by
Biopsy reveals hyperplasia with or without metastasis
fleas from infected rodents or other wild animals.
with neoplastic disorders.
The disease is highly zoonotic.
● Humans may be infected by flea-bites and con- Differential diagnosis
tact with infected animals or their tissues.
Differential diagnoses for mandibular lymphadenopathy
● There is a high risk for developing primary pneu-
include hyperplasia due to regional skin disorders,
monic plague following inhalation of Y. pestis-
FeLV/FIV infection, lymphoma, metastatic lymph-
infected droplets expelled from cats with secondary
adenopathy and atypical hyperplasia.
pneumonic plague.
Treatment
Treat the primary disease.
Prevention
Minimize cat contact with rodents and fleas in endemic CUTANEOUS/SUBCUTANEOUS FOREIGN
areas. BODY REACTION*
● Eliminate rodents indoors; control rodent habitats
near domestic dwellings (e.g. garbage piles). Classical signs
● Keep cats indoors; neuter outdoor cats to reduce
roaming and hunting. ● Lymphadenopathy in local node draining
● Flea control. from foreign body region.
Use post-exposure prophylaxis for other cats: tetracy- See main reference on page 1073 (The Cat With Skin
cline or doxycycline at standard doses for 7 days. Lumps and Bumps.
Clinical signs be subclinical or cause chronic weight loss, vomit-

ing, diarrhea and mesenteric lymphadenopathy.
Signs of aseptic or septic inflammation are present at ● The infection occasionally disseminates to virtu-
the foreign body site (cutaneous, subcutaneous or ally all organs with corresponding systemic and
deeper) and local lymphadenopathy may or may not be local signs.
present. ● Peripheral lymphadenopathy occurs with dis-
seminated disease.
Diagnosis Leprosy is caused by M. lepraemurium and is charac-
Exploration of area reveals foreign body. terized by chronic single to multiple, freely moveable,
non-painful intact or ulcerated and abscessed fleshy
Lymph node biopsy reveals hyperplasia or uncom- cutaneous nodules, with or without subcutaneous
monly lymphadenitis. lesions. Systemic signs are rare.
● Painless regional lymphadenopathy is typical.
Differential diagnoses Atypical mycobacteriosis is caused by several non-

Bite wound cellulitis, chronic bacterial and fungal infec- tubercular, non-lepromatous Mycobacterium sp., and is
tions, neoplasia and eosinophilic granuloma complex. usually characterized by chronic, local or regional
subcutaneous lesions with multiple draining tracts.
Differentiation is based on cytology, histology and culture. Lesions are most often found on the caudal abdomen,
inguinal region or lumbar region, but also on the thorax.
Treatment Systemic signs are uncommon but may occur.
● Disseminated infection (systemic non-tuberculous
See The Cat With Skin Lumps and Bumps (page 1074). mycobacteriosis), which is clinically similar to
tuberculosis, is most likely with organisms from
MYCOBACTERIAL INFECTIONS* the M. avium complex,
● Local, regional or generalized lymphadenopathy
Classical signs may occur.
● Chronic vomiting, diarrhea, mesenteric

lymphadenopathy (tuberculosis).
Diagnosis
● Multiple chronic ulcerated fleshy
cutaneous nodules on head and limbs Cytology and histology of affected tissues reveal
(leprosy) and regional lymphadenopathy. granulomatous to pyogranulomatous inflammation.
● Chronic ulcerated subcutaneous lesions on
Lymph node biopsy reveals hyperplasia (all clinical
caudal abdomen, inguinal and groin
forms) or granulomatous lymphadenitis (tuberculosis,
regions (atypical mycobacteriosis) ± local
systemic non-tuberculous mycobacteriosis).
or regional lymphadenopathy.
Acid-fast bacteria are usually detectable in affected
See main reference, page 1085 (The Cat With Non- tissues with tuberculosis and leprosy, but may be diffi-
Healing Wounds). cult to find with atypical mycobacteriosis.
Culture is possible at selected laboratories, and
Clinical signs particularly useful for identifying fast-growing
mycobacteria, the most common causes of atypical
There are three categories of Mycobacterium sp. infec-
mycobacteriosis.
tion in cats: tuberculosis, leprosy and atypical.
Tuberculin testing is not reliable in cats.
Tuberculosis is caused by M. tuberculosis, M. bovis,
M. tuberculosis-bovis variant, and M. microti. It may Immunoassays may be available for some organisms.
Differential diagnosis These organisms typically produce chronic ulcerating

lesions or masses (abscesses and mycetomas) that are
Differential diagnoses for disseminated mycobacter- cutaneous or subcutaneous. The lesions have usually
ial infections include multicentric lymphoma, widely developed at sites of penetrating wounds and have not
metastatic tumors, other pyogranulomatous bacterial resolved with typical wound treatment. Localized
infections and systemic fungal infections. infections in other organs and disseminated infections
Differential diagnoses for leprosy include neoplasia, may also occur. Accompanying signs vary with organ
eosinophilic granuloma complex, other chronic bacter- involvement.
ial infections and fungal infections. Local, regional, generalized peripheral and internal
Differential diagnoses for local or regional atypical lymphadenopathy may occur.
mycobacteriosis include neoplasia, foreign body reac- Systemic signs may be absent or mild with local cuta-
tion, eosinophilic granuloma complex, panniculitis, neous and subcutaneous infections. Mild to severe
pansteatitis, other chronic bacterial infections and fun- signs occur with internal or disseminated infections.
gal infections.
Differentiation is based on cytology, histology and culture.
Diagnosis
Treatment Pyogranulomatous-granulomatous inflammation is
evident on cytology and histology of exudates and
Tuberculosis. biopsy specimens.
● Notify public health officials. Euthanasia is often
advised because of the zoonotic risk. If treatment is Cytology may reveal Gram-positive bacteria in
attempted, drug doses are provided in the reference macrophages (Rhodococcus equi), mats of Gram-positive
at the end of the chapter. filamentous organisms (Actinomyces sp.), Gram-
positive, weakly acid-fast beaded filamentous organ-
Treatment of leprosy and atypical mycobacteriosis are isms (Nocardia sp.), or Gram-positive branching
discussed in The Cat With Non-Healing Wounds filamentous organisms with transverse longitudinal
(page 1086). divisions resulting in paired rows of coccoid spores
(Dermatophilus congolensis).
Lymph node biopsy reveals hyperplasia or lymph-
(PYO)GRANULOMATOUS BACTERIAL adenitis.
INFECTIONS* Definitive diagnosis is by culture of the organism
from lesions.
Classical signs
There may be a history of exposure to horses with
● Chronic ulcerating rhodococcosis.
cutaneous/subcutaneous lesions.
● ± Local, regional or generalized
lymphadenopathy. Differential diagnosis
Eosinophilic granuloma complex, mycobacterial infec-
See main reference, page 1086 (The Cat With Non-
tions, fungal infections, neoplasia, panniculitis and
Healing Wounds).
steatitis.
Differentiation is based on cytology, histology and culture.
Clinical signs
Chronic ulcerating lesions occur with a number of Treatment
bacteria, including Rhodococcus equi, Actinomyces sp.,
Treat the primary disease. See page 1087 (The Cat With
Nocardia sp., and Dermatophilus congolensis.
Non-Healing Wounds).
METASTATIC NEOPLASTIC Treatment

LYMPHADENOPATHY: MAST CELL TUMOR* See page 1075 (The Cat With Skin Lumps and Bumps).
Classical signs
● Firm cutaneous nodule (cutaneous form). METASTATIC NEOPLASTIC
● Marked splenomegaly (lymphoreticular LYMPHADENOPATHY: OTHER TUMORS*
form).
Classical signs
See main reference, page 1074 (The Cat With Skin
Lumps and Bumps).
● Signs of primary tumor.
lymphadenopathy.
Clinical signs
See main reference, page 1067 (The Cat With Skin
Most primary cutaneous mast cell tumors present as Lumps and Bumps).
single, or less commonly, multiple dermal nodules
without other clinical signs.
● Histologically they may be classified as compact Clinical signs
mastocytic, diffuse mastocytic and histiocytic. The
average age of cats with mastocytic tumors is 10 The cat is usually presented for signs of the primary
years, while the average age with histiocytic tumor.
tumors is 2.4 years. Occasionally the cat is presented because of local,
Cutaneous mast cell tumors may infrequently metas- regional or rarely generalized lymphadenopathy.
tasize to local, regional and distant peripheral lymph Most metastatic neoplasia occurs in older cats.
nodes causing lymphadenopathy. This is most likely
with diffuse mastocytic tumors and tumors with
> four mitoses/ten high-power fields. Diagnosis
Cutaneous and lymphoreticular (splenic) mast cell Lymph node biopsy reveals hyperplasia and infiltration
tumors may occur together with variable involvement by carcinoma, uncommonly sarcoma, and rarely non-
of internal and peripheral lymph nodes. The average lymphoid, non-mast cell round cell tumors.
age of cats with lymphoreticular tumors is 10 years. ● Carcinomas include squamous cell carcinoma,
bronchogenic carcinoma, mammary carcinoma and
Diagnosis others.
● Sarcomas include fibrosarcoma, osteosarcoma and
Biopsy of the cutaneous mass and/or spleen reveals others.
numerous normal or atypical mast cells. ● Round cell tumors include plasma cell tumors,
Lymph node biopsy reveals hyperplasia and increased myeloid leukemia, malignant histiocytosis and
numbers of mast cells. melanoma.
If the cat is presented for lymphadenopathy, reviewing
the history and physical examination, and performing
routine laboratory evaluation, and thoracic and
Other neoplasia, eosinophilic granuloma complex, abdominal radiographs and ultrasound examina-
chronic bacterial infections, fungal infections, and pro- tions, will help identify and stage the primary
tothecosis. tumor.
Differentiation is based on cytology, histology and Normal and enlarged regional lymph nodes should be
culture. biopsied as part of clinical staging of the cat with cancer.
Differential diagnosis Lymph node cytology reveals hyperplasia; histology

reveals multifocal necrosis.
For a cat presented for lymphadenopathy, differential
diagnoses include lymphoma and most chronic causes The organism, a small Gram-negative coccobacilli, is
of hyperplasia. difficult to see on routine cytology and Gram-stain.
● FA test of air-dried smears of tissues or exudate
Differentiation is based on cytology, histology and helps identify the organism.
culture.
The organism may be cultured from an aspirate of
lymph node, bone marrow (not blood), or other tissue.
Treatment ● Not all laboratories will attempt culture and special
See page 1067 (The Cat With Skin Lumps and Bumps). media is required – check before submitting.
A single titer ~ 1:80 gives a presumptive diagnosis,
TULAREMIA* while acute (as early as possible once illness is
detected) and convalescent (14 days later) antibody
Classical signs titers demonstrating a four-fold rise give a confirma-
tory diagnosis. Titers are useful to confirm a zoonotic
● Acute high fever. disease when treatment is based on a tentative diag-
● Peripheral and internal lymphadenopathy nosis.
See main reference, page 382 (The Pyrexic Cat).

Clinical signs Other acute viral, bacterial, fungal and parasitic (e.g.
Signs appear within 2–7 days of infection with toxoplasmosis) infectious processes.
Francisella tularensis subsp. tularensis or palaearctica. ● These are distinguished on the basis of exposure
risk, serologic testing and organism identification.
High fever (> 40˚C), lethargy, inappetence, dehydration. ● Acute Gram-negative bacteremia, e.g. secondary to
Moderate to marked painful lymphadenopathy due myelosuppression, is not usually associated with
to lymphadenitis is common; site of infection affects lymphadenopathy.
distribution:
● Cats exposed by mouthing or ingesting a rabbit
Treatment
or rabbit tick will have initial mandibular, cervical
or mesenteric lymphadenopathy. Treat early on the basis of tentative diagnosis.
● Cats exposed by a mosquito, tick bite or innocu-
Antibiotics (optimal treatment is not known).
lation will have initial lymphadenopathy in the ● Recommended antibiotics include tetracycline,
node draining the region. doxycycline, chloramphenicol, streptomycin and
Other variable signs include multifocal white oral ulcers, gentamicin at standard recommended doses.
abdominal pain, hepatosplenomegaly, vomiting and diar- Fluoroquinolones have been effective experimen-
rhea. tally.
● Localized tularemia causing a chronically draining ● Recommended duration of therapy is 7–14 days.
subcutaneous mass has also been reported. ● Use parenteral treatment initially to minimize
contact of nursing personnel with oral cavity. Use
Diagnosis follow-up treatment with oral antibiotics to min-
imize hospitalization and aminoglycoside toxi-
History of exposure to wild rabbits (North America, coses.
F. tularensis tularensis).
Treat animal for ticks.
History of exposure to infected rodents, ticks and mos-
quitoes, or contaminated soil and water (Northern Highly zoonotic from tissues and ticks – strict isolation
hemisphere, F. tularensis palaearctica). and barrier nursing procedures must be followed.
● Treat in an isolation area using isolation gowns, Diagnosis

high-density filter masks and gloves.
● Clean and decontaminate all surfaces with usual Lymph node biopsy reveals hyperplasia or lymph-
hospital disinfectants. adenitis.
● Place all contaminated material in double-layer bio- Culture of bacteria from lymph node or other lesions.
hazard bags and incinerate. Bacteria include Pseudomonas mallei (glanders),
Notify public health officials; veterinary personnel Burkholderia pseudomallei (meliodosis), Yersinia ente-
should contact a physician. rocolitica, Yersinia pseudotuberculosis, Serratia
marscecens, Listeria monocytogenes, and Chriseomonas
luteola.
OBSTRUCTIVE EDEMA*
With glanders there is a history of exposure to diseased
Classical signs horses or other solipeds, or contaminated meat, and
there may be respiratory tract nodules similar to tuber-
● Localized edema. culosis.
● ± Local or regional lymphadenopathy.
Clinical signs MISCELLANEOUS FUNGAL INFECTIONS*

Lymphatic obstruction due to a tumor or other
mass causes edema (e.g. head and neck, limb). Classical signs
Local or regional nodes may be enlarged.

● Chronic ulcerating
cutaneous/subcutaneous lesions.
Diagnosis lymphadenopathy.
Biopsy of the primary lesion.
Lymph node biopsy reveals edema with or without Clinical signs
hyperplasia, metastasis or infection. Chronic ulcerating lesions or masses that are cuta-
neous or subcutaneous. Usually they have developed at
sites of penetrating wounds and have not resolved with
MISCELLANEOUS BACTERIAL typical wound treatment.
INFECTIONS* Infections of mucosal surfaces, localized infections in
other organs and disseminated infections may also
Classical signs occur with accompanying signs varying with organ
● Localizing signs of inflammation. involvement. Internal infections are more common with
● Local, regional or generalized certain organisms.
lymphadenopathy. Local, regional or generalized lymphadenopathy
may occur.
Systemic signs may be absent or mild with local cuta-
Clinical signs
neous and subcutaneous infections, and mild to severe
Solitary to generalized lymphadenopathy. with internal or disseminated infections.
Oral or skin wounds may be present indicating the site
of entry. Infection may also be via the intestinal tract Diagnosis
and cause mesenteric lymphadenopathy.
Culture of the organism and histologic demonstration
Systemic signs are usually present, and more severe of tissue invasion in biopsy specimens. Organisms
with more generalized infections. include Pythium insidiosum (oomycete), Trichosporon
sp. (yeastlike fungus), Candida sp. (dimorphic fungus), Pathogenesis

dermatophytes (pseudomycetoma) and numerous
hyphae-producing organisms. The latter infections are Two forms have been described.
● In cats ~ 2 years of age, lymphadenopathy was due
termed zygomycosis, hyalohyphomycosis and phaehypho-
mycosis based on characteristics of fungal hyphae, and to a distinctive hyperplasia resembling that seen
eumycotic mycetoma if pyogranulomatous nodules in experimental FeLV infection.
containing tissue grains are formed. – Some cats were FeLV positive.
– It was postulated that lymphadenopathy was due
Lymph node biopsy reveals hyperplasia or lymph- to FeLV infection.
adenitis. ● In cats ~ 4 years of age, marked lymphadenopathy
Rule out immunosuppression (diabetes mellitus, was due to hyperplasia resembling lymphoma.
hyperadrenocorticism, lymphoma, FeLV/FIV infection, – Tested cats were FeLV negative.
immunosuppressive therapy) and neutropenia, espe- – Cats were recovering from urinary tract, upper
cially if internal or disseminated mycosis is present. respiratory, and FeLV infections.
– It was postulated that lymphadenopathy was due
to an immune response to infection.
STEATITIS ● A follow-up report used silver staining to identify
tiny bacteria in the nodes of some cats from both
Classical signs studies. These bacteria may have been Bartonella
● Depression, anorexia, reluctance to move henselae, the causative agent of cat-scratch disease
and pain on landing. in humans. Cats harboring B. henselae are usually
● ± Lymphadenopathy. young and recent studies show that Bartonella
henselae may induce lymph node hyperplasia in
cats.
Clinical signs – Could the acute phase of FIV infection have
Depression, anorexia, reluctance to move because of been responsible for some of the cases?
pain, and pain upon handling. – FIV status was not known – reports antidated
routine testing for FIV infection.
Firm and lumpy subcutaneous fat with or without – A recent study shows that co-infection with
accompanying lymphadenopathy. Bartonella henselae and FIV increases the risk
Other clinical signs include fever and abdominal dis- for lymphadenopathy.
tention from fluid and firm abdominal fat. – Unusual infections in some of the cases suggest
immunodeficiency.
Diagnosis – However, no cases of atypical hyperplasia have
been reported in FIV-infected cats.
History of a diet high in oxidized unsaturated fats (e.g.
rancid tuna) and/or deficient in vitamin E. Rare in cats
fed commercial foods.
Clinical signs
Biopsy of fat confirms steatitis – the fat may be grossly
yellow to brown. Moderate to marked, regional to generalized non-
painful peripheral lymphadenopathy in a cat ~ 4
Lymph node biopsy reveals hyperplasia. years of age.
● Lymphadenopathy is usually the chief com-
plaint; most cats are otherwise normal.
IDIOPATHIC ATYPICAL HYPERPLASIA
Other signs variably present include lethargy, inap-
Classical signs petence, weight loss, fever, pale mucous mem-
branes, hepatosplenomegaly (first case series) and
● Moderate to marked generalized
signs due to concurrent infections (e.g. sneezing,
lymphadenopathy in young cats.
hematuria).
Diagnosis sound examinations, bone marrow biopsy, lymph

node bacterial/fungal culture, biopsies of other
Lymph node cytology consistent with hyperplasia, abnormal organs (submit for cytology/histology
lymphoma, or suspicious for lymphoma. and culture), tests for Bartonella henselae and
Lymph node histology reveals marked hyperplasia with Ehrlichia sp. infection (see page 417), serologic
disruption of lymph node architecture. tests for fungal agents, and antinuclear antibody
● Characteristic findings in the first case series were and lupus erythematosus cell tests.
paracortical hyperplasia with histiocytes, lympho- – Although FIP may cause mesenteric lymph-
cytes, plasma cells, and immunoblasts, and post- adenopathy, peripheral lymphadenopathy has not
capillary venular proliferation. been reported.
● Characteristic findings in the second case series
were paracortical, follicular or diffuse lymphoid
expansion, but other findings typical of lymphoid Differential diagnosis
malignancy were variably absent. Lymphadenopathy is a problem and not a diagnosis,
Idiopathic lymphadenopathy is not a diagnosis in and as such this discussion of idiopathic generalized
itself. Lymph node hyperplasia is an immune reaction lymphadenopathy is an extension of the Introduction.
to a cause. Atypical hyperplasia represents either an The most common causes of generalized lymph-
unusual cause or an atypical response to a usual cause. adenopathy are generalized skin diseases, FeLV/FIV
Aggressive diagnostic evaluation should be performed infections and lymphoma.
to reveal infection or neoplasia, especially since multi- ● Skin lesions are usually obvious if lymphadenopa-
system immune-mediated diseases such as systemic thy is due to a skin disease.
lupus erythematosus are rare in cats. Work-up ● If a cat is FeLV- and/or FIV-positive, the possibility
includes: of concurrent neoplasia or infection contributing to
● FeLV test.
lymphadenopathy should be considered.
● If an ELISA (enzyme-linked immunosorbent assay)
● Nodal lymphoma is one of the less common
test on blood is negative, and another cause of lymph- forms of lymphoma.
adenopathy has not been found, obtain a FA (fluo- – It may be solitary, regional or generalized, simi-
rescent antibody) or PCR (polymerase chain lar to cats with atypical hyperplasia.
reaction) test on blood. If negative, obtain a FA or – Cats may have no historical signs other than
PCR test on a bone marrow or lymph node aspirate, lymphadenopathy, similar to cats with atypical
or immunohistochemistry test on a bone marrow hyperplasia.
core or lymph node biopsy. It should be noted that – Excisional biopsy is mandatory and communi-
PCR testing has not been standardized and is more cation with the pathologist essential to rule in or
likely to give false-positive results than ELISA and rule out lymphoma.
FA if the laboratory does not maintain the highest – There may be evidence of lymphoma at another
standards of quality control. site, e.g. bone marrow, liver, spleen or the dis-
● FIV test.
ease will progress to involve these sites.
● Search for other infections and neoplasia.
Hepatosplenomegaly was not reported in the
– Detailed review of history of physical examina- case series where lymph node histology resem-
tion for subtle signs, including ophthalmologic bled lymphoma.
examination.
– Further work-up will depend on clinical signs,
exposure risks for infectious agents and financial Treatment
considerations.
Treatment should be supportive if needed pending a
– Diagnostic evaluation may include complete
diagnosis.
blood count, serum chemistry profile, urinalysis,
blood culture, urine culture, abdominal and tho- If the owner refuses a work-up, and the cat is otherwise
racic radiographs, cardiac and abdominal ultra- normal, encourage observation rather than euthanasia.
Pending a diagnosis, or if owner refuses a work-up, if FeLV/FIV status has not been reported in most cases,
the cat is febrile or has localizing signs of infection, but cats have not had signs of such infections.
consider empirical antibiotic treatment. Acceptable
choices include amoxicillin 10–20 mg/kg PO bid,
Clinical signs
amoxicillin-clavulanate 62.5 mg (combined dose) PO
bid, doxycycline 5 mg/kg PO bid, enrofloxacin 5 mg/kg Unilateral cervical, or unilateral and bilateral
PO once daily, orbifloxacin 2.5–7.5 mg/kg once daily, inguinal masses.
and marbofloxacin 2.5–5.0 mg/kg once daily, for
Mass has been painless on palpation in 2/3 of cases.
2 weeks. Cats receiving fluoroquinolones should be
monitored for visual disturbances. No sex predilection; the majority of cases have been
reported in cats 3–8 years of age.
Do not treat for lymphoma unless lymph node his-
tology is unequivocal or there is evidence of lym- Cervical mass may cause dyspnea from tracheal com-
phoma at another site. pression.
● Waiting to treat is probably not harmful.
No other clinical signs.
● An indolent lymphoma is unlikely to respond to
aggressive chemotherapy.
Do not treat with corticosteroids. Diagnosis
● Corticosteroids may allow an infectious process to
Histology of excised lymph node reveals capillary vaso-
worsen that may otherwise resolve spontaneously.
proliferation, lymphoid atrophy and preservation of
● Corticosteroids may induce lymphoma cell resist-
architecture.
ance to other anticancer drugs.

Dependent on cause of lymphadenopathy. Differential diagnoses for superficial masses include
benign and malignant solid tumors of skin, subcuta-
In the two case series, lymphadenopathy resolved
neous tissue, and muscle; epidermal cyst, granuloma,
within 4 months in 60% of cats with follow-up in the
abscess, hematoma, and scar tissue; typical and atypi-
first study, and all cats with follow-up in the second
cal lymph node hyperplasia, lymphoma, metastatic
study.
lymphadenopathy, and lymphadenitis.
Additional diagnoses for cervical masses include
PLEXIFORM VASCULARIZATION OF LYMPH
enlarged thyroid or parathyroid gland, and salivary
NODES
mucocele.
Classical signs Additional diagnoses for inguinal masses include
prominent inguinal fat pads.
● Unilateral cervical mass.
● Unilateral or bilateral inguinal mass(es). Differentiation is based on biopsy for cytology, his-
tology and culture.
Pathogenesis Presence of other clinical signs, laboratory findings,
radiographs and ultrasound examination of the mass
A single case series and individual cases have been
may help narrow the list of differential diagnoses prior
reported.
to biopsy, and in some cases exclude biopsy (e.g.
Pathogenesis is not known. hyperthyroidism).
● An ischemic pathogenesis has been postulated,
but cats have not been evaluated with respect to
Treatment
thromboembolic disease nor have other throm-
boembolic events been identified. Surgical excision of the affected node(s).
Prognosis adenopathy. Unlike in other species, minimal sys-

temic signs have been noted.
Complete resolution reported for all cats.
Local edema for several weeks may occur post- Diagnosis
operatively.
Lymph node biopsy reveals lymphadenitis with or
without abscessation; chains of cocci are seen.
JUVENILE STREPTOCOCCAL
LYMPHADENITIS Biopsy of distant nodes reveals hyperplasia.
Culture of organism from lymph nodes, or skin (fasci-
Classical signs itis) and tonsil (cervical lymphadenitis).
● Kittens.
● Fever. Differential diagnosis
● Cervical lymphadenopathy. In the initial febrile phase, other infections could
mimic juvenile streptococcosis, and lymphadenitis
from other organisms could rarely occur. Acute
Pathogenesis FeLV/FIV infection can also cause fever and lymph-
adenopathy, although cats are not usually as ill and nor
Streptococcus canis (Group G β-hemolytic strepto-
is lymphadenopathy as prominent. Differentiation is on
cocci) may cause a variety of infections in cats including
the basis of lymph node culture and FeLV/FIV tests.
bacteremia, wound sepsis, pyoderma/cellulitis, pyo-
thorax, pneumonia, urogenital infections, arthritis, dis- Differential diagnoses for necrotizing fasciitis include
cospondylitis, acute neonatal death, and fading kittens. eosinophilic granuloma complex, other chronic bacter-
ial (e.g. nocardiosis) and fungal infections, panniculitis
In 3–7-month-old kittens, streptococcal lymphadeni-
and steatitis. Differentiation is based on cytology, his-
tis may occur.
tology and culture.
● The organism colonizes the tonsils (pharyngeal
trauma is not necessary) and then disseminates
along lymphatics to the lymph nodes of the head Treatment
and neck. Reported treatments include procaine penicillin
In mature cats necrotizing fasciitis has been reported. 50 000 IU SC once daily, or procaine and benzathine
The pathogenesis of increased streptococcal virulence penicillin 75 000–100 000 IU (combined dose) q 48–72
is not known. hours, or penicillin V 20 mg/kg PO q 8 h, for 5 days.
Penicillin G, ampicillin, amoxicillin and amocillin-
In dogs, the use of fluoquinolones has been incrimi- clavulanate should also be effective.
nated as a risk factor for streptococcal infections.
Lance and irrigate abscesses.
Clinical signs
Prognosis
Juvenile lymphadenitis is characterized by acute
Prognosis is excellent with early treatment.
fever, lethargy and inappetence.
● Marked unilateral or bilateral cervical lymph- Untreated cases of juvenile lymphadenitis may
adenopathy with or without generalized lymph- progress to pyothorax, pneumonia and acute death,
adenopathy occurs. likely due to streptococcal toxic shock syndrome.
● Single to multiple kittens in a litter may be
affected; they are usually litters from a young Transmission
queen.
Streptococci do not live in the environment; the source
Necrotizing fasciitis in mature cats is characterized by of infection is other cats harboring streptococci in a
multifocal ulcerative purulent skin lesions and lymph- carrier state.
Juvenile streptococcal lymphadenitis is usually a cat- Clinical signs

tery problem, with concurrent neonatal infections.
● Vaginal colonization in young nulliparous
Lymphadenopathy may be present but is not the salient
queens is the main source of neonatal infection; feature of chronic progressive polyarthritis.
older queens eliminate the infection and pass Lymphadenopathy is one of the “minor signs” of sys-
colostral antibodies to their young. temic lupus erythematosis.
● Epidemics may occur following introduction of an
infected queen or tom (preputial colonization) into Lymphadenopathy was present in a series of cats with
a naïve cattery. progressive lymphocytic cholangitis.
Transmission with juvenile lymphadenitis is presum-

ably from oral to oral contact (e.g. grooming) with Diagnosis
carrier cats with pharyngeal/tonsillar colonization. ● Work-up of the primary disease.
● Lymph node biopsy reveals hyperplasia.
Prevention
The carrier state cannot be eliminated by antibiotic HYPEREOSINOPHILIC SYNDROME
therapy. While short-term penicillin treatment of
queens at parturition will reduce neonatal mortality, Classical signs
chronic treatment in a cattery as prophylaxis against
juvenile infections is not recommended as this will pro-
● Lethargy, inappetence, weight loss,
mote resistant organisms. As herd immunity increases, vomiting, diarrhea.
epidemics will resolve.
See main reference page 758.
POST-VACCINAL LYMPHADENOPATHY
Clinical signs
Classical signs Most cats are presented for chronic lethargy, inappe-
● Mild incidental lymphadenopathy. tence, weight loss, vomiting and diarrhea.
● History of recent vaccination. Other clinical signs include fever, pruritus and seizures.
Clinical signs Abdominal palpation may reveal thickened intestines,

mesenteric lymphadenopathy and hepatosplenomegaly.
Mild generalized lymphadenopathy or local lymph-
adenopathy draining the vaccination site may be noted Peripheral lymphadenopathy is present infre-
for several weeks post-vaccination. quently.
Diagnosis Diagnosis
History of vaccination and no other clinical signs. Marked mature eosinophilia, increased synchronous
Lymph node biopsy reveals hyperplasia. eosinopoiesis on bone marrow biopsy, and exclusion of
other causes of eosinophilia.
Lymph node biopsy reveals hyperplasia with or without
NON-CUTANEOUS IMMUNOLOGIC/ eosinophilic infiltration.
INFLAMMATORY DISORDERS
Classical signs BACTEREMIA

● Signs of polyarthritis.
Classical signs
● Signs of systemic lupus erthematosus.
● Signs of lymphocytic cholangitis. ● Fever, lethargy, inappetence.
Clinical signs EHRLICHIOSIS

Lymphadenopathy is not usually present in acute
bacteremia or endotoxemia due to conventional Classical signs
Gram-negative (e.g. Escherichia coli), Gram-positive ● Lethargy, inappetence, weight loss.
(e.g. Staphylococcus sp.) and anaerobic (e.g. Clostridium ● ± Lymphadenopathy.
perfringens) organisms unless lymphadenitis occurs.
Mild–moderate generalized lymphadenopathy may be
present with chronic bacteremia regardless of origin. Clinical signs
Most cats have lethargy, inappetence and weight loss.
Diagnosis Other signs variably present include fever, anemia,

hyperesthesia, arthralgia, irritable disposition, lymph-
Documenting infection and identifying the site may adenopathy and splenomegaly.
require routine laboratory tests, imaging, and blood,
urine and lymph node cultures.
Diagnosis
adenitis. Variable laboratory findings include non-regenerative
anemia, neutropenia, neutrophilia, lymphopenia, lym-
phocytosis, monocytosis, thrombocytopenia and hyper-
proteinemia due to polyclonal gammopathy.
MYCOPLASMA AND L-FORM INFECTIONS
Lymph node biopsy reveals hyperplasia.
Classical signs A positive FA test for antibodies against Ehrlichia
● Chronic limb wound and lameness. canis and Ehrlichia risticii or positive PCR test for
● ± Local or regional lymphadenopathy. ehrlichial DNA is diagnostic of infection. Preliminary
evidence suggests that cats may be PCR positive but FA
negative.
Clinical signs Resolution of clinical signs with treatment with tetra-

cyclines.
Non-healing bite wound (cellulitis) and lameness due
to (poly)arthritis/synovitis.
Local or regional lymphadenopathy may be present. BARTONELLOSIS
Classical signs
Diagnosis
● Asymptomatic cats.
Cytology of skin lesions or joint fluid lesions reveals ● ± Lymphadenopathy.
suppurative inflammation but no organisms.
See main reference page 530 (The Anemic Cat).
adenitis.
Clinical signs
Culture of organism is necessary for a definitive diagnosis.
Culture requires special transport and culture media – con- Cats usually harbor Bartonella henselae, the main
tact the laboratory prior to submitting specimen. causative agent of human cat-scratch disease, without
clinical signs.
Response to a tetracycline or a fluoroquinolone
gives a presumptive diagnosis. Failure to respond Mild popliteal lymphadenopathy occurs during acute
does not rule-out the diagnosis. experimental infection.
Lymph nodes are normal during chronic experimental

CYTAUXZOONOSIS
infection.
Bacteria resembling B. henselae have been seen in Classical signs
some clinical cases with moderate to marked lymph-
● Fulminant disease with fever and
adenopathy due to atypical hyperplasia.
hemolytic anemia.
Diagnosis See main reference page 389 (The Pyrexic Cat).

Lymph node biopsy reveals follicular hyperplasia in
Clinical signs
grossly normal lymph nodes during chronic experimen-
tal infection. Acute onset of fever, lethargy, inappetence, dyspnea,
anemia and jaundice.
Silver staining of lymph nodes of cats with lymph-
adenopathy may reveal bacteria. In such cases blood Lymphadenopathy is usually identified at necropsy.
culture and/or serologic testing and/or PCR testing for
B. henselae should be performed. Diagnosis
Exposure history (tick exposure in south-central or
south-eastern North America).
PROTOTHECOSIS Identification of the protozoan, Cytauxzoon felis, on
red cells, as tiny dot, tetrad, safety-pin or signet ring
Classical signs forms.
● Firm cutaneous nodule on foot. Lymph node histology reveals hemorrhage and edema.
Clinical signs ANTHRAX

Large firm cutaneous nodule(s), which may be ulcer-
ated, on foot, limb, head or base of tail. Nodules are not Classical signs
painful on palpation, but may cause discomfort and ● Edema of the head and neck.
other signs from local mass effect. ● Acute death with no promontory signs.
Local lymph node is usually normal.
No systemic signs. Clinical signs
Rare – cats are resistant to anthrax.
Diagnosis Lingual and pharyngeal edema cause oral serosan-
guineous discharge and dyspnea.
Cytology and histology of biopsy specimens reveal
granulomatous inflammation. Cervical regional lymphadenopathy due to edema,
hemorrhage and necrosis may occur.
Lymph node biopsy may reveal hyperplasia or lymph-
adenitis. In one case acute death occurred with no promontory
signs and there were no significant necropsy findings
Identification of Prototheca sp. (algae), in specimens by
other than congested lungs and unclotted blood.
cytology, histology or culture.
● Mature organisms are round, have a hyaline cell
Diagnosis
wall, small central nucleus, may show internal cleav-
age into endospores, and vary from smaller to larger History of ingesting potentially contaminated raw
than neutrophils. meat or animal by-products.
Do not perform necropsy if anthrax suspected. Diagnosis

Identification of a large bacillus on stained blood smear Exposure history (Glossina spp. [tsetse flies] vectors),
from marginal ear vein or other peripheral vein, or on clinical signs, serologic testing for antibodies to
stained smear from aspiration biopsy of tissue. Trypanasoma sp.
Culture of Bacillus anthracis from aspirated material. The cat is highly susceptible to experimental infection
with certain African Trypanasoma sp., but natural
infection is rarely encountered clinically.
AMERICAN TRYPANOSOMIASIS
Classical signs
TOXOPLASMOSIS
● Acute and chronic right-sided heart failure.
Classical signs
Clinical signs ● Anorexia, fever, dyspnea and signs of
The cat is susceptible to infection in South America and ocular inflammation in mature cats.
may act as a reservoir host.
● Fading neonate.
Clinical disease has not been formally described but is See main reference on page 432 for details (The Yellow
stated to be similar to dogs. Cat or Cat With Elevated Liver Enzymes), page 375
Generalized lymphadenopathy is present during acute (The Pyrexic Cat).
infection in dogs, in addition to signs due to myocardi-
tis (acute death, collapse, hypothermia, pale mucous
membranes, weak pulses, arrhythmias, dyspnea). Clinical signs
Common signs include fever, uveitis, dyspnea (pneu-
Diagnosis monia), vomiting, diarrhea, icterus (hepatitis and
hepatic necrosis), mesenteric lymphadenopathy,
Diagnosis is based on exposure history (Triatomae muscle pain and neurologic signs.
[kissing bugs] vectors), clinical signs, serologic testing
for antibodies to Trypanosoma cruzi, and identification Generalized peripheral lymphadenopathy may be
of trypomastigotes in buffy coat smears. present, which is due to reactive lymphoid hyperplasia
and not Toxoplasma-induced lymphadenitis.
AFRICAN TRYPANOSOMIASIS
Diagnosis
Classical signs Acute systemic toxoplasmosis typically affects kittens,
● Fulminant disease resembling or immunosuppressed cats, which usually have a his-
overwhelming sepsis. tory of chronic disease.
Confirmation is by measuring serum IgM antibodies
Clinical signs or demonstrating rising serum IgG antibodies.
Fever, generalized edema, purulent nasal and ocu- The organism occasionally may be seen in airway wash
lar discharges, signs of disseminated intravascular cytology of cats with pneumonia.
coagulation, lymphadenopathy, splenomegaly and Peripheral lymph node biopsy may reveal hyperplasia.
neurologic signs. Mesenteric lymph node biopsy may reveal necrosis.
RECOMMENDED READING
Greene CE (ed) Infectious Diseases of the Dog and Cat, 2nd edn. London, W.B. Saunders Company, 1998.
Lucke VM, Davies JD, Wood CM, Whitbread TJ. Plexiform vascularization of lymph nodes: An unusual but dis-
tinctive lymphadenopathy in cats. J Comp Path 1987; 97: 109–119.
Mooney SC, Patnaik AK, Hayes AA, MacEwen EG. Generalized lymphadenopathy resembling lymphoma in cats:
Six cases (1972–1976). J Am Vet Med Assoc 1987; 190: 897–900.
Moore FM, Emerson WE, Cotter SM, DeLellis RA. Distinctive peripheral lymph node hyperplasia of young cats. Vet
Pathol 1986; 23: 386–391.
Teske E, Van Straten G, Van Noort R, Rutteman GR. Chemotherapy with cyclophosphamide, vincristine, and pred-
nisolone (COP) in cats with malignant lymphoma: new results with an old protocol. J Vet Intern Med 2002; 16:
179–186.
Walton RM, Hendrick MJ. Feline Hodgkin’s-like lymphoma: 20 cases (1992–1999). Vet Pathol 2001; 38: 504–511.
21. The yellow cat or cat with elevated
liver enzymes
Albert E Jergens
KEY SIGNS
● Jaundiced cat.
MECHANISM?
● Jaundice occurs when serum bilirubin values exceed 2.0 mg/dl.
Jaundice results from either increased erythrocyte hemolysis or hepatobiliary disease.
WHERE?
● Pre-hepatic (hemolytic processes), hepatic (parenchymal disease), or post-hepatic (extra-
hepatic biliary obstruction).
WHAT?
● Most cats with jaundice have hepatic lipidosis, cholangiohepatitis syndrome (CHS), or extrahepatic
biliary obstruction (EHBO).
Non-jaundiced cats with elevated liver enzymes may or may not have liver disease. The degree
of dysfunction is assessed by bile acid analysis and the cause determined by liver cytology
and/or biopsy if indicated.

Diseases causing a yellow cat or cat with elevated liver enzymes
PRE-HEPATIC
● Hemolytic processes causing clinical signs are usually associated with PCV < 18%.
INFLAMMATION
INFECTION
● Mycoplasma haemofelis *(Hemobartonella felis)* (p 424)
Bacterial (Mycoplasma) parasite which infects red blood cells and causes RBC destruction.
Jaundice, lethargy, inappetance and occasional vomiting.
continued
421
continued
IMMUNE
● Immune-mediated anemia (p 424)
Jaundice, lethargy, inappetance, occasional vomiting, and respiratory distress with severe ane-
mia.
HEPATIC
● Jaundice caused by primary hepatic parenchymal diseases.
DEGENERATIVE
●Cirrhosis (p 435)
Rare and usually follows severe chronic hepatopathy. Jaundice, anorexia, weight loss and/or
hepatomegaly.
METABOLIC
Polyuria, polydipsia, increased appetite, weight loss, plantigrade stance with neuropathy.
●Hyperthyroidism (p 437)
Generally seen in cats greater than 8 years old. Often have an increased appetite, weight loss, poor
hair coat, vomiting.
●Hepatic lipidosis*** (p 425)
Often previous history of obesity and/or anorexia. Jaundice, weight loss, and anorexia are
common.
NEOPLASTIC
●Lymphosarcoma* (p 431)
Usually a manifestation of multicentric lymphosarcoma. Jaundice, anorexia, weight loss, vomiting
and/or diarrhea.
● Non-hematopoietic liver tumors (biliary cyst adenoma, hepatocellular carcinoma) (p 436)
Vast majority are benign tumors seen in old cats. Anorexia, lethargy, and weight loss
predominate.
INFLAMMATION
● Feline cholangitis (cholangitis/cholangiohepatitis syndrome)*** (p 427)
The neutrophilic form is seen most commonly in male cats. It may be associated with other
inflammatory disorders (IBD, pancreatitis) concurrently affecting the gastrointestinal tract. It
occurs as an acute phase associated with signs of systemic illness such as fever, anorexia,
lethargy, vomiting and jaundice. Signs in the chronic phase are milder and weight loss domi-
nates. The lymphocytic form is associated with jaundice, hepatomegaly, vomiting, diarrhea
and/or ascites.
21 – THE YELLOW CAT OR CAT WITH ELEVATED LIVER ENZYMES 423
INFECTIOUS
Mycotic:
● Histoplasmosis (p 438)
Of regional significance in the central US. Seen primarily in young cats with depression, weight
loss, fever and anorexia. Dyspnea, tachypnea and abnormal lung sounds seen in 50% of cats.
Viral:
●Feline infectious peritonitis (FIP)* (p 430)
Progressive anorexia, weight loss, jaundice, fever and/or ascites with effusive forms of disease.
●Feline leukemia virus* (p 437)
May cause pre-hepatic jaundice, immunosuppression and/or lymphosarcoma. Salient signs include
mucus membrane pallor, anorexia, weight loss, lymphadenopathy and/or jaundice.
Protozoan:
Jaundice, cyclical fever, and anterior uveitis are commonly observed. Dyspnea and central nervous
system signs may or may not occur concurrently.
Toxic:
●Acetaminophen (paracetamol) toxicity (p 433)
Acetaminophen toxicity causes cyanosis, dyspnea and facial edema.
●Diazepam toxicity (p 434)
Diazepam toxicity causes anorexia, depression and jaundice.
POST-HEPATIC
Jaundice caused by decreased or impaired biliary excretion.
Mechanical:
●Extrahepatic biliary obstruction (EHBO)** (p 439)
May be caused by pancreatic diseases, neoplasia or extrinsic compression. Jaundice, anorexia,
weight loss, vomiting and abdominal pain seen with pancreatitis.
Inflammation:
●Pancreatitis** (p 439)
Anorexia, lethargy and abdominal pain predominate. Jaundice may occur several days after mild signs.
●Cholecystitis (p 440)
Uncommonly recognized, but may cause abdominal pain, fever, vomiting and jaundice.
Trauma:
●Ruptured bile duct (p 441)
Low-grade abdominal pain, malaise, weight loss and/or effusion.
or storage is suspected. This phenomena is observed

INTRODUCTION with a variety of non-hepatic primary disorders (e.g.,
renal and gastrointestinal diseases) which may cause
MECHANISM? these cats to later develop primary liver disease. Bile
acid analysis determines hepatic function and the
Jaundice results when serum bilirubin is increased
need to obtain cytologic/biopsy specimens for defini-
above 2 mg/ml.
tive diagnosis.
Most bilirubin originates from senescent erythrocytes
and is processed in the liver for excretion in the bile.
Jaundice results from either increased erythrocyte INCREASED BILIRUBIN PRODUCTION
hemolysis, which exceeds the processing capacity of (PRE-HEPATIC CAUSES OF JAUNDICE
the liver, or hepatobiliary disease. OR INCREASE\D LIVER ENZYMES)
WHERE? MYCOPLASMA HAEMOFELIS

(HEMOBARTONELLA FELIS)*
Pre-hepatic jaundice is due to hemolytic processes.
IMMUNE-MEDIATED ANEMIA
Erythrocyte hemolysis causes release of increased
heme pigments, which overwhelm hepatic process-
ing/excretion of bilirubin. Classical signs
Hepatic jaundice is seen with severe diffuse hepatic ● Pale mucus membranes, PCV usually
cholestasis (via inflammation) or major bile duct < 18%; hemoglobin < 10 g/dl.
obstruction. Inflammation in portal or periportal areas ● Lethargy, in appetence, and anorexia may
causes jaundice early in the disease course; whereas, be observed.
parenchymal injury away from periportal areas results ● +/- fever.
in jaundice development late in the disease course. ● Occasional vomiting.
Post-hepatic jaundice is caused by intraluminal or
See main reference on page 530 for details (The Anemic
extraluminal disorders that mechanically occlude the
Cat).
biliary tree (e.g., gall bladder and common bile duct).
Post-hepatic (extrahepatic biliary obstruction).
Pathogenesis
Rapid destruction of red cells exceeds the liver’s capa-
WHAT?
city to metabolize increased hemoglobin breakdown
Pre-hepatic causes for jaundice are primarily attributable products (bilirubin).
to erythrocyte parasitemia (hemobartellosis), infectious
Most commonly associated with Mycoplasma haemofe-
disease (FeLV), and immune-mediated hemolysis (rare).
lis infection and less commonly with immune-mediated
Hepatic causes for jaundice may be caused by hepatic anemia. Hemolysis may also be caused by feline
lipidosis, cholangiohepatitis syndrome and hepatic leukemia viral (FeLV) infection.
lymphosarcoma.
Pre-hepatic causes for jaundice in the cat are
Post-hepatic causes for jaundice are caused by pancre- uncommon.
atitis and neoplasms involving the gallbladder and bil-
iary tree (less common).
Clinical signs
Non-jaundiced cats with elevated liver enzymes may
Pale mucus membranes, PCV< 18% and often
or may not have significant hepatic disease. An
12–15%; hemoglobin < 10 g/dl.
underlying defect in bilirubin metabolism affecting
conjugation reactions or cytosolic pigment transport Lethargy, inappetance, anorexia.
+/− fever and vomiting. sion include increased heart and respiratory rates which
usually occur when the PCV < 15–18% for acute loss
Lymphadenopathy, or skin, respiratory, and gastro-
and < 12% for more chronic loss. See page 531 (The
intestinal infections secondary to immunosuppression
Anemic Cat).
are seen with FeLV infection.
Antivirals and immunotherapy for FeLV infection.
Diagnosis
Typically anemia is moderate to severe (PCV 12–17%) HEPATOCELLULAR DISEASES
with a reduced hemoglobin < 10 g/dl. (JAUNDICE OR INCREASED LIVER
ENZYMES CAUSED BY HEPATIC
Examine blood smears closely with a reduced PCV for
PARENCHYMAL DISEASES)
presence of red cell parasites (hemobartonellosis).
Saline agglutination and direct Coomb’s tests confirm HEPATIC LIPIDOSIS***
immune-mediated anemia but the Coomb’s test
requires feline specific antibody to be meaningful. Classical signs
Liver enzymes (ALT, ALP) are often normal or ● Obese anorectic female cats are
insignificantly elevated. predisposed.
Serologic testing (ELISA or fluorescent antibody) for ● Progressive anorexia, vomiting, and
FeLV infection. diarrhea are common.
● Severe jaundice and hepatomegaly are
Polymerase chain reaction assays may be of great ben- present.
efit in documenting infection if available.

Hepatic and post-hepatic disorders are often chronic The etiopathogenesis is poorly understood and ill-
diseases and are associated with some anemia. In these defined.
instances, the anemia is mild (PCV of 18–27%), non-
Triglycerides accumulate in the liver as a consequence
regenerative and is attributable to anemia of chronic
of imbalanced fat metabolism which is likely multifac-
disease.
torial in origin. These imbalances may include uptake
Hemolytic anemia is usually regenerative unless it is of fatty acids, use of fatty acids for energy (e.g., ketone
detected early (< 4 days) or if stem cells are involved; as production and fatty acid oxidation), production and
may occur with Mycoplasma haemofelis infection or dispersal of lipoproteins throughout the body, and de
immune-mediated red cell destruction. novo synthesis of triglycerides. Many metabolic condi-
tions, nutritional factors, drugs and toxins can cause
Hemolytic anemia associated with FeLV infection may
excessive hepatic fat accumulation (see below).
or may not be regenerative.
Approximately 50% of cats have idiopathic (primary)
hepatic lipidosis in which no underlying medical con-
Treatment dition is detected.
● History of previous obesity is observed in nearly all
Supportive care and antibiotics (doxycycline 5 mg/kg
cats.
PO q 12 h for 21 days or enrofloxacin 5 mg/kg PO q 12 ● Anorexia or rapid weight reduction contributes to
h for 7–14 days) for cats with hemobartonellosis.
hepatic fat accumulation. Anorexia may be preceded
Whole blood/packed red cell transfusions, cortico- by a stressful event such as a move to a new house.
steroids (prednisone 1–2 mg/kg PO q 12 h as needed), ● Imbalanced nutrition using caloric- or protein-
and supportive care for immune-mediated anemia. restricted diets, especially if unpalatable, can trig-
Clinical parameters which suggest the need for transfu- ger marked weight loss. Experimentally, dietary
energy must be restricted 50–75% for at least hepatic lipidosis. Histologic confirmation is the pre-
2 weeks to induce hepatic lipidosis. ferred modality, as recent reports have noted poor cor-
● Hepatic lipidosis occurs either as a primary idio- relation between cytologic interpretation and histologic
pathic event or secondary to another disease findings in cats with liver disease.
process. Frequently it occurs secondary to underly-
Histopathologic confirmation requires specialized pro-
ing diseases, most commonly cholangiohepatitis,
cessing to assess.
inflammatory bowel disease, and acute or chronic
● Both hematoxylin/eosin and specific staining for fat
pancreatitis. A recent study for 30% of cats had
should be performed.
acute pancreatitis.
● Greater than 50% of hepatocytes contain lipid vac-
● Acquired carnitine deficiency may be related to the
uolation.
development of hepatic lipidosis. Carnitine is pri-
marily synthesized in the liver and is essential for Abdominal ultrasonography may suggest hepatic lipi-
enzyme-mediated uptake of fatty acids into mito- dosis versus extrahepatic biliary obstruction, cholan-
chondria. In health, it also facilitates fatty acid giohepatitis and neoplasia.
product transport and the oxidation of long-chain ● Cats with hepatic lipidosis have diffuse hyper-
fatty acids. Starved cats have diminished capacity echogenicity, hepatomegaly, and an absence of bil-
for fatty acid beta-oxidation or export of VLDL, iary tract abnormalities.
leading to hepatic triglyceride sequestration.
Non-regenerative anemia is seen in 30% of cats.
● Less commonly observed in association with dia-
betes mellitus and toxicity (e.g., aflatoxins, bacter- Biochemical liver parameters are often suggestive of
ial toxins). hepatic lipidosis.
● Marked but discrepant increases of serum ALP in
Fat accumulation in hepatocytes results in cholestasis
comparison to ALT and AST.
and hepatic jaundice.
● Total bilirubin values exceed 2 mg/dl as most cats
Progressive liver dysfunction causes anorexia, vomiting are severely jaundiced.
and dehydration.
Approximately 30% of cats are hypokalemic.
Signs of overt hepatic encephalopathy (ptyalism,
Abnormal coagulation tests are observed in > 50% of
seizures) are uncommon.
cats. Approximately 20% have clinical evidence of
excessive bleeding. Vitamin K deficiency is the most
Clinical signs common coagulation abnormality.
● Carefully appraise coagulation status prior to liver
Most commonly seen in middle-aged to older cats of
aspirate or biopsy.
either sex. There is no breed predisposition.
The most common early signs are progressive anorexia
and depression with intermittent vomiting over several
weeks. Cats with inflammatory liver disease (cholangiohepati-
tis) are often febrile and may have ascites. Increased
Common presenting complaints include, weight loss,
ALT +/− AST and hyperglobulinemia are prominent
prolonged (> 2 weeks) anorexia, vomiting and lethargy.
features in these cats and are not observed in cats with
Jaundice, hepatomegaly and dehydration are detected hepatic lipidosis.
on physical examination.
Sonographic abnormalities to the biliary excretory
Ascites, fever and ptyalism are uncommon. pathway or hepatic parenchyma are evident in most
cats with extrahepatic biliary obstruction and neopla-
sia, respectively.
Diagnosis
Cytologic examination of hepatic parenchyma obtained
Treatment
via fine-needle aspirate, or histologic examination of
a liver biopsy specimen is usually diagnostic for Cats must be fed 65–90 kcal/kg/day until eating.
● Gastrostomy or jejunostomy tube alimentation with Thiamine supplementation (100 mg of thiamine

high-energy commercial enteral diets is necessary if hydrochloride, q 12 h by oral, subcutaneous or IM
vomiting is frequent. routes) is generally advised.
● Esophagostomy tubes can be used when vomiting is
The potential value of carnitine (1250 mg L-carnitine/cat
not frequent, and may be simpler and safer to place
q 24 h) and taurine (250–500 mg q 24 h) supplementa-
than gastrostomy tubes.
tion has not been critically assessed but is unlikely to be
● Nasoesophageal tubes are indicated in cats too ill
harmful.
for a gastrostomy tube.
● They are often used for short-term support until
placement of gastrostomy tube. Prognosis
● Nasoesophageal and some esophageal tubes require
Survival rates are up to 60% with aggressive therapy.
liquified commercial diets (Iams Nutritional
Recovery Formula, Clinicare, or Hill’s A/d mixed Evaluate closely for concomitant diseases (pancreatitis)
with water). as they warrant a more guarded prognosis.
● It takes several days before the caloric requirements
can be fed in 3–4 meals per day without inducing
Prevention
vomiting. Initially small volumes, e.g., 5 ml, should
be fed every 2 hours, and the volume is increased It is important to use sensible restriction diets for obese
while reducing the frequency over several days. cats. Feed 60–75% of maintenance requirements (60
Alternatively, feeding can begin with a constant rate kcal/kg) to promote slow but steady weight loss. Food
infusion over 24 hours using a syringe infusion intake should be adjusted monthly for the individual cat
pump with the volume increased gradually until the to produce a weight loss of 1–2% per week.
daily caloric requirements are met. Cats can then be ● A variety of commercial, nutritionally balanced but
transitioned to bolus feeding four times daily. Tubes reduced caloric rations are available.
should be left in place until the cat is voluntarily
eating its full caloric requirements for 2 weeks and
has a stable and increasing weight.
FELINE CHOLANGITIS (CHOLANGITIS/
Avoid benzodiazipines as they are inadequate to stimu- CHOLANGIOHEPATITIS SYNDROME)***
late appetite and may aggravate CNS signs.
Classical signs
Vomiting is controlled with metoclopramide
(0.2–0.5 mg/kg q 8 h or using a constant rate infu- ● Anorexia, weight loss, and vomiting.
sion 1–2 mg/cat/24 h). Two periods of exercise total- ● Jaundice, +/- fever, +/- ascites.
ing 45–60 min/day help reduce vomiting and high ● Often palpable hepatomegaly.
gastric residual volumes. This can be accomplished
by letting the cat free in a consulting room, prefer-
Pathogenesis
ably with a window.
Cholangitis is the cause of jaundice in 30% of cats.
Correct dehydration and electrolyte imbalances with
fluid therapy. Etiology is unknown but may involve causative factors
● Monitor serum potassium and phosphorous and such as bacterial infection. The different forms of
supplement with KCl and potassium dihydrophos- cholangitis may represent different stages of the same
phate as needed to combat hypokalemia and disease process. One hypothesis suggests that the
hypophosphatemia. unique anatomic relationship in which the bile duct and
major pancreatic duct form a short common duct enter-
Ursodeoxycholic acid (10–15 mg PO q 24 h) for intra-
ing the duodenum may predispose cats to inflammatory
hepatic cholestasis.
hepatic disease. This connection might favor the ascen-
Vitamin K1 is often given (3–5 mg per cat q 12 h ini- sion of luminal bacteria or the entrance of pancreatic
tially) due to the frequency of coagulation disturbances. enzymes into the biliary tract. Supporting this theory is
the observation that inflammatory disease of other ali- ● Mild to severe infiltration of portal areas by plasma
mentary organs, such as pancreatitis and inflammatory cells, lymphocytes and neutrophils, without or
bowel disease, are associated with cholangitis. without macrophages is present. Leukocytes are
within walls and/or lumina of bile ducts, and are
A new classification scheme by the World Small
associated with biliary epithelial degeneration or
Animal Veterinary Association Liver Diseases and
necrosis. Lymphoid aggregates may be present in
Pathology Standardisation Research Group recognizes
portal areas. Biliary hyperplasia, periductal fibrosis
three distinct forms of cholangitis in cats.
or bridging portal fibrosis may be present.
In the traditional classification scheme, cholangitis ● It is usually associated with partial or complete bil-
denoted inflammation of the biliary tree and cholangio- iary obstructive lesions resulting in cholestasis.
hepatitis referred to inflammation around bile ducts and ● Signs and liver enzyme elevations tend to be milder
peribiliary hepatocytes. than with the acute neutrophilic phase, and reflect a
smoldering inflammatory hepatic disease. Weight
However, with the new classification scheme, the term
loss is a dominant sign. Signs may wax and wane.
cholangitis is used in preference to cholangiohepatitis,
Jaundice may or may not be present. Ascites is not
because inflammatory disruption of the limiting plate to
a feature of the acute or chronic phase. In general,
involve hepatic parenchyma is not always a feature and,
the chronic phase appears less common than the
when present, is an extension of a primary cholangitis,
acute phase.
and inflammation is centered on intrahepatic bile ducts.
Lymphocytic cholangitis.
Three separate syndromes occur as defined by clini-
● Lymphocytic cholangitis is postulated to be
cal and histologic criteria: neutrophilic cholangitis,
immune-mediated in origin.
lymphocytic cholangitis and chronic cholangitis.
● Histologically there is moderate to marked infiltra-
Cirrhosis may occur as an end-stage of cholangitis but tion of portal areas by small lymphocytes. With
is rare. chronicity, the intensity of portal infiltration tends
● The lymphocytic form is more common than the to abate. Lymphocytic infiltrates may also be pres-
neutrophilic form of cholangitis in the UK and ent that are centered on and infiltrating walls of bile
Australia, but the neutrophilic form appears to be ducts, but this is an inconsistent feature, especially
the most common form in some other locations. in the chronic phase. Inflammation may or may not
extend into the periportal parenchyma. Histologic
Neutrophilic cholangitis.
evidence of intrahepatic cholestasis may be present.
● This is usually referable to ascending bacterial infec-
● It occurs primarily in middle-aged cats with chronic
tion but is also rarely reported in protozoal infec-
(> 3 weeks) signs. Recurrent episodes of clinical
tions. E. coli is sometimes cultured from the bile, and
signs are often interspersed with weeks or months of
occasionally Gram-positive anaerobes are cultured.
normalcy, with a normal or even increased appetite.
● Two phases of neutrophilic cholangitis are recog-
● Cats are often less ill than with the acute neu-
nized; an acute phase and a chronic phase.
trophilic form, and may have ascites.
Neutrophilic cholangitis – Acute phase.
Chronic cholangitis associated with liver fluke infes-
● Neutrophils are within walls and lumina of intra-
tation.
hepatic bile ducts and within portal areas. Bile duct
● Lesions result from infection by liver flukes such as
epithelial degeneration and necrosis is present.
Amphimerus pseudofelineus, (Opisthorchis pseudo-
There is variable extension of inflammation through
felineus), Opisthorchis tenuicollis, Metorchis albidus,
the limiting plate to involve periportal parenchyma.
M. conjunctus (M. complexus), Platynosomum
Bacteria may be visible. There is usually minimal
concinnum (page fastosum).
biliary hyperplasia or periductal fibrosis.
● Generally, there is an acute onset of signs with marked
systemic illness (fever, anorexia, lethargy, vomiting). Clinical signs
Neutrophilic cholangitis – Chronic phase. Often observed in middle-aged cats.
Intermittent episodes of inappetance or anorexia and Differential diagnosis

lethargy.
Cholangitis produces greater increases of serum ALT
Weight loss. as compared to HL.
● Cats with lymphocytic cholangitis may have con-
Fever occurs with neutrophilic cholangitis.
current inflammation involving pancreatic, intes-
Ascites is sometimes observed with lymphocytic tinal and renal tissues.
cholangitis. Ascitic fluid had a high total protein con-
tent attributable primarily to globulins. Fever and ascites are common with cholangitis but are
not observed with HL.
Jaundice +/− hepatomegaly occur with both types.
Cats with HL have higher ALP activity as compared to
cholangitis-affected cats.
Diagnosis Feline infectious peritonitis (FIP) may appear similar to
Definitive diagnosis requires histologic evaluation of the lymphocytic form, particularly if there is ascitic
liver biopsy specimens. fluid with a high protein content. The syndromes clini-
● Tissues may be obtained via ultrasound-guided per- cally look similar, although fever is more common with
cutaneous biopsy, laparoscopically or by laparo- FIP. Liver biopsy, especially a wedge section, is usually
tomy. However, 18-gauge needle biopsies are less diagnostic.
reliable than wedge biopsies. In one study, less than
60% of cats with cholangitis had needle biopsy
results that were in accordance with the diagnoses Treatment
based on the wedge biopsy.
Specific treatment is dictated by results of hepatic
● Perform coagulation tests (ACT or APTT/OSPT or
biopsy.
PIVKA) prior to hepatic biopsy. Initiate vitamin K1
therapy if abnormal (see dosage below). Neutrophilic cholangitis.
● Empiric antibiotic choices are amoxicillin (22
Bile and liver culture are recommended in cats with
mg/kg PO q 12 h) and metronidazole (10 mg/kg PO
suspected neutrophilic cholangitis.
q 12 h) or enrofloxacin (2.2 mg/kg bid PO) until
Survey abdominal radiographs are usually normal but bile culture results are known.
are useful to confirm hepatomegaly and the presence of ● Continue antibiotic therapy for 6–8 weeks.
peritoneal effusion. Abdominal sonography shows bil- ● Ursodeoxycholic acid (10–15 mg/kg PO q 24 h)
iary tract thickening and distention (neutrophilic may be useful for choleresis following correction of
cholangitis) or increased parenchymal echogenicity biliary obstruction.
(lymphocytic cholangitis). ● S-adenosylmethionine (20 mg/kg PO q 24 h) is rec-
ommended to replenish glutathione stores and scav-
Biochemical liver parameters show high ALT, ALP
enge free radicals.
and total bilirubin concentrations. Total bilirubin con- ● Surgical correction (biliary diversion) is indicated
centrations may increase 2–10 times normal values,
in cats with clinical signs or imaging features (e.g.,
with ALT concentration increased to a greater extent
distended and tortuous common bile duct, large gall
relative to ALP.
bladder and/or prominent intrahepatic bile ducts)
Increased plasma globulin and decreased albumin are indicative of obstructive biliary tract lesions.
often present in the lymphocytic form.
Lymphocytic cholangitis.
Leukocytosis may be present in suppurative form. ● Use immunosuppressive doses of steroids (pred-
nisone 2 mg/kg PO q 24 h) for 4–6 weeks to reduce
Biliary obstruction should be suspected in cats with
hepatic inflammation. If a favorable response is
lethargy, intermittent fever and progressive jaundice.
observed, then steroids may be tapered at 25% of
These cats will require surgical correction for obstruc-
the dose q 2 weeks as determined by clinical signs,
tive jaundice.
liver enzymes and/or bile acid tests.
● Administer ursodeoxycholic acid for choleresis and

FELINE INFECTIOUS PERITONITIS (FIP)*
modulation of “noxious” bile acids.
● Long-term immunosuppressive therapy (steroids
+/− metronidazole) is often required in cats with Classical signs
persistent clinical signs or abnormal laboratory
● 50% of cats are < 2 years of age.
values. Some cats that fail to respond to pred-
● Weight loss, anorexia, vomiting and
nisone may respond to chlorambucil (0.2 mg/kg
lethargy.
PO q 48 h).
● Jaundice +/- cyclical fever.
Supportive care as dictated by the animal’s needs. ● Protein-rich ascites in “effusive” form.
● Vitamin K for coagulopathy (3–5 mg per cat PO q
1
24 hours as needed). See main reference, page 372 (The Pyrexic Cat).
● Fluid therapy to combat dehydration and electrolyte
disturbances.
● Nutritional therapy is important to reduce the Clinical signs
hepatic workload and augment recovery.
Young cats (< 2 years old) and from a multicat envi-
– Jejunostomy or gastrostomy tubes and feeding a
ronment are most susceptible.
pureed commercial or esophagostomy tubes and
feeding a commercial liquified diet are best tol- Signs are referable to chronic inflammation of the kid-
erated. neys, liver, visceral lymph nodes, intestines, lungs, eyes
– Feed a protein-modified diet as dictated by the and brain.
status of renal function and signs of hepatic
Chronic, progressive inappetance, weight loss, fever
encephalopathy (rare).
and depression.
– Control vomiting with famotidine (0.2 mg/kg
SID PO) or metoclopramide (0.2–0.5 mg/kg q Signs may be cyclical at first.
8 h) or constant rate infusion at 1–2 mg/cat/24 h.
Jaundice and ascites may occur in cats with chronic
liver involvement.
Prognosis Dyspnea from pleural effusion occurs in about one in
five cats.
Long-term follow-up on a large number of cats with
cholangitis has not been performed. CNS signs include seizures, personality changes, nys-
tagmus, head tremor and hyperesthesia.
The prognosis with neutrophilic cholangitis is less
favorable than for cats with lymphocytic cholangitis. Vomiting may occur with granuloma formation in the
intestines, or inflammation in other organs such as the
Cats with the neutrophilic form that survive the initial
liver.
treatment period of several months have a reasonable
chance for long-term survival. Ocular signs include bilateral uveitis, perivascular exu-
dates, retinal hemorrhage or detachment.
Cats with lymphocytic cholangitis may survive com-
fortably for months to years with appropriate therapy.
Diagnosis
Prevention Diagnosis is based on history, clinical signs and char-
acteristic histologic lesions on tissue biopsy.
Medical/surgical correction of biliary obstructive
● Parenchymal lesions are characterized by multi-
lesions when recognized.
focal hepatic necrosis with pyogranulomatous
Treatment of inflammatory (lymphocytic-plasmacytic) inflammation.
lesions involving the intestinal mucosa (i.e., inflamma- ● Pyogranulomas may be grossly evident on the cap-
tory bowel disease). sule of the liver.
Increased activities of ALT and ALP are common. – Give human interferon-β 30 IU/day for 7 days at
Total bilirubin values may be increased above 2–3 alternate weeks to boost immunity.
mg/dl (jaundice). – Nutritional support via force feedings,
esophagostomy or gastrostomy tube, or naso-
Diagnostic sampling of effusions is useful as they are
esophageal catheter.
generally high protein but low to moderate cellularity
● Because of the extremely poor prognosis, euthana-
(modified transudate) with non-lytic neutrophils.
sia is recommended if there is no response to pal-
Serologic testing for FIP antibodies may give con- liative therapy.
founding results. Coronaviral antibodies are wide-
spread in the general cat population and the new 7B FIP
antibody test appears to have problems with false neg- LYMPHOSARCOMA*
atives and false positives in the field.
● Reverse transcriptase-PCR detection of coronaviral Classical signs
antigens in effusion fluid or tissues presently lacks
● Most cats > 10 years of age.
high diagnostic accuracy. False positives occur
● Lethargy, anorexia, weight loss.
because enteric coronavirus may be present system-
● Jaundice may be present.
ically, and false-negative results also occur.
● Hepatomegaly +/- effusion (ascites or
● Immunocytochemistry demonstrating coronavirus
hemoperitoneum).
antigen within circulating monocytes or tissue
macrophages appears to be specific, but low num-
bers of infected cells in tissue samples limit the sen-
sitivity for use in biopsy samples. The technique is Pathogenesis
only available at some laboratories.
Generally presents as a manifestation of multicentric
lymphosarcoma. Lesions may occur in conjunction
Differential diagnosis with neoplastic infiltrates involving other lymphoid
organs, such as peripheral lymph nodes, or the alimen-
Abdominocentesis in FIP-infected cats may yield a tary mucosa.
protein-rich exudate which is dissimilar from other
inflammatory/degenerative hepatopathies except lym- Neoplastic lymphocytes gradually replace normal
phocytic cholangiohepatitis. Histopathology of the hepatocytes causing organ enlargement and hepatic
liver is diagnostic. Also, differentiate FIP from car- failure.
diomyopathy and neoplasia which may cause chronic ● Cholestasis and jaundice result from involvement of
illness similar to FIP or cavity effusion. intrahepatic biliary structures.
Cats with FIP will often have involvement of multiple

organ systems (eyes, lungs, CNS). Clinical signs
Mostly seen in middle-aged and older cats.
Treatment Lethargy, anorexia, and weight loss predominate.
There is no definitive therapy for FIP and the disease is Hepatomegaly +/− jaundice are common.
almost uniformly fatal in cats with signs.
● Supportive care is palliative at best.
– Immunosuppressive doses of steroids (2–4 mg/kg Diagnosis
PO q 24 h) +/− other cytotoxic drugs (e.g.,
Suspicion of hepatic neoplasia is raised by older age,
cyclophosphamide 2.2 mg/kg/day on four consec-
history of chronic illness and suggestive clinical signs.
utive days each week or chlorambucil 20 mg/m2
every 2–3 weeks) are recommended for vasculitis. Increased serum ALT and ALP activities are common.
– Administer broad-spectrum antimicrobials for In general, relatively greater increases in ALT versus
secondary bacterial infections. ALP are observed.
Radiographic imaging may aid diagnosis. Clinical signs

● Symmetrical hepatomegaly is often observed on
survey radiographs. Infection with the obligate intracellular coccidia causes
● Hepatic sonography shows generalized hyper-
inflammation and cell necrosis in affected tissues.
echogenicity or multifocal hypoechogenicity to the Lung, brain, gut, liver and eye are most affected.
liver parenchyma. Diverse but are generally referable to respiratory, neu-
Definitive diagnosis requires cytologic or histologic romuscular or gastrointestinal systems.
evaluation of liver specimens. Anorexia, cyclical fever, dyspnea and lethargy are
common.
Differential diagnosis Uveitis may involve one or both eyes.
Rule out benign conditions, such as hepatic cysts, hepa- Cystic involvement of the CNS may cause pronounced
tocellular/bile duct adenomas, and regenerative nodules neurologic deficits (with the type of observed CNS
which may mimic hepatic lymphosarcoma. These other deficit dependent upon involvement of the brain, brain
diseases may be definitively ruled out by performance stem and/or spinal cord), or may be rapidly fatal with
of liver biopsy with histologic interpretation. advanced disease.
Cysts located within skeletal muscles are painful, and
Treatment often cause hyperesthesia on muscle palpation, stiff-
Combination chemotherapy using cyclophosphamide ness of gait and shifting leg lameness.
(300 mg/m2 PO q 3 weeks), vincristine (0.75 mg/m2 IV Hepatic involvement may follow dissemination causing
weekly for 4 weeks), and prednisone (2 mg/kg/day) is jaundice due to hepatitis or cholangiohepatitis. Cystic
recommended. See page 676 for treatment details. involvement of the intestinal mucosa may cause lympho-
Provide supportive therapy (including provision of cytic-plasmacytic enteritis.
enteral feeding if needed) as needed.
Diagnosis
Prognosis
Non-regenerative anemia and leukopenia.
The prognosis is guarded. Approximately 50% of cats
with hepatic lymphosarcoma will respond to multi- Marked increases in serum ALT and AST activities
drug chemotherapy. occur with hepatic infection.
Concurrent FeLV infection shortens survival times but Hyperproteinemia occurs in some cats with chronic
does not influence response to chemotherapy. toxoplasmosis.
Thoracic radiographs may demonstrate diffuse intersti-
tial to alveolar opacities.
TOXOPLASMOSIS* Serologic testing provides useful diagnostic information.
● IgM and IgG titers are assessed by ELISA tech-
Classical signs niques.
● Anorexia, lethargy, neurologic signs and – A high (> 256) IgM titer is suggestive of active
dyspnea. infection.
● Cyclical fever. – A 4 × rise in IgG titer over 2–3 weeks is sugges-
● +/- icterus, vomiting and diarrhea. tive of active infection.
● Anterior or posterior uveitis. Demonstration of the organism (cysts) in affected
biopsy/necropsy tissues is helpful in making a
See main reference, page 375 (The Pyrexic Cat). diagnosis.
Differential diagnosis Increasing depression, weakness and panting occur.

Increasing harsh lung sounds are secondary to worsen-
Toxoplasmosis should be differentiated from other ing pulmonary edema.
feline systemic infections including feline leukemia
and immunodeficiency viral infections and feline infec- Vomiting and generalized weakness are less common.
tious peritonitis. Jaundice may occur 3–6 days post-ingestion.
Hemoglobinuria occurs in some cats or a dark brown
Treatment urine containing increased amounts of hemoglobin,
Available drugs suppress replication of T. gondii but do bilirubin and protein may be seen.
not completely kill the parasite. Death occurs within 18–36 hours of ingestion of a toxic
● Use clindamycin (12.5 mg/kg PO q 12 h) for dose.
3 weeks.
● Cats with ocular inflammation should be judi-
ciously treated with topical glucocorticoids (topical Diagnosis
0.5 % prednisolone acetate drops q 6–12 h). Diagnosis is based on a history of recent drug exposure
and the presence of “unique” clinical signs.
ACETAMINOPHEN (PARACETAMOL) Anemia is typically non-regenerative within 4–6 days

INTOXICATION of intoxication.
● Heinz-bodies may be visualized with new methyl-
Classical signs ene blue stain.

● Increased numbers of nucleated red cells reflecting
● Often history of recent drug exposure. hypoxemia may be evident.
● Acute onset of cyanosis, dyspnea and facial
edema. Neutrophilic leukocytosis reflects stress.
● +/- jaundice occurs several days post- Unexplained and rapid increase in liver biochemical
ingestion. parameters are observed.
● ALT, AST, ALP and total bilirubin concentrations
may be elevated.
Pathogenesis
Histologic examination of hepatic biopsy specimens
Cats have impaired ability to readily metabolize acet- reveals hepatocellular necrosis, lipid accumulation
aminophen. Ingestion of 50–60 mg/kg may be fatal and/or biliary duct proliferation.
for cats. This is equivalent to one child tablet or half
an adult tablet.
Large doses of acetaminophen produce toxic interme-
diates which cause oxidative damage in cells, espe- The features of acetaminophen toxicosis (drug expo-
cially erythrocytes and hepatocytes. sure classic signs, clinico-pathologic findings and acute
● Oxidative damage to hemoglobin leads to methemo- hepatic injury) make most other diseases unlikely.
globinemia and reduced oxygen-carrying capacity.
● Tissue hypoxia and vascular injury occur. Treatment
Hepatic injury is characterized by hepatocellular necrosis. Attempt to minimize drug absorption in acute (< 4
hours) intoxications.
● Perform orogastric lavages (several cycles each at
Clinical signs
5–10 ml/kg of tepid water) to mechanically remove
Pale mucous membranes or acute cyanosis with blue- gastric contents.
tinged mucous membranes, dyspnea, facial edema, ● Give activated charcoal (2 g/kg body weight) to
salivation and depression are typical signs of poisoning. bind residual luminal toxicants via orogastric tube.
Fluid therapy may be required to correct dehydration, Clinical signs

acid–base imbalances and electrolyte abnormalities
occurring from vomiting. Most cats become lethargic, ataxic and anorectic
within 96 hours following ingestion.
Specific antidotal therapy.
● N-acetylcysteine (Mucomyst, Mead Johnson &
Jaundice is common and occurs during the first 11 days
Co.) helps to neutralize toxic intermediates. of illness.
– Administer a loading dose of 140 mg/kg orally,
followed by doses of 70 mg/kg every 4–6 hours Diagnosis
for upto 3 days.
● Ascorbic acid is used in combination with N-
History of recent drug exposure.
acetylcysteine. Unexplained and rapid increase in liver biochemical
– Its use is controversial. It works slowly and is parameters.
used as adjunctive therapy. ● Profound increases in ALT, AST and total bilirubin
– Give 30 mg/kg q 6 h PO for seven or more treat- are present.
ments. ● Hypoglycemia/hypocholesterolemia indicates severe
● Cimetidine inhibits hepatic production of toxic hepatic insufficiency.
intermediates. ● Abnormal coagulation tests (OSPT, APTT) suggest
– Give 5 mg/kg q 8 h PO or parenterally for 3 days disseminated intravascular coagulation.
minimum.
Death occurs from acute hepatic failure.
Blood transfusions and oxygen therapy should be given ● Histologic review of tissue specimens reveals pro-
as needed. found hepatocellular necrosis.

The prognosis is guarded and is highly dependent on A history of diazepam administration associated with
severity of intoxication and time lapse prior to treatment. fulminate hepatic failure make most other diseases
unlikely.
Prevention
Treatment
Avoid drug overdosage.
Supportive care as dictated by the patient.
Store medication safely away from pets.
Fluid therapy for hydration maintenance.
● Add dextrose to combat hypoglycemia.
DIAZEPAM INTOXICATION Meet nutritional needs to facilitated hepatic regeneration.

● Total parenteral nutrition or nasoesophageal
Classical signs catheter feeding.
● Lethargy, ataxia and anorexia < 3–4 days Plasma transfusions to replace consumed coagulation
post-ingestion. factors.
● Jaundice commonly observed.
Prognosis
Poor: cats presented in an obtunded condition warrant a
Pathogenesis
grave prognosis.
Idiosyncratic hepatotoxicity is suspected. The dosage
causing toxicity may range from 1 mg once daily to 2.5 Prevention
mg twice daily.
Evaluate baseline ALT and AST activities in cats prior
Prior sensitization to diazepam is not required. to initiating daily oral treatment with diazepam.
● Retest again 1 week after initiating therapy. Ultrasound may reveal diffuse parenchymal nodules
● Discontinue diazepam therapy in cats with unex- and an irregular liver margin.
plained increases in liver enzyme activities.
Histologic evaluation of liver biopsy specimens is
Peractin is a more effective appetite stimulant, and has required for definitive diagnosis.
not been reported to have serious idiosyncratic reactions. ● Microscopic lesions show both fibrosis and abnor-
mal regenerative nodules.
● Tissues may be obtained by ultrasound-guided
CIRRHOSIS
biopsy, laparoscopy or via laparotomy.
● Cirrhosis may be difficult to confirm by needle
Classical signs
biopsy unless multiple sites are sampled. In practice,
● Anorexia, weight loss, lethargy and a small laparotomy incision and wedge biopsy of the
jaundice. liver gives a better diagnostic sample and is quick
● Hepatomegaly or a normal-sized liver may and simple. In cats with chronic hepatitis/cirrhosis,
be palpated. less than 40% of paired needle biopsy results may
be in accordance with the wedge biopsy diagnosis.
● Patients with cirrhosis may have occult bleeding
Pathogenesis tendencies. Screen for the presence of coagulopathy
prior to liver biopsy by performing evaluation of a
Cirrhosis is a relatively uncommon disease in the cat
PIVKA assay or APTT/OSPT.
but may occur as a progression of specific feline
hepatopathies (e.g cholangiohepatitis, chronic biliary
obstruction), systemic disorders (e.g., pancreatitis, Differential diagnosis
inflammatory bowel disease, chronic renal disease),
Cirrhosis is the end result of many different chronic
and possibly vascular and immune-mediated diseases.
liver disorders. Therefore, differentiation of the pri-
Cirrhosis would appear to occur most frequently with dis- mary parenchymal disease leading to cirrhosis is gener-
eases affecting the portal areas, specifically the bile ducts. ally not clinically relevant.
Cirrhosis is characterized by both fibrosis and the con-
version of normal hepatic architecture into structurally Treatment
abnormal (regenerative) nodules.
Strategies for therapeutic support in cats with cirrhosis
are first prioritized as to severity, and approached in a
Clinical signs logical step-wise fashion. The presence of jaundice or
ascites does not indicate a hopeless situation for med-
Anorexia, weight loss and lethargy predominate.
ical treatment.
Hepatomegaly and intermittent diarrhea may also be
Feed adequate calories (1.25–1.50 MER) to prevent
observed.
further malnourishment. Use of enteral nutrition is
Ascites is uncommon. strongly recommended in anorectic cats. Reduce
dietary protein intake in cats with overt signs of hepatic
Jaundice is often present.
encephalopathy (HE).
Supplement water-soluble vitamins as needed at
Diagnosis
twice the normal dose. Use vitamin K in cats with bil-
Cats usually have a previous diagnosis of chronic iary occlusion and elevated PIVKA or APTT/OSPT
hepatopathy, such as cholangitis (cholangitis/cholan- assays.
giohepatitis).
Control signs of HE with antimicrobials, reduced pro-
Liver enzyme activities are variably increased depend- tein diets and mucosal protectants (e.g., sucralfate).
ing upon the relative magnitude of cholestasis or hepa- Vitamin K therapy may reduce GI bleeding which also
tocellular inflammation. contributes to HE.
Correct hydration deficits with intravenous fluids. Fluid Persistent hyperglycemia observed on 2–3 occasions at
choices are based on the presence of ascites and elec- least 3 hours apart over 24 hours.
trolyte status.
Urinalysis shows glucosuria, +/− ketonuria, +/− pro-
Use low-salt diets, cage rest and diuretics for control of teinuria and +/− bacteriuria.
ascites.
Liver biochemical parameters (ALT, ALP) are mildly to
Antibiotics are indicated in patients with suppurative moderately increased.
inflammation, fever and/or leukocytosis.
Use anti-inflammatory (e.g., prednisone, azathioprine) NON-HEMATOPOIETIC LIVER TUMORS
drugs to reduce mononuclear cellular infiltrates. (BILIARY CYST ADENOMA,
HEPATOCELLULAR CARCINOMA)
Anti-fibrotic agents, such as colchicine, D-penicillamine,
may reduce hepatic fibrosis.
Classical signs
Actigal may cause choleresis and promote a more bene-
● Most cats are > 10 years old.
ficial bile acid milieu.
● More common in DSH.
Reduce free radical damage to hepatocytes by adminis- ● Hepatomegaly +/- mass lesion is often
tration of S-adenosyl. palpable.
Prognosis Pathogenesis
The prognosis in most animals with cirrhosis is poor. Most (60%) of cats have benign tumors.
Bile duct tumors may progress from benign to malig-
nant lesions.
DIABETES MELLITUS ● Benign lesions are usually focal and cystic; malig-
nant tumors often involve multiple lobes.
Classical signs
Hepatomegaly is associated with extensive infiltrative
● Polyuria and polydipsia. disease.
● Increased appetite.
● Weight loss with palpable hepatomegaly. Metastasis is common with bile duct carcinomas.
Clinical signs
Clinical signs
Generally seen in geriatric cats (> 10 years old).
Polyuria/polydipsia (PU/PD) are common.
More common in DSH than in Siamese.
Increased to ravenous appetite, although terminally it
may be decreased. Anorexia, lethargy and weakness are seen.
Weight loss with or without hepatomegaly. Hepatomegaly +/− mass lesion is often palpable.
Jaundice is an uncommon complication of diabetes. It

is more commonly associated with sulfonylurea (e.g., Diagnosis
glipizide) therapy. Approximately 20% of cats on sul- Variable elevation in hepatic biochemical parameters.
fonylurea therapy develop increased liver enzymes and In general, relative increases in ALP versus ALT activ-
a small percentage become jaundiced. ity are observed. However, dramatic increases in either
liver enzyme may not be present even with moderately
Diagnosis sized tumors.
Suggested by salient clinical signs (PU/PD, alterations Abdominal imaging (survey radiographs, sonography)
in appetite, weight loss). confirms hepatomegaly or mass.
● Ultrasonography is useful in detecting involvement Weight loss, polyphagia and unkempt haircoat are com-
of multiple hepatic lobes and in obtaining a guided mon.
core biopsy of lesions.
Vomiting and small bowel diarrhea may be observed.
Definitive diagnosis requires histologic evaluation of
A reduced appetite is seen in about one in ten cats with
liver biopsy specimens.
hyperthyroidism.
Panting and respiratory distress are observed with con-
Differential diagnosis comitant cardiac disease.
It is important to distinguish benign from malignant Seen primarily in middle-aged and older cats.
hepatic tumors, as treatment and prognosis are widely
divergent. Differentiation may only be made by histo- Physical examination is suggestive.
● Palpable thyroid gland enlargement is evident in
logic interpretation of hepatic biopsy specimens.
90% of cats if the examiner is experienced.
● Patchy alopecia/unkempt haircoat, overgrown toe
Treatment nails are often present.

● Reduced muscle mass; most cats are thin.
Surgical resection (lobectomy) of benign hepatocellu-
lar or biliary tumors is recommended. Cardiac auscultation may reveal cardiac disturbances.
● Tachycardia (>240 bpm), murmurs and/or a gallop
Chemotherapy is not useful for treatment of malignant rhythm suggest cardiac manifestations of thyrotoxi-
neoplasia. cosis.
Prognosis Diagnosis
The prognosis for cats with benign tumors after resection Increased liver enzyme (ALT, ALP) activities are seen
is good. Most cats are disease free at least 1 year later. in > 75% of hyperthyroid cats.
The prognosis for malignant neoplasia is poor. Closely assess renal parameters (BUN, creatinine, uri-
nalysis) as concomitant renal disease may be present.
HYPERTHYROIDISM Demonstration of elevated basal serum thyroxine (T4)
concentration provides definitive diagnosis.
Classical signs ● Suspicious cats with a “borderline” T value should
4
● Rarely seen in cats < 8 years of age. be retested.
● Weight loss, polyphagia and unthrifty ● Increased free T may be observed in some cats
4
appearance predominate. with high normal total T4 concentrations.
● Polyuria/polydipsia +/- vomiting/diarrhea ● Alternatively, performance of a T suppression test
3
may be seen. may discriminate between normal and mildly
hyperthyroid cats.
See main reference, page 304 (The Cat With Weight Perform thoracic radiography, electrocardiography
Loss and a Good Appetite). (ECG), +/− echocardiography to rule out cardiac disease.
Clinical signs
Clinical signs result from overproduction/secretion of FELINE LEUKEMIA VIRUS
thyroid hormones. Malignant thyroid tumors are rare.
See page 424 under pre-hepatic causes for jaundice and
More than 70% of hyperthyroid cats have bilateral thy- page 432 for hepatic causes for jaundice (e.g. lympho-
roid adenomas or adenomatous hyperplasia. sarcoma).
HISTOPLASMOSIS Diagnosis
Non-regenerative anemia is typically present and neu-
Classical signs trophilic leukocytosis. Severe pancytopenia is occa-
● Young, outdoor cats (< 4 years old). sionally observed when there is bone marrow
● Lethargy, anorexia and weight loss. involvement.
● Pale mucous membranes. Hyperproteinemia, hyperglobulinemia, +/− mild eleva-
● Mild to moderate respiratory signs (fever, tions of ALT may be observed.
dyspnea, tachypnea).
● Occurs in central United States. Radiographic imaging may aid diagnosis.
● Survey thoracic radiographs show a diffuse pul-
monary interstitial pattern suggesting fungal pneu-
Pathogenesis monia.
● Symmetrical hepatomegaly is observed on survey
The etiologic agent is a soil-borne dimorphic fungus,
Histoplasma capsulatum. The organism is likely abdominal radiographs/ultrasonography.
inhaled and disseminates from the respiratory tract to Definitive diagnosis requires demonstration of organ-
multiple other sites in the body (e.g. liver). isms in infected tissues.
● Potential diagnostic modalities include bron-
Granulomatous inflammation occurs in response to
fungal infection. choalveolar lavage, fine-needle aspiration and exfo-
liative cytology, and tissue biopsy.
The disease is of regional significance in the central
United States, especially the Mississippi and Ohio Serologic tests for antibodies directed against
River Valleys and Texas. Histoplasma antigens are not recommended, as false-
negative results are common in cats with naturally
occurring disease.
Clinical signs
Primarily disease of young (< 4 years of age) outdoor
cats. Neoplasia and other systemic mycoses may produce
similar signs to histoplasmosis.
Cats present with a vague history of an insidious ● Cats with histoplasmosis (and other mycoses) tend
chronic illness. to be younger than cats with neoplasia.
● Serologic testing may be useful in detecting cats
Lethargy, anorexia, weight loss and pale mucous mem-
brane color are common. with cryptococcosis.
Respiratory distress (dyspnea/tachypnea) is seen in Treatment

50% of infected cats and occasionally coughing.
Combination chemotherapy with amphotericin B and
Lymphadenopathy, splenomegaly and hepatomegaly itraconazole (5 mg/kg PO q 12 h), or high loading
are common. doses (10 mg/kg PO q 12–24 h) of itraconazole.
Mild to moderate fever is usually present, but the tem- Generally treat for 4–6 months but dependent on remis-
perature may be normal. sion of signs.
Intestinal involvement may result in diarrhea and weight See page 26 for details of amphotericin treatment in cats
loss. On palpation thickened intestinal loops, mesenteric (Cryptococcus in The Cat With Signs of Chronic Nasal
lymphadenopathy and/or hepato/splenomegaly may be Disease).
evident.
Prognosis
Ocular involvement may cause granulomatous chori-
oretinitis, retinal detachment with blindness and optic Fair to good with disseminated disease depending on
neuritis. the severity of fungal involvement and the chronicity.
Emaciated cats with advanced disseminated disease Cyclical vomiting and fever.
have a poor prognosis and they may not live long
Hepatomegaly may be palpable.
enough for the treatment to take effect.
Acholic feces are occasionally seen with complete
POST-HEPATIC CAUSES OF JAUNDICE obstruction.
OR INCREASED LIVER ENZYMES Acute pancreatitis may cause anorexia, lethargy,
abdominal pain and jaundice as a consequence of extra-
EXTRAHEPATIC BILIARY OBSTRUCTION hepatic biliary obstruction.
(EHBO)** PANCREATITIS** Pancreatic abscesses, cysts and neoplasia may cause
signs of extrahepatic biliary obstruction.
Classical signs
● Progressive anorexia, lethargy and marked
jaundice. Diagnosis
● Vomiting and fever may be episodic. Non-regenerative anemia and possibly a neutrophilic
● Hepatomegaly. leukocytosis are seen.
● +/- acholic feces.
Increased liver biochemical parameters are commonly
observed.
● Dramatic elevations in serum total bilirubin con-
Pathogenesis
centration. Elevations may occur as rapidly as
Obstruction of the extrahepatic biliary system has 4 hours following complete biliary obstruction.
diverse causes, including pancreatic disease, neoplasia, ● Increased ALP and GGT activities occur secondary
cholelithiasis and extrinsic compression (masses). to cholestasis. A 3–5-fold increase in GGT and
Consequences of biliary obstruction include cell mem- 2–10-fold rise in ALP are often present.
brane and organelle injury due to stagnation of bile ● Increased ALT (up to 10-fold) and 3–10-fold
acids and other injurious substances. Pancreatitis and increased AST activities reflect hepatocellular
neoplasia are the most common causes. injury.
● Pancreatitis may cause obstructive jaundice through
direct cholangiohepatic injury via refluxed pancre- An antemortem diagnosis of pancreatitis causing
atic secretions, pancreatic fibrosis and/or obstruc- obstructive jaundice is elusive.
● Variable leukocytosis with elevation of liver bio-
tion of the common bile duct within a few weeks
following pancreatic injury. chemical parameters (total bilirubin, ALP, ALT) are
● Neoplasia (e.g., pancreatic adenocarcinoma) may
present.
● Recent studies show that elevation in feline
cause slowly progressive external compression of
the major bile ducts, resulting in obstructed biliary pancreatic-like immunoreactivity assay (fPLI) may
flow and jaundice. provide presumptive serologic evidence of pancreati-
tis. Serum fPLI appears to be more sensitive and more
Complete occlusion leads to cholestasis, hepatomegaly specific than serum feline trypsin-like immunoreactiv-
and dilatation of intrahepatic biliary structures. ity assay (fTLI) or abdominal ultrasonography.
● Ultrasonography demonstrates a generalized loss of
Obstruction of bile flow incites biliary tract/hepatocel-
lular inflammation and injury. pancreatic echogenicity with pancreatitis in most
● Permanent biliary tract dilatation and hepatic fibro-
cases.
sis may be seen with chronic extrahepatic biliary Ultrasonography may confirm the presence of a pan-
obstruction. creatic mass and/or extrahepatic biliary obstruction
causing extrahepatic biliary obstruction.
Clinical signs ● Diagnosis of extrahepatic biliary obstruction is
Anorexia, lethargy and marked jaundice which are pro- confirmed on ultrasonographic evaluation or
gressive. exploratory surgery.
● Sonography shows a distended/tortuous common

CHOLECYSTITIS
bile duct, large gall bladder and distended intrahep-
atic biliary ducts. These findings may be observed
Classical signs
as early as 5–7 days post-obstruction when viewed
by an experienced sonographer. ● Abdominal pain, fever, vomiting.
● +/- jaundice.
● Palpable right cranial abdominal mass.
The historical, clinical and laboratory features of extra-
Clinical signs
hepatic biliary obstruction may be indistinguishable
from other severe cholestatic hepatopathies. Abdominal pain, fever, vomiting and jaundice.
Abdominal ultrasonography is the quickest and least A mass lesion may be palpable in the cranial abdomen.
invasive means to confirm extrahepatic biliary obstruc-
Animals may present in endotoxic shock with gall blad-
tion.
der rupture.
Treatment Pathogenesis
First stabilize the patient with fluid and electrolyte therapy. Inflammation of the gall bladder is uncommon.
Perform a laparotomy for inspection/correction of the Inflammation may occur from occlusion of the cystic
biliary tract obstructive lesion. duct, with resultant gall bladder inflammation resulting
● Prompt correction of complete obstruction via per- from bile stasis. Occlusion may occur due to extralu-
formance of cholecystoduodenostomy or cholecysto- minal compression (e.g., mass, adhesion) or intralumi-
jejunostomy is recommended. nal obstruction as seen with cholelithiasis.
● Broad-spectrum antibiotics are indicated if biliary-
Emphysematous cholecystitis is most commonly
enteric anastomosis is performed. observed in association with diabetes mellitus, acute
Extrahepatic biliary obstruction caused by pancreatitis cholecystitis with/without cholelithiasis, and traumatic
may be amenable to medical therapy (dietary modifica- ischemia of the gall bladder.
tion, IV fluids, antiemetics, etc.). E. coli bacteria are most commonly cultured from the
● Biliary decompression is recommended in pan-
biliary tree of affected cats.
creatitis patients with rising hype bilirubinemia or
sonographic evidence of worsening gall bladder
distention. Diagnosis
Specific therapy for hepatocellular inflammation (con- Most animals have a variable leukocytosis.
firmed by biopsy) and intrahepatic cholestasis may be Hepatic biochemical parameters (total bilirubin, ALT
required. and ALP) are modestly increased.
● Use ursodeoxycholic acid (10 mg/kg PO q 12 h) for
5–7 days post-operatively to reduce cholestatic Ultrasonography or laparotomy is usually necessary for
injury. a diagnosis.
● Gas accumulation within the biliary tree/gall blad-
der indicates cholecystitis.
Prognosis ● Choleliths may be an uncommonly recognized inci-
dental finding.
Guarded to good depending upon the underlying cause.
● Cranial abdominal fluid accumulation indicates bil-
Biochemical abnormalities associated with extraheptic iary rupture and peritoneal inflammation. Analysis of
biliary obstruction subside quickly following success- peritoneal effusion reveals the presence of inflamma-
ful surgery. tory cells (e.g., neutrophils, macrophages) and biliru-
bin crystals in a turbid golden-brown or green fluid.
Laparotomy allows for cholecystectomy and treatment Pathogenesis

of peritonitis.
Rupture of the extrahepatic biliary tree may occur with
blunt or penetrating abdominal trauma, necrotizing
Treatment cholecystitis and cholelithiasis (rare). Leakage of sig-
Surgically remove calculi causing clinical signs of nificant volumes of bile into the peritoneal cavity
hepatobiliary disease. induces tissue inflammation. Unconjugated bile acids
are most irritating, as they alter the permeability of vas-
Assess patency of biliary tree during surgery. If the gall- cular structures within the peritoneal membranes.
bladder appears inflamed, consider cholecystectomy.
● Administer vitamin K 12–24 hours prior to surgical Altered membrane permeability promotes transmural
intervention. bacterial migration into the peritoneal cavity, septic
● Perform concurrent liver biopsy to assess the extent inflammation and septicemia.
of hepatic inflammation. Non-septic inflammation causes intra-abdominal fluid
Culture bile fluid for the presence of aerobic/anaerobic sequestration, contraction of circulating blood volume
bacterial pathogens. and dehydration which may induce hypovolemic shock.
● Use broad-spectrum antibiotic therapy effective
against enteric pathogens. Good first-choice drugs Diagnosis
which reach therapeutic biliary concentrations
include cephalosporins, penicillins, doxycycline, Suggestive history with other evidence of trauma.
metronidazole, clindamycin and the quinolones. Liver enzymes (ALP, ALT) are mildly to moderately
Base antimicrobial therapy on the results obtained increased. Moderate-to-severe hyperbilirubinemia is
from biliary culture and susceptibility testing. often present.
Fluid therapy is administered to hypovolemic cats or Cytologic examination of abdominal effusion confirms
those requiring correction of electrolyte derangements. the diagnosis.
● The effusion is turbid and golden brown-to-green in
Prognosis appearance. Inflammatory cells (macrophages and
neutrophils) and bilirubin crystals are generally seen.
The prognosis in most cases is guarded. Those cats
which are not extremely debilitated or that have necro-
tizing cholecystitis have a more favorable prognosis. Treatment
Immediate surgical correction of bile leakage.
● Perform cholecystectomy if concurrent necrotizing
RUPTURED BILE DUCT
cholecystitis is present.
● Provide adequate post-operative drainage.
Classical signs
● Malaise, weight loss. Correct fluid and electrolyte derangements intra-
● Low-grade abdominal pain. venously using a balanced electrolyte solution with
● Abdominal effusion +/- jaundice. electrolyte supplements as needed. Colloids may be
needed for correction of hypoalbuminemia if present.
Broad-spectrum antibiotic therapy, as per cholecystitis,
Clinical signs if septicemia is present.
There is often a history of trauma.
General malaise, weight loss and abdominal pain pre- Prognosis
dominate. A guarded prognosis is warranted in most cats. Cats
Abdominal effusion +/− jaundice may be present. having pronounced effusion, chronic debilitation, or
Intervals ranging from 3 days to 3 weeks before the clinical evidence of sepsis at the time of diagnosis have
presentation may be observed. a poor prognosis.
RECOMMENDED READING
Addie DD, Jarrett O. Feline coronavirus infection. In: Greene CE (ed) Infectious Diseases of the Dog and Cat, 2nd
edn. Philadelphia, PA, W.B. Saunders, 1998, pp. 58–69.
Bunch SE. Hepatobiliary diseases in the cat. In: Nelson RW, Cuoto CG (eds) Small Animal Internal Medicine, 3rd
edn. St. Louis, MO, Mosby, 2003, pp. 506–524.
Center SA, Warner K, Corbett J, et al. Proteins invoked by vitamin K absence and clotting times in clinically ill cats.
J Vet Intern Med 2000; 14: 292–297.
Charles JA, Histologic Classification of Cholangitis in Cats Proceedings of 12th ECVIM - CA/ESVIM Congress.
Ogilvie GK, Moore AS. Lymphoma in cats. In: Ogilvie GK, Moore AS (eds) Managing the Veterinary Cancer
Patient. Trenton, NJ, Veterinary Learning Systems Co, 1995, pp. 249–259.
WSAVA Standards for Histological and Clinical Diagnosis of Canine and Feline Liver Diseases. Elsevier, 2005
22. The cat with abdominal distention
or abdominal fluid
Anthony Abrams-Ogg
KEY SIGNS
● Abdominal distention or pendulous abdomen.
● Fluid wave on ballotment.
● Abdominal mass.
MECHANISM?
● In the “8F” classification scheme the causes of abdominal distention are fluid, fat, food, feces,
flatus, fetus, formidable organomegaly and feeble abdominal musculature.
WHERE?
● Abdomen. The primary disease process may be intra-abdominal, extra-abdominal or systemic.
WHAT?
● The most common causes of moderate to marked abdominal distention in cats are physiologic –
pregnancy and obesity. The most common pathologic cause is abdominal fluid.

Diseases causing abdominal distention or abdominal fluid
ANOMALY
● Intrahepatic arteriovenous fistula (p 474)
The pressure differential between the artery and portal vein leads to ascites (transudate) secondary
to portal hypertension.
● Portal vein atresia or hypoplasia (p 475)
Congenital underdevelopment of the portal vein leads to ascites (transudate) secondary to portal
hypertension.
● Inherited coagulation defects (p 473)
Inherited coagulation factor deficiencies or deficiencies in vitamin K metabolism may cause spon-
taneous abdominal bleeding and re-bleeding after trauma.
continued
443
continued
● Umbilical or inguinal hernia* (p 478)

Owners may misinterpret a change in abdominal contour due to herniation of abdominal fat or
organs as abdominal distention.
METABOLIC
● Obesity*** (p 452)
A round abdominal contour results from excessive intra-abdominal and abdominal subcutaneous fat.
●Pregnancy*** (p 455)
Abdominal distention is usually apparent by the last 2 weeks of gestation.
●Hepatic lipidosis* (p 472)
Ascites (usually transudate or modified transudate) occasionally occurs with hepatic lipidosis.
Abdominal bleeding may occur secondary to coagulopathy.
● Juvenile abdominal fluid** (p 465)
A mild increase in normal peritoneal fluid compared to a mature animal may be encountered during
laparotomy of an immature animal. Fluid is a transudate.
● Hyperadrenocorticism* (p 470)
A pendulous abdomen results from feeble abdominal musculature and increased abdominal fat.
NEOPLASTIC
● Abdominal lymphoma*** (p 458)
Alimentary lymphoma may cause abdominal distention due to marked intestinal thickening,
mesenteric lymphadenopathy or obstructive effusion. Splenic or hepatic lymphoma may sponta-
neously bleed.
● Visceral mast cell tumor** (p 461)
Marked splenic enlargement with a mast cell tumor may cause abdominal distention. Abdominal
mast cell tumors may spontaneously bleed or cause obstructive ascites. Abdominal fluid often con-
tains mast cells.
●Solid tumors*** (p 460)
Hepatic or splenic hemangiosarcoma and other solid tumors may spontaneously bleed. A tumor
may cause portal hypertension. Carcinomatosis may cause obstructive effusion.
● Neoplasia obstructing or compressing lower urinary tract (p 474)
Tumors obstructing or compressing the trigone region of the bladder or the urethra and causing para-
doxical incontinence may cause abdominal distention secondary to marked enlargement of the bladder.
NUTRITIONAL
●Overeating* (p 471)
An unusually large meal may cause transient abdominal distention.
PHYSICAL
●Aerophagia* (p 471)
Dyspneic or tachypneic cats may swallow sufficient air to cause mild abdominal distention.
22 – THE CAT WITH ABDOMINAL DISTENTION OR ABDOMINAL FLUID 445
IDIOPATHIC
●Megacolon** (p 465)
Obstipation results in marked colonic enlargement that may cause abdominal distention.
●Peliosis hepatis (p 476)
Hepatomegaly and/or spontaneous abdominal hemorrhage may cause abdominal distention.
●Hepatic amyloidosis (p 475)
Hepatomegaly, splenomegaly, intestinal dilation and/or spontaneous intra-abdominal hemorrhage
may cause abdominal distention.
● Hepatic necrosis (p 475)
Ascites or spontaneous abdominal hemorrhage may occur secondary to hepatic necrosis due to
various causes.
● Hepatic cirrhosis (p 472)
Ascites may occur with hepatic cirrhosis. The fluid may be transudate, modified transudate or exudate.
●Gastric-dilation volvulus (p 478)
Gastric dilation with air results in tympanic abdominal distention.
● Perirenal pseudocysts (p 476)
Fluid-filled sacs surrounding the kidneys cause abdominal distention. Chronic renal failure is com-
monly present.
●Right heart failure** (p 462)
Ascites may occur in cats with right heart failure. The fluid is a modified transudate.
●Extra-uterine fetuses (p 477)
Ascites occasionally occurs with “ectopic pregnancy”.
● Budd–Chiari-like syndrome (p 477)
Obstruction of the cranial vena cava or venous vasculature of the liver causes ascites. Ascitic fluid
is a modified transudate.
●Idiopathic chylous ascites (p 479)
Chylous ascites is usually due to neoplasia. Idiopathic chylous ascites is rare.
INFLAMMATION
● Gastroenteritis* (p 468)
Flatus formation and intestinal thickening in cats with diarrhea may cause mild abdominal distention.
● Non-suppurative cholangiohepatitis* (p 472)
Ascites occasionally occurs with cholangiohepatitis. The fluid may be a transudate, modified tran-
sudate or exudate.
● Pancreatitis** (p 466)
Cats with pancreatitis may have abdominal effusion, which is occasionally detectable on physical
examination. Fluid may be a modified transudate or exudate.
● Pneumoperitoneum (p 477)
Acute pneumoperitoneum is usually due to gastric perforation or gastrointestinal rupture.
continued
continued
● Steatitis (p 472)
Inflammation of abdominal fat may cause peritoneal effusion with high protein content and mature
neutrophils (exudate).
● Granulomatous urethritis and urethral stricture (p 474)
Chronic narrowing of the urethra leads to massive enlargement of the bladder and urine dribbling
from paradoxical incontinence.
● Glomerulonephritis (p 473)
Glomerulonephritis may cause nephrotic syndrome and ascites, which is a transudate.
● Sclerosing encapsulating peritonitis (p 479)
The abdominal mesothelial lining becomes replaced by fibrous tissue. Ascites may occur.
INFECTIOUS:
Viral:
● Feline infectious peritonitis (FIP)*** (p 456)
Immune-complex vasculitis results in a marked peritoneal exudate. Fluid is typically straw-
colored, viscous like egg white and highly proteinaceous (exudate) with mature neutrophils.
Hepatic infection may also cause ascites due to portal hypertension.
Bacterial:
● Septic peritonitis* (p 467)
Bacterial infection results in a septic suppurative exudate.
● Intestinal tuberculosis* (p 469)
Effusion may occur secondary to mesenteric lymphadenopathy. The fluid may be a transudate,
modified transudate, exudate or chylous effusion and may contain macrophages containing acid-
fast bacteria.
● Leptospirosis (p 478)
Leptospirosis has been associated with liver disease and ascites in cats.
●Hepatic abscess (p 476)
Hepatic abscesses may be associated with septic and non-septic effusions.
Protozoal:
Toxoplasmosis may cause peritoneal effusion secondary to liver and mesenteric lymph node infec-
tion. Fluid is a transudate or modified transudate and may contain tachyzooites.
Parasitic:
●Abdominal fluke infection (p 479)
Metorchis spp. are bile duct parasites that may cause hepatic cysts and ascites.
Iatrogenic:
● Fluid overload* (p 471)
Excessive fluid therapy tends to cause pulmonary edema leading to dyspnea or subcutaneous edema.
● Ligation of portosystemic shunt (p 475)

Ligation of a portosystemic shunt may lead to ascites secondary to portal hypertension.
Toxic:
● Anticoagulant rodenticide poisoning (and other acquired coagulopathies)* (p 473)
Acquired coagulopathy may cause abdominal hemorrhage.
Trauma:
● Traumatic hemorrhage*(p 471)
Abdominal hemorrhage may occur with blunt trauma (e.g. motor vehicle accident, falling from
heights), penetrating trauma (e.g. abdominal bite wound), or post-operatively.
● Traumatic rupture of the urinary bladder or urethra* (p 463)
The urinary bladder may rupture from motor vehicle trauma, falling from heights, bladder expression,
cystocentesis, penetrating trauma and as a complication of urethral obstruction. Abdominal fluid is
urine ± blood.
● Umbilical, inguinal and traumatic abdominal wall hernia (p 478)
Owners may misinterpret change in abdominal contour due to herniation of abdominal fat or
● Ruptured gall bladder or bile duct (p 478)
Motor vehicle trauma, falling from heights, gunshot wounds and cholelithiasis may cause rupture of
the gall bladder or a major bile duct. Fluid is dark bile-stained and a modified transudate to exudate.
● Traumatic abdominal wall hernia* (p 478)
Owners may misinterpret a change in abdominal contour due to herniation of abdominal fat or
bile or urine. In narrow definitions, peritoneal effu-

INTRODUCTION sion and ascites refer to transudates and modified
transudates. Characteristics of the various types of
fluids vary somewhat with laboratories, but the fol-
MECHANISM?
lowing definitions are typical.
– Transudate – clear and colorless, specific grav-
Abdominal distention has several causes. These causes
ity (SG) ≤ 1.013–1.018, total protein <25 g/L
may be present alone or in combination. A mnemonic
(2.5 g/dl), low cellularity (total nucleated cell
classifies the causes using an “8F scheme”: fluid, fat,
count < 1.0–1.5 × 109/L [1000–1500/μl]).
food, feces, flatus, fetus, formidable organomegaly
– Modified transudate – clear to slightly cloudy,
and feeble abdominal musculature.
straw-colored to pink-white, SG > 1.013–1.018,
Fluid accumulation in the peritoneal cavity is the most total protein between 25 and 50 g/L (2.5–5.0
common cause of pathologic abdominal distention and g/dl), and total nucleated cell count < 5.0–7.0 ×
of marked abdominal distention, but it is not as com- 109/L (< 5000–7000/μl). Nucleated cells consist
mon in cats as in dogs. of mesothelial cells, non-degenerate neutrophils,
● In broad definitions (used here), fluid in the peri- macrophages and lymphocytes.
toneal cavity is referred to as peritoneal effusion or – Exudate – turbid to opaque white to yellow or
ascites. In terms of clinical pathology, the type of red, SG > 1.018, high protein (> 25 g/L [2.5
fluid may be a transudate, modified transudate, g/dl]), highly cellular (total nucleated cell count
septic exudate, non-septic exudate, chyle, blood, > 5.0 × 109/L [5000/μl]).
– Cell types in a non-septic exudate are similar to a does not clot further after withdrawal. Platelets
modified transudate, except for feline infectious disappear within several hours, and erythrophago-
peritonitis, where the predominant cells are non- cytosis by macrophages begins within 1 day, and
degenerate neutrophils, and in some neoplastic this can be used to help age the effusion.
effusions, where malignant cells predominate. – Bile – clear to cloudy and dark yellow with
– Cells in a septic exudate are predominantly neu- a green or orange tinge, SG > 1.018, protein > 25
trophils. The fluid is further characterized by the g/L (2.5 g/dl), total nucleated cells > 5 × 109/L
presence of intracellular bacteria, degenerate (5000/μl) with cell composition similar to mod-
changes in the neutrophils and a foul odor. ified transudate, but may become a highly cellu-
– Degenerate and non-degenerate neutrophils lar septic exudate. Bilirubin may be confirmed
are distinguished on the appearance of their using a urine dipstick or by seeing bilirubin crys-
nuclei. Non-degenerate neutrophils appear simi- tals free in the fluid or in macrophages.
lar to peripheral blood neutrophils and have – Urine – clear to slightly cloudy and pale yellow,
tightly clumped, basophilic nuclear chromatin. variable SG and protein content. It may be a
As the neutrophils age, the nuclei become hyper- transudate, but total nucleated cells are often > 3
segmented, and then pyknotic (tightly clumped × 109/L (3000/μl) with cell composition similar
sphere), and then eventually break up into sev- to modified transudate, and it may become a
eral smaller tightly clumped spheres (karyor- highly cellular septic exudate.
rhexis). This aging change should not be ● While in theory a specific disease process causes a
confused with degenerative change. Degenerate specific type of fluid, in reality the type of fluid
neutrophils have swollen pale eosinophilic may vary somewhat. In particular, the disorders that
nuclei resulting from increased membrane per- generally cause pure transudates are occasionally
meability to water. Toxic changes in the cyto- associated with modified transudates, and vice
plasm (basophilia, vacuolation and Dohle versa. This may be due to modification of fluid pro-
bodies) may also be present. duction by concurrent disorders as well as variable
– In a recent report, a nucleated cell count > 13 × criteria for characterizing the fluids. The implica-
109/L (13 000/μl) was highly sensitive and spe- tion of this fact is that a specific differential diag-
cific for septic peritonitis, although cats with FIP nosis should not be ruled out strictly on the
were not included. grounds that the type of fluid is not the classic
– Protein content characteristic of an exudate may type for that disorder.
be confirmed by Rivalta’s test (see Feline infec- – Although protein content is one of the classic
tious peritonitis). clinicopathologic values by which to categorize
– Chyle – opaque and white to pink (slightly fluids, protein levels were recently reported to be
cloudy and straw-colored in fasting animals), SG similar in septic and non-septic peritoneal fluids.
variable, protein 2.0–7.0 g/L (20–70 g/dl), and ● The peritoneal cavity is lined by a serous membrane
total nucleated cell count < 10 × 109/L (10 000/μl) (serosa) and normally contains a small amount of
containing a large number of small lymphocytes fluid that serves as a lubricant for the abdominal
(chyle is comprised of lymph and chylomicrons). organs. Normal peritoneal fluid is a transudate
The fluid in the tube separates into a cream-like (ultrafiltrate) that comes from interstitial fluid pro-
layer when refrigerated. Chylous effusions are duced by local capillary beds, which diffuses across
also characterized by fluid triglyceride level the serosa into the peritoneal cavity. The serosa is
greater than serum triglyceride level, fluid choles- equally permeable to diffusion of the fluid back into
terol level lower than serum cholesterol level, and the interstitium, but most is reabsorbed from the
a fluid cholesterol:triglyceride ratio < 1 (with the abdomen by uptake by lymphatics, especially of the
values measured in mg/dl). diaphragm. The ultrafiltrate contains protein that is
– Blood – cloudy and red (centrifugation results in in equilibrium with plasma protein. The mecha-
a clear supernatant above red sediment), SG, pro- nisms that promote formation of subcutaneous
tein and total nucleated cell count consistent with edema will thus promote formation of peritoneal
peripheral blood. Effusion may contain clots but fluid. These mechanisms are:
– Reduced plasma colloidal osmotic (oncotic) thrombosis (not reported in the cat). The fluid is
pressure due to hypoalbuminemia. Hypo- usually a transudate.
albuminemia occurs by the same mechanisms as – Pre-sinusoidal hepatic portal hypertension may
in dogs, i.e. reduced hepatic production, or renal, be caused by an arterioportal fistula and surgi-
gastrointestinal or cutaneous loss. Hypoalbumi- cal ligation of a portosystemic shunt. The fluid
nemia severe enough to cause spontaneous is usually a transudate.
effusions or edema (typically ≤ 10–15 g/L – Sinusoidal hepatic portal hypertension results
[1–1.5 g/dl) is rare in cats. As albumin levels from liver disease. The most common cause is
drop there is a progressive risk for exacerbation cirrhosis, which is uncommon in cats. Severe
of ascites formed by other mechanisms, for hepatocyte swelling in hepatic lipidosis, and
example, increased hydrostatic pressure. When chronic cholangiohepatitis and hepatic neoplasia
spontaneous fluid accumulation occurs, subcuta- may also cause sinusoidal hypertension. Other
neous edema may develop preferentially to pleu- mechanisms contribute to ascites in liver dis-
ral and peritoneal effusions. Peritoneal fluid is ease, including hypoalbuminemia, water and salt
a transudate. retention (see below) and non-septic peritonitis.
– Increased capillary hydrostatic pressure. This The fluid may thus be a transudate, modified
may occur from fluid overload, decreased arte- transudate or exudate. Although liver diseases
riolar resistance, and increased venous pres- are common in cats, ascites sufficient to cause
sure. Cats with fluid overload usually develop abdominal distention is not.
pulmonary or subcutaneous edema preferen- – Post-sinusoidal hepatic portal hypertension is
tially to pleural and peritoneal effusions. Fluid caused by veno-occlusive disease. The fluid is a
overload causes a transudate. modified transudate.
– Portal venous hypertension is an increase in – Post-hepatic (post-sinusoidal) portal hyperten-
venous pressure unique to the abdomen. It is sion results from obstruction of the hepatic
classified anatomically as pre-hepatic (which is veins or caudal vena cava and right heart fail-
also pre-sinusoidal), hepatic (pre-sinusoidal, ure. Increase in vena caval pressure increases
sinusoidal, or post-sinusoidal), or post-hepatic hepatic vein pressure, which increases sinu-
(which is also post-sinusoidal) in origin. soidal and portal pressures. The fluid is a modi-
Anatomic location affects protein content of the fied transudate.
ascitic fluid and is relevant to differential diag- – Obstruction of the venous outflow of the liver,
noses. Pre-sinusoidal disorders usually cause a from the hepatic venules to the right atrium, is
pure transudate. Sinusoidal and post-sinusoidal referred to as Budd–Chiari-like syndrome. It is
disorders increase hepatic sinusoidal pressure, rare in cats.
which, in addition to portal hypertension, causes ● Reduced lymphatic uptake. This usually occurs
effusion of hepatic lymph from the hepatic lym- with tumors obstructing a substantial portion of the
phatics through the surface of the liver. Hepatic serosal surface or mesenteric lymph nodes (±
lymph is high in protein. The resulting fluid is a venous obstruction). The fluid is a transudate to
modified transudate, i.e. a transudate modified modified transudate, but may contain neoplastic
by increased levels of protein. The fluid may cells. Lymphatic obstruction occurs occasionally
also have a mild increase in red blood cells, with inflammation, in which case the fluid is a
resulting in a serosanguineous fluid. modified transudate to exudate.
– Pre-hepatic portal hypertension results from ● Increased permeability of the capillary endothe-
obstruction of the portal vein, usually by a lium and blood vessels. This occurs secondary to
tumor. The fluid is a transudate, but may contain inflammation.
neoplastic cells. Other potential causes include – In feline infectious peritonitis a type III hyper-
surgical ligation of a portosystemic shunt or sensitivity reaction leads to leukocytoclastic
of the portal vein, portal vein atresia or hypopla- (neutrophil-mediated) vasculitis. The fluid is a
sia (anecdotal reports in the cat), and portal vein non-septic exudate, containing increased levels
of inflammatory proteins and neutrophils from Bile in the peritoneal cavity results from traumatic
the vasculitis. injury to the gall bladder or bile ducts. It is rare in cats.
– In septic peritonitis the fluid is a septic exudate The presence of bile may be associated with septic or
containing bacteria and increased levels of pro- non-septic peritonitis, with increases in bacteria and/or
tein, neutrophils and bacteria. protein and neutrophils accordingly.
– In pancreatitis the fluid is a modified transudate
Urine in the peritoneal cavity usually results from trau-
to non-septic exudate, depending on the increase
matic injury to the urinary bladder. It is uncommon in
in protein and cells.
cats. Rarely direct effusion of urine may occur with
– Ascites may be associated with a decreased
severe cystitis. The presence of urine may be associated
effective plasma volume, which promotes salt
with septic or non-septic peritonitis, with increases in
and water retention by the renin-angiotensin-
bacteria and/or protein and neutrophils accordingly.
aldosterone system, antidiuretic hormone, and
Rupture of the bladder may also cause abdominal hem-
the sympathetic nervous system, thereby helping
orrhage.
to maintain the ascitic state. (Water retention
may result in hyponatremia. Hyperkalemia may Fat accumulates because of overeating and underactiv-
also result from a decreased effective plasma ity. Fat accumulates within the abdomen as well as
volume and other mechanisms in cats with within the abdominal subcutaneous tissue, especially of
ascites. The combination of hyponatremia and the caudal ventral abdomen.
hyperkalemia mimics hypoadrenocorticism.)
Food may cause increased distention of the stomach
Chyle in the peritoneal cavity is an uncommon non- and small intestine after a large meal. This is a physio-
specific finding indicating that lymphatic rupture has logic cause of organomegaly.
occurred. Chylous effusion may occur with any of the
Feces may cause increased distention of the large intes-
basic mechanisms that promote peritoneal fluid pro-
tine after a large meal. This is a physiologic cause of
duction except for hypoalbuminemia. Most cases are
organomegaly. More often, increased accumulation of
caused by neoplasia, and fewer are caused by inflam-
feces in the large intestine is a sign of constipation.
mation, right heart failure and liver disease. Other
Severe constipation (obstipation, megacolon) may
causes are rare in cats, including primary abdominal
result in marked abdominal distention.
lymphangiectasia and traumatic rupture of a major
lymphatic vessel. Flatus (gastrointestinal air) is not physiologically com-
mon in cats. Flatus may develop secondary to aeropha-
Blood in the peritoneal cavity results from injury to
gia in dyspneic cats and as a sign of primary intestinal
blood vessels, spontaneous or traumatic rupture of
disorders. Gastric dilation-volvulus is rare. Abdominal
abnormal blood-filled spaces, or a coagulopathy.
distention may also develop from pneumoperitoneum.
Hemoperitoneum is not as common in cats as dogs,
Sources of air include gastric perforation, gastrointesti-
because abdominal trauma does not commonly cause
nal rupture, extension of air from the thoracic cavity,
severe abdominal hemorrhage in cats, and heman-
penetrating abdominal wounds and intra-abdominal
giosarcoma is rare. Other causes of hemoperitoneum in
gas-forming bacteria.
the dog such as anticoagulant rodenticide poisoning,
perforated gastrointestinal ulcers, and splenic torsions, Fetuses are a cause of physiologic organomegaly.
are also uncommon in cats. Clinical signs due to acute
Formidable organomegaly usually results from
anemia and local effects of hemorrhage vary with the
markedly distended hollow organs (bladder, intestinal
severity of bleeding. Signs of acute hypovolemia, e.g.
tract, uterus) or neoplasia. Granulomatous inflammation,
weakness, lethargy, hypothermia, pale mucus mem-
cyst and pseudocyst formation is less common. Rare
branes, tachycardia and weak pulses, occur with a
causes include heterotopic ossification. Acute inflamma-
smaller volume of blood loss than do abdominal dis-
tion of an organ usually causes minimal to moderate
tention. In most cases of hemoperitoneum in cats,
organomegaly and does not cause abdominal distention.
abdominal distention is not noted. In converse, cats
with abdominal distention due to acute blood loss will Feeble abdominal musculature is caused by hyper-
have signs of hypovolemia. adrenocorticism.
Organomegaly is easily detected on abdominal palpa-

WHERE?
tion, with the exception of hepatomegaly where falci-
Abdominal distention and/or fluid may be signs of: form fat may preclude palpation of the liver.
● A primary abdominal disorder or physiologic ● Mild distention of the intestines with air may make
change. Any abdominal organ may be involved. them less distinct than usual on palpation.
● An extra-abdominal disorder. ● Free-living toms may have firm abdominal muscula-
● A systemic disorder. ture and be more difficult to palpate.
Peritoneal fluid may be accompanied by pleural fluid, Abdominal pain may be signaled by contraction of
pericardial fluid or subcutaneous edema. abdominal musculature, vocalization on abdominal
palpation, attempting to escape, and defensive aggres-
A large volume of abdominal fluid, in addition to caus-
sion. Some clinicians believe that cats with abdominal
ing abdominal distention, may cause dyspnea
pain may not react, and that inactivity and remaining
(diaphragmatic compression), anorexia (compression
hunched-up also signify abdominal pain. Abdominal
of the stomach), increased frequency of urination (com-
pain may be caused by trauma, inflammation of a spe-
pression of the bladder), abdominal discomfort, and
cific organ, peritonitis, acute over-distention of the
difficulty walking. A large volume of fluid can also
bladder or gastrointestinal tract, and over-exuberant
compress the caudal vena cava and decrease venous
palpation. Abdominal pain may be mimicked by back
return to the heart.
pain (uncommon in cats), or the cat objecting to veteri-
nary examination. Fluid distention due to transudates
WHAT? and modified transudates is not painful.
The chief complaint may be abdominal distention, per- Abdominal radiography, abdominal ultrasound exami-
ceived weight gain, signs due to abdominal distention, nation, and abdominocentesis will reveal the cause of
or signs of an underlying or associated disease. abdominal distention if clinical findings are inconclusive.
● If imaging is planned it should be performed prior
Most causes of abdominal distention may result in min- to abdominocentesis (1) to identify organomegaly,
imal to marked distention, but most commonly result in and (2) because a small amount of air may enter the
minimal to mild distention. The most common causes abdomen during abdominocentesis, which may cre-
of abdominal distention in cats are physiologic – preg- ate imaging artifacts.
nancy and obesity. The most common pathologic cause – Radiography will not detect small volumes of
of moderate to marked abdominal distention is abdom- fluid. There is progressive loss of abdominal
inal effusion. The most common causes of marked detail with increasing amounts of fluid, and
abdominal effusion are right heart failure, feline infec- large-volume ascites creates a homogeneous soft-
tious peritonitis and neoplasia. tissue density. Radiography is not very useful to
distinguish the type of fluid, except that exudates
tend to produce a “ground-glass appearance”
DIAGNOSIS
because the presence of flocculent material pro-
Fat is easily confused with fluid, both peripherally and duces variation in radiographic density.
in the abdomen, and the two cannot always be distin- – Ultrasonography will detect small volumes of
guished by palpation alone. However, cats with severe fluid, and may identify flocculent densities in
abdominal distention due to fluid will have a more exudates and debris on the serosa.
taught abdomen than severely obese cats, and body con- ● Abdominocentesis will usually be positive if there
tour will change more with position when distention is is > 4–5 ml/kg of fluid.
due to fluid. Fluid is confirmed on physical examination – If fluid is detected during an ultrasound exami-
only if a fluid thrill or abdominal organ is noted with nation, ultrasound-guided aspiration of the fluid
ballottement, which requires a large volume of fluid. is recommended.
Smaller amounts of fluid may cause the abdominal – For blind abdominocentesis, the cat is best sup-
organs, especially the loops of intestine, to feel more ported in the standing position or held in the
slippery than usual, or to be less distinct than usual, on restrainer’s arms with the ventrum parallel to the
palpation. ground. Ideally the bladder should be empty.
– If a large volume of fluid is known to be present, the catheter more difficult to advance and
a regular needle, butterfly needle, intravenous more prone to kinking or breakage) or peri-
catheter or peritoneal lavage catheter attached to toneal dialysis/lavage catheter (preferred) is
a syringe ± three-way stopcock may be used to inserted caudally, or right laterally, to the
remove the desired volume. Following surgical umbilicus (dissection may be used), and
preparation of the skin, the needle or catheter is directed caudally and towards the right.
inserted along the ventral midline caudal to the – 20 ml/kg warm saline is infused by gravity or
umbilicus. injected over 2–5 minutes. The cat is gently
– If the procedure is being used to diagnose the rolled from side-to-side (catheter in place),
presence of a small volume of fluid, a 1-inch, 22-G and then after 2–5 minutes a diagnostic sam-
needle should be inserted along the ventral mid- ple is retrieved by gravity or by aspiration (it
line caudal to the umbilicus, and the fluid is neither necessary nor possible to retrieve all
allowed to drip out by gravity. Samples should the infused fluid). The catheter is removed
be collected into an EDTA (purple top) tube and and the skin incision sutured.
into a clot tube (red top). If no fluid appears, the – Complications from presence of a large
needle should be gently twisted, and, if this is volume of ascites may necessitate large-volume
unsuccessful, a syringe may be attached and abdominocentesis. This is normally a safe proce-
gentle suction applied. If midline abdominocen- dure, however:
tesis is negative, the abdomen may be “divided” – The fluid may rapidly re-accumulate, espe-
into four quadrants with the umbilicus as the cially if intra-abdominal pressure from the
center point, and the procedure repeated in each fluid (tamponade) was in equilibrium with the
quadrant, stopping when a sample is obtained. forces promoting fluid accumulation. Very
– Minimal analysis of the fluid consists of visual rapid re-accumulation could lead to acute
inspection, specific gravity, packed cell volume hypovolemia. This is most likely to occur
and total protein (measured by refractometer or with hypoproteinemia and right-sided heart
urine dipstick), and cytologic examination using failure.
a routine hematology stain. Fluids with high cel- – Repetitive large-volume abdominocentesis
lularity may be examined using a smear similar will promote hypoproteinemia because of
to a blood smear or using a squash smear. Fluids repetitive loss of protein in the ascitic fluid.
with low cellularity should be centrifuged prior – For these reasons it is recommended to
to examination and/or examined using a line- remove enough fluid to resolve secondary
smear technique, a technique similar to a blood problems, but not to try to empty the
smear, but where the spreader slide is rapidly abdomen.
drawn back several millimeters before the end of
The prognosis for cats with peritoneal effusion is
the sample slide, thus concentrating the cells in a
generally poor, especially if accompanied by pleural
line. More extensive evaluation may include cell
effusion.
counts, bilirubin, urea, creatinine, potassium,
glucose, bibarbonate, lactate, pH, albumin, glob-
ulin, cholesterol, triglyceride, amylase and DISEASES CAUSING ABDOMINAL
lipase levels, RT-PCR for feline coronavirus, DISTENTION OR ABDOMINAL FLUID
Gram-stain and microbial culture.
– If abdominocentesis is unsuccessful, diagnostic
peritoneal lavage may be performed. OBESITY***
– The bladder is emptied and the cat is
restrained in dorsal or left lateral recumbency. Classical signs
– The skin is surgically prepared. An intra- ● Disproportionately large abdomen
venous catheter (which may be fenestrated compared to head, thorax and distal limbs.
with a scalpel blade, although this may make
Pathogenesis Obesity causes or increases the risk for insulin resist-

ance, impaired glucose tolerance, diabetes mellitus,
Obesity results from caloric intake in excess of that hepatic lipidosis, feline lower urinary tract disease,
required for basal metabolism and physical activity. musculoskeletal problems, bacterial skin infections,
Overfeeding prior to maturity may cause adipocyte pro- increased risk of surgical and anesthetic complications
liferation predisposing to obesity in maturity. and impaired immune function. Obesity as a risk factor
for cardiovascular disease and neoplasia in cats has not
Adipocyte numbers gradually increase with aging and been reported.
basal metabolic rate decreases.
Some cats are probably more likely to become obese by Clinical signs
genetic predisposition.
Obesity is typically most pronounced in the abdomi-
Neutering promotes obesity in part because sex hor- nal region, although the thorax, neck and upper limbs
mones affect appetite and protein and fat metabolism. will also have increased subcutaneous fat.
Neutered cats have lower basal energy requirements ● If abdominal distention is due to intra-abdominal
and are also less likely to roam. fat, it will be accompanied by deposition of sub-
● Neutered male cats are more prone to obesity than
cutaneous fat. Large subcutaneous fat depots may
neutered female cats. accumulate in the inguinal area.
● Obesity in neutered male cats is primarily due to
increased food intake. Signs of adult-onset hypothyroidism include lethargy,
inappetence, mild hypothermia and heat-seeking
Physical activity is reduced in many housecats and with behavior, skin changes (dry lusterless hair, scale forma-
aging. Reduced physical activity reduces caloric needs, tion, alopecia, myxedema), bradycardia and reproduc-
and also results in reduced muscle mass, which in turn tive problems. Obesity may be severe.
lowers basal metabolic rate.
Signs of acromegaly include signs of diabetes mellitus,
Offering highly palatable foods and boredom may facial and carpopedal dysmorphism, and cardiomegaly.
increase calorie intake. Signs of hyperadrenocorticism include signs of dia-
Appetite stimulation is a side effect of certain drugs. betes mellitus, abdominal distention, alopecia and frag-
This effect is most pronounced with megesterol acetate ile skin. The signs of insulinoma are those of
and benzodiazepines, but may occur occasionally with hypoglycemia.
glucocorticoids and phenobarbital. Various drugs may
also reduce physical activity. Diagnosis
Endocrine disorders causing obesity are rare in cats. Diagnosis of obesity is usually made on the basis of
● Hypothyroidism is usually caused by treatment of
physical examination. Abdominal radiography or ultra-
hyperthyroidism. Naturally occurring hypothy- sound examination can be used to confirm obesity as a
roidism in mature cats is rare, but may be idiopathic cause of abdominal distention if necessary.
or immune-mediated as in the dog.
● Acromegaly may cause initial obesity by appetite There is usually a history of a highly palatable, high-
stimulation and weight gain by stimulation of bone calorie diet being consumed and physical inactivity.
and muscle growth. Cats with acromegaly ultimately There is absence of other clinical signs of other causes
develop diabetes mellitus, which causes weight loss. of abdominal distention.
● Hyperadrenocorticism may cause initial obesity by
appetite stimulation. Many cats with hyperadreno- If there are signs of endocrinopathy, it should be con-
corticism develop diabetes mellitus, which causes firmed by appropriate testing. Endocrinopathies are
weight loss. rare causes of obesity.
● Insulinoma could theoretically promote obesity ● Hypothyroidism may be suspected on the basis of
because of the anabolic effects of insulin, but this clinical signs, a low T4 and/or free T4 (measured by
has not been reported. equilibrium dialysis validated for cats), and absence
of evidence for a concurrent disorder causing Primary obesity is best treated by offering a
euthyroid sick syndrome. hypocaloric diet designed for weight loss in cats.
– If there is a history of treatment for hyperthy- These diets generally have reduced fat and higher car-
roidism, the above findings plus response to bohydrate than maintenance diets, and a higher con-
therapy are sufficient for a diagnosis. centration of essential nutrients. Some are also high in
– If naturally occurring hypothyroidism is sus- fiber. Newer weight-loss diets for cats have restricted
pected, additional testing is recommended. carbohydrate (<25% ME) and are high in protein.
Similar to testing for hypothyroidism in dogs,
A satiety effect of insoluble fiber (e.g. cellulose) used
interpretation of tests is controversial.
as a bulking agent has not been proven in cats, and
– TSH response tests using animal-origin TSH
foods rich in such fiber increase the risk of constipa-
have been used in the past, but such TSH is no
tion. Fermentable fiber may promote satiety.
longer widely available. Recombinant human
TSH is now available, and protocols using this Because some obese cats have very low metabolic
preparation should be defined in the future. rates, it is best to calculate the amount of energy being
– TRH response test may be used: Obtain baseline consumed by the cat, and then reduce energy fed to
serum sample, give 0.1 mg/kg IV, obtain post 80% of current consumption. Using current energy
serum sample at 4 hours. A normal response is a consumption as a basis for restricting calories, makes it
> 50% increase from baseline. more likely that successful weight loss will be achieved
– The assay for canine TSH has been used anec- in the first month of the program, which makes it more
dotally but has not been validated for the cat. likely the owner will continue the program.
– Thyroid biopsy may be obtained, demonstrating ● If current energy consumption cannot be deter-
atrophy or thyroiditis. mined, a guideline is to offer 60–75% of energy the-
– If there is a response to therapy, thyroid supple- oretically required for maintenance of ideal body
ment can then be withdrawn to observe for weight (i.e. 60–75% of 60 kcal/kg ideal body
recurrence of signs. weight/day) and adjust every 2–4 weeks to achieve
a loss of about 1% of body weight per week.
Differential diagnosis At 1% weight loss per week, about 90% of weight will
The principal cause of abdominal distention that may be lost from fat and <10% from lean body tissue. More
be confused with fat is fluid. However, many cats with severe calorie restriction decreases the proportion lost
ascites are chronically ill and have muscle wasting. from fat and increases the proportion of weight lost
from lean body tissue. Losses of body weight greater
Pregnancy – in pregnant cats the degree of abdominal than 2% per week are dangerous as hepatic lipidosis
distention may be disproportionate to the amount of may develop. During a weight loss program it is impor-
subcutaneous fat. tant to verify that the cat is eating regularly. Fasting will
Obesity is a common disorder and may make diagnosis increase the risk for developing hepatic lipidosis.
of other concurrent causes of abdominal distention dif- It is important not to restrict calories by restricting protein.
ficult by interfering with palpation.
Dietary additives may help promote weight loss and/or
ameliorate secondary glucose intolerance, and are
Treatment being added to commercial diets for cats.
For successful management of obesity, it is essential ● l-carnitine increases fatty acid oxidation and pro-
that the owner is committed to the goal that their cat motes fat loss, while preserving muscle mass. It
achieves a healthy body weight. The owner needs to also appears beneficial in treating cats with hepatic
understand and believe that appropriate management of lipidosis. Supplemental l-carnitine can be dosed
obesity leads to a more active and healthier pet, and a orally (250 mg/cat q 24 h of pharmacological grade
longer life of their pet. The evidence that only 53% of product added to food or formulated as aqueous
obese cats were alive after 4 years compared to 83% suspension).
of cats with optimum body weight may help to con- ● Vitamin A promotes weight loss by stimulating
vince some owners of the importance of weight loss. uncoupling protein formation, which increases
energy loss as heat. Vitamin A also decreases leptin

PREGNANCY***
(a hormone involved in fat metabolism) concentra-
tions, which may improve insulin sensitivity.
Classical signs
● Chromium, fermentable fiber and low glycemic
index starch sources (corn, sorghum) may ● Mild to marked abdominal distention in
improve glucose tolerance status by improving breeding cats.
insulin sensitivity, increasing insulin secretion and
decreasing post-prandial glucose concentrations, Pathogenesis
respectively.
● Increasing physical activity is also beneficial, but Intentional or unintentional breeding.
is not as easy to achieve in cats as in dogs. The most
practical approach is to encourage the owner to Clinical signs
engage in regular active play with the cat, such as
having the cat chase an object on a string or a light Previous signs of estrus.
spot, although it is not known what constitutes a Abdominal distention usually does not become appar-
proper “feline exercise program”. Other alternatives ent until the last 1–2 weeks of gestation. It is easiest to
for indoor cats are to provide an outdoor enclosure detect in queens that are thin, have a short haircoat,
or leash-controlled outdoor activity sessions. have had previous pregnancies, and have large litters.
– Cats given environmental enrichments such as
additional food dishes, water bowls and litter Mammary gland development (“milk bar”) usually
boxes, plus climbing towers, window perches, does not become apparent until the last week of ges-
scratching posts, cat spas, grooming supplies tation, although pinking of the nipples may be noted
and toys, had increased activity levels sooner. Abdominal distention is usually noted before
and greater weight loss compared to cats that development of a milk bar.
did not have an enriched environment Nesting behavior does not begin until 1–2 days before
Surgical debulking of fat or liposuction has not been delivery.
reported in cats and is not recommended.
Diagnosis
The use of drugs is currently not recommended.
Dehydroepiandrosterone may cause severe adverse reac- History of estrus, indoor/outdoor lifestyle, escape from
tions in cats. Thyroid hormone should only be used in indoors, or intentional breeding.
cases of proven hypothyroidism. The initial dose is
Fetal membranes can usually be palpated from day
0.05–1.0 mg once a day, with a goal of maintaining
17–25 of gestation, and occasionally up to day 35. The
serum T4 between 20–40 nmol/L 4–6 hours after dosing.
fetuses palpate as distinct water-filled spheres (“tiny
bladders”). An enlarged uterus is palpable as a tubular
Prognosis organ between the colon and bladder from day 25 of
The prognosis for weight reduction is dependent upon gestation and on.
compliance. Fetuses can be seen by ultrasound examination begin-
The prognosis for complications of obesity depends ning day 11–14 of gestation; fetal heartbeats can be
upon the severity of obesity and other factors affecting seen by day 22–24.
the complicating disorder. Fetal mineralization is first detectable by radiography
The prognosis for hypothyroidism is excellent. beginning day 38 of gestation, but is most reliable for
identifying fetal skeletons after day 45 of gestation.
This corresponds to the period that abdominal disten-
Prevention tion becomes apparent.
The ration should be restricted or a hypocaloric diet ● The above times are based on breeding dates and
offered as soon as the propensity for obesity is noticed. are not as reliable as times based on days prior to
Physical activity should be encouraged. parturition. In a recent report, fetal mineralization
was first detectable 25–29 days prior to parturition, lent FIP strains arise from mutations in the avirulent
and the vertebral column detectable by day 22–27 (enteric) strains during replication of the latter. Both
prior to parturition. The pattern of progressive min- type I (genuine) FCoV and type II FCoV (which result
eralization was used to accurately predict day of from recombination between FCoV and canine coron-
parturition. avirus) can give rise to FIP strains.
The virus initially replicates in epithelial cells of the
Differential diagnosis pharynx, respiratory system and intestinal tract.
Cats with uncomplicated pregnancies are healthy, and Antibodies are produced, which fail to eliminate the
as such the main differential diagnosis is obesity. virus and facilitate its uptake by macrophages, where
However, obese cats are more often neutered, and the virus further replicates.
obese cats also have evidence of increased subcuta-
Macrophages migrate in the blood to venules of various
neous inguinal fat. Palpation of an enlarged uterus is
tissues, e.g. the serosa of the abdomen. The macrophages
usually possible in pregnant cats, and palpation find-
exit the venules, and virus replication continues.
ings can be confirmed by imaging.
Antigen–antibody complexes form around the
If a sick cat with abdominal distention with an venules, attracting neutrophils. The result is a pyo-
unknown pregnancy is presented for examination, all granulomatous vasculitis, resulting in effusion.
other causes for abdominal distention should be con-
FIP is more common in cats infected with feline
sidered. If the only cause of abdominal distention found
leukemia virus (FeLV) in areas where FeLV is fre-
during work-up appears to be an enlarged uterus, then
quent.
acute metritis or spontaneous abortion should be
considered, as well as an unrelated disorder complicat-
ing pregnancy. Clinical signs
Most common in cats 3 months to 3 years old. There
Treatment may also be an increased prevalence in geriatric cats.
Ovariohysterectomy if the pregnancy is unwanted. FIP occurs in two main forms: wet (effusive) and dry.
Non-specific signs (depression, anorexia, weight
loss, fever) are common in both forms.
Prognosis
In wet FIP, pericardial, pleural and/or peritoneal
Good – dystocia is uncommon in cats.
effusions occur.
● Initially abdominal organs, especially the intes-
Prevention tines, may not feel as distinct as usual.
● Later, as fluid accumulates, marked painless dis-
Ovariohysterectomy; isolate from toms during heat.
tention of the abdomen occurs.
In dry FIP, signs are referable to the organ involved.
FELINE INFECTIOUS PERITONITIS (FIP)***
● FIP may cause chronic hepatitis, which could
result in abdominal distention from hepatomegaly
Classical signs
and ascites from portal hypertension.
● Depression, anorexia, weight loss, fever, ● Massive mesenteric lymphadenopathy has also
pleural or peritoneal effusion. been reported.
FIP is caused by strains of feline coronavirus (FCoV). No routinely performed test has 100% sensitivity or
These virulent stains have the ability to replicate in specificity, and diagnosis always relies on a combina-
macrophages as well as in epithelial cells. The viru- tion of clinical signs and laboratory test results.
A complete blood count may reveal a mature neutro- of 1 was reported to have a negative predictive value
philia (chronic inflammation), lymphopenia (stress), of 91% (and a higher ratio would presumably have a
and high plasma total protein (increased globulins and higher negative predictive value.)
fibrinogen). – Rivalta’s test is useful to confirm that the fluid is
an exudate, by testing for coagulation of protein
A serum chemistry profile may reveal hyperglobuline-
in an acetic acid solution. Five ml of distilled
mia and a decreased albumin to globulin ratio. (Total
water and one drop of 98% (glacial) acetic acid
serum protein is less than plasma protein because of the
are mixed in a test tube. Vinegar should be a
absence of fibrinogen.) Liver enzymes ± bilirubin will
practical alternative to use as a point-of-care test.
be elevated if there is hepatic involvement.
One drop of the effusion is carefully layered on
“FIP tests”, which include various serum antibody the surface of the solution. If the drop disappears
tests and RT-PCR assays for FCoV viral antigens, and the solution remains clear, the test is nega-
are often non-contributory. Positive tests indicate tive and the fluid is a transudate. If the drop
exposure or presence of FCoV and not necessarily the retains its shape, remains on the surface, or
FIP strains. Tests are likely to be positive with classic slowly floats down, the test is positive and the
effusive FIP, but a negative test result does not rule out fluid is an exudate. Rivalta’s test may also be
the disease if the clinical, laboratory and pathologic positive in septic peritonitis and lymphoma (i.e.
findings are typical of the disease. Cats with very high other causes of exudates), but these disorders
titers are likely to have FIP. Furthermore, because the can usually be ruled in or out with other tests.
negative predictive value of the antibody test is high – Glucose may be detected with a urine dipstick but
overall, cats with abdominal effusion and a negative the diagnostic value of glucose level is not known.
antibody test result are unlikely to have FIP (although – Direct immunofluorescence of FCoV antigen
serum antibody titers may be low because of binding by in the peritoneal fluid macrophages. This has
the large viral load in the effusion). been reported to have a specificity and positive
predictive value of 100%, and negative predic-
Abdominal radiography or ultrasonography will
tive value of 57–89%.
demonstrate peritoneal fluid, typically containing
– Utility of measuring FCoV antibody in the
echogenic debris.
effusion varies, but it is at least as good as, and
Abdominocentesis. Cytologic, biochemical and probably better, than a serum test.
immunologic tests on the abdominal fluid are more – Preliminary results indicate that RT-PCR for FCoV
useful than blood tests. These tests include: in the effusion is of high sensitivity and specificity.
● Cytology. Peritoneal fluid from a cat with wet FIP – Adenosine deaminase activity. The level in the
will typically reveal a non-septic exudate. The fluid fluid is usually higher than with other causes, but
is pale to straw-colored, may contain white flecks the test is not routinely available.
(fibrin) and may clot upon standing. Cytology
An FeLV test should be performed.
reveals a high-protein background (stippling, cres-
cent formation) and mature neutrophils. Chylous Exploratory surgery or laparoscopy with reveal multi-
effusion may also occur. focal small (e.g. 1–5 mm) white serosal plaques.
● Total protein, albumin and globulin levels. As in Biopsies of abdominal lesions seen at surgery or
serum, but of more diagnostic value: the higher the laparascopy reveal pyogranulomatous to granuloma-
total protein and globulin level, and lower the albu- tous inflammation. Immunohistochemistry may be
min to globulin ratio, the more likely the cat has FIP. used to demonstrate FCoV antigen within tissues. Viral
Total protein ≥ 120 g/L (12 g/dl) had a specificity of culture may be available through research facilities.
99% and positive predictive value of 89% in one
study, while gamma-globulins ≥ 30 g/L (3.0 g/dl)
and gamma-globulin content >32% in the fluid as
demonstrated by protein electrophoresis have been Differential diagnoses for cats with non-specific signs
reported to have 100% specificity and positive pre- and peritoneal fluid include neoplasia, pancreatitis
dictive values for FIP. An albumin to globulin ratio and right heart failure.
The main differential diagnoses for abdominal disten- An important time of transmission is from asympto-
tion due to a non-septic exudate are steatitis and matic queens to kittens at 5–7 weeks of age.
cholangiohepatitis. With steatitis, the abdomen is usu-
In utero infection may occur, but this usually leads to
ally painful on palpation and abdominal fat is yellow to
abortion or neonatal loss.
brown.
Differential diagnoses for liver disease include cholan-
Prevention
giohepatitis, lipidosis and neoplasia.
Routine disinfection is important because the virus is
readily inactivated.
Treatment
Do not introduce FCoV test-positive cats into a house-
Supportive care.
hold. Identifying FCoV carriers prior to introduction in
Large-volume abdominocentesis. a multi-cat facility is the main value of FIP tests.
Corticosteroids and immunosuppressive agents at stan- For catteries with a history of FCoV infections, isolate
dard doses have been used with limited success. queens 2–3 weeks before parturition, quarantine queen
and kittens after parturition, and then wean kittens at
Antiviral drugs have been used with limited success.
4–5 weeks of age and isolate.
Recombinant human and recombinant feline interfer-
Modified-live intranasal vaccine is recommended for
ons appear to prolong survival in some cats.
open multiple-cat households.
Recombinant feline interferon has been used at a dose
of 1 million U/kg SC every other day until remission of FeLV vaccination is recommended for open, multiple-
clinical signs, followed by 1 million U/kg SC once a cat households.
week. Prednisolone has been given concurrently at an
initial dose of 2 mg/kg once a day and then tapered to
ABDOMINAL LYMPHOMA***
0.5 mg/kg every other day. A common recommenda-
tion is to use low-dose human recombinant interferon-
Classical signs
alpha at 30 U/cat/day PO for 7 days on alternate weeks,
although there are little firm data documenting benefit. ● Painless lymphadenopathy (multicentric
lymphoma).
The thromboxane synthetase inhibitor ozagrel
● Anorexia, weight loss, vomiting, diarrhea
hydrochloride, 5–10 mg/kg, combined with pred-
(alimentary lymphoma).
nisolone, 2 mg/kg, dramatically improved clinical
signs in two cases, but ozagrel is not readily available.
Pathogenesis
Dapsone is effective in the treatment of vasculitis but
has not been evaluated for FIP. Multicentric nodal lymphoma, characterized by
peripheral lymphadenopathy, frequently involves
the liver and/or spleen. This form is often associated
Prognosis
with FeLV infection and is occasionally associated
Effusive FIP is almost always fatal within a few days with FIV infection.
to months of onset of signs.
Alimentary lymphoma may affect various sites in the
gastrointestinal tract and mesenteric lymph nodes,
Transmission and may extend into the liver, spleen or kidneys.
Extra-abdominal sites (e.g. lung, bone marrow) may
FIP is most common in multiple cat households
also be involved. Alimentary lymphoma is infrequently
where cats are exposed to FCoV.
associated with FeLV infection, and is occasionally
FCoV transmission occurs by inhalation of virus shed associated with FIV infection.
from oronasal secretions or ingestion of virus shed in ● It has long been believed that chronic inflammatory
feces. bowel disease may progress to lymphoma.
Alternatively, severe inflammatory bowel disease Biopsy of gastrointestinal tract or other abdominal
may actually represent an indolent lymphoma. organ.
A progressive course of disease is more consistent ● In addition to making a diagnosis, the biopsy
with lymphoma while a waxing and waning course should be used to grade the lymphoma with respect
is more consistent with inflammatory bowel disease. to its aggressiveness. High-grade lymphomas are
● Alimentary lymphoma has historically been consid- poorly differentiated and may be further character-
ered to be primarily of B-cell origin. There is ized as immunoblastic or lymphoblastic. Low-
increasing evidence of T-cell alimentary lymphoma, grade lymphomas are well differentiated and may
especially with low-grade lymphomas. also be referred to as lymphocytic. Intermediate
forms also occur. The percentage of cell types
Solitary hepatic, splenic or renal lymphoma may also
varies between studies, but overall low-grade lym-
occur.
phomas are less common than intermediate and
Abdominal lymphoma may cause abdominal disten- high-grade lymphomas.
tion by hepatomegaly, splenomegaly, gastrointesti- ● Lymphocytic gastrointestinal lymphoma may have
nal thickening or dilation, or fluid. a tendency to be epitheliotropic (to involve the
● Abdominal lymphoma may cause ascites by portal mucosa) and to be of T-cell origin.
vein compression, lymphatic obstruction, septic
FeLV and FIV tests should be obtained.
peritonitis secondary to intestinal perforation and
spontaneous hemorrhage. Iron-deficiency anemia from chronic gastrointestinal
hemorrhage may occur with alimentary lymphoma.
Clinical signs Peritoneal fluid may be a transudate, modified tran-
sudate, septic exudate, chylous or hemorrhagic effu-
Multicentric nodal lymphoma:
sion, and may contain neoplastic cells.
● Variable lethargy, inappetence and weight loss.
Some cats have no systemic signs.
● Generalized moderate to marked painless periph- Differential diagnosis
eral lymphadenopathy.
● Variable hepatomegaly and icterus, splenomegaly, Differential diagnoses for generalized lymphadeno-
abdominal distention (uncommon). pathy include atypical hyperplasia, hyperplasia in response
to generalized skin diseases, immunologic disorders and
Alimentary lymphoma: systemic infections, widely metastatic neoplasia, and
● Anorexia, inappetence and weight loss. generalized bacterial or fungal lymphadenitis.
● Variable vomiting and diarrhea, but absence of
these signs does not rule out alimentary lymphoma. Differential diagnoses for lethargy, anorexia, weight
● Variable intestinal mass or thickening, organomegaly,
loss, vomiting and diarrhea include inflammatory
icterus and abdominal distention. bowel disease, other gastrointestinal neoplasia, pancre-
● Peripheral lymphadenopathy is uncommon.
atitis, systemic mycoses and cholangiohepatitis. Other
than inflammatory bowel disease, these disorders may
Other abdominal extra-nodal lymphoma: also cause lethargy, anorexia and weight loss without
● Signs of specific organ failure, e.g. icterus with vomiting and diarrhea.
hepatic lymphoma.
● Variable organomegaly and abdominal distention.
Differential diagnoses for marked splenomegaly
include mast cell tumor and other tumors.
Diagnosis
Treatment
Abdominal radiography or ultrasonography may
demonstrate an intestinal mass or intestinal thickening, Chemotherapy as described in Chapter 31 Aggressive
splenomegaly, hepatomegaly, lymphadenopathy or lymphomas should be treated aggressively and indolent
peritoneal fluid. lymphomas should be treated more conservatively.
Cats with high-grade lymphoma should be treated intestinal epitheliotropic lymphoma have a better prog-
with a multi-agent protocol. nosis than with other forms of abdominal lymphoma.
In one report, 69% achieved complete remission with
Cats with low-grade lymphoma (usually alimentary)
a median survival of 22.8 months.
may be treated with less aggressive protocols such as
prednisone and chlorambucil. Most cats tolerate chemotherapy for lymphoma and
fatal complications of chemotherapy are rare.
Splenectomy may be considered for splenic lymphoma
if there is no evidence of lymphoma at another site.
Because there is always the possibility of undetected Solid tumors***
microscopic lymphoma at another site, surgery should
be reserved for cats where there is poor response to, Classical signs
or unacceptable side effects with, chemotherapy. ● Chronic anorexia, lethargy, weight loss.
Surgical removal of a gastrointestinal lymphomatous
mass should be reserved for cats where the tumor is Clinical signs
causing gastrointestinal obstruction or perforation.
Surgical removal in addition to chemotherapy in Anorexia, lethargy and weight loss.
other cases does not appear to be of added benefit. Variable fever, vomiting, diarrhea, icterus, palpable
mass, depending upon the location of the tumor.
● Absence of vomiting or diarrhea does not rule out a
Prognosis
gastrointestinal tumor.
Response to chemotherapy in several case series pro-
vides general information, but it is difficult to give a Abdominal fluid ± abdominal distention may be
prognosis for an individual cat. Ultimately the only way present because of pre-hepatic or hepatic portal
to determine prognosis is to treat the cat and observe hypertension, lymphatic obstruction or hemor-
response. rhage. A large abdominal mass may contribute to
abdominal distention.
The prognosis for multicentric lymphoma is discussed ● Splenic or hepatic hemangiosarcoma is the most
in The Cat With Enlarged Lymph Nodes. common neoplastic cause of hemoperitoneum, but
In recent reports, about one-third to two-thirds of cats it is much less common than in the dog. Other
with alimentary lymphoma achieved a complete tumors may also spontaneously bleed.
● Abdominal fluid has been recognized with many
remission with chemotherapy, many of the other cats
achieved a partial remission (with overall response solid tumors, including those of the liver, pan-
rates up to 90%), and 1-year survival about 20–40%. creas, kidney, intestinal tract and peritoneum
Some of these cats will become long-term survivors (mesothelioma).
and are considered to be cured. Iron-deficiency anemia from chronic gastrointestinal
Regardless of anatomic location, usually only cats that hemorrhage may occur with gastrointestinal adenocar-
achieve a complete remission with induction chemother- cinomas.
apy have the possibility of being cured.
Diagnosis
FeLV status, FIV status, sex, tumor burden and loca-
tion, histologic grade and immunophenotype do not Abdominal radiography or ultrasonography may
independently consistently predict achievement of demonstrate an abdominal mass, organomegaly or peri-
remission, duration of remission or survival. Some of toneal fluid.
the weakness of prognostic factors may reflect differ-
Biopsy of suspected neoplastic tissue.
ent criteria for anatomic location and histologic grade
as well as the poor statistical power of relatively small Abdominal fluid may be a transudate, modified
case series. Certain combination of factors may affect transudate, chylous or hemorrhagic effusion, and
prognosis. For example, cats with well-differentiated may contain neoplastic cells.
Differential diagnosis VISCERAL MAST CELL TUMOR**

Differential diagnoses for a cat with subacute to
chronic non-specific signs and peritoneal fluid include Classical signs
cholangiohepatitis, pancreatitis, tuberculosis, pyogran- ● Depression, anorexia, weight loss, marked
ulomatous bacterial infections, systemic mycoses and splenomegaly (splenic mast cell tumor).
toxoplasmosis. ● Depression, anorexia, weight loss,
Differential diagnoses for an abdominal mass vomiting, diarrhea (intestinal mast cell tumor).
include cyst, focal necrosis, abscess, granulomatous
inflammation, intussusception and heterotopic ossifica- Pathogenesis
tion of the liver. Most of these will not commonly cause
abdominal distention or fluid. Mast cell tumor is a spontaneously arising neoplasm
and is not related to FeLV or FIV infection.
Differential diagnosis for a thickened peritoneum or
peritoneum covered with multiple plaques or nodules Splenic mast cell tumor frequently metastasizes;
other than mesothelioma or metastatic neoplasia organs involved, in decreasing order of frequency, are
include FIP, tuberculosis and sclerosing encapsulating liver, abdominal or thoracic lymph nodes, bone
peritonitis. marrow and peripheral blood, lung and intestine.
Intestinal mast cell tumor most commonly involves
the small intestine, and may involve multiple sites.
Treatment Metastasis to liver and mesenteric lymph nodes is com-
mon; metastasis to spleen, lung and bone marrow may
Most solid tumors are best treated by surgical exci- also occur.
sion, but they are often unresectable by the time ascites
develops. Visceral mast cell tumor may cause abdominal dis-
tention by splenomegaly, effusion or spontaneous
Benefit of chemotherapy for most abdominal solid hemorrhage.
tumors is not known, but effect is likely to be poor in
most cases, and anorexia is common with aggressive Clinical signs
combination protocols. Use of carboplatin or lomus-
tine as single agents may be considered in that side Splenic mast cell tumor:
● Variable depression, anorexia, weight loss, inter-
effects in most cats are minimal.
mittent vomiting, dyspnea.
Radiation therapy may be considered, but in many ● Marked splenomegaly.
cases will not be feasible. ● Abdominal fluid may be detectable on physical
Abdominocentesis may be used to reduce signs attrib- examination.

utable to marked abdominal distention. Intestinal mast cell tumor:
● Variable depression, anorexia, weight loss, fever,
Rutin, 50 mg/kg PO tid, may be considered to reduce
effusion if it is chylous. (It may also be used to help dyspnea, intermittent vomiting, diarrhea. Melena or
alleviate chylous effusions due to other causes.) hematochezia may be present.
● Intestinal mass(es) or thickened intestines may be
Intracavitary chemotherapy with carboplatin or palpable.
thiotepa may be considered in an effort to alleviate ● Peritoneal fluid may be detectable on physical
effusion due to widespread metastasis or mesothe- examination.
lioma.
Diuretics may reduce malignant ascites in some Diagnosis
cases. Furosemide, 1 mg/kg PO/SC/IV once to twice Abdominal radiography or ultrasonography may
daily, or spironolactone, 1–2 mg/kg PO, bid may be demonstrate splenomegaly, hepatomegaly, intestinal
tried. mass, lymphadenopathy or peritoneal fluid.
● Sonographic abnormalities of the spleen include The benefit or detriment of chemotherapy in addition to
splenomegaly, irregular contour, mottled appear- surgery is not known. Prednisone alone or protocols
ance, and hyperechoic and hypoechoic nodules. used to treat lymphoma may be considered.
Lymph nodes may be hypoechoic. Intestinal masses
are hypoechoic and there is loss of normal wall lay-
Prognosis
ering. Effusion is anechoic.
The prognosis for splenic mast cell tumor is good,
Fine-needle biopsy of spleen, gastrointestinal mass
even with evidence of widespread dissemination.
or other organ based on clinical signs will often reveal
Median survival post-splenectomy is 12–19 months,
neoplastic mast cells. Surgical biopsy of intestinal
and peripheral mastocytosis declines.
masses may be required for diagnosis. Intraoperative
cytology is recommended, so that wide surgical exci- The prognosis for intestinal mast cell tumor is poor,
sion of the tumor(s) may follow. with most cats being euthanized soon after diagnosis or
● Abdominal fluid usually contains mast cells with treatment.
or without eosinophils. Occasionally no mast cells
are present.
RIGHT HEART FAILURE**
Fifty percent of cats with splenic mast cell tumor
will have mast cells in the peripheral blood on cyto- Classical signs
logic examination of direct smear or buffy coat smears.
● Dyspnea due to pleural effusion.
Other laboratory findings include hyperglobulinemia
and coagulation abnormalities.
Pathogenesis
Iron-deficiency anemia from chronic intestinal hem-
orrhage may occur with intestinal mast cell tumor. Cats with right heart failure usually develop pleural
effusion. Peritoneal effusion is a less common occur-
Eosinophilia may occur with visceral mast cell tumors.
rence.
● Peritoneal effusion has been observed with congen-
ital tricuspid valve dysplasia, patent ductus arte-
riosus and intrapericardial heterotopic liver.
The main differential diagnosis for marked ● Peritoneal effusion has been observed with
splenomegaly is lymphoma, but it does not typically acquired pericardial effusion (which in-itself may
cause the massive splenomegaly seen in cats with mast be a sign of right heart failure), persistent atrial
cell tumor. standstill, traumatic tricuspid valvular insuffi-
ciency, tricuspid valvular endocarditis, myocarditis,
The main differential diagnoses for an intestinal mass
heartworm disease, severe chronic anemia, and
and abdominal distention are adenocarcinoma and
dilated, hypertrophic and restrictive cardiomy-
lymphoma. Chronic intussusceptions are rare, and
opathy. Of these various disorders, dilated car-
would not typically be associated with abdominal dis-
diomyopathy is most likely to cause peritoneal
tention or fluid.
effusion.
The presence of eosinophils in peritoneal fluid is not
Pulmonary edema may also be present due to left heart
specific for mast cell tumor, and has also been seen
failure.
with lymphoma, septic peritonitis and pneumotho-
rax. However, the presence of mast cells is highly spe-
cific for visceral mast cell tumor. Clinical signs
Peritoneal effusion is usually accompanied by pleu-
ral effusion. Pleural effusion ± pulmonary edema will
Treatment
cause dyspnea.
Splenectomy or excision with 5–10 cm margins of ● Most peritoneal effusion due to right heart failure
intestinal masses. causes undetected to minimal abdominal distention.
● Marked abdominal distention is occasionally the Large-volume abdominocentesis should be considered

predominant clinical sign. for ascites not responsive to diuretic treatment that is
causing diaphragmatic compression, stomach compres-
Other signs of heart disease variably present include
sion or abdominal discomfort.
jugular distention, murmur, gallop rhythm, tachycardia,
bradycardia and irregular rhythm.
Prognosis
Diagnosis The prognosis for cats with ascites due to right heart
failure is poor, because of the poor prognosis of most of
Radiography is useful to demonstrate pleural effusion the underling heart diseases.
and large-volume peritoneal effusion.
For a specific heart disease, it is not known if the pres-
Echocardiography will assess myocardial function, ence of peritoneal effusion in addition to pleural effu-
and valvular competency, and may demonstrate trans- sion changes prognosis.
diaphragmatic peritoneal effusion. If echocardiography
is not available, non-selective angiocardiography is
useful to diagnose dilated and hypertrophic cardiomy- TRAUMATIC RUPTURE OF THE URINARY
opathy. BLADDER OR URETHRA**
Electrocardiography will characterize arrhythmias. Classical signs
Abdominal ultrasonography will demonstrate peri- ● Acute depression, anorexia, dehydration,
toneal fluid. vomiting, anuria.
Abdominocentesis usually reveals a modified transu-
date. Pathogenesis
Causes are listed in approximate decreasing order of
Differential diagnosis frequency. These causes include:
● Blunt abdominal trauma.
The main differential diagnosis for a cat presented in
acute heart failure characterized by cardiogenic – Motor vehicle trauma is the most common
shock, dyspnea and abdominal fluid is acute abdomi- cause, followed by falling from heights,
nal hemorrhage. Pulmonary crackles will usually be although a ruptured urinary bladder is not a com-
present in heart failure. mon injury, especially compared to other trau-
matic injuries (e.g. pelvic fractures, facial
The main differential diagnosis for a cat with chronic injuries). Trauma usually causes rupture at
heart failure characterized by pleural and peritoneal the apex of the bladder.
effusions is neoplasia. Other differential diagnoses ● Urethral catheterization.
include iatrogenic volume overload, hypoalbuminemia, – This is most likely to occur when treating ure-
feline infectious peritonitis and systemic bacterial and thral obstruction. Rupture usually occurs in the
mycotic infections. urethra or neck of the bladder. Urethral
obstruction may also spontaneously lead to ure-
thral rupture without catheterization.
Treatment
● Expression of the urinary bladder.
The treatment of heart failure is discussed in The Cat – This is most likely to occur when trying to
With an Enlarged Heart or Abnormal Heart Sounds. express the bladder in an unsedated cat with ure-
thral spasm following relief of urethral obstruc-
Specific treatment of peritoneal effusion is usually not
tion, or following cystocentesis.
required.
● Cystocentesis.
Diuretic therapy (e.g. furosemide, initial dose 1–2 – This rarely causes rupture of the bladder, but has
mg/kg bid) will help reduce abdominal fluid. occurred when performing cystocentesis on cats
with a severely distended bladder following ure- ● Creatinine or potassium levels in the abdominal
thral obstruction. fluid greater than that of the serum are strongly
● Penetrating abdominal trauma. suggestive of uroperitoneum. (It is not sufficient to
– Bite wounds, staking injuries and bullet wounds simply measure those parameters in the peritoneal
are uncommon causes of urinary tract trauma. fluid because azotemic animals with ascites will
also have creatinine and potassium in the ascitic
Acute bladder rupture occasionally causes marked
fluid.) The higher the abdominal fluid:serum creati-
hemorrhage into the abdomen or into the bladder (with
nine and potassium ratios, the more likely the cat
massive clot formation).
has uroperitoneum. In one study of cats with
uroperitoneum, the abdominal fluid:serum creati-
Clinical signs nine ratio ranged from 1.1:1 to 4:1, with a mean of
2:1, and the abdominal fluid:serum potassium ratio
Clinical signs are due to post-renal uremia and asso-
ranged from 1.2:1 to 2.4:1, with a mean of 1.9:1.
ciated disorders.
Abdominal fluid:serum urea ratios are not as reli-
Non-specific signs of uroperitoneum include variable able because of more rapid equilibration of urea.
depression, lethargy, anorexia and dehydration.
Contrast radiography will demonstrate a rupture of the
Body temperature and heart rate may be elevated, nor-
bladder or urethra. To demonstrate a rupture of the
mal or low. Vomiting is common. Abdominal pain may
bladder, the radiograph should be obtained just as
be present.
the final amount of contrast material is injected. If
Many cats are not urinating, but presence of urination only a small amount of contrast material leaks out of
does not rule out urinary tract rupture. (If urination the bladder, it may be rapidly diluted in the peritoneal
is present, there may be hematuria.) fluid resulting in a false-negative study.
Similarly, a palpable bladder does not rule out rup-
ture of either the bladder or urethra. Differential diagnosis
Abdominal distention and a fluid wave are occasionally Differential diagnoses for a cat presented for no urina-
evident. Urethral rupture may also cause inguinal sub- tion include ethylene glycol or lily poisoning, or ure-
cutaneous edema (there may also be signs of inflam- thral obstruction.
mation due to cellulitis). Differential diagnoses for a cat presented with acute
depression and peritoneal fluid include right heart
Diagnosis failure, acute pancreatitis, liver disease with ascites
and hepatic encephalopathy, and acute abdominal
A serum chemistry profile will reveal mild to marked hemorrhage (mucous membranes will be pale).
elevations in urea and creatinine levels unless the
animal is tested shortly after injury. Hyperkalemia may Other rare causes of uroperitoneum include spontaneous
also be present. leakage at the site of a bladder tumor, traumatic avulsion of
a ureter, transudation of urine through a severely inflamed
Abdominal ultrasonography will demonstrate peri- bladder wall and leakage post-nephrotomy. Radiographic
toneal fluid. contrast studies will facilitate diagnosis. An excretory uro-
Peritoneal fluid is initially a pale yellow to serosan- gram may be required to demonstrate an avulsed ureter.
guineous transudate, and cytology will be unremark-
able, unless the cat is a tom, where sperm may be Treatment
present. Cell counts may increase with time (> 3×109/L,
Fluid therapy to correct dehydration and reduce uremia.
3000/μl) resulting in a modified transudate. Secondary
septic peritonitis will result in an exudate with degen- Antibiotics if there is secondary septic peritonitis, e.g.
erate neutrophils and bacteria. ampicillin, cefoxitin at standard doses.
Large-volume abdominocentesis to reduce uremia. Diagnosis

Peritoneal dialysis will further reduce uremia but is not
usually required. Abdominal radiography will demonstrate marked
accumulation of feces in the colon.
Ruptured urinary bladders are usually surgically
repaired.
Non-surgical management (catheterization to keep the
bladder empty) has been described in other species. It The main differential diagnosis for a cat with chronic
may be considered if the cat is too unstable for surgery, dyschezia, tenesmus and abdominal distention is
but will not usually reduce costs because of the longer colonic neoplasia with metastases resulting in obstruc-
hospitalization period. tive ascites.
Ruptured urethras may be treated by surgical repair

or by placement of an ante-pubic urinary catheter, Treatment
or less optimally by chronic urethral catheterization. For the cat with megacolon sufficiently severe to cause
abdominal distention, subtotal colectomy is recom-
Prognosis mended.
Uroperitoneum in-itself carries a good prognosis. If medical therapy is desired, correct dehydration,
Uremia will rapidly resolve once the urinary tract is administer parenteral antibiotics (e.g. ampicillin) to
repaired. Chemical peritonitis from urine also usually protect against bacterial translocation, and administer
rapidly resolves. Prognosis is largely determined by multiple small volume enemas with lactulose prior to
associated injuries. anesthetizing the cat for manual disimpaction. Use of
enema soap will facilitate the latter (do not use
chlorhexidine soaps). If disimpaction is successful,
MEGACOLON** chronic therapy consists of a low-residue diet, lactulose
and prokinetic agents (e.g. cisapride).
Classical signs
● Chronic straining to defecate. JUVENILE ABDOMINAL FLUID**
See main reference on page 783 for details (The Classical signs
Constipated or Straining Cat).
● Mild excess in abdominal fluid encountered
during pediatric ovariohysterectomy.
Clinical signs
Variable anorexia, lethargy, weight loss, unkempt hair- Clinical signs
coat and vomiting.
More peritoneal fluid may be encountered when spay-
Straining to defecate, with the resultant minimal pas- ing a cat at an early age (e.g. 3 months) than at a tradi-
sage of feces that may be dry or mucoid. tional age (e.g. 6 months).
Large volume of firm feces in the colon on abdominal
palpation. Digital rectal examination may reveal nar- Diagnosis
rowing of pelvic canal secondary to fractures or tumor.
Neurologic examination may reveal sacral nerve The fluid is a transudate.
injury.
Marked colonic dilation may occur causing abdominal Differential diagnosis
distention. FIP, where the fluid is a non-septic exudate.
Treatment feline pancreatic lipase immunoreactivity. No laboratory

abnormality appears to be correlated with the develop-
None required. ment or severity of effusion.
● Peritoneal effusion is usually a modified transudate,
PANCREATITIS** but may be a non-septic exudate.

Diagnostic imaging findings are also variable.
Classical signs ● On abdominal radiographs, decreased contrast may
● Acute depression and anorexia. be present due to effusion. This may be restricted to
● Ascites may develop. the cranial abdomen or be more generalized.
● Other radiographic findings supportive of pancre-
See main reference on page 272 (The Cat With atitis include a mass effect in the right cranial quad-
Depression, Anorexia or Dehydration). rant (displacement of organs), and localized
dilation of loops of intestine (ileus). Normal find-
ings do not rule out pancreatitis.
Clinical signs ● On abdominal ultrasonography, accumulation of
Cat may be of any age, with no sex or breed predilec- peritoneal fluid around the pancreas is a highly
tion, except perhaps for Siamese cats. specific finding for pancreatitis. Generalized peri-
toneal effusion is a less specific finding.
Duration of clinical signs prior to presentation varies ● Other ultrasonographic findings with a high speci-
from several days to more than 3 weeks. ficity for pancreatitis include pancreatic regular or
Depression and/or anorexia are the most common irregular enlargement, pancreatic hypoechogenic-
historical signs and may be the only signs present. The ity, hyperechogenicity of peripancreatic fat (may be
most common physical abnormalities are dehydra- difficult to appreciate), and dilation of the pancre-
tion and hypothermia. Fever is uncommon. atic duct in the left lobe. Normal findings do not
rule out pancreatitis.
Other inconsistent signs include weight loss, vomit- ● Definitive ante-mortem diagnosis requires biopsy
ing, diarrhea, cranial abdominal pain, cranial abdomi- obtained by exploratory laparotomy or laparoscopy.
nal mass, dyspnea, ataxia and disorientation, and
shock. Polydipsia may be present, but is usually due to
concurrent diabetes mellitus. Differential diagnosis
● Peritoneal effusion may occur, and in some cases Differential diagnoses for cats with pancreatitis caus-
may be of sufficient quantity to cause abdominal ing acute depression and abdominal fluid include
distention. Peritoneal effusion may be more likely septic peritonitis, acute abdominal hemorrhage, right
to occur when there is concurrent liver disease. heart failure, ruptured urinary bladder, ruptured gall
Pleural effusion may also occur. bladder, steatitis, toxoplasmosis, ligation of a porto-
systemic shunt and, uncommonly, hepatic encephalo-
Diagnosis pathy where liver disease is also causing ascites.
Because clinical and laboratory findings are non- For cats with pancreatitis causing subacute depres-
specific, diagnosis requires a high index of suspicion. sion and abdominal fluid, the primary differential
diagnoses are neoplasia, feline infectious peritonitis
Pancreatitis should be considered in any cat with and right heart failure.
unexplained acute depression. Pancreatitis should
also be considered in any critically ill cat developing
ascites, pleural effusion or hypothermia. Treatment
Laboratory findings are variable and are most valu- Address the inciting cause if one is identified.
able in ruling out other causes of depression and
The remainder of therapy is largely supportive.
anorexia. The most sensitive and specific tests are ele-
vations in feline trypsin-like immunoreactivity and Antiemetics and analgesics.
Surgical debridement of grossly necrotic tissue and of raw meat (source of Salmonella spp.), or inappropri-
therapeutic abdominal lavage, or closed therapeutic ate use of NSAIDs. In some cases no cause can be found.
abdominal lavage using a technique similar to diagnos- Septic peritonitis is less common in cats than dogs.
tic peritoneal lavage, should be considered if peritoneal
A complete blood count usually reveals hemoconcen-
fluid is an exudate.
tration and a left shift and toxic neutrophils. The
If there is a large volume of ascites that is a modified total neutrophil count may be elevated, normal or low,
transudate, therapeutic abdominocentesis should be con- depending upon the severity and acuteness of inflam-
sidered, and it should definitely be performed if there is mation. Mild anemia may be present.
a problem secondary to a volume effect (e.g. dyspnea
A serum chemistry profile may reveal hyperalbu-
from diaphragmatic compression), but the benefit of the
minemia (dehydration), hypoalbuminemia (abdominal
procedure on the course of the disease is not known.
exudation), hyperglycemia (stress) or hypoglycemia
(severe sepsis).
SEPTIC PERITONITIS*
Abdominal radiography may demonstrate loss of detail
and “ground-glass” appearance and/or free gas in
Classical signs
the abdomen. Abdominal ultrasonography may demon-
● Acute depression, anorexia, fever, strate peritoneal fluid and ileus. Imaging may also
abdominal pain. reveal evidence of pleural fluid.
Abdominocentesis may yield fluid. The fluid is a septic
exudate, although intra-cellular bacteria may not be seen.
Clinical signs
Sensitivity of cytology is reported as approximately
Acute onset of depression and anorexia; the cat may be 60–90%, although in a recent case series peritoneal fluid
moribund. cytology and a nucleated cell count > 13×109/L
(13 000/μl) had a diagnostic accuracy of 100% in cats.
Variable vomiting and diarrhea. These are most likely if
Abdominal fluid should be Gram-stained and cultured for
the cause is a perforating intestinal foreign body.
aerobic and anaerobic bacteria. The most frequently iso-
Initial fever, tachycardia ± dark pink mucous mem- lated organisms are Escherichia coli, Enterococcus spp
branes, but these signs may progress rapidly to nor- and Clostridium spp.
mothermia or hypothermia, bradycardia and pale ● In a recent report, glucose levels in septic peritoneal
mucous membranes with severe sepsis or septic fluid were usually lower than blood glucose levels,
shock (see The Cat With Acute Depression, Anorexia and a difference of > 1.1 mmol/L (20 mg/dl) was
and Dehydration). highly specific for septic peritonitis. In contrast,
glucose levels in non-septic effusions were equal or
Pain is present on abdominal palpation in about 2/3 of
higher than blood levels. (This study did not include
cases. The cat is probably less likely to react if it is
cats with FIP.) In addition, septic effusions tended to
moribund. Mild abdominal distention may be present.
have a lower pH and higher lactate levels than non-
Polypnea and icterus may be present. septic effusions.
● Food particles may be seen with gastrointestinal
perforation.
Diagnosis
● If abdominocentesis is unsuccessful, and pre-surgi-
History or signs of abdominal surgery, sharp or blunt cal confirmation of septic peritonitis is desired,
trauma to abdomen, linear or sharp gastrointestinal diagnostic peritoneal lavage should be performed.
foreign body, pre-existing infection of abdominal
organ (e.g. hepatic abscess, pyometra), pre-existing
abdominal neoplasia, pre-existing disorder with ascites,
pre-existing infection outside of abdomen causing peri- Differential diagnoses for an acutely depressed cat
tonitis by extension or hematogenous spread, ingestion with abdominal distention and/or pain include trauma,
urethral obstruction, panleukopenia and other Abdominal distention may occur because of ileus,
causes of acute enteritis, acute pancreatitis and acute with intestinal fluid retention, flatus (especially in
pyelonephritis. acute gastroenteritis), thickening of the intestinal wall
(especially in chronic gastroenteritis, e.g. inflammatory
Differential diagnoses for a moribund cat with abdom-
bowel disease), or rarely because of ascites due to
inal distention include urethral obstruction, hepatic
protein-losing enteropathy. Enlarged intestines con-
encephalopathy, feline infectious peritonitis, advanced
tribute to the prominent abdominal contour characteris-
neoplasia, heart failure and hemoperitoneum.
tic of malnourished kittens with a heavy roundworm
burden.
Treatment ● Abdominal distention is usually mild except in
neonatal kittens where it may be severe.
Supportive care and treatment for hypotension or
● Distended loops of intestine may feel more or less
shock, including intravenous fluids, is required.
distinct than usual. Palpation may yield a
Broad-spectrum intravenous antibiotics, e.g. ampi- “squishy” or spongy sensation and create borbo-
cillin and gentamicin; cefoxitin (second-gener- rygmus.
ation cephalosporin); cefazolin (first-generation ● Thickened loops of intestine will feel more promi-
cephalosporin) combined with enrofloxacin and nent on abdominal palpation.
metronidazole or clindamycin; or imipenem-cilastatin
as a single agent. It should be remembered that
Diagnosis
enrofloxacin is not licensed for parenteral use in the cat,
and there are anecdotal reports of blindness following a Abdominal radiographs will always demonstrate
single injection. If “sulfur granules” are seen suggestive dilation of the intestines with air, and may demon-
of Actinomyces spp. or Nocardia spp., then initial strate dilation of the intestines with fluid. Neither
empirical therapy should consist of penicillin G or plain nor contrast radiographs are very useful to
ampicillin and trimethoprim-sulfa, or imipenem-cilas- evaluate thickness of the intestinal walls.
tatin.
Abdominal ultrasonography is very useful to rule out
Exploratory laparatomy to address underlying cause of peritoneal fluid, to demonstrate intestinal wall thick-
peritonitis and to lavage abdomen. Post-operative open- ening and to evaluate intestinal motility.
abdomen management or closed-suction drainage sys-
tems are often required to treat severe generalized
peritonitis. With such management, the prognosis for
cats appears to be similar to dogs, with average survival Differential diagnoses for cats with vomiting, diarrhea
rates of 60–80%. and abdominal distention include acute pancreatitis,
cholangiohepatitis, hepatic lipidosis, gastrointestinal
neoplasia and acute renal failure with volume over-
GASTROENTERITIS*
load.
Classical signs
Treatment
● Vomiting and/or diarrhea.
Treatment of the primary disease.
Severe gastrointestinal distention by flatus in
Clinical signs neonates should be relieved by intubation (stomach
Cats with acute or chronic gastroenteritis will have vom- air) or trans-abdominal enterocentesis (intestinal
iting and/or diarrhea of variable frequency and severity. air).
Other variable clinical signs include depression, Simethicone is not of proven value to reduce flatus
anorexia, dehydration, weight loss, reduced growth rate formation in humans, and is likely of no benefit in
in kittens, abdominal pain, melena and hematochezia. cats.
with multiple 1–3 mm spots, thickened pancreas with

TOXOPLASMOSIS*
saponification of peripancreatic fat, lymphadenopa-
thy and focal thickening of the intestines.
Classical signs
Biopsies of abdominal organs may reveal mixed
● Anorexia, fever, dyspnea and signs of
inflammation, tachyzooites, and occasionally cysts.
ocular inflammation in mature cats.
Histology will also reveal multifocal necrosis.
● Fading neonate.
Elevated IgM titer; four-fold rise in IgG titers 3 weeks
See main references on page 375 for details (The apart. Serology gives the most interpretable informa-
Pyrexic Cat ). tion if both acute and convalescent IgM and IgG titers
are obtained.
Clinical signs
Non-specific signs of depression, anorexia, weight Differential diagnosis
loss and fever are common. Differential diagnoses for cats with hepatopathy, mesen-
Specific clinical signs vary with the various organs teric lymphadenopathy and peritoneal fluid include con-
involved. current inflammatory bowel disease and pancreatitis,
● Common signs include uveitis, dyspnea (pneumo- alimentary lymphoma, FIP, tuberculosis and systemic
nia) and muscle pain. fungal infections. Of these, only the infectious diseases
● All abdominal organs may be infected by are likely to also cause pleural fluid, pneumonia (except
Toxoplasma gondii. Specific clinical signs of for FIP), or uveitis.
abdominal infection are usually due to hepatitis
and hepatic necrosis (icterus), and mesenteric
lymphadenopathy (palpable nodes). Vomiting,
Treatment
diarrhea and pain on abdominal palpation may be Clindamycin 10–25 mg/kg PO, IM, IV bid continuing
present. Peritoneal fluid may also be present, but is at least 2 weeks beyond resolution of clinical signs.
unlikely to cause abdominal distention.
Sulfadiazine (30 mg/kg PO bid) and pyrimethamine
Specific signs may also be due to concurrent disorders (0.5 mg/kg PO bid) may be used if clindamycin is not
causing immunosuppression. available or not tolerated. Folinic acid (5 mg/day) or
brewer’s yeast (100 mg/kg/day) may be required to
correct myelosuppression resulting from folinic acid
Diagnosis
deficiency caused by therapy.
Routine laboratory results are variable. Neutrophilia is
Trimethoprim-sulfonamide 30 mg/kg bid may be con-
common with systemic infection. Hepatitis is common,
sidered if these are the only drugs available.
causing elevations in liver enzymes and bilirubin.
Supportive care.
Abdominal imaging may reveal hepatomegaly, changes
consistent with pancreatitis (see The Cat With Acute
Anorexia, Depression or Dehydration), mesenteric
INTESTINAL TUBERCULOSIS*
lymphadenopathy and peritoneal fluid.
Peritoneal fluid is presumably a transudate or modi- Classical signs
fied transudate, which may contain tachyzooites.
● Chronic weight loss, vomiting, diarrhea,
Abnormalities at exploratory laparatomy include mesenteric lymphadenopathy.
hepatomegaly, reticular pattern to the surface of the liver
Clinical signs HYPERADRENOCORTICISM*

Cats with the intestinal form of tuberculosis (caused by
Mycobacteria tuberculosis, M. bovis, M. tuberculosis- Classical signs
bovis variant, and M. microti) and intestinal involvement ● Polyuria, polydipsia, polyphagia.
with non-tubercular mycobacteria (M. avium complex) ● Abdominal distention, alopecia, fragile skin.
may show signs varying from subclinical infection to
chronic enteritis characterized by weight loss, fever, See main reference on page 251 for details (The Cat
vomiting, diarrhea and mesenteric lymphadenopathy. With Polyuria and Polydipsia).
Cats with advanced disease may develop obstructive
ascites. Clinical signs
Many cats with hyperadrenocorticism have diabetes
Diagnosis mellitus, which causes the polyuria and polydipsia.
Laboratory results are variable, but non-regenerative Polyphagia may be due to both diabetes and hypera-
anemia is common. drenocorticism, and may be severe.
Abdominal radiographs may reveal mesenteric lym- Muscle wasting is due to both disorders. This con-
phadenopathy and peritoneal fluid. Abdominal ultra- tributes to abdominal distention, which is manifested
sonography may reveal intestinal thickening, as a “pot-bellied” appearance, similar to the dog.
mesenteric lymphadenopathy, and peritoneal fluid. Dermatologic signs include unkempt haircoat, patchy
Lymph nodes may be calcified. alopecia, and skin that tears and bruises easily.
Peritoneal fluid may presumably be a transudate,
modified transudate, chylous or exudate. Macro- Diagnosis
phages containing acid-fast bacteria may be seen.
Confirmatory testing and distinguishing a pituitary
Cytology and histology of a biopsy of the intestinal tumor from an adrenal tumor is similar to the dog,
tract and mesenteric lymph nodes reveal granuloma- involving urine cortisol:creatinine ratio, ACTH stimu-
tous to pyogranulomatous inflammation. Acid-fast lation test, dexamethasone suppression tests, plasma
bacteria are usually detectable in biopsies. ACTH level, abdominal ultrasonography and CT-scan-
Culture is possible at selected laboratories, but may ning or magnetic resonance imaging.
take weeks for a positive result.
Differential diagnosis Other causes of insulin-resistant diabetes mellitus.
Differential diagnoses for intestinal tuberculosis Muscle wasting from another chronic disease plus
include alimentary lymphoma, widely metastatic marked obesity or peritoneal fluid can mimic the pot-
tumors, other pyogranulomatous bacterial infections bellied appearance of hyperadrenocorticism.
and systemic fungal infections.
Treatment
Treatment Hypophysectomy and adrenectomy have historically
Notify public health officials. Euthanasia is often provided the most consistent results.
advised with true tuberculosis because of the zoonotic Trilostane has alleviated clinical signs of pituitary-
risk. If treatment of a mycobacterial infection is dependent hyperadrenocorticism in all reported cases.
attempted, drug doses are provided in references in The
Cat With Non-Healing Wounds and The Cat With Mitotane and ketoconazole have inconsistent results.
Enlarged Lymph Nodes. Pituitary irradiation has inconsistent results.
FLUID OVERLOAD* AEROPHAGIA*

● Dyspnea due to pulmonary edema, and/or ● Mild abdominal distention in a dyspneic
subcutaneous edema. cat.
Clinical signs
Clinical signs
Dyspnea.
Excessive fluid therapy tends to cause pulmonary or
subcutaneous edema more than pleural or peritoneal Mildly distended stomach or loops of intestine on
effusions. abdominal palpation. Loops of intestine may feel more
or less distinct than usual. Palpation may yield a
Fluid therapy may exacerbate pre-existing ascites
“squishy” or spongy sensation and create borboryg-
by causing increased hydrostatic pressure or exacerbat-
mus.
ing hypoalbuminemia. The presence of a mechanism
for ascites formation may divert fluid away from the
lungs or subcutaneous tissue into the peritoneal space. Diagnosis
History of dyspnea.
Diagnosis
Palpable distention of gastrointestinal tract by air.
History of fluid therapy and improvement of ascites
with decreasing fluid rates or diuretic therapy. Radiography will confirm air in the gastrointestinal
tract and rule out dyspnea due to diaphragmatic com-
pression by a large volume of fluid causing abdominal
distention.
OVEREATING*
Classical signs TRAUMATIC HEMORRHAGE*

● Abdominal distention following a large
Classical signs
meal.
● Pale mucous membranes, weak pulses,
tachycardia.
Clinical signs ● External signs of trauma.
Mild abdominal distention is commonly noted in kit-
tens following nursing or drinking.
Clinical signs
Occasionally a mature cat may eat an unusually large
With blunt trauma in cats (e.g. motor vehicle accidents,
quantity of food sufficient to cause noticeable abdomi-
falling from heights), thoracic injuries and resulting
nal distention. This is most likely to happen when offer-
dyspnea are more common or clinically important than
ing a new, highly palatable food, in cats that have
abdominal injuries. Abdominal hemorrhage may occur
fasted, and in cats with polyphagia.
but is rarely life threatening.
● Signs of blunt trauma may be present, including
Diagnosis shorn nails, excoriations of the skin, fractured teeth
and mandible, epistaxis and pelvic fractures.
History of consuming a large meal.
Penetrating trauma is less common than blunt trauma,
Palpable distention of gastrointestinal tract.
and includes bite wounds, staking injuries and bullet
Radiography will demonstrate a large quantity of wounds. Bacterial peritonitis is more common or clini-
ingesta. cally important than acute abdominal hemorrhage.
● The wound may be difficult to visualize or palpate, Abdominal ultrasonography may reveal a normal or
but palpation of the abdominal wall at the wound enlarged liver, altered hepatic echogenicity and peri-
site will usually incite a painful response. The toneal fluid.
severity of bleeding varies with the organs and
Peritoneal fluid is usually a transudate or modified
blood vessels that are injured.
transudate. Occasionally, high protein fluid typical of
Abdominal hemorrhage may occur following surgery an exudate occurs with non-suppurative cholangiohep-
or external biopsy procedures (e.g. percutaneous liver atitis.
biopsy).
Definitive diagnosis requires liver biopsy.
Regardless of the type of trauma, the signs of
abdominal hemorrhage are those of acute hypo- Differential diagnosis
volemia. Abdominal distention is unlikely.
Differential diagnoses for a cat with signs of liver
abnormalities and peritoneal fluid include hepatic neo-
Diagnosis plasia and other chronic liver diseases, acute pancreati-
Abdominal ultrasonography will usually demonstrate tis, right heart failure, feline infectious peritonitis and
peritoneal fluid. Abdominocentesis may yield blood. toxoplasmosis.
● Following percutaneous biopsy of an abdominal
organ, tachycardia is the first sign of hemorrhage
Treatment
and this finding is more sensitive than ultrasound or
abdominocentesis to detect active bleeding. Nutritional support.
Corticosteroids for cholangiohepatitis.
HEPATIC LIPIDOSIS, NON-SUPPURATIVE
CHOLANGIOHEPATITIS AND HEPATIC Therapeutic abdominocentesis is not required.
CIRRHOSIS*
STEATITIS
Classical signs
● Anorexia, lethargy, weight loss, icterus. Classical signs
● Depression, anorexia and reluctance to
See main reference on page 425 for details (The Yellow move.
Cat or Cat With Elevated Liver Enzymes).

Anorexia, lethargy and weight loss. Depression, anorexia, fever and reluctance to move
Variable icterus, vomiting, diarrhea. because of pain.
Ascites is uncommon, especially ascites sufficient to Abdominal distention may occur from fluid and
cause abdominal distention. firm abdominal fat, and the abdomen may be tense
● Ascites is reported more frequently in some case
because of pain.
series, which may represent distinct sub-types of Other clinical signs include fever and firm and lumpy
chronic liver diseases. subcutaneous fat with or without accompanying lymph-
Hepatomegaly is common with lipidosis, but is usually adenopathy.
not sufficient to cause abdominal distention.
Diagnosis
Diagnosis History of a diet high in oxidized unsaturated fats
These liver diseases may be suspected on the basic of (e.g. rancid tuna) and/or deficient in vitamin E. Rare
clinical signs and variably elevated liver enzymes. in cats fed commercial foods.
Biopsy of fat – may be grossly yellow to brown. partial thromboplastin time. If the prothrombin time
is elevated, it may normalize with vitamin K therapy.
Abdominal ultrasound examination may reveal peri-
toneal fluid. Abdominocentesis may reveal a sterile
exudate high in protein and mature neutrophils, Differential diagnosis
similar to that seen with feline infectious peritonitis,
Hemorrhage due to abdominal neoplasia, trauma, or
or a chylous effusion. Associated sclerosing encapsu-
hepatic necrosis, amyloidosis, or peliosis.
lating peritonitis has also been reported.
Treatment
INHERITED AND ACQUIRED
(ANTICOAGULANT RODENTICIDE Transfusion.
POISONING) COAGULATION DEFECTS
Vitamin K for Devon Rex cats, vitamin K antagonist
rodenticide poisoning, and cats with liver disease with
Classical signs
prolonged prothrombin times (see main references on
● Spontaneous bleeding and re-bleeding page 509 for details, The Bleeding Cat).
after trauma.
Environment that minimizes trauma.
Clinical signs
GLOMERULONEPHRITIS
Spontaneous bleeding and re-bleeding may occur at
various sites, including within the abdomen, although Classical signs
thoracic hemorrhage tends to be more common.
● Chronic depression, anorexia, weight loss.
Signs due to acute anemia and abdominal distention ● Polyuria/polydipsia if chronic renal failure.
vary with the severity of blood loss. ● Subcutaneous edema and/or ascites if
nephrotic syndrome.
Diagnosis
Clinical signs
Abdominal ultrasonography will demonstrate peri-
toneal fluid. Abdominocentesis will confirm that the Signs are those of chronic renal failure and/or
fluid is blood. nephrotic syndrome. Concurrent signs may be present
from an underlying disease (FeLV infection, FIP,
Cats bleeding from hemophilia A or hemophilia B
Mycoplasma arthritis and other chronic infections, sys-
will have prolonged activated partial thromboplas-
temic lupus erythematosus and other immune-mediated
tin time. Definitive diagnosis is by quantification of
disorders, mercury intoxication). Dyspnea may occur
factor VIII or factor IX, respectively.
due to pleural effusion or pulmonary thromboembolism.
Devon Rex cats bleeding from inherited vitamin K
responsive coagulopathy will have prolonged pro-
Diagnosis
thrombin time and activated partial thromboplastin
time, which resolve with vitamin K therapy. A serum chemistry profile will reveal azotemia with
chronic renal failure, and severe hypoalbuminemia
Cats bleeding from coagulopathy due to vitamin K
with nephrotic syndrome.
antagonist rodenticide poisoning will have pro-
longed prothrombin time, activated partial throm- Urinalysis will reveal inappropriately low urine spe-
boplastin time, and PIVKA clotting time, which cific gravity with chronic renal failure, and marked
resolve with vitamin K therapy. proteinuria with nephrotic syndrome (note that pro-
teinuria will raise specific gravity).
Cats bleeding from coagulopathy due to liver disease
(e.g. hepatic lipidosis or cholangiohepatitis) will have Abdominal imaging may reveal small kidneys, altered
prolonged prothrombin time and/or activated renal echogenicity or peritoneal fluid.
Peritoneal fluid is a transudate. Urinary bladder may be markedly enlarged (±

atonic), sufficient to cause abdominal distention.
Kidney biopsy will reveal glomerulonephritis.
Potential underlying diseases should be investigated.
Diagnosis
Littermates should be evaluated for familial disease.
Difficulty in passing urinary catheter.
Differential diagnosis Abdominal radiography will confirm enlargement of
the bladder. Contrast urethrogram or excretory uro-
Other causes of chronic weight loss and ascites include
gram may identify narrowing of urethra or a mass at
FIP, neoplasia, pancreatitis, liver diseases, right heart
the trigone.
failure, steatitis and tuberculosis. If the peritoneal fluid
is a transudate, the main differential diagnosis is neo- Abdominal ultrasonography will confirm enlargement
plasia. of the bladder and may identify a mass at the trigone.
Definitive diagnosis requires biopsy, which may
Treatment require surgery.
Treat the underlying disorder if possible.
Prednisone (initial dose 2–4 mg/kg/day) has been rec- INTRAHEPATIC ARTERIOVENOUS FISTULA
ommended but is of questionable value.
Classical signs
Treatments that are ineffective in most dogs include
cytotoxic drugs and cyclosporine. ● Ascites.
Treatments of potential benefit in dogs include ACE-
inhibitors (e.g. enalapril, benazepril) to reduce
Clinical signs
hypoproteinemia, n-3 fatty acids to reduce inflam-
mation and inhibit platelets, and low-dose aspirin A fistula between the hepatic arterial system and portal
(0.5 mg/kg PO every other day) to inhibit platelets. venous system causes ascites from pre-sinusoidal
portal hypertension. Other signs could include poor
Plasma transfusions will temporarily ameliorate
weight gain, reduced appetite, and dyspnea secondary
hypoalbuminemia.
to ascites. Congestive heart failure and hepatic
encephalopathy from secondary porto-systemic shunt-
ing are theoretical sequelae.
NEOPLASIA OBSTRUCTING OR
Usually a congenital lesion, therefore seen in young
COMPRESSING THE LOWER URINARY
animal, but could occur secondary to trauma or surgery.
TRACT, GRANULOMATOUS URETHRITIS
AND URETHRAL STRICTURE
Diagnosis
Classical signs
Rare.
● Chronic straining to urinate and
Abdominal ultrasound examination will confirm peri-
incontinence.
toneal fluid and may detect a cavernous lesion.
Doppler ultrasound may detect high-velocity turbulent
blood flow through the fistula.
Clinical signs
Abdominocentesis reveals a transudate.
Dysuria characterized by increased time in litter box,
straining, and dribbling urine from paradoxical inconti- Angiography may be used to confirm the diagnosis.
nence.
Exploratory laparotomy may reveal prominent subcap-
Tumors affecting mucosa may cause hematuria. sular hepatic blood vessels.
PORTAL VEIN ATRESIA OR HYPOPLASIA HEPATIC AMYLOIDOSIS

● Ascites. ● Lethargy, anorexia, weight loss, anemia,
● Hepatic encephalopathy. hepatomegaly.

An underdeveloped portal venous system causes Amyloidosis is a systemic disease with deposition of
ascites from pre-sinusoidal portal hypertension in a amyloid protein AA in numerous tissues including the
young animal. Other signs could include hepatic liver.
encephalopathy, poor weight gain, reduced appetite ● In most cases, including familial amyloidosis in
and dyspnea secondary to ascites. Abyssinian cats, renal failure from renal amyloi-
dosis dominates the clinical presentation.
Nephrotic syndrome causing ascites is rare because
Diagnosis amyloid affects primarily the renal medulla.
● In some cases, including as a familial disease in
Rare.
some lines of Siamese cats and Oriental short-
Elevated serum bile acids. hair cats, amyloid deposition in the liver is clini-
Abdominal ultrasound examination will confirm peri- cally most important.
toneal fluid and a small liver. – Signs are mostly due to chronic liver disease
(lethargy, anorexia, weight loss), or acute hemor-
Abdominocentesis reveals a transudate. rhage (anemia, hemoperitoneum) resulting from
Angiography or exploratory laparatomy may be used to spontaneous hepatic rupture. Signs of liver failure
confirm the diagnosis. (icterus, hepatic encephalopathy) are not common.
– Abdominal distention may occur due to
hepatomegaly, splenomegaly, intestinal dila-
LIGATION OF PORTOSYSTEMIC SHUNT tion and hemoperitoneum.

● Ascites. Liver enzymes are normal to variably elevated.
Liver biopsy will demonstrate amyloid. If amyloidosis is
Clinical signs suspected, biopsy of the intestinal tract may be consid-
ered to demonstrate amyloid deposition because there is
Ligation of a portosystemic shunt may cause ascites an increased risk of hemorrhage from liver biopsy.
from pre-sinusoidal portal hypertension.
HEPATIC NECROSIS
Diagnosis
Common for 2 days following surgical ligation of a Classical signs
portosystemic shunt. Ascites is less likely to occur with ● Acute depression and anorexia.
an ameroid constrictor or cellophane banding.
Abdominal ultrasound examination will confirm peri-
toneal fluid. Clinical signs
Abdominocentesis reveals a transudate to modified Hepatic necrosis may result from a wide variety of
transudate. mechanisms (e.g. tissue hypoxia, free radical forma-
tion) and specific etiologies (e.g. feline infectious in a dog, so testing for this organism should be consid-
peritonitis, virulent systemic feline calicivirus infec- ered.
tion, toxoplasmosis, acetaminophen and diazepam
toxicosis).
HEPATIC ABSCESS
Clinical signs are due to the specific cause and to acute
liver injury, which may range from subclinical to ful- Classical signs
minant hepatic failure with hepatic encephalopathy.
● Lethargy, anorexia, and weight loss.
Necrotic liver tissue may spontaneously hemorrhage
resulting in peritoneal fluid and acute anemia.
Clinical signs
Non-specific signs are most common.
Diagnosis
In a case series about a quarter of cats had a fever and
Liver biopsy will demonstrate necrosis.
about a third were hypothermic. One third of cats had
Abdominal ultrasonography will confirm the presence abdominal pain.
of peritoneal fluid. Abdominocentesis will confirm that
the fluid is blood.
Diagnosis
Rare disorder.
PELIOSIS HEPATIS
Variable neutrophilia, anemia, hypoalbuminemia,
Classical signs hyperbilirubinemia and elevation in liver enzymes.
● Spontaneous abdominal hemorrhage. Ultrasound may demonstrate hypoechoic or mixed
hypoechoic/hyperechoic lesions in the liver and
abdominal effusion.
Clinical signs
Abdominal fluid cytology usually reveals degenerate
Variable clinical signs include: neutrophils and bacteria. Degenerate neutrophils with-
● Spontaneous abdominal hemorrhage from irregu- out bacteria and hemorrhagic effusion have also been
lar blood-filled cystic spaces, which may result in seen.
pale mucous membranes, collapse or abdominal
Culture of hepatic lesions.
distention.
● Signs of liver disease, including hepatomegaly or
jaundice. Telangiectasia is often present. PERI-RENAL PSEUDOCYSTS
● Weight loss, dyspnea.
Classical signs
Diagnosis ● Abdominal distention.
● Polyuria and polydipsia.
Abdominal radiographs may reveal hepatomegaly or
● Inappetence and weight loss.
loss of abdominal detail.
Abdominal ultrasound examination will reveal hypo-
Clinical signs
echoic regions in liver ± peritoneal fluid.
Abdominal distention occurs due to the formation of
Fine-needle aspiration of liver lesions should yield
unilateral or bilateral fluid-filled sacs. The sacs lack an
blood. Abdominocentesis may yield blood.
epithelial lining and contain either a transudate of
Histology of liver biopsy will confirm the diagnosis. serum, urine, or uncommonly, blood.
Peliosis hepatis may be caused by Bartonella henselae About 75% of cats have concurrent chronic renal fail-
infection in humans, and the two have been associated ure, but cause and effect are not known.
Cats are presented for abdominal distention and/or clin- Clinical signs
ical signs of chronic renal failure such as polyuria,
polydipsia, inappetence and weight loss. Budd-Chiari-like syndrome is congenital or acquired
obstruction of the venous outflow of the liver, includ-
ing the hepatic venules, hepatic veins and caudal vena
Diagnosis cava, causing post-sinusoidal portal hypertension. It
Abdominal radiography will demonstrate large kid- is rare in cats. Cases have included veno-occlusive dis-
neys. Ultrasonography will demonstrate small kidneys ease and fibrous webs in the caudal vena cava.
within fluid-filled structures. The predominant clinical sign is progressive abdomi-
Presence of fluid may be confirmed by abdominocente- nal distention due to fluid.
sis. Analysis of fluid will reveal a transudate, urine or
blood. Diagnosis
Routine hematology and serum biochemistry may Angiography will demonstrate caudal vena caval
reveal changes consistent with chronic renal failure. obstruction.
Liver biopsy will demonstrate veno-occlusive disease.
Abdominocentesis will reveal a modified transudate.
EXTRA-UTERINE FETUSES
Classical signs
PNEUMOPERITONEUM
● None.
Classical signs
Clinical signs ● Marked abdominal distention.
Most “ectopic pregnancies” are not associated with
clinical signs, and are an incidental finding during ovar-
iohysterectomy. Clinical signs
Because extra-uterine fetuses usually occur second- Mild pneumoperitoneum usually occurs following
ary to uterine rupture, marked hemorrhage at the time laparotomy and intentional marked pneumoperitoneum
of rupture or septic peritonitis may occur, which may occurs during laparascopy.
result in peritoneal fluid.
Marked spontaneous pneumoperitoneum usually
Ascites without systemic signs of illness may also results from a perforating gastric ulcer or neoplasm,
occur. rupture of the stomach or large intestine, or less
often as an extension from pneumothorax or pneu-
Diagnosis momediastinum. Small intestinal rupture usually does
not cause marked pneumoperitoneum unless it is a
Abdominal radiography or ultrasonography will complication of endoscopy, which uses insufflation.
demonstrate a mummified fetus ± peritoneal fluid. Gas may also enter from penetrating abdominal
wounds or perforation of the bladder during traumatic
urinary tract catheterization, or may be produced by
BUDD–CHIARI-LIKE SYNDROME intra-abdominal bacteria, but such gas does not usually
cause abdominal distention.
Classical signs The predominant clinical sign of marked pneumoperi-
● Marked abdominal distention due to toneum is marked abdominal distention due to air,
ascites. and acute onset of depression if associated with gas-
trointestinal tract rupture.
● Perforating gastric ulcers may result in marked

LEPTOSPIROSIS
pneumoperitoneum without generalized peritonitis
and may be associated with minimal systemic
Classical signs
signs.
● Gastrointestinal perforation may occur with mini- ● Undefined.
mal-to-absent pneumoperitoneum.
Clinical signs
Diagnosis
Positive titers and seroconversion to Leptospira spp.
Radiography will demonstrate free air in the have been documented in various sick cats.
abdomen. This is best seen along the peritoneal sur-
Clinical signs are variable and many are attributable to
face of the diaphragm and the fundus of the stom-
concurrent diseases.
ach. Lateral views obtained in dorsal or sternal
● Abdominal distention due to ascites has been
recumbency will demonstrate the air if standard
reported.
views are inconclusive.
With marked pneumoperitoneum, abdominocentesis
Diagnosis
will reveal air. Abdominocentesis may also reveal
abdominal fluid, the characteristics of which will vary The disease in cats is rare compared to dogs.
with the cause.
Most cats with positive titers have had some evidence
of liver disease, e.g. increased liver enzymes, bilirubin
UMBILICAL, INGUINAL, TRAUMATIC or ascites.
ABDOMINAL WALL HERNIA* Currently diagnosis in dogs relies on demonstrating a
four-fold rise in acute and convalescent titers, and
Classical signs arguably the same criteria should be applied to cats.
● Localized swelling of the abdomen.
GASTRIC DILATION-VOLVULUS

Congenital or acquired hernias are usually evident as ● Tympanic cranial abdomen, shock.
localized changes in abdominal contour.
● Owners may misinterpret marked displacement of
Clinical signs
abdominal fat or organs into the hernia as
abdominal distention. Gastric dilation-volvulus is rare in cats. Clinical
signs are similar to dogs.
With acquired traumatic abdominal hernias there are
usually also internal or external signs of motor vehicle Abdominal distention occurs because of dilation of
trauma or fight wounds. the stomach with air.
● Ventral abdominal herniation may be associated
with rupture of the cranial pubic ligament.
Diagnosis
Abdominal radiography will demonstrate marked gas-
Diagnosis tric distention with air.
The focal nature of the lesion is usually evident on
abdominal palpation, especially if the hernia is RUPTURED GALL BLADDER OR BILE DUCT
reducible.
Classical signs
Abdominal imaging or surgical exploration may be
necessary to confirm the hernia. ● Progressive icterus and abdominal distention.

Rupture of the gall bladder or biliary tract is rare Infection is usually diagnosed by finding characteristic
in cats. Causes include motor vehicle trauma, falling operculated eggs on fecal floatation.
from heights, penetrating trauma (e.g. bullet wound)
Abdominal ultrasonography may demonstrate hepatic
or cholelithiasis.
tumors or cysts and peritoneal fluid.
Bile peritonitis causes mild systemic signs in dogs
Abdominocentesis may rarely reveal peritoneal fluid
unless secondary infection occurs.
containing single-end operculated eggs.
Diagnosis
SCLEROSING ENCAPSULATING
Abdominal ultrasonography will demonstrate peri- PERITONITIS
toneal fluid. The gall bladder is small with gall blad-
der rupture and small-to-large with bile duct Classical signs
rupture.
● Variable (rare disorder).
Abdominocentesis will reveal a dark bile-stained
modified transudate to (usually septic) exudate con-
taining high levels of bilirubin pigment with or without Clinical signs
crystals. It should be noted that ascites in an animal that The abdominal mesothelial lining becomes replaced by
is icteric from pre-hepatic or hepatic causes also con- fibrous tissue resulting in encasement of abdominal
tains some bilirubin, because of diffusion of bilirubin organs. Clinical signs reported in dogs and cats due to
from the blood into the ascitic fluid. If there is question the peritonitis or underlying disorders include anorexia,
as to whether the source of bile is the blood or the bil- vomiting, abdominal pain, abdominal mass and ascites.
iary tract, the bilirubin level in the abdominal fluid
may be compared to serum, with a higher level in
the fluid indicating biliary tract rupture. (In one Diagnosis
case series of dogs and cats, bilirubin level in the fluid Biopsy of peritoneum reveals fibrous tissue.
was consistently at least two times the serum level.)
IDIOPATHIC CHYLOUS ASCITES

ABDOMINAL FLUKE INFECTION
Classical signs
Classical signs
● Ascites.
● Chronic weight loss, anorexia, vomiting,
diarrhea, jaundice.
Clinical signs
Clinical signs Idiopathic chylous ascites is rare compared to idio-
Platynosomum spp., Metorchis spp.,Opisthorchis spp., pathic chylothorax.
Clonorchis spp. and Amphimerus spp. are bile duct
Peritoneal effusion with or without concurrent pleural
parasites in numerous mammals, including cats.
effusion.
Infections may be subclinical or may cause chronic
weight loss, anorexia, vomiting, diarrhea and jaundice.
Diagnosis
Some infections may cause hepatic neoplasia or hepatic
cysts. Abdominocentesis reveals chylous effusion.
Fluke infection of the peritoneal cavity causing ascites Neoplasia or other underlying causes of effusion are
has been reported rarely. not identified.
RECOMMENDED READING
Auman M, Worth LT, Drobatz KJ. Uroperitoneum in cats: 26 cases (1986–1995). J Am Anim Hosp Assoc 1998; 34:
315–324.
Bonczynski JJ, Ludwig LL, Barton LJ, Loar A, Peterson ME. Comparison of peritoneal fluid and peripheral blood
pH, bicarbonate, glucose, and lactate concentration as a diagnostic tool for septic peritonitis in dogs and cats. Vet
Surg 2003; 32: 161–166.
Center SA, Harte J, Watrous D, et al. The clinical and metabolic effects of rapid weight loss in obese pet cats and the
influence of supplemental oral L-canitine. J Vet Intern Med 2000; 14: 598–608.
Connallly H. Cytology and fluid analysis of the acute abdomen. Clin Tech Small Anim Pract 2003; 18: 39–44.
Costello MF, Drobatz KJ, Aronson LR, King LG. Underlying cause, pathophysiologic abnormalities, and response
to treatment in cats with septic peritonitis: 51 cases (1990–2001). J Am Vet Med Assoc 2004; 225: 897–902.
Fossum TW, Wellman M, Relford RL, Slater MR. Eosinophilic pleural or peritoneal effusions in dogs and cats: 14
cases (1986–1992). J Am Vet Med Assoc 1993; 202: 1873–1876.
Haney DR, Levy JK, Newell SM, Graham JP, Gorman SP. Use of fetal skeletal mineralization for prediction of par-
turition date in cats. J Am Vet Med Assoc 2003; 223: 1614–1616.
Hartmann K, Binder C, Hirschberger J, et al. Comparison of different tests to diagnose feline infectious peritonitis.
J Vet Intern Med 2003; 17: 781–790.
Mandell DC, Drobatz K. Feline hemoperitoneum: 16 cases. Vet Emerg Crit Care 1995; 5: 93–97.
Paltrinieri S, Parodi MC, Cammarata G. In vivo diagnosis of feline infectious peritonitis by comparison of protein
content, cytology, and direct immunofluorescence test on peritoneal and pleural effusions. J Vet Diagn Invest
1999; 11: 358–361.
Steyn PF, Wittum TE. Radiographic, epidemiologic, and clinical aspects of simultaneous pleural and peritoneal effu-
sions in dogs and cats: 48 cases (1982–1991). J Am Vet Med Assoc 1993; 202: 301–312.
Tasker S, Gunn-Moore D. Differential diagnosis of ascites in cats. In Practice 2000; 22: 472–479.
Wright KN, Gompf RE, DeNovo RC. Peritoneal effusion in cats: 65 cases (1981–1997). J Am Vet Med Assoc 1999;
214: 375–381.
23. The bleeding cat
Anthony Abrams-Ogg
KEY SIGNS
● Rule out a local lesion.
● Confirm a bleeding tendency.
● Identify a vascular, platelet or clotting disorder.
MECHANISM?
● Bleeding is caused by vascular injury or a disturbance of one or more stages of normal hemostasis.
● The stages of normal hemostasis are: vasoconstriction and formation of a platelet plug
(primary hemostasis), formation of a fibrin clot (secondary hemostasis) and clot dissolution
(fibrinolysis).
WHERE?
● Bleeding caused by a vascular injury may occur at any site.
● Bleeding caused by a non-traumatic vascular disorder varies with the specific disorder.
● Bleeding due to a platelet disorder tends to be cutaneous and mucosal.
● Bleeding due to a coagulopathy tends to be subcutaneous and internal.
WHAT?
● The most common causes of bleeding are local lesions. These result from trauma, inflamma-
tion or neoplasia.
● The most common causes of bleeding tendencies are liver diseases, neoplasia, and infectious
diseases. Most of this is subclinical.
● The most common causes of abnormal clinical bleeding are hepatic lipidosis, retroviral-induced
megakaryocytic hypoplasia and vitamin K antagonist poisoning.

Diseases causing a bleeding cat
VASCULAR DISORDERS
ANOMALY
● Cutaneous asthenia (Ehlers–Danlos syndrome) (p 519)
Inherited fragile skin and/or fragile vessels may lead to vascular trauma.
continued
481
continued
METABOLIC
● Renal failure*** (p 494)
Uremia causes alimentary tract ulceration, systemic hypertension causes retinal hemorrhages, a
platelet function defect may be present, coagulation defects may be present, and hemolytic-uremic
syndrome is an uncommon complication of renal transplantation.
●Hyperadrenocorticism (p 520)
Acquired fragile skin may lead to vascular trauma.
● Systemic hypertension** (p 495)
Systemic hypertension may cause retinal hemorrhages and, less often, epistaxis. The most com-
mon cause of hypertension is chronic renal failure. Other causes include hyperthyroidism, diabetes
mellitus, hyperadrenocorticism and polycythemia vera. Rare disorders that may cause hypertension
include multiple myeloma, pheochromocytoma and hyperaldosteronism.
NEOPLASTIC, INFLAMMATION, TRAUMA
● Local lesions causing localized hemorrhage *** (p 492)
Tumors (e.g. cutaneous squamous cell carcinoma), local inflammation (e.g. cat bite abscesses,
idiopathic cystitis), and trauma (e.g. lacerations) may cause local bleeding at the site.
●Motor vehicle and other major blunt trauma*** (p 493)
Major trauma can cause mild to severe local bleeding at numerous sites.
● Strangulation (p 519)
External choking injury may cause scleral hemorrhage.
TOXIC
● Snake bite envenomation (p 503)
Snake venom toxins may cause edema and bleeding around the bite.
PLATELET DISORDERS
ANOMALY
●Chediak–Higashi syndrome (p 520)
An inherited platelet function defect causes prolonged bleeding after trauma.
●Idiopathic thrombocytopathia (p 520)
An inherited platelet function defect causes spontaneous mucosal bleeding.
● Von Willebrand’s disease (p 521)
An inherited von Willebrand’s factor (a platelet adhesion protein) deficiency causes prolonged
bleeding after trauma.
METABOLIC
● Megakaryocytic hypoplasia** (p 495)
Reduced platelet production may be due to hematopoietic neoplasms in the bone marrow, retrovi-
ral infections, histoplasmosis infecting the bone marrow, idiopathic causes (which are probably
immune-mediated) and toxicoses. Severe thrombocytopenia causes spontaneous mucosal bleeding
and prolonged bleeding after injury.
23 – THE BLEEDING CAT 483
● Disseminated intravascular coagulation* (p 501)

Acute and chronic DIC are characterized by variable thrombocytopenia, although clinical bleeding
is uncommon.
● Splenomegaly (p 521)
Splenic sequestration may contribute to thrombocytopenia when there is marked splenomegaly.
● Feline leukemia virus (FeLV) infection** (p 499)
Bleeding tendencies may be caused by megakaryocytic hypoplasia, immune-mediated platelet
destruction, and DIC secondary to infections and neoplasia. Clinical bleeding is uncommon except
with severe thrombocytopenia.
● Feline immunodeficiency virus (FIV) infection** (p 500)
Bleeding tendencies may be caused by megakaryocytic hypoplasia, prolongation of clotting times
due to unknown mechanisms, and DIC secondary to infections and neoplasia. Clinical bleeding is
uncommon except with severe thrombocytopenia.
INFLAMMATION (IMMUNE)
● Immune-mediated thrombocytopenia (ITP) (p 506)
ITP may be primary or secondary to neoplasia, infectious diseases or drugs. Transient thrombocy-
topenia may occur following vaccination in dogs, but has not been documented in cats. Severe
thrombocytopenia causes spontaneous mucosal bleeding and prolonged bleeding after injury.
IDIOPATHIC
● Miscellaneous diseases (p 505)
Thrombocytopenias due to unknown mechanisms have been seen with a variety of diseases not
typically associated with abnormal bleeding. Clinical bleeding with these abnormalities is uncom-
mon.
TOXIC
● Antibiotics (p 523)
Antibiotics may have various effects on hemostasis including idiosyncratic megakaryocytic
hypoplasia, impaired platelet function, and exacerbating vitamin K deficiency and antagonism.
● Antiplatelet cardiac drugs (p 520)
Aspirin and n-3 fatty acids are given to impair platelet function in an attempt to prevent throm-
boembolism in cardiomyopathy. Effect, if any, is subclinical. Risk for spontaneous bleeding with
newer drugs that block specific platelet receptors is probably low.
● Non-steroidal anti-inflammatory drugs (p 524)
Non-steroidal anti-inflammatory drugs given for analgesia may impair platelet function. Effect on
risk for bleeding is probably minimal.
● Miscellaneous drugs (p 524)
Sedatives, anesthetic agents and anti-histamines may impair platelet function. Effect on risk for
bleeding is probably minimal.
continued
continued
COAGULOPATHIES
ANOMALY
● Hemophilia A (classical hemophilia) (p 510)
Inherited factor VIII deficiency causes spontaneous internal bleeding and re-bleeding after trauma.
● Hemophilia B (Christmas disease) (p 513)
Inherited factor IX deficiency causes spontaneous internal bleeding and re-bleeding after trauma.
● Hageman trait* (p 504)
Inherited factor XII deficiency causes markedly prolonged activated clotting time and activated
partial thromboplastin time without clinical signs.
● Vitamin K responsive coagulopathy in the Devon Rex (p 515)
An inherited defect in vitamin K metabolism causes spontaneous internal bleeding and re-bleeding
after trauma.
● Factor X deficiency (p 522)
Inherited factor X deficiency causes spontaneous internal bleeding and re-bleeding after trauma.
● Hemophilia C (p 514)
Inherited factor XI deficiency causes excessive bleeding after trauma.
METABOLIC
● Liver disease** (p 498)
Vitamin K deficiency (several causes), failure of coagulation factor synthesis, and chronic DIC
may cause excessive bleeding after venepuncture and liver biopsy. The liver may be friable.
● Pancreatitis (p 518)
Hemostatic abnormalities are usually subclinical. Clinical bleeding is unlikely unless there is
severe DIC or concurrent liver disease.
● Exocrine pancreatic insufficiency (EPI) (p 516)
Vitamin K malabsorption may cause spontaneous or excessive bleeding.
● Inflammatory bowel disease (IBD) (p 517)
Vitamin K malabsorption may cause spontaneous or excessive bleeding.
● Disseminated intravascular coagulation* (p 501)
Acute and chronic DIC are characterized by variable prolongation of clotting times, although clini-
cal bleeding is uncommon. DIC may be caused by hematopoietic and solid neoplasms, viral infec-
tions (panleukopenia, feline infectious peritonitis), bacterial and fungal sepsis, systemic protozoal
infections and hyperthermia. Clinical bleeding is uncommon.
NUTRITIONAL
● Vitamin K deficient diet (p 523)
A diet severely deficient in vitamin K1 or containing a vitamin K antagonist may cause sponta-
neous internal bleeding and re-bleeding after trauma. Anorexia may contribute to vitamin K defi-
ciency in liver disease.
INFLAMMATION (IMMUNE)
● Circulating anti-coagulant (p 522)
Circulating anti-coagulants may be acquired in immune-mediated diseases and cause spontaneous
or excessive bleeding.
IDIOPATHIC
● Miscellaneous diseases* (p 505)
Prolongation of clotting times due to unknown mechanisms have been seen with a variety of dis-
eases not typically associated with abnormal bleeding. Clinical bleeding with these abnormalities
is uncommon.
TOXIC
● Antibiotics (p 523)
Some antibiotics may exacerbate vitamin K deficiency and antagonism.
● Vitamin K antagonist rodenticides and drugs (p 507)
Poisoning with these compounds may cause severe spontaneous internal bleeding and excessive
bleeding following trauma.
● Anti-convulsants (p 523)
Phenobarbital may cause a subclinical vitamin K antagonism.
●Anti-thyroid drugs (p 524)
Anti-thyroid drugs may cause a subclinical vitamin K antagonism.
●Anti-coagulants (p 522)
Anti-coagulant drug overdose may cause spontaneous bleeding.
● Snake bite envenomation* (p 503)
Snake venom hematoxins may cause subclinical and clinical bleeding tendencies.
into a stable fibrin clot. Calcium (factor IV) is

INTRODUCTION needed for most steps in the cascade.
– Secondary hemostasis is classically divided into
MECHANISM? the extrinsic, intrinsic, and common system,
although there is extensive interaction between
Hemostasis following injury to a blood vessel is classi- these pathways.
cally divided into primary hemostasis, secondary – The extrinsic system (tissue factor pathway) is
hemostasis and fibrinolysis, although there is extensive initiated when tissue factor (factor III) is
interaction between these parts. expressed on the surface of activated subendo-
● Primary hemostasis consists of: thelial fibroblasts and monocytes at sites of vas-
– Vasoconstriction. cular injury or inflammation. In a simplified
– Formation of the initial platelet plug. view, tissue factor interacts with factor VII to
● Secondary hemostasis consists of a cascade of form a tissue factor–activated factor VII com-
coagulation proteins that converts the platelet plug plex that amplifies itself and directly activates
factor X (the start of the common system). The ● Neoplasia. Neoplasia may disrupt blood vessels,
extrinsic system is the main pathway for the ini- promote inflammation, promote angiogenesis and
tiation of coagulation in vivo, but it cannot sus- promote fragile vasculature (e.g. endothelium with-
tain coagulation. out a vessel wall).
– The intrinsic system (contact activation path-
Bleeding is less often caused by a disorder of pri-
way) is activated by exposure to subendothe-
mary or secondary hemostasis. Such disorders may
lial tissue following vascular injury. Activation
cause subclinical abnormalities in test results or
of contact activating factors (factors XII
abnormal clinical bleeding.
[Hageman], high-molecular-weight kininogen,
prekallikrein), XI, IX and VIII occurs. Contact Abnormal bleeding is spontaneous or excessive.
activation by factor XII is probably of minimal ● Spontaneous bleeding occurs as a result of the
importance in initiating normal coagulation minor trauma of daily activity.
in vivo. However, while the extrinsic system is ● Similar to other organ systems, hemostasis has
most important for initiating coagulation, the a large reserve capacity – a severe deficiency
intrinsic system is important in sustaining coagu- is required for spontaneous bleeding to occur,
lation. In a simplified view, thrombin resulting for example, a platelet count < 10–20 × 109/L
from extrinsic system activation ultimately (10 000–20 000/μl), or a factor VIII level < 10% nor-
results in factors IX and VIII (together with cal- mal is required for spontaneous bleeding to occur.
cium and platelet phospholipid) forming a – Bleeding diatheses are less common in cats than
“tenase complex” on the surface of activated in dogs.
platelets, which activates factor X. The contact ● Excessive bleeding occurs following trauma or
activation factors are important in inflammation development of other local lesions. The degree of
and fibrinolysis. bleeding is inappropriate for the severity of the
– The common system is activated by the end- lesion.
products of the extrinsic and intrinsic systems
Bleeding disorders may be inherited or acquired.
(i.e. the tissue-factor-activated factor VII and
● Inherited disorders are as common in mixed-breed
tenase complexes, respectively). In a simplified
cats as in purebreds.
view, the initial step is activation of factor X,
which then activates factor V. Activated factors Multiple mechanisms may contribute to bleeding in an
X and V (together with calcium and platelet individual patient.
phospholipid) form a “prothrombinase complex”
Acute blood loss causes acute anemia and hypo-
on the surface of activated platelets, which acti-
volemia. Signs include lethargy, anorexia, hypother-
vates thrombin (factor II), which in turn converts
mia, pallor, tachycardia, weak pulses and dyspnea.
fibrinogen (factor I) to fibrin. Factor XIII then
stabilizes the fibrin clot, converting the fibrin Chronic blood loss causes iron-deficiency anemia.
monomer to a fibrin polymer.
Regardless of cause, acute substantial bleeding may
● Fibrinolysis refers to clot dissolution by the plas-
cause signs due to a space-occupying effect and/or
minogen-plasmin system.
inflammation incited by the presence of blood. Signs
Bleeding is most often caused by local vascular include mucosal and cutaneous swellings (hematomas);
injury. Normal hemostasis ensues and the degree of neurologic signs from bleeding into or around the cen-
bleeding is appropriate for the injury. Causes of vas- tral nervous system; lameness, muscle pain, muscle
cular injury include: stiffness, joint swelling and joint pain (hemorrhage into
● Sharp and blunt trauma. This includes clinical muscles and joints); uveitis; dyspnea from pulmonary
procedures (e.g. venepuncture, dentistry, surgery). or pleural hemorrhage, or tracheal compression by a
● Tissue inflammation. Inflammation disrupts blood jugular hematoma; acute cardiac tamponade from peri-
vessels and causes vasodilation. The latter increases cardial hemorrhage (causing tachycardia and hypoten-
blood flow to the area and promotes extravasation sion similar to hypovolemia), abdominal distention
of red blood cells. and abdominal pain (presumably due to hemorrhage
within organs), dysuria due to a clot within the bladder, – Bleeding from mucosal surfaces – epistaxis,
and possibly vomiting due to a clot within the stomach. melena and hematuria.
– Intraocular hemorrhage.
– Risk of spontaneous bleeding is related to the
WHERE? platelet count, but quantification of the risk is
imprecise, in part because of imprecision in
Bleeding may be the result of a local lesion or a distur-
platelet counting, especially in cats (see discus-
bance in primary or secondary hemostasis.
sion below). The following values are derived
Bleeding from a local lesion may occur into or from from humans and dogs; cats are at less risk of
any tissue and is appropriate for the severity of the bleeding for a given platelet count. Indeed, signs
lesion. of clinical bleeding in cats are usually absent or
● Bleeding varies with the severity, type and location mild until almost no platelets are evident on a
of lesion. Hemostasis may be insufficient to stop blood smear. Bleeding is worse at a given platelet
bleeding, and manipulation of the lesion may reac- count if there is concurrent vasculopathy, platelet
tivate bleeding. function defect, coagulopathy, fever, or, possibly,
● Presence of blood clots in shed blood rules out a anemia.
typical coagulopathy, but not a platelet disorder, as – Platelets < 80 × 109/L (< 80 000/μl) – increased
the cause of bleeding. bleeding at surgery.
– Platelets < 50 × 109/L (< 50 000/μl) – micro-
Absence of blood clots in shed blood does not rule in a
scopic spontaneous bleeding.
coagulopathy.
– Platelets < 20 × 109/L (< 20 000/μl) – mild risk of
● Initial bloodshed may be too rapid to immediately
spontaneous clinical bleeding.
activate coagulation (e.g. laceration of a large vessel).
– Platelets < 10 × 109/L (< 10 000/μl) –moderate
● Clots may have been removed (e.g. swallowed) and
risk of spontaneous clinical bleeding.
only red blood cells not incorporated into the clot
– Platelets < 5 × 109/L (< 5 000/μl) – severe risk of
remain.
spontaneous clinical bleeding.
● Clot lysis may have occurred.
● Excessive bleeding may be characterized by:
● Blood in body cavities and the intestinal tract may
– Occurrence immediately following injury,
not clot because of defibrination on epithelial sur-
because the initial platelet plug does not form.
faces and clots may be digested.
– Increased rate of bleeding.
Vascular disorders may result in either spontaneous or – Prolonged bleeding.
excessive bleeding at the site of the disorder. – Prolonged bleeding after venepuncture is
● Vascular disease secondary to systemic hyperten- one of the most common initial signs of
sion commonly causes retinal hemorrhages and less thrombocytopenia. It should not be dismissed
commonly epistaxis. and attributed to the venepuncture technique in
● Other vascular disorders are not common causes of a cat at risk for a bleeding disorder.
bleeding in cats.
Coagulopathies may result in either spontaneous or
Platelet disorders may result in either spontaneous or excessive bleeding.
excessive bleeding. ● Spontaneous bleeding occurs because vasocon-
● Spontaneous bleeding occurs because blood ves- striction and platelet plugs are insufficient to stop
sel walls are continuously sustaining minute bleeding from larger vessels. Coagulation is neces-
injuries and being plugged by platelets. A platelet sary, and a coagulopathy permits bleeding from
disorder permits bleeding at sites of minute injury larger vessels into tissues and body cavities result-
in small vessels resulting in the following signs: ing in the following signs:
– Bleeding at multiple sites. – More localized bleeding (although widespread
– Petechiation and ecchymoses, especially in hemorrhage may occur).
dependent areas and areas subject to normally – Subcutaneous hematomas and intramuscular
high wear and tear (e.g. gums). hemorrhages.
– Bleeding into body cavities (pleural space, peri- If the blood sample is being collected by using a winged-
toneal cavity, joints). infusion set (“butterfly”), jugular catheter, or vacuum
– Scleral hemorrhage. tube draw, then the first 2–5 ml should be discarded or
● Excessive bleeding may be characterized by: used for serum chemistry determinations. This may
– Delayed bleeding and rebleeding because the ini- reduce platelet clumping and premature activation of
tial platelet plug is not stabilized by a fibrin clot. coagulation. In most cases a blood sample is obtained by
– Detection of a bruise following venepunc- venepuncture using a syringe and needle, in which case
ture is one of the most common initial signs the EDTA (platelet count) and citrate tubes (coagulation
of coagulopathy. It should not be dismissed tests) should be filled first, and the remaining blood used
as a result of venepuncture technique in a cat for serum chemistry determinations.
at risk for a bleeding disorder.
Routine tests of hemostasis include:
– Increased rate of bleeding if a larger vessel is
● Platelet count.
injured.
– Used for detecting thrombocytopenia.
Differences are not absolute between bleeding due – Platelet counts may be obtained by estimation
to platelet disorders and coagulopathy, and clinical from a blood smear, manual counting, or with
signs overlap. Bleeding patterns seen with both automated cell counters.
include cutaneous and subcutaneous bleeding at – To estimate platelet count, prepare a routinely
venepuncture sites, gingival bleeding, retinal hemor- stained blood smear. Examine the blood smear
rhages, cerebral hemorrhages, pulmonary hemor- monolayer where red cells are close together
rhages and widespread bleeding. and 50% are touching. Normally there are
about 10–30 platelets/oil immersion field
(magnification = × 1000); each platelet ≈ 20 ×
WHAT? 109/L (20 000/μl). This requires a properly pre-
pared blood smear. An alternative method that
To diagnose the cause of bleeding:
avoids a blood smear uses a disposable count-
● Rule out a local lesion.
ing chamber and supravital stain (ZynoStain,
● Confirm abnormal bleeding with tests of hemostasis.
Zynocyte, MA, USA) (Tasker et al, 2001).
● Characterize abnormal bleeding as a defect in pri-
– Manual counting may be performed using a
mary and/or secondary hemostasis based on clinical
Unopette microcollection system (Becton
signs and tests of hemostasis.
Dickinson) and a hemocytometer.
● Determine if the hemostatic defect is inherited or
– Automated cell counters use impedance
acquired.
(Coulter principle), quantitative buffy coat
● Determine the mode of inheritance if inherited.
(QBC) or light scattering properties (flow
● Determine an underlying cause if defect is acquired.
cytometry).
The most common causes of bleeding are local – Platelet counting in cats has historically been
lesions – trauma, inflammation and neoplasia. problematic because cats are prone to artifac-
tual thrombocytopenia due to platelet clump-
The most common causes of impaired hemostasis
ing. Platelet clumping results from difficulties in
are liver diseases, neoplasia and infectious diseases.
obtaining blood samples and increased aggre-
Most of the alterations in hemostasis are subclinical.
gatability of platelets.
The most common causes of abnormal clinical bleed- – Citrate samples are superior to EDTA samples,
ing are hepatic lipidosis, retroviral-induced megakar- although platelet clumping may still occur.
yocytic hypoplasia and vitamin K antagonist poisoning. – If a citrated blood sample has been
obtained for coagulation testing (see
below), consider using this sample for
TESTS OF HEMOSTASIS
platelet counting.
Tests of hemostatic function are necessary to determine – A solution containing citrate, theophylline,
what stage of the hemostatic process is abnormal. adenosine and dipyradamole (CTAD) con-
tains platelet inhibitors and reduces platelet – The test is used most often for screening cats
clumping. It is commercially available in a with uremia prior to kidney biopsy.
vacuum tube (CTAD tube [formerly Diatube- – Do not routinely perform if cat has thrombocyto-
H], Becton Dickinson). penia. BMBT is usually prolonged when the
– Manual agitation and vortex mixing of blood platelet count is < 50 × 109/L (50 000/μl), and
samples does not reliably break up platelet progressive prolongation is expected with wors-
clumps. ening thrombocytopenia. A platelet count of
– The effect of delay in processing the sample 10–15 × 109/L (10 000–15 000/μl) is likely to
on the platelet count is controversial, but the result in a BMBT of 5–6 minutes. BMBT may be
general recommendation is to perform the performed in a cat with thrombocytopenia to
platelet count as soon after collection as pos- detect a concurrent platelet function defect, if
sible. bleeding is considered to be excessive for the
– Automated cell counters that use light- platelet count and clotting tests are normal.
scattering technology may detect platelet – Ketamine-acepromazine sedation is normally
clumps. used, but BMBT with other sedatives or anes-
– Some clumping may occur without dropping thetics is similar.
the platelet count below normal range. – Place cat in lateral recumbency and fold up the
– Examination of a blood smear is always rec- upper lip. Secure the lip with a tightly tied gauze
ommended. This can be used to verify a platelet strip passed through the mouth, around the head
count obtained by manual or automated methods. rostral to the ipsilateral ear, and caudal to the
This is especially important when platelet counts contralateral ear.
are obtained in-house using quantitative buffy – Avoiding obvious blood vessels, make a 5–6 mm
coat technology. long by 1 mm deep incision in the buccal mucosa
– Closely examine the feather edge of the blood of the everted lip above the molars or premolars;
smear to identify platelet clumps. Also examine this is best done using a spring-loaded device
the blood sample to identify a blood clot in the (e.g. Triplett Bleeding Time Device, Helena Labo-
tube. ratories). Blot the blood with a filter paper 1–2 mm
– Evaluation of a blood smear in a bleeding cat from the incision. The incision should not be
will rapidly determine whether or not the cat stretched or touched during the test. However, if a
is bleeding due to thrombocytopenia. fibrin film forms over the incision it should be
– If there are ≥ 1–2 platelets per oil field, it is teased away using the filter paper to touch the
unlikely the cat is suffering from sponta- blood as it wells up.
neous hemorrhage. If there are ≥ 3–4 – Normal BMBT is 1–3.25 min.
platelets per oil field, it is unlikely that the – Prolonged BMBT in an animal with a normal
cat will bleed excessively. platelet count indicates a vascular defect,
– If platelet clumps are present, the platelet platelet function defect or von Willebrand’s
count is probably adequate and bleeding is disease. Anemia will prolong bleeding time in
not due to thrombocytopenia. humans, rabbits, and dogs, but this effect has not
– The most reliable results are obtained with man- been evaluated in cats. A coagulopathy will not
ual counting, estimation from a well-prepared immediately affect BMBT, but rebleeding may
blood smear, and automated cell counters using occur. If the incision is made in an inflamed area,
flow cytometry. bleeding time will be prolonged.
– Reference ranges vary with the method of – In general, the longer the BMBT value, the more
counting – a typical range is 200–600 × 109/L likely the risk of bleeding, but there are no pre-
(200 000–600 000/μl). cise values defining the risk.
● Buccal mucosal bleeding time (BMBT). ● Activated clotting (coagulation) time (ACT).
– BMBT is typically used for detecting disorders – The intrinsic system is initiated by contact acti-
of platelet function when platelet numbers are vation. In the ACT siliceous (diatomaceous)
normal. earth or glass particles are used to provide a very
large surface for contact activation. Blood clots – There is no direct correlation between the
via the intrinsic and common pathways. degree of prolongation of ACT and the risk
– Add 2 ml fresh blood to an ACT tube pre- for bleeding. The risk for bleeding at a given
warmed to 37˚C using a heating block or human ACT value will vary with the underlying dis-
axilla. Invert the tube rapidly five times and order causing the coagulation abnormality. In
incubate at 37˚C for 60 s. Quickly tip the tube general, for a given disorder, the longer the ACT
gently to observe for clot formation. If no clot is value the more likely the risk of bleeding, but
observed, quickly re-incubate for another 10 sec- there are no precise values defining the risk.
onds, and then re-examine for clot formation. ● Activated partial thromboplastin time (aPTT).
Repeat observations every 10 seconds until the – In this test, calcium, a contact activator and a
very first signs of a clot appear. Time to first platelet phospholipid substitute are added to
clot formation is the activated clotting time. plasma, and the time to clot formation is meas-
After clot formation is first noted, re-incubate ured. Normal blood clotting via the intrinsic
and re-examine every 10 seconds. A complete system requires contact activation and the
solid clot, which is detected by tipping the tube thromboplastin effect of platelet phospholipid.
upside down, normally forms within another 10 (A thromboplastin is a substance having proco-
s. The formation of an incomplete “soft” clot is agulant activity.) The various platelet phospho-
indicative of the presence of heparin (in low con- lipid substitutes used in the test have only partial
centration) or low fibrinogen levels. thromboplastin activity, hence the name of the
– Earlier reported ranges for ACT in cats vary test.
from < 65–75 s to 60–125 s. In the author’s prac- – Most laboratories perform this assay with a
tice the accepted range is 60–90 s. In a recent study fibrometer or photo-optical device, which
(Bay et al, 2000), normal range was 55–165 s. detects the formation of fibrin strands. The assay
– In that study, blood was collected by direct should only be performed in a laboratory that
draw into ACT vacuum tubes. The most com- has validated its assay for use in cats.
mon practice is to collect blood with a – Blood is collected into 3.2% citrate anti-coagulant
syringe, and then inject the blood into the (9 parts blood:1 part citrate). Underfilling, over-
ACT tube. It is possible that syringe collec- filling or a clot in the citrate tube invalidates the
tion and injection shortens ACT by increasing results. The margin for error in the blood:citrate
platelet activation (although this is not impor- ratio in cats is not known. Citrate vacuum tubes
tant in humans), and by initiating coagulation are designed to draw the correct amount of blood.
before the blood enters the ACT tube. – The sample should be centrifuged promptly and
– Traumatic venepuncture inconsistently pro- kept refrigerated or frozen until assayed. If the
longs ACT. sample cannot be centrifuged promptly, it should
– Prolonged ACT indicates a defect in the be refrigerated until assayed.
intrinsic or common system of coagulation. – Prolonged aPTT > 20–25% of a control sample
– The clotting process requires phospholipid (prepared from a pool of donors) and/or outside
from the platelets in the blood, so it has been the normal range indicates a defect in the intrin-
suggested that severe thrombocytopenia sic or common system of coagulation.
(<10 × 109/L [< 10 000/μl]) may also prolong – It may also be beneficial to submit an addi-
ACT. This has not been proven in the cat, and tional control sample from a clinically normal
probably a virtual absence of platelets would cat collected and handled in exactly the same
be necessary. manner as the patient sample in order to detect
– ACT is not affected by sedation with ketamine artifactual prolongation of the aPTT.
and acepromazine. – When comparing serial test results, results
– Although ACT depends to some extent on the from one laboratory cannot be directly com-
operator, a defect in the intrinsic or common path- pared against results from another laboratory
way causing clinical bleeding will usually result in because of differences in methodology,
an ACT > 1.5–2 min. including use of different thromboplastins.
– As with ACT, there is no direct correlation – PIVKA clotting time is similar to PT, but a
between the degree of prolongation of aPTT and different thromboplastin is used to activate
the risk for bleeding. The risk for bleeding at a coagulation, and the plasma is diluted,
given aPTT value will vary with the underlying resulting in longer clotting times. The test
disorder causing the coagulation abnormality. In was introduced as a more sensitive assay
general, for a given disorder, the longer the aPTT than the standard PT for monitoring war-
value the more likely the risk of bleeding, but farin therapy in humans. The assay is more
there are no precise values defining the risk. sensitive both because the thromboplastin is
● Prothrombin time (PT). more sensitive to factor X deficiency, and
– This test is similar to the aPTT, except that a because the longer clotting times facilitate
thromboplastin with tissue factor-like activity is detection of subtle changes. It is also believed,
added in excess to the test system, thus mimick- but not proven, that the test is more sensitive
ing the extrinsic system. The assay should only than the PT to detect vitamin K deficiency or
be performed in a laboratory that has validated antagonism because the PIVKAs (uncarboxy-
its assay for use in cats. lated clotting factors, see Vitamin K antago-
– Collect sample as for aPTT. nist poisoning, below) inhibit the thromboplastin
– Prolonged PT > 20–25% of control sample and the factor X conversion of prothrombin to
and/or outside the normal range indicates a thrombin.
defect in the extrinsic or common system of – PIVKA time is a modified PT, and does not
coagulation. actually measure concentration of PIVKAs.
– It may also be beneficial to submit an addi- – The test was first introduced as the Throm-
tional control sample from a clinically nor- botest™, and this name is used interchangeably
mal cat collected and handled in exactly the with PIVKA. The former is recommended to
same manner as the patient sample in order avoid the confusion that arises from the term
to detect artifactual prolongation of the PT. PIVKA.
When comparing serial test results, results – PIVKA time is more sensitive than PT to detect
from one laboratory cannot be directly com- subclinical and clinical coagulopathies in cats
pared against results from another laboratory due to vitamin K deficiency.
because of differences in methodology, includ- – Most cats (> 95%) with a bleeding tendency
ing use of different thromboplastins. To facili- due to vitamin K deficiency will have a pro-
tate comparison in humans an international longed PIVKA time.
normalized ratio (INR) may be calculated as – It is controversial whether or not PIVKA time
INR = (patient PT/mean normal PT)ISI, where is more sensitive than the PT for the detection
ISI represents the international sensitivity of vitamin K antagonism in dogs. This has not
index of the thromboplastin. The validity of been evaluated in cats. Certainly any cat with
using INR in cats has not been extensively clinical hemorrhage due to vitamin K antago-
evaluated. nist poisoning will have a prolonged PT.
– PT results are typically shorter than aPTT PIVKA time may be more useful than PT for
results. the monitoring of warfarin therapy for pro-
– As with ACT and aPTT, there is no direct corre- phylaxis of thromboembolism in cats with
lation between the degree of prolongation of PT cardiomyopathy.
and the risk for bleeding. The risk for bleeding at – PIVKA time is not specific for vitamin K defi-
a given PT value will vary with the underlying ciency or antagonism. Similar to the PT, it will
disorder causing the coagulation abnormality. In be prolonged in any disorder affecting fac-
general, for a given disorder, the longer the PT tors II, VII, IX and X, including congenital
value the more likely the risk of bleeding, but factor VII deficiency and some cases of DIC.
there are no precise values defining the risk. – Collect sample as for PT and aPTT.
● Proteins induced by vitamin K antagonism or – Although the Thrombotest is a simple test for a
absence (PIVKA). reference laboratory to perform, it is not as
widely offered by such laboratories as are PT and inhibition of clotting in samples from patients
aPTT. Point-of-care instruments are available. treated with heparin.The venom typically
● Thrombin time (TT) and fibrinogen (factor I) causes hemolysis of the sample.
level. – Assays that use citrated plasma are now avail-
– Thrombin measures the time required for throm- able. This facilitates measurement of FDPs as
bin to convert fibrinogen to fibrin. The test is part of a coagulation screen.
performed by adding thrombin to diluted citrated – Increased FDPs suggest accelerated fibrinoly-
plasma. sis by the plasmin system.
– Collect sample as for aPTT and PT. – The test is infrequently positive in cats.
– Prolonged TT is due primarily to hypofibrino- – D-dimers, measured by immunologic assays,
genemia and thus TT is a precise method to are another marker of fibrinolysis, and repre-
assay fibrinogen level. Thrombin time is also sent breakdown products of cross-linked fib-
prolonged by inhibitors such as heparin and rin. Little is currently known of the utility of
fibrin degradation products. d-dimer measurement in cats.
– Fibrinogen level can also be measured in a clinic ● Schistocytes and other poikilocytes.
or laboratory by heat precipitation as follows – Fragmented and other abnormal red cells may
(this method is best for measuring increased lev- appear with disseminated intravascular coagula-
els of fibrinogen and may not be sufficiently sen- tion (DIC).
sitive to measure decreased levels): ● Specialized tests of hemostasis.
– Fill two microhematocrit tubes with EDTA Other tests of hemostasis are used in research labo-
(or citrated) blood. ratories and may be required to investigate a novel
– Immerse one of the tubes in a 56–58˚C bleeding disorder.
(133–136˚F) water bath for 3 minutes to pre- – Platelet aggregation is the test most often used
cipitate fibrinogen. to further investigate a defect of primary hemo-
– Centrifuge both tubes at standard rate and stasis. In the most widely used method, various
time, and measure microhematocrit and total aggregating agents are added to platelet-rich
protein (using a refractometer). plasma, and a change in plasma turbidity is
– [Total Protein in the room temperature sample detected by a spectrophotometer as the platelets
(albumin + globulin + fibrinogen)] – [Total aggregate. Whole blood aggregometry is an alter-
Protein in the heated sample (albumin + glob- native, but less widely used, technique. Platelet
ulin)] = fibrinogen. aggregation is very sensitive, and in vitro defects
– An alternative, less precise, method is to may not result in clinically relevant effects.
obtain serum from a separate clot tube and
subtract total protein in the serum sample from
DISEASES CAUSING BLEEDING
total protein in the plasma sample.
– Several other methods for measuring fibrinogen
level, including immunologic assays, are in use LOCAL LESIONS CAUSING LOCALIZED
in reference laboratories. HEMORRHAGE***
● Fibrin-degradation products (FDPs).
– FDPs are the breakdown products of fibrinogen Classical signs
and fibrin monomers by plasmin.
● Clinically evident localized bleeding.
– The latex agglutination test is most commonly used.
● Local signs of trauma, inflammation or
– This was originally exclusively a serum test,
neoplasia.
where blood is collected in a special tube
containing a soybean trypsin inhibitor and fer-
de-lance (Bothrops atrox) venom to promote
Clinical signs
rapid and complete clotting of the sample.
The rapid clotting facilitates emergency test- Diseases where clinical bleeding may be the chief com-
ing, while the complete clotting circumvents plaint or a clinical problem include:
● Bleeding into or from skin, underlying tissues, Tests of hemostasis (platelet count, BMBT, ACT,
ears and footpads with lacerations, puncture aPTT, PT) are either normal or not sufficiently abnor-
wounds, blunt trauma, ruptured cat bite abscesses mal to account for the hemorrhage.
and bleeding tumors (see The Cat With Skin Lumps
and Bumps, page 1067 and The Cat With Non-Heal-
ing Wounds, page 1081). Vasculitis usually results in Differential diagnosis
edema, but may rarely cause local bleeding. If a local lesion is not apparent, a hemostatic defect is
● Bleeding from oral cavity due to lacerations and likely.
puncture wounds, periodontal disease, and oral
neoplasms (see The Cat With Bad Breath or Oral Local lesions and hemostatic defects may be concurrent.
Lesions, page 602). Systemic hypertension may cause retinal hemorrhages
● Epistaxis from nasal trauma, rhinitis and neo- and epistaxis.
plasms (see The Cat With Upper Respiratory Tract
Signs of Chronic Nasal Disease, page 19).
● Ocular hemorrhage from corneoscleral lacera- Treatment
tions, severe uveitis, and ocular neoplasms (see The
Treat the local lesion – see the appropriate chapters
Cat With Eye Problems, page 1165).
listed above.
● Hematuria from major trauma to the kidney or
bladder, idiopathic lower urinary tract disease, neo- Use fluid therapy and/or whole blood transfusion
plasms of the kidney or bladder (see The Cat With (10–20 ml/kg) to correct acute hypovolemia and
Urinary Tract Signs, page 173). Clot formation in anemia.
the bladder may cause or exacerbate signs of lower
urinary tract disease.
● Vaginal bleeding from pyometra, spontaneous abor- MOTOR VEHICLE AND OTHER MAJOR
tion or lochia (see The Infertile Queen, page 1145). BLUNT TRAUMA***
● Melena from intestinal neoplasia, which may cause
iron-deficiency anemia (see The Cat With Signs of Classical signs
Gastrointestinal Tract Disease, page 578).
● Hematochezia from colitis (and rarely acute enteri- ● Shorn nails, fractured mandible, fractured
tis), and colonic and anorectal neoplasms (see The pelvis, dyspnea.
Cat With Signs of Gastrointestinal Tract Disease,
page 578). Clinical signs
● Hemoptysis from major blunt trauma, acute heart
failure and less commonly lung lobe torsion and External signs of trauma include shorn nails, and
primary lung neoplasms (see The Dyspneic or bleeding from skin and oral cavity lacerations.
Tachypneic Cat, page 47). Internal signs of trauma include palpable fractures,
● Hemothorax from major blunt trauma, penetrating non-palpable bladder, hemoperitoneum and dyspnea
trauma and spontaneous bleeding from the thymus from pneumothorax, hemothorax, diaphragmatic her-
(see The Dyspneic or Tachypneic Cat, page 47). nia, pulmonary contusions, neurogenic pulmonary
● Hemopericardium from major blunt trauma, pen- edema, shock and pain.
etrating trauma or neoplasia (rare) (see The Dysp-
neic or Tachypneic Cat, page 47). The cat may be in shock with pale mucous membranes
● Hemoperitoneum from major blunt trauma, pene- and weak pulses.
trating trauma, liver disorders (especially hepatic
amyloidosis and peliosis hepatis), and bleeding
Diagnosis
neoplasms (see The Cat With Abdominal
Distention or Abdominal Fluid, page 443). Diagnosis is facilitated if the event is witnessed, e.g. hit
by motor vehicle, fall from a height, kicked by a horse.
Diagnosis
Physical examination findings consistent with trauma
See the appropriate chapters listed above. are supportive evidence.
Radiographic findings often reveal fractures and tho- Uremic stomatitis and uremic gastroenteritis may
racic abnormalities. Intra-abdominal bleeding may cause bleeding in acute and chronic renal failure, con-
cause loss of detail on abdominal radiographs, but ultra- tributing to anemia in the latter.
sound, abdominocentesis and diagnostic peritoneal
Hypertension may cause retinal hemorrhages and/or
lavage are superior for its detection.
retinal detachment.
● Thoracic injuries and resulting dyspnea are more
common and clinically important than abdominal Hemolytic-uremic syndrome is an uncommon compli-
injuries following blunt trauma in cats. Abdominal cation of renal transplantation.
hemorrhage may occur, but is rarely life threatening.
Hemostatic testing is usually normal in traumatized
Diagnosis
cats, although mild thrombocytopenia may occur sec-
ondary to massive bleeding. Trauma does not appear to Hemostatic testing is usually normal.
be an important trigger for DIC in cats. ● Mildly prolonged aPTT and mild thrombocytope-
nia (mechanisms not known) have been seen in
● Uremic thrombocytopathia has not been docu-
Differential diagnoses for hemoperitoneum include mented in cats, but probably occurs. Determining
anti-coagulant rodenticide poisoning, inherited coagu- BMBT prior to renal biopsy is recommended.
lopathy (e.g. hemophilia A and B), ruptured neoplasm ● Hemolytic-uremic syndrome results in thrombocy-
(e.g. hemangiosarcoma) and spontaneous bleeding from topenia.
a diseased liver (e.g. amyloidosis, peliosis hepatis).
Differential diagnoses for hemothorax include anti- Differential diagnosis
coagulant rodenticide poisoning, inherited coagulo-
If a cat with chronic renal failure is showing signs of
pathy (e.g. hemophilia A and B), and spontaneous
acute bleeding other than retinal hemorrhages, a con-
bleeding from the thymus.
current local or hemostatic disorder should be pursued.
Treatment
Treatment
See the appropriate chapters for treatment of specific
The use of H2-blockers and/or sulcralfate may
traumatic disorders.
reduce gastrointestinal bleeding.
Dental prophylaxis may reduce oral cavity bleeding.
RENAL FAILURE***
Amlodipine, enalapril or benazapril is recommended
Classical signs for treatment of hypertension (see The Blind Cat or
Cat With Retinal Disease, page 1171).
polyuria, polydipsia. No specific treatment is recommended for the hemosta-
● Pale mucous membranes (anemia). tic disorders. If BMBT is prolonged and requires cor-
rection prior to an invasive procedure, treatments useful
See main reference, page 235 (The Cat With Polyuria in humans and/or dogs include:
and Polydipsia). ● Whole blood or packed red cell transfusion, or
recombinant human erythropoietin therapy to
improve anemia, because uremic bleeding is worse
Clinical signs
at a lower hematocrit.
Cats with chronic renal failure show varying lethargy, ● Fresh-frozen plasma or cryoprecipitate trans-
inappetence, weight loss, polyuria, polydipsia, inter- fusion, or desmopressin to improve von Willebrand’s
mittent vomiting and anemia. factor level and/or function, because defects in von
Willebrand’s factor may contribute to the thrombo- Hemostatic testing is normal or may identify abnor-
cytopathia (in humans) and augmenting von malities secondary to underlying (e.g. myeloma) or
Willebrand’s factor may compensate for non-von concurrent (e.g. FIV infection) diseases.
Willebrand’s factor-dependent defects. Fresh-
frozen plasma and cryoprecipitate may also contain
functional platelet microparticles. Recombinant
factor VIIa is beneficial in humans. Differential diagnoses for retinal hemorrhages include a
● Peritoneal or hemodialysis, to reduce uremic toxins platelet disorder or coagulopathy.
that contribute to bleeding.
Differential diagnoses for epistaxis include trauma,
rhinitis, neoplasia, a platelet disorder or coagulopathy.
SYSTEMIC HYPERTENSION**
Treatment
Classical signs
Amlodipine, enalapril or benazapril are used most often
● Retinal hemorrhages.
to treat renovascular hypertension (see The Blind Cat
● Epistaxis.
or Cat With Retinal Disease, page 1171).
● Signs of the underlying disease.
For other conditions, treatment of the primary disease
may be sufficient to resolve hypertension.
Clinical signs
Sustained systemic blood pressure leads to vascular
MEGAKARYOCYTIC HYPOPLASIA**
damage manifested clinically most often as retinal
hemorrhages and less frequently as epistaxis.
Classical signs
● Signs of the primary disease such as
Cats with chronic renal failure (the most common
leukemia, lymphoma, FeLV/FIV infection,
cause of hypertension) will have varying lethargy,
histoplasmosis (e.g. fever, inappetence,
inappetence, weight loss, polyuria, polydipsia and
weight loss, gingivitis, lymphadenopathy,
intermittent vomiting.
hepatosplenomegaly, dyspnea, diarrhea).
Cats with hyperthyroidism, diabetes mellitus and ● Signs of concurrent cytopenias (e.g. pale
hyperadrenocorticism may have systemic hyper- mucous membranes from anemia, fever
tension but bleeding and other signs of organ dam- secondary to neutropenic sepsis).
age do not commonly occur without concurrent renal ● History of drug use known to cause
failure. myelosuppression.
● Platelet disorder bleeding (e.g. prolonged
Cats with multiple myeloma show non-specific signs
bleeding after venepuncture, melena,
of lethargy, inappetence and weight loss.
epistaxis, petechiation).
Cats with polycythemia vera have dark mucous mem-
branes and may seizure.
Hyperaldosteronism (may cause weakness and
Pathogenesis
polyuria/polydipsia due to hypokalemia) and pheochro- Megakaryocytic hypoplasia reduces platelet production
mocytoma (may cause polyuria/polydipsia) can cause (hypoproliferative thrombocytopenia).
hypertension, but the risk for abnormal bleeding is not
Megakaryocytic hypoplasia occurs most commonly as
known. These disorders are both rare in the cat.
part of generalized bone marrow failure or dyshemato-
poiesis resulting in pancytopenia. Causes of bone mar-
Diagnosis row failure include:
Routine work-up is required to identify the primary dis- ● Hematopoietic neoplasia causing myelophthisis.
ease. Neoplasms include lymphoid leukemia, myeloid

leukemia, myelodysplastic syndrome, multiple mye- Signs due to anemia (e.g. pale mucous membranes,
loma, malignant histiocytosis and mast cell tumor. tachycardia) and local effects of hemorrhage (e.g.
● Infections causing generalized bone marrow failure hematoma formation) vary with severity and acuteness
or dyshematopoiesis. Infectious agents include of blood loss.
feline leukemia virus, feline immunodeficiency
Signs of underlying hematopoietic neoplasia, FeLV
virus, Histoplasma capsulatum, and, possibly,
or FIV infection, or histoplasmosis include fever,
Ehrlichia spp.
inappetence, weight loss, lymphadenopathy, hepato-
– Feline panleukopenia virus infection causes
splenomegaly, dyspnea and diarrhea.
transient myelosuppression, but acute thrombo-
● FeLV or FIV infection may cause gingivitis.
cytopenia is due to disseminated intravascular
coagulation. Fever may be present due to spontaneous infection
● Cytotoxic anticancer drugs and large-field radia- secondary to concurrent neutropenia.
tion therapy produce predictable dose-dependent
effects.
– Cats are more sensitive to azathioprine toxicosis
than dogs, probably because of decreased levels
Diagnosis
of thiopurine methyltransferase, the enzyme History and physical examination findings are consis-
responsible for the drug’s metabolism. tent with a primary disease (e.g. drug therapy).
● Idiosyncratic, immune-mediated, and toxic drug
A complete blood count will reveal thrombocytopenia.
reactions have been reported with chlorampheni-
● Artifactual thrombocytopenia is common in cats.
col, griseofulvin (especially in FIV-infected cats),
A platelet count generated by a laboratory instru-
cephalosporins, ribavirin, albendazole, anti-thyroid
ment or manual count should be verified with a
drugs (propylthiouracil, methimazole, carbima-
blood smear, and the blood smear should be closely
zole), and phenobarbital.
examined for platelet clumps.
Occasionally no cause is found and/or megakaryocytic
Bone marrow biopsy will reveal megakaryocytic
hypoplasia is the only bone marrow abnormality. Some
hypoplasia. Concurrent erythroid hypoplasia, myeloid
of the idiopathic cases are due to immune-mediated
hypoplasia and neoplasia may also be identified.
mechanisms. A diagnosis of immune-mediated hypo-
● If feline leukemia virus infection is suspected but
plasia is usually based on ruling out other causes of
peripheral blood tests are negative, then obtain a
megakaryocytic hypoplasia, presence of other disorders
fluorescent antibody (FA) or PCR test on a bone
that are typically immune-mediated, and response to
marrow aspirate or ELISA test on a bone marrow
immunosuppressive therapy.
core biopsy. It should be noted that PCR testing
has not been standardized and is more likely to
Clinical signs give false-positive results than ELISA and FA if
the laboratory does not maintain the highest
In most cases thrombocytopenia is noted during work- standards of quality control.
up of the primary disease or work-up of other signs, e.g.
fever.
Clinical bleeding is occasionally the chief complaint or
noted during examination or work-up.
Other causes of thrombocytopenia are usually asso-
Spontaneous bleeding includes petechiation, ecchy-
ciated with normal to increased platelet counts on bone
moses, epistaxis, ocular hemorrhages, hematuria and
marrow biopsy. For many of these causes the primary
melena.
disease is sufficiently characterized on routine work-up
Excessive bleeding is usually first noted as bleeding to explain thrombocytopenia without the need for bone
from venepuncture sites. Biopsy sites, suture lines marrow biopsy. Other causes of thrombocytopenia
and other local lesions may also bleed excessively. include:
● DIC (platelet consumption). ● Handle gently in the hospital and provide a well-
● Immune-mediated thrombocytopenia (platelet padded cage.
destruction). This is a rare disorder in the cat. ● Feed soft food to minimize gingival trauma.
● Marked splenomegaly (platelet sequestration). ● Minimize invasive procedures and injections. If
This is an uncommon cause of thrombocytopenia in injection is required, use 25-G or smaller needles.
the cat. The intravenous route is preferred (with the excep-
● Severe bleeding (platelet loss). tion of vitamin K). Subcutaneous and especially
– Severe bleeding may result in mild thrombo- intramuscular injections may cause hematomas that
cytopenia. In a series of cats with anticoagulant may impair absorption of the drug in addition to
rodenticide poisoning, a platelet count as low as causing discomfort.
58 × 109/L (58,000/μl) was noted (reference 9). ● Apply moderate manual pressure or pressure band-
If severe bleeding is associated with mild throm- ages to sites of active bleeding when possible.
bocytopenia, it is more likely that the low ● Do not drain hematomas unless they are causing a
platelet count is a result of, rather than the cause problem (e.g. tracheal compression).
of, the bleeding. ● Avoid over-exuberant intravenous fluid therapy,
which dilutes platelet and coagulation factor con-
centrations. Synthetic colloids may cause platelet
Treatment dysfunction.
● Avoid drugs that significantly decrease platelet
Treat the primary disease if possible.
function (e.g. aspirin), antagonize vitamin K, or
Thrombocytopenia may be transiently improved by have direct anti-coagulant effects (e.g. heparin).
transfusion of fresh whole blood, platelet-rich – Penicillins, some cephalosporins, tetra-
plasma, or fresh-frozen plasma (which contains func- cyclines, gentamicin and sulfa drugs have
tional platelet particles), 10–20 ml/kg, or platelet con- been demonstrated to variably impair platelet
centrate, 1–2 units/cat. function in vitro or in vivo in humans, rabbits
● This is recommended before biopsy of internal or dogs. Worsening hemorrhage is likely to be
organs if the platelet count is < 50 × 109/L seen only in severely thrombocytopenic patients.
(50 000/μl ). Effects of these drugs in cats are not known.
● Platelet transfusions may be used prophylactically However, amoxicillin, cefazolin, cephalexin,
against spontaneous hemorrhage in humans with doxycycline, and enrofloxacin at standard doses
platelet counts < 10–20 × 109/L (10 000–20 do not impair platelet function in normal dogs
000/μl). This is not recommended in cats because and are unlikely to have any clinically relevant
spontaneous critical hemorrhage is rare in thrombo- hemostatic effects in cats.
cytopenic cats, and because most practices have a – Acepromazine and some antihistamines impair
limited donor blood supply. platelet function in humans. Acepromazine does
not impair platelet function in dogs and these
Augmenting one part of hemostasis compensates to
drugs are unlikely to have any clinically relevant
some extent for a deficiency in another part. To this end
hemostatic effects in cats.
inhibitors of fibrinolysis (e.g. aminocaproic acid),
which augment coagulation, have been useful in treat-
ing thrombocytopenia in humans but have not been
Prognosis
evaluated in cats.
Prognosis is determined by the primary disease.
General treatment measures for cats with a bleeding
tendency include the following recommendations. If megakaryocytic hypoplasia cannot be promptly cor-
These are most important in cats with moderate to rected and if the cat is clinically bleeding from severe
marked defects in hemostasis: thrombocytopenia, the prognosis for long-term transfu-
● Minimize exuberant exercise and risk for trauma at sion support is poor because of donor exhaustion and
home (keep indoors). possibly platelet alloimmunization.
toneum may occur with amyloidosis and peliosis

LIVER DISEASE**
hepatis.
Classical signs Coagulation abnormalities are more likely to be pres-
ent if there is concurrent pancreatitis.
vomiting, icterus.
● Spontaneous or excessive bleeding may
occur. Clinical signs
More than 80% of cats with liver disease may have a
See main reference page 421 (The Yellow Cat or Cat
coagulation abnormality, but abnormal clinical bleed-
With Increased Liver Enzymes).
ing is uncommon.
Excessive bleeding may occur following venepunc-
Pathogenesis
ture and liver biopsy.
The most common causes of liver disease in the cat are
Severity of coagulopathy correlates to some extent
lipidosis, cholangiohepatitis and lymphoma. Less
to increase in alkaline phosphatase value, likely due
common causes include congenital portosystemic shunts,
to cholestasis.
amyloidosis, non-lymphoid neoplasia, feline infectious
peritonitis, peliosis hepatis, toxoplasmosis and toxins In other species acute bleeding into the intestinal tract
(e.g. diazepam). may precipitate hepatic encephalopathy, but this has
not been documented in the cat.
Liver disease may cause bleeding tendencies by several
mechanisms including:
● Acquired platelet function defects (not proven in cats).
● Decreased synthesis of coagulation factors. Diagnosis
– Primary hepatocellular failure affecting syn-
Combining results of several studies, coagulation
thesis of all factors.
abnormalities may be categorized as follows:
– Vitamin K deficiency (contributing to coagu-
● Vitamin K deficiency: Normal platelet count, pro-
lopathy in about 50% of cases).
longed PT, ± prolonged aPTT, normal TT.
– Intrahepatic cholestasis and extrahepatic bile
● Synthesis failure: Normal platelet count, pro-
duct obstruction prevent release of bile acids
longed PT, prolonged aPTT, prolonged TT.
into the small intestine that are needed for
● Indeterminate: Normal platelet count, normal PT,
absorption of vitamin K1 and K2.
prolonged aPTT, normal TT.
– Anorexia and antibiotic therapy contribute to
● DIC: Low platelet count, prolonged PT, prolonged
vitamin K deficiency.
aPTT, prolonged TT; or 3 of the following: low
● Synthesis of abnormal prothrombin (not proven in
platelet count, prolonged PT or aPTT, prolonged
cats).
TT or hypofibrinogenemia, decreased antithrombin
● DIC causing consumption of platelets and coagula-
III (not routinely available), presence of FDPs, red
tion factors.
blood cell fragments.
● Decreased clearance of plasminogen activators
thus promoting fibrinolysis (not proven in cats). Vitamin K deficiency may also be identified by improve-
ment in coagulation following vitamin K1 therapy.
In general, fever decreases the half-life of coagula-
tion factors and wound healing increases consumption PIVKA time is more sensitive in identifying abnor-
of coagulation factors (e.g. after exploratory laparo- mal coagulation than are PT and aPTT. Cats may show
tomy). Both of these may be present with liver disease. a bleeding tendency with a prolonged PIVKA time and
normal PT and aPTT.
The liver may be more fragile with hepatic lipidosis,
amyloidosis and peliosis hepatis increasing the risk of More than one mechanism may contribute to coagu-
bleeding after liver biopsy. Spontaneous hemoperi- lopathy.

In most cases the cat with liver disease is presented for Clinical bleeding is uncommon except with severe
subacute to chronic non-specific signs and coagulopa- thrombocytopenia, in which case bleeding is typical of
thy is identified in the work-up of liver disease. platelet disorders, e.g. petechiation, epistaxis, melena,
prolonged bleeding after venepuncture.
A large number of disorders may be associated with
subacute non-specific signs and subclinical coagulopa-
Diagnosis
thy, including neoplasia, retroviral infections, FIP, heart
disease and pancreatitis. Routine work-up will help FeLV antigen test.
identify the primary disease. ● Bleeding tendencies are most likely to occur dur-
ing persistent viremia, in which case ELISA and
FA tests are usually both positive.
Treatment
● If peripheral blood tests are negative and another
Vitamin K1, 2.5–5 mg/kg SC for 1–2 days, will usually cause of megakaryocytic hypoplasia has not been
normalize PT and aPTT in 1–2 days if vitamin K determined, obtain a FA or PCR test on a bone mar-
deficiency is solely responsible for coagulopathy. row aspirate or ELISA test on a bone marrow core
(PIVKA values take 3–5 days to normalize.) The biopsy. It should be noted that PCR testing has
need for further vitamin K1 therapy will depend on suc- not been standardized and is more likely to give
cess of managing the primary disease. false-positive results than ELISA and FA if the
laboratory does not maintain the highest stan-
dards of quality control.
Prognosis
Hemostatic testing may reveal thrombocytopenia, and
Prognosis is determined by the primary liver disease.
prolonged PT, ACT, and aPTT and hypofibrinogenemia
Prognosis for resolution of a vitamin K deficient state if DIC is present.
is excellent.
The main cause of clinical bleeding in FeLV-infected
FELINE LEUKEMIA VIRUS (FELV) cats is megakaryocytic hypoplasia. If a FeLV-positive
INFECTION** cat is bleeding without severe thrombocytopenia
(usually platelets < 20 × 109/L, <200 000/μl), another
Classical signs hemostatic disorder should be investigated.
● Lethargy, inappetence, weight loss, A concurrent disease may be responsible for sub-
unkempt haircoat, fever, anemia, gingivitis, clinical hemostatic defects including liver disease,
recurrent upper respiratory infections, cardiomyopathy, pancreatitis, renal failure, other sys-
opportunistic infections. temic infections, lymphoma and other neoplasms, and
● Cats with megakaryocytic hypoplasia may snakebite envenomation and other toxicoses.
have platelet disorder type bleeding. Feline immunodeficiency virus (FIV) infection
causes similar signs to FeLV infection and may also
See main reference on page 540 (The Anemic Cat). cause megakaryocytic hypoplasia and other hemosta-
tic defects. An FIV test may be used to rule this out.
Pathogenesis Most causes of megakaryocytic hypoplasia, ITP and
DIC may be identified by routine work-up.
FeLV infection can cause bleeding tendencies by
several mechanisms. These include:
Treatment
● Megakaryocytic hypoplasia.
● Immune-mediated platelet destruction. Thrombocytopenia and other hemostatic defects may
● DIC secondary to infections and neoplasia. be transiently improved by transfusion of fresh
whole blood, platelet-rich plasma, or fresh-frozen processes, e.g. neoplasia, bone marrow failure with
plasma (which contains functional platelet particles), griseofulvin therapy.
10–20 ml/kg. Bleeding due to thrombocytopenia – FIV infection in-itself does not commonly cause
may also be treated with platelet concentrate, 1–2 severe megakaryocytic hypoplasia.
units/cat. – FIV infection in-itself does not appear to cause
● Transfusion is recommended before biopsy of platelet function defects.
internal organs if the platelet count is < 50 × 109/L ● Prolongation of aPTT. The mechanism is not
(50,000/dl). known, but it is not due to specific factor deficien-
cies, DIC, or a circulating inhibitor.
Treat infections and neoplasia.
● Prolongation of TT. The mechanism is not known,
Recombinant human interferon-α, 1 unit/cat PO q but it is not due to hypofibrinogenemia or dysfib-
24 h may ameliorate myelosuppression. rinogenemia.
● DIC secondary to infections and neoplasia.
Bone marrow transplantation for megakaryocytic
hypoplasia may be considered if available.
Clinical signs
Clinical bleeding is uncommon.
Prognosis
Severe thrombocytopenia may cause bleeding typical
Prognosis for severe FeLV-induced megakaryocytic
of platelet disorders, e.g. petechiation, epistaxis,
hypoplasia is poor.
melena, prolonged bleeding after venepuncture.
Long-term prognosis with other hemostatic defects
Prolongation of the aPTT and TT do not result in
is determined by the FeLV-associated underlying
abnormal bleeding.
disease.
Diagnosis
FELINE IMMUNODEFICIENCY VIRUS (FIV)
INFECTION** FIV antibody test (ELISA, FA, western blot).
● Antibody is usually detectable within 2 months of
Classical signs infection, but may take up to 6 months, therefore a
negative test should be repeated if FIV is being con-
sidered in the differential diagnoses of a cat with
unkempt haircoat, fever, generalized
thrombocytopenia.
lymphadenopathy, gingivitis, diarrhea,
● PCR test for viral DNA. It should be noted that
dermatitis, recurrent upper respiratory
PCR testing has not been standardized and is
infections, opportunistic infections,
more likely to give false-positive results than
neurologic signs, uveitis.
antibody tests if the laboratory does not main-
● Various hemostatic abnormalities may
tain the highest standards of quality control.
occur but are usually subclinical.
Neutropenia and lymphopenia are common con-
See main reference on page 339 (The Thin, Inappetent current hematologic abnormalities in symptomatic
Cat). cats.
Hemostatic testing may reveal the following abnormal-
ities due to FIV infection: low to normal platelet count,
Pathogenesis
normal BMBT unless thrombocytopenic, shortened to
The following hemostatic defects may occur with normal PT, normal to prolonged ACT and aPTT, nor-
FIV infection: mal to prolonged TT and normal to increased fibrino-
● Thrombocytopenia. This may be due to the pri- gen. In addition, prolonged PT, ACT and aPTT and
mary infection or secondary to other disease hypofibrinogenemia may occur if DIC is present.
Differential diagnosis DISSEMINATED INTRAVASCULAR

FeLV infection causes similar signs to FIV infection. COAGULATION (DIC)*
FeLV infection causes severe megakaryocytic hypopla-
sia more commonly than FIV infection, and other Classical signs
hemostatic defects may also occur. A FeLV antigen test ● Signs of underlying sepsis or non-septic
may be used to rule this out. inflammation (e.g. anorexia, depression,
Most other causes of megakaryocytic hypoplasia and fever, hypothermia, tachycardia, abdominal
DIC may be identified by routine work-up. pain).
● Signs of underlying neoplasia (e.g.
Concurrent disease may be responsible for the hemo- inappetence, weight loss,
static defect. Subclinical coagulation abnormalities lymphadenopathy, hepatosplenomegaly,
have been identified with a number of disorders includ- abdominal mass, dyspnea).
ing liver disease, cardiomyopathy, pancreatitis, renal ● Signs of underlying FIP (e.g. inappetence,
failure, other systemic infections, lymphoma and other weight loss, fever, abdominal distention,
neoplasms, and snake bite envenomation and other dyspnea).
toxicoses. ● Signs of underlying liver disease (e.g.
inappetence, weight loss, icterus).
● Signs of other underlying diseases, e.g.
Treatment hyperthermia (temperature ≥ 42˚C
The prolonged aPTT and TT may be corrected by [107.6˚F]), shock, snake bite wound.
transfusion of fresh or fresh-frozen plasma, 10–20
● Spontaneous and excessive bleeding at
ml/kg. various sites may occur, but is uncommon.
● This is recommended before biopsy of internal
organs, although the need for such transfusion is not Pathogenesis
known.
Concurrent intravascular activation of hemostasis
Bleeding due to thrombocytopenia may be transiently and accelerated fibrinolysis lead to microvascular
improved by transfusion of fresh whole blood, thrombosis and embolism.
platelet-rich plasma or fresh-frozen plasma (which
contains functional platelet particles), 10–20 ml/kg, or Thrombosis and embolism may lead to organ failure.
platelet concentrate, 1–2 units/cat. Bleeding tendencies occur secondary to consump-
● This is recommended before biopsy of internal tion of platelets and coagulation factors, increased
organs if the platelet count is < 50 × 109/L (50 plasmin activity, and circulating anti-coagulants,
000/dl). including fibrin degradation products (FDPs).
Numerous disease processes may trigger DIC,
Prognosis including thromboembolism due to cardiomyopathy,
neoplasia (e.g. hemangiosarcoma, hepatic, biliary and
Prognosis for severe FIV-induced megakaryocytic pulmonary carcinomas, mesothelioma, lymphoma,
hypoplasia is poor. myeloid leukemia, malignant histiocytosis), infections
Myelosuppression associated with griseofulvin or other (e.g. bacterial sepsis, tuberculosis, histoplasmosis,
drug therapy will usually resolve, but intensive sup- cytauxzoonosis, toxoplasmosis), non-infectious inflam-
portive care is required. mation (e.g. pancreatitis, immune-mediated diseases),
heat stroke, major trauma, penetrating head trauma,
There is no specific prognosis associated with the shock and snake bite envenomation.
unique FIV-associated coagulation defects.
DIC has wide clinical and pathological spectra and may
Long-term prognosis is usually determined by other be acute to chronic, localized to generalized, and
FIV-associated diseases. subclinical to fulminant. A broad definition is used
here to include most cases of consumptive thrombocy- – In the author’s opinion, firm diagnostic criteria
topenia and microangiopathic disorders. should not be used. Rather, the probability of
DIC increases with the number of consistent lab-
Acute DIC is not as common in cats as in dogs. The
oratory abnormalities: e.g. it is possible that a cat
most common causes are panleukopenia virus infec-
with only thrombocytopenia has DIC, it is more
tion, other overwhelming infections (e.g. cytaux-
likely that a cat with thrombocytopenia and pro-
zoonosis), and neoplasia.
longed ACT has DIC, while it is highly probable
The most common causes of subacute to chronic that a cat with thrombocytopenia, prolonged PT
DIC are liver diseases, neoplasia and FIP (due to and aPTT, hypofibrinogenemia and increased
vasculitis). FDPs has DIC. Scoring systems based on this
approach have been used in humans.
Thrombocytopenia has also been noted with several
● Measuring antithrombin III, which tends to be
other diseases (see Miscellaneous diseases, page 505),
consumed in DIC, may add specificity but probably
where the thrombocytopenia is likely consumptive in
does not increase sensitivity to the diagnosis of
origin.
DIC.
● Measurements of D-Dimer are being used with
Clinical signs increasing frequency to support the diagnosis of
DIC in dogs. Little is currently known of the utility
Signs of the primary disease. of D-dimer assay in the diagnosis of DIC in cats.
Most DIC is subclinical. D-dimer is a more specific marker of thrombosis
than are FDPs, but D-dimer is not specific for DIC.
Superficial and deep spontaneous bleeding may occur, D-dimer levels will be increased in thromboem-
but it is uncommon. bolic disorders including arterial and pulmonary
Venepuncture and biopsy sites, suture lines, and inter- thromboembolism.
● There is poor correlation between degrees of coagu-
nal and external injuries may bleed excessively.
lation abnormalities, severity of underlying clinical
Signs due to anemia and local effects of hemorrhage disease and risk for hemorrhage.
vary with severity of blood loss.
Diagnosis
Differential diagnoses for the various primary diseases
Identification of a primary disease. are discussed throughout this book. If a hemostatic
defect is identified in the work-up of the primary dis-
Diagnosis is controversial in all species and there is not
ease, the possibility of a defect unrelated to the primary
a single test or combination of tests that rules in or rules
disease should be considered, e.g. Hageman trait.
out DIC.
Differential diagnoses for abnormal hemostasis with
Laboratory abnormalities consistent with DIC
liver disease include vitamin K deficiency, synthesis
include:
failure and undetermined causes (which might be mild
● Low platelet count, prolonged ACT, prolonged
DIC).
aPTT, prolonged PT, prolonged TT, hypofibrino-
genemia, decreased antithrombin III concentration, In cats with neutropenia due to myelosuppression and
presence of FDPs, and red blood cell fragments. secondary sepsis, thrombocytopenia may be due to
● One approach uses presence of three of the above concurrent megakaryocytic hypoplasia rather than DIC.
abnormalities (counting prolonged PT and/or
aPTT as one abnormality) as criteria for diagnosing
Treatment
DIC.
– Another approach uses low platelet count, pro- Treat the primary disease.
longed PT, prolonged aPTT, and prolonged TT ● This is the most important treatment. If this is not
as diagnostic of DIC in liver disease. possible, other treatments will ultimately fail.
Adequate fluid therapy to promote microvascular cir- ● Resistance to hematoxins may in part reflect
culation, but not excessive fluid therapy, which will cats playing with, and subsequently being bitten,
promote edema and bleeding. by smaller snakes (thus receiving less venom),
and/or only cats with mild–moderate envenomation
If clinically bleeding, transfuse to replace platelets
surviving long enough to be presented to a veteri-
and/or clotting factors and anti-thrombin III with fresh
narian.
whole blood, platelet-rich plasma, or fresh/fresh-frozen
plasma, 10–20 ml/kg. Venoms from Elapidae snakes (e.g. Australian tiger
snake and brown snake, North American coral snakes,
Heparin therapy is controversial.
Indian cobras) are predominantly neurotoxic, although
● It is recommended because, although bleeding is
procoagulants and myolysins may cause significant
clinically more obvious, thrombosis causes most
complications.
of the organ damage.
● Signs include areflexic dilated pupils, dysphagia
● The goal is to block microvascular thrombosis
(salivation), dyspnea (respiratory paralysis),
while not aggravating bleeding.
hindlimb ataxia and flaccid quadriplegia.
● In cats with fulminant DIC, doses of 50–200 units/kg
● Local reaction to the bite wound may be minimal.
SC q 6–8 h have been recommended; 75–100 units SC
● Although neurologic signs predominate, cats with
q 8 h is used most often. The dose may be incubated
tiger or brown snake bites may have significant dis-
for 30 minutes in the blood product prior to transfu-
turbances of hemostasis.
sion to activate antithrombin III, although the value of
– Potent procoagulants, especially in the brown
this practice is unproven. An initial goal is prolonga-
snake venom, act as prothrombin converters,
tion of the ACT or aPTT to 1.5–2 times the mean
resulting in consumption of fibrinogen.
value of normal range or aPTT control value.
– 10–30% of cats show evidence of hemostatic
● It should not be used in cats with subclinical, subacute
abnormalities. Typical signs include non-clotting
or chronic DIC, unless thromboembolism is present.
blood, prolonged coagulation times (ACT typ-
– If thromboembolism is present, an initial dose of
ically 180–240 s), continuous bleeding from
200 units/kg SC q 6–8 h is recommended.
wounds and venepuncture sites, hematemesis
and hematuria.
Prognosis
Venoms from Viperidae (e.g. common adder in Britain
The prognosis is largely determined by the primary
and continental Europe, Vipera palaestina in the
disease.
Middle East) are predominantly hematoxic, although
Acute diffuse DIC has a very poor prognosis. some have neurotoxic properties.
● Edema ± bleeding/bruising around the bite is
typical, but is not predictive of systemic toxicosis.
SNAKE BITE ENVENOMATION* ● Widespread bleeding is uncommon with bites from
the common adder and V. palaestina, but may occur.
Classical signs
Venoms from Crotalidae (e.g. North American rattle-
● Bite wound on cranial half of body ± local snakes, copperhead, cottonmouth, and South American
swelling or bleeding (Viperidae, fer-de-lance and bushmaster) are predominantly hema-
Crotalidae). toxic, although some (e.g. Majove rattlesnake, Asian
● Paresis/paralysis or bleeding tendency habu snake) are potent neurotoxins.
depending upon species of snake. ● Severe regional swelling may occur surrounding
the bite from massive extravasation of plasma and
red cells, but local reaction is not predictive of sys-
Clinical signs
temic toxicosis.
Cats are believed to be less likely to be bitten by most ● Hypotension may result from pooling of blood in
snake species than dogs, and to be more resistant to lungs and thoracic vessels.
hematoxins. ● Widespread bleeding may occur.
– Clinical reports of Massassauga rattlesnake bites Treatment

to cats are lacking. In dogs envenomation may
cause marked prolongation of clotting times but Keep animal calm.
clinical bleeding is rare. If a bite on a limb is witnessed, application of a tourniquet
Venoms from most Colubridae are mild and clinical or cold pack by the owner for 10–20 min may be benefi-
reports of bites to cats lacking. cial, but should not delay transport to a veterinarian.
● The boomslang of central and South Africa pro- Supportive care.
duces a powerful hematoxin that is procoagulant
and causes DIC in humans and dogs. Specific antivenom (antivenin) therapy.
● Observe for allergic reactions.
● Premedication with an anti-histamine, e.g. diphenhy-
Diagnosis dramine, 1 mg/kg IV as a slow bolus over 10–15 min
is recommended. This will not potentiate the venom.
Diagnosis is based on a history of exposure to the snake
(try to identify species) and/or physical examination If there are signs of hemostatic abnormalities, treat as
findings. for DIC (page 502) (see Disseminated intravascular
coagulation, above) with transfusions of fresh whole
CBC may reveal hemoconcentration, hemolysis, blood, fresh plasma or fresh-frozen plasma.
echinocytosis, rubricytosis or thrombocytopenia.
Antibiotic therapy for secondary wound infection and
Serum chemistry profile may reveal hypoproteinemia, delayed surgical management of the wound may be
hypokalemia and elevated CK, ALT, urea and creati- necessary.
nine levels.
Urinalysis may reveal myoglobinuria or hemoglobin- HAGEMAN TRAIT*
uria, and glucosuria.
Hemostatic testing may reveal variable thrombocy- Classical signs
topenia, prolonged PT and/or ACT, aPTT, and ● None.
increased FDPs (i.e. DIC).
A Snake Venom Detection Kit (CSL Limited, Pathogenesis
Australia) can be used for identification of the presence
and type of Australian snake venom. Testing is also Hageman trait refers to reduced synthesis, release or
available from commercial veterinary laboratories. function of factor XII (Hageman factor).
Urine is preferred over blood because of non-specific Activation of factor XII to XIIa is the first step in the
binding with plasma proteins. A swab of the bite site is intrinsic system. As previously noted, this does not
most accurate, but is rarely identifiable in cats with appear to be an important mechanism for the initiation
bites from Australian snakes. of coagulation in vivo.
Factor XII is involved in the conversion of plasmino-
Differential diagnosis gen to plasmin, which is responsible for clot dissolu-
tion (fibrinolysis).
See The Weak and Ataxic or Paralyzed Cat (page 952)
for differential diagnosis of neurologic signs. Factor XII is also involved in inflammation.
Differential diagnoses for the local reaction include

angioedema from insect envenomation, animal bite
Clinical signs
wounds, sharp and blunt trauma. Spontaneous bleeding does not occur.
Differential diagnoses for hemostatic abnormalities Prolonged ACT and aPTT are usually noted inciden-
include other causes of DIC. tally, e.g. when hemostasis is evaluated prior to biopsy.
Concurrent thrombocytopenia or thrombocytopathia Vitamin K antagonist poisoning – PT is prolonged as

was believed to have triggered bleeding in a cat follow- well as aPTT.
ing modified-live virus vaccination. This would appear
DIC – thrombocytopenia is often present, in addition to
to be an uncommon event, and is not reported in
signs of a primary disease.
humans with Hageman trait.
Acquired factor XII deficiency has been reported in
Humans with Hageman deficiency are at increased risk
humans but not in cats.
for thromboembolic events as a result of a deficient fib-
rinolytic system. It is not known if cats with Hageman
trait and cardiomyopathy are at increased risk of arte- Treatment
rial thromboembolism.
None required.
It is not known if cats with Hageman trait have blunted
inflammatory responses.
Prognosis
Diagnosis Normal life expectancy.
No signs of abnormal bleeding unless another disease
process affecting hemostasis is present. Transmission
Hageman trait is the most common inherited coagu- Factor XII deficiency is a heritable single-gene defect
lation factor deficiency in cats, but prevalence is not that is autosomal recessive.
known. Although stated to be common, recent large retro-
spective reviews of hemostatic disorders in sick cats
Prevention
have not identified any cases.
Probably none is required.
Hemostatic testing reveals normal platelet count and
BMBT, normal PT, and markedly prolonged ACT and
aPTT (e.g. aPTT > 50 s, often > 100 s, where the upper
MISCELLANEOUS DISEASES*
limit of normal range is 25 s).
Definitive diagnosis is based on quantification of fac- Classical signs
tor XII activity (FXII:C), similar to the diagnosis of
● Signs of the primary disease.
hemophilia A, and ruling-out acquired factor XII defi-
ciency (see Circulating anti-coagulant, below).
Clinical signs
Differential diagnosis Thrombocytopenia, increased ACT/aPTT/PIVKA
time, or decreased antithrombin III levels have been
Hemophilia A, B (and C) are the main differential
noted in various diseases not typically associated with
diagnoses for markedly prolonged ACT and aPTT as
bleeding tendencies. Diseases include hypertrophic car-
solitary abnormalities.
diomyopathy, congenital cardiac disorders, pleural
If a cat is presented with bleeding and a prolonged ACT effusions not due to feline infectious peritonitis, dia-
and aPTT are found, a judgment must be made as to betes mellitus, hyperthyroidism, hypertension, chronic
whether the bleeding is appropriate for the injury. For renal failure, urinary tract infection, urethral obstruction,
example, a cat with hemothorax and prolonged ACT rhinitis, Mycoplasma haemofelis infection (haemo-
and aPTT could have hemophilia A or chest trauma and bartonellosis), primary neurologic diseases, and non-
Hageman trait, but in the former case there would be no anti-coagulant toxicoses.
evidence of injury.
DIC may be the mechanism for at least some of these
Hemophilia B and Hageman trait have occurred con- abnormalities. The close interaction between the
currently. intrinsic system and inflammation via factor XII
may be responsible for some alterations in ACT and trait, page 504 and Vitamin K responsive coagu-
aPTT. lopathy in the Devon Rex, page 515).
Hemostatic abnormalities are subclinical. ITP may be concurrent with other autoimmune dis-
eases, e.g. hemolytic anemia, myasthenia gravis, and
systemic lupus erythematosus.
Diagnosis
Clinical signs and work-up of the primary disease.
Clinical signs
Primary ITP is rare. There is usually marked thrombo-
IMMUNE-MEDIATED
cytopenia and signs are typical of platelet disorder
THROMBOCYTOPENIA (ITP)
bleeding, including petechiation, epistaxis, melena
and hematuria.
Classical signs
Signs of an underlying disease may be present, e.g.
● Platelet disorder bleeding (e.g. prolonged
lymphadenopathy with lymphoma.
bleeding after venepuncture, melena,
epistaxis, petechiation). Splenomegaly may be present due to hyperplasia,
extra-medullary hematopoiesis and neoplasia.
Thrombocytopenia may be an incidental finding in a
Pathogenesis work-up.
In ITP, platelets become antigenic leading to acceler- Anemia and associated signs vary.
ated platelet destruction by the macrophage–mono-
cyte system, particularly in the spleen.
Diagnosis
In primary, or idiopathic, ITP an underlying disease
is not found and the disease is considered to be auto- Rule out other causes of thrombocytopenia based on
immune. clinical signs and work-up.
In secondary ITP, a primary, or underlying, disease is Hemostatic testing reveals thrombocytopenia, normal
found, e.g. FeLV infection, where there is immune- PT and aPTT, and normal to increased fibrinogen
complex deposition on the surface of infected platelets. level. Platelet counts < 10 × 109/L (10 000/μl) are stated
● Lymphoma is another primary disease associated to mildly prolong ACT, but this effect is poorly docu-
with ITP, and ITP may be the mechanism of throm- mented.
bocytopenia associated with various other neo-
Bone marrow biopsy reveals increased numbers of
plasms.
megakaryocytes.
● Thrombocytopenia caused by anti-thyroid drugs
(propylthiouracil, methimazole, carbimazole) is Demonstration of platelet or megakaryocyte-associated
presumed to be immune-mediated because affected antibody by immunofluorescence (test may not be
cats may have antinuclear antibodies. readily available). Platelet and megakaryocyte-associated
● Modified live virus vaccination has been associ- neutrophils have also been reported.
ated with thrombocytopenia and thrombocytopathia
Response to immunosuppressive therapy.
in dogs, typically occurring within 2–4 weeks of
vaccination. Thrombocytopenia varies from a sub-
clinical, self-limiting fall within normal range to
severe thrombocytopenia requiring immunosup-
pressive therapy. Post-vaccinal thrombocytopenia Megakaryocytic hypoplasia is distinguished from ITP
or thrombocytopathia has been suspected in cats on the basis of identification of a disease that causes
based on post-vaccinal bleeding in cats with other- decreased platelet production, e.g. myeloid leukemia,
wise sub-clinical hemostatic defects (see Hageman on bone marrow biopsy.
● Note that idiopathic megakaryocytic hypoplasia Prognosis

and pancytopenia may be immune-mediated in ori-
gin. If there are any megakaryocytes present in the Based on a limited number of cases, the prognosis is
marrow biopsy, testing by immunofluorescence for good.
megakaryocyte-associated antibody should be per-
formed. ITP and immune-mediated megakary- VITAMIN K ANTAGONIST RODENTICIDES
ocytic hypoplasia are both uncommon but well- AND DRUGS
documented causes of thrombocytopenia in cats.
Whether or not concurrent immunologic attack on Classical signs
platelets and megakaryocytes is occurring in some
cases is not known.
● Spontaneous or excessive internal or
● Note that FeLV infection may cause both external bleeding.
megakaryocytic hypoplasia and decreased platelet
lifespan.
In DIC a primary disease can usually be identified, Pathogenesis
thrombocytopenia tends to be mild–moderate, and Vitamin K is normally obtained from the diet and intes-
there may be prolongation of PT, aPTT, and TT, tinal flora, and absorbed in the intestinal tract.
hypofibrinogenemia, increased FDPs, and red cell frag-
ments. Vitamin K is essential for carboxylation of clotting
factors II, VII, IX and X. The uncarboxylated clotting
Splenomegaly as a cause of thrombocytopenia is prob- factors cannot bind calcium, a necessary step in clot
ably rare. If it is due to neoplasia it may be identified by formation.
splenic biopsy, but this does not rule out that thrombo-
cytopenia is due to secondary ITP. An increase in the Vitamin K is converted to inactive vitamin K-epoxide
platelet count with prednisone treatment of a non- during the carboxylation process.
hematopoietic neoplasm, e.g. hemangiosarcoma, gives The enzyme, epoxide reductase, converts vitamin K-
putative evidence that ITP is present. epoxide back to active vitamin K. This cycle conserves
Severe bleeding may result in mild thrombocytopenia. vitamin K and precludes the need for daily intake.
In a series of cats with anti-coagulant rodenticide poi- Anti-coagulant rodenticides inhibit epoxide reduc-
soning, a platelet count as low as 58 × 109/L (58 000/μl) tase preventing the re-cycling of vitamin K, such that
was noted. If severe bleeding is associated with mild hepatic stores become rapidly depleted, leading to coagu-
thrombocytopenia, it is more likely that the low platelet lopathy.
count is a result of, rather than the cause of, the bleeding.
There are numerous products classified chemically as
hydroxycoumarins (e.g. warfarin) and indandiones
Treatment (e.g. diphacinone). Second-generation products are
Prednisone 2–4 mg/kg PO until platelet count is nor- those effective against warfarin-resistant rats and are
mal or stable (usually within one week). The dose is more potent. Potency is related to degree and duration
slowly tapered after 2 weeks with re-measurement of of enzyme inhibition. The half-life of second-genera-
platelet count. tion products is much longer than warfarin.
If there is no response, then strategies used in dogs may be Most toxicity data are based on other species or limited
tried, e.g. vincristine 0.02 mg/kg IV, cyclophosphamide data. As rules-of-thumb, single-dose oral LD50 for war-
50 mg/m2 PO alternate days, cyclosporine 5 mg/kg farin is 5–50 mg/kg, for diphacinone 15 mg/kg, and for
PO bid. bromadialone and brodifacoum 25 mg/kg. Ten percent
of the LD50 is a rule-of-thumb to determine the mini-
If the cat is acutely weak from blood loss, a transfu- mum toxic dose. The lack of information is not a big
sion should be given (10–20 ml/kg whole blood), espe- concern since ingestion is rarely observed or quantifi-
cially if the PCV < 15. able with cats.
Anti-coagulant rodenticide poisoning may occur ● Mucosal surface bleeding (petechiation, melena,
from either ingesting the poison (primary toxicosis) hematochezia) may also occur.
or a poisoned rodent (secondary toxicosis). Secondary
Sudden death may occur due to cerebral hemorrhage,
toxicosis is unlikely with warfarin, but may occur
hemopericardium, pulmonary or mediastinal hemor-
with second-generation products, and indeed may be
rhage, or exsanguination into the pleural or abdominal
the most common cause of anti-coagulant rodenti-
cavities.
cide poisoning in cats. Secondary toxicosis was sus-
pected as the cause of poisoning in a recent case
series.
Diagnosis
Cats with cardiomyopathy may be treated with vitamin
Anti-coagulant poisoning is less common in cats than
K antagonists as prophylaxis for thromboembolism.
dogs because of difference in eating habits.
Feces may be colored (e.g. green) from dye in bait
with primary toxicosis.
Clinical signs
Measuring hematocrit and total protein may help
Signs appear 2–5 days after exposure.
identify blood loss as a cause of lethargy, bearing in
● Severity and time to onset of signs depends on
mind that in the first few hours of bleeding these
amount of poison ingested and the animal.
parameters may not change appreciably.
– The higher the dose of poison the earlier and
more severe the signs. For a given amount of Reticulocytes will appear after 4 days of the onset of
poison, exposure over several days is more hemorrhage, but this is late in the disease process and not
toxic than a single large exposure. usually useful to identify blood loss as a cause of acute
– Because cats put less physical stress on their tis- anemia.
sue compared to dogs, signs tend to appear later
Radiographs and ultrasound examinations may detect
in cats after exposure than in dogs.
fluid accumulation in organs and body cavities.
– Signs appear earlier and are more severe in very
young and old animals. Maintaining a high index of suspicion when a cat at risk
● The newer generation poisons do not necessarily has appropriate signs will lead to hemostatic testing.
cause earlier onset of signs. ● PT is the most valuable routine test.
– Factor VII has the shortest half-life of the vita-
Signs of acute anemia and hypovolemia are present.
min K dependent factors and is in the extrinsic
Other non-specific signs include depression (which
system. The other vitamin K dependent factors
may appear before detectable anemia), non-localizable
have longer half-lives and are in the intrinsic or
pain and fever.
common system.
Localizing signs of hemorrhage include scleral hemor- – PT becomes prolonged before aPTT does, but by
rhages, otic hemorrhages, epistaxis, cough, hemoptysis the time a cat is presented with clinical bleeding,
and dyspnea (pulmonary hemorrhage), inspiratory both PT and aPTT are usually prolonged.
dyspnea or restrictive breathing (hemothorax), abdom- – If PT is not prolonged, then a prolongation of
inal pain (presumably due to hemorrhage within aPTT is not due to vitamin K antagonism.
organs), abdominal distention (hemoabdomen), lame- ● Platelet count is normal, or may be mild to moder-
ness, muscle pain and stiffness (hemorrhage into mus- ately decreased if there is marked hemorrhage.
cles), lameness and joint swelling (hemarthrosis), BMBT should be normal, but rebleeding may
neurologic signs (cerebral hemorrhage), ecchymoses, occur.
subcutaneous hematomas and excessive bleeding from ● Response to vitamin K1 (see Treatment, below).
wounds. ● PIVKA time is increased (see Tests of hemostasis,
● Pleural hemorrhage, mediastinal hemorrhage, and above). PIVKA time is more sensitive than PT to
subcutaneous hematomas appear to be most vitamin K antagonism, but is not necessary to make
common. the diagnosis in the bleeding animal, nor, despite its
name, is it specific for a vitamin K dependent coagu- son is witnessed or suspected within several hours
lopathy. prior to consultation. (See Acute poisoning in The Cat
● Analytic confirmation of the poison in the blood is With Depression, Anorexia or Dehydration,
possible through some diagnostic laboratories. page 285). Examine vomitus for evidence of bait
(some are colored green) or a rodent; consider saving
vomitus for toxicologic analysis.
● Administer an adsorbent and cathartic by stom-
Trauma, e.g. by a motor vehicle, can result in similar ach tube if the cat is sufficiently cooperative and:
patterns of hemorrhage and systemic signs. This is dif- – Examination of vomitus confirms ingestion and
ferentiated on the basis of evidence of injury (e.g. a toxic dose is suspected.
sheared nails, lacerations, fractured pelvis) and hemo- – Ingestion is known, induced vomiting did not
static testing. adequately eliminate poison, and it is less than
12 hours post-ingestion.
Differential diagnoses for bleeding at a specific site
– Ingestion is suspected, it is considered to be too
include local lesions at that site. These are differenti-
late to induce vomiting, and it is less than 12
ated on the basis of other signs of these processes and
hours post-ingestion.
normal hemostatic test results.
– Give a slurry of activated charcoal, 1.0–5.0
Liver and gastrointestinal diseases may result in vita- g/kg, preferably using a preparation that
min K deficiency, but the signs of the primary disease includes sorbitol as a cathartic. If activated
are present (e.g. jaundice, diarrhea) and are usually charcoal without cathartic is used, follow with
subacute to chronic. sodium sulfate, 1/2 level teaspoon per kg in
5–10 volumes of tepid water, by stomach
Fulminant DIC causing overt bleeding is not common
tube. If sorbitol or sodium sulfate is not avail-
in cats, and there will be clinical or laboratory signs of
able, use lactulose, 3 ml/kg PO.
an underlying disease. If in doubt, response to vitamin
● Measure PT at 48 and 72 hours and begin vitamin
K therapy rules out DIC.
K1 therapy if PT is prolonged. Obtaining a baseline
Hemophilia A, B and C are characterized by a normal PT may be helpful to facilitate detection of early
PT and prolonged aPTT. changes in PT. A less desirable alternative is to
measure baseline ACT and then at 72 and 96 hours,
Acute heart failure causes dyspnea and the same sys-
and begin vitamin K1 therapy if ACT is > baseline.
temic signs as acute hypovolemia due to hemorrhage,
● In some cases it may be less expensive or more con-
and nasal and oral cavity blood-tinged liquid may be
venient (e.g. cat is obstreperous in hospital) to
present. A heart murmur and arrhythmia may be pres-
empirically treat with vitamin K1 than to monitor
ent with both. Pulmonary crackles are more likely to
coagulation.
be caused by heart failure. Acute heart failure is more
common than anti-coagulant poisoning, and, while Vitamin K1. The synthetic product is phytonadione
radiographic pulmonary changes may be the same, which has the same activity as natural phylloquinone.
cardiomegaly is usually present with heart failure and ● The purpose of therapy is to provide a daily source
the heart may be smaller with hemorrhage. Echocar- of vitamin K until the toxin is eliminated and the
diography and hemostatic testing will definitively dis- vitamin K–vitamin K epoxide cycle can resume.
tinguish the two. Vitamin K1 is expensive but the small size of the
doses makes therapy less expensive in cats com-
pared to most dogs and allows empirical use of
Treatment
higher, longer doses.
Post-exposure treatment. ● Improvement in the PT is expected within 8–12
● Induce vomiting with xylazine, 0.44 mg/kg IM, or hours and normalization by 24–48 hours.
with hydrogen peroxide, 2 ml/kg, or syrup of ● Preferred route is PO as it has the best absorption.
ipecac, 3–6 ml/kg diluted 1:1 with water, PO or – The injectable products may be given orally.
preferably by stomach tube, if ingestion of the poi- Feed canned food as fat promotes absorption.
The daily dose may be given in one or two lost red cells, coagulation factors, and provide
daily treatments. Some prefer the latter to volume.
ensure that the cat ingests at least some vita- – Plasma (10–20 ml/kg). The vitamin K dependent
min K1 each day. factors are stable in plasma so fresh-frozen plasma
– If animal is vomiting give SC. is not necessary. Packed red cells are then given
– Avoid IV injection because of the risk for ana- for red cell replacement.
phylactoid reactions associated with vehicles – If only stored whole blood is available, this will
in the preparation (this risk may be less with provide some coagulation factor activity in addi-
some newer formulations). If IV injection is tion to red cells.
necessary (e.g. severe hematoma formation at
Thoracocentesis should be used to relieve life-threat-
injection site), pre-treat with diphenhydramine
ening pleural blood, and pericardiocentesis to relieve
or tripelenamine, or equivalent anti-histamine,
life-threatening cardiac tamponade.
1 mg/kg IV over 20 minutes (rapid injection
causes hypotension), or acepromazine, 0.05– Crystalloid or synthetic colloid fluid therapy may be
0.1 mg/kg IV. Dilute the vitamin K1 product in necessary for the animal in shock, but minimum
5% dextrose or other approved diluents listed required volumes should be used to minimize dilution
in the product circular, give slowly over 60 of clotting factors and platelets.
minutes, and observe closely for anaphylactoid
Avoid drugs that may enhance toxicosis by altering
reactions and urticaria.
metabolism of poison. Such drugs commonly used in
● Vitamin K1 dose:
cats include sulfonamides, metronidazole, fluoro-
– Warfarin, fumarin, pindone, valone − 1 mg/kg
quinolones and cimetidine. Ranitidine and famotidine
for 1–2 weeks.
are safe to use.
– Bromadiolone, diphacinone, chlorophacinone,
brodifacoum − 2.5–5 mg/kg for 3–4 weeks.
Prognosis
– If product is not known − 2.5–5 mg/kg for 3–4
weeks (assume secondary poisoning with a sec- Prognosis is excellent with prompt treatment.
ond-generation product).
– Do not give higher doses – response is not better Prevention
and there may be a risk of causing Heinz body
Prevent exposure to anti-coagulant poisons by proper
hemolytic anemia.
storage of products and confining cats when products
– Measure PT 2, 3 and 5 days after discontinu-
are in use.
ing treatment, especially if poison is not
known, to ensure treatment was sufficiently For weeks to months after the initial episode, ani-
long. Alternatively measure ACT at 3, 4 and 6 mals are more sensitive to toxicosis upon re-exposure
days. to long-acting rodenticides. This is likely because the
poison is still present in the liver and stores of vitamin K
Provide supplemental oxygen using an oxygen tent (do
have not yet fully recovered.
not use a nasal catheter) if the cat is dyspneic or tachyp-
neic.
HEMOPHILIA A (CLASSICAL HEMOPHILIA)
Transfusion is required for the actively bleeding cat
with existing or potential hypovolemic shock or other
Classical signs
life-threatening hemorrhage.
● 3–8 hours are required for vitamin K to raise ● Excessive internal or external bleeding in
coagulation protein levels. young male cats.
● Transfusion is preferred for volume support since
fluid therapy will dilute remaining clotting factors
Pathogenesis
and platelets.
– Fresh whole blood (10–20 ml/kg) is the most Hemophilia A is caused by reduced synthesis, release
practical blood product to use and will replace or function of factor VIII (anti-hemophilic factor).
● It is a heritable single-gene defect that is X-linked longed ACT and aPTT (typically aPTT is > 1.5–2
recessive (see Transmission). times control value, and aPTT > 40 s where the upper
limit of normal range is 25 s).
Factor VIII is probably synthesized in the liver.
● Prolonged aPTT is corrected by adding plasma
Severity of clinical signs correlates with factor VIII (which contains factor VIII), but not serum (which
level. does not contain factor VIII), to the sample. This
● Bleeding tendency is worst if levels < 1%. result allows a presumptive diagnosis of hemophilia
● Bleeding tendency is less if levels are 5–30%. A as inherited deficiencies of the other coagulation
● Carriers are clinically normal with levels ≈ 50%. factors consumed during clotting are not known.
The various individual cases and hemophiliac families Definitive diagnosis is based on quantification of
reported are probably due to new and different muta- factor VIII activity (FVIII:C) and ruling out acquired
tions in the large factor VIII gene and subsequent in- factor VIII deficiency (see Circulating anti-coagulant,
breeding. Hemophiliac cats may thus vary in the below). Measuring factor VIII activity quantifies the
severity of factor VIII deficiency. ability of the patient’s plasma to correct the prolonged
aPTT of factor VIII deficient plasma. In hemophiliacs
FVIII:C is < 25–30% of normal.
Clinical signs
Clinical signs are usually noted in cats less than a year
of age, but occasionally the diagnosis is made in an
older cat. Differential diagnoses for bleeding at a specific site
include local lesions at that site. These are differenti-
Most cases are diagnosed as a result of investigation of
ated on the basis of other signs of injury or inflamma-
persistent or recurrent bleeding after neutering or
tion and normal hemostatic test results.
declawing.
Abnormal bleeding due to a platelet disorder is ruled
History may reveal previous excessive bleeding from
out on the basis of a normal platelet count and BMBT.
wounds, hematomas, lameness (hemarthrosis), and
unexplained internal bleeding. Hemophilia B and C are characterized by a prolonged
ACT and aPTT that is corrected by adding serum to
Although umbilical bleeding in neonates and bleeding
sample, and by a low factor IX or XI quantification.
at the time of teething have not been specifically
reported, some family histories have reported fatal Cats with coagulopathy secondary to liver failure will
bleeding diatheses in related kittens. have clinical and laboratory signs of liver disease, e.g.
subacute to chronic inappetence, jaundice, hepatic
Hematomas probably form at subcutaneous vaccination
encephalopathy, and increased liver enzymes, respec-
sites but go unnoticed. Vaccination does not trigger
tively, and may have a prolonged PT.
bleeding at other sites.
Cats with vitamin K antagonist poisoning and other
Signs due to anemia and local effects of hemorrhage
vitamin K related disorders have a prolonged PT and
vary with severity of blood loss. Signs are acute to sub-
will respond to vitamin K therapy.
acute in onset.
Fulminant DIC causing overt bleeding is not common
Males are affected the most. However, because cats
in cats, and there will be clinical or laboratory signs of
may have minimal signs, males may breed, resulting in
an underlying disease.
affected females (see Transmission).
Acquired factor VIII deficiency has been reported in
humans but not in cats.
Diagnosis
Hemophilia A is rare. Treatment
Hemostatic testing reveals normal platelet count and Transfusion with 10–20 ml/kg fresh whole blood,
BMBT (may rebleed), normal PT, and markedly pro- fresh plasma, or fresh-frozen plasma (frozen within 8
hours of collection and stored for < 1 year), or 2 units Transmission

cryoprecipitate.
● By definition, fresh products are those used
Factor VIII deficiency is a heritable single-gene defect
within 8 hours of collection. Factor VIII levels that is X-linked recessive.
begin to decline after 8 hours of refrigeration, and Based on classical mendelian inheritance, where “X”
in humans only 50% of factor VIII activity is pres- and “Y” are sex-chromosomes, “H” is the normal fac-
ent after 24 hours, but in dogs 85% of activity tor VIII gene, “h” is the abnormal factor VIII gene, and
remains. Some factor VIII activity is probably pres- approximately half the litter are males and half females:
ent in both up to two weeks. The stability of feline ● Breeding an unaffected male (XH,Y) to a normal
factor VIII is not known. While ideally fresh blood female (XH,XH), will result in all normal males and
products should be used, blood or plasma that is all normal females, i.e. none in litter are bleeders.
more than 8 hours old is still likely be beneficial to This is, of course, the normal situation.
a hemophiliac. ● Breeding an unaffected male (XH,Y) to a carrier
● If plasma products are used, 25–70 ml packed red female (XH,Xh), will result in 50% of the males in
cells may also be needed. the litter being affected, and 50% of the females
● Transfusion may be used during a bleeding episode being carriers, i.e. approximately 25% of the litter
or prophylactically before a procedure. (all males) are bleeders. This is the most likely nat-
● Collect sufficient blood samples for hemostatic ural scenario in the random appearance of hemo-
testing prior to transfusion. philia.
● A single transfusion may stop active bleeding in a ● Breeding an unaffected male (XH,Y) to an affected
cat if there is no underlying injury or inflammatory female (Xh,Xh), will result in all males being
disorder. affected and all females being carriers, i.e. approxi-
● Half-life of factor VIII post-transfusion is probably mately 50% of litter are bleeders (all males).
only 8–12 hours, so repetitive transfusions every ● Breeding an affected male (Xh,Y) to a normal
12–24 hours may be necessary. female (XH,XH), will result in all males being nor-
● Cats with absolute factor VIII deficiency may theo- mal and all females being carries, i.e. none in litter
retically become refractory to transfused factor VIII are bleeders.
because of antibody formation. ● Breeding an affected male (Xh,Y) to a carrier
Treatment with vitamin K1 is of no benefit, except as a female (XH,Xh), will result in 50% of the males
diagnostic test to rule out vitamin K antagonist poison- being affected, and 50% of the females being
ing. affected females, i.e. 50% of litter are bleeders (half
male, half female).
Treatments in dogs and/or humans not evaluated in cats ● Breeding affected male (Xh,Y) to an affected
include desmopressin, lyophilized factor VIII, recombi- female (Xh,Xh), will result in all males being
nant human factor VIII, recombinant factor VIIa, affected and 50% all females being affected, i.e.
inhibitors of fibrinolysis (e.g. aminocaproic acid), liver 75% in litter are bleeders (all male, half female).
transplantation, and gene therapy. This is the least likely naturally occurring situation.
Prognosis
Prevention
In most cases spontaneous bleeding is minimal or
mild. Parents and littermates may be tested for factor
VIII:C to identify affected cats (males and homozy-
Prognosis is good for cats kept in an environment gous females) and carriers (heterozygous females).
that minimizes trauma and exuberant exercise. ● Normal cats have normal factor VIII:C levels.
● In most species, carrier females have ≈ 40–60%
Bleeding tendency appears to be less in mature cats
compared to juveniles. An explanation for this may be normal factor VIII:C, but the upper range may
factor VIII levels increasing with age, as has been seen overlap with the lower range of normal. One con-
in normal cats. firmed carrier had a factor VIII:C of 69%. Breeding
studies are the only way to identify carriers with Excessive bleeding following injury or procedures,
low normal factor VIII:C. e.g. neutering, declawing, venepuncture.
● Clinically affected cats have < 25–30% factor
Family history may reveal fatal bleeding diathesis/unex-
VIII:C.
plained death in related kittens.
A breeder should be advised not to breed affected and
Other than bleeding tendencies being more severe,
carrier/suspected carrier cats. One strategy would be to
signs are otherwise identical to hemophilia A.
only breed cats with factor VIII:C ≥ 100%.
Males are affected the most. Because signs are more
For clients who are not breeders, or if factor VIII test-
apparent than in hemophilia A, males are less likely
ing of related cats is cost-prohibitive, neuter and spay
to breed and produce affected female offspring (see
all related cats. Measure ACT first to identify affected
Transmission).
cats that will require transfusion prior to surgery.
Diagnosis
HEMOPHILIA B (CHRISTMAS DISEASE) Hemophilia B is rare.
Classical signs
BMBT (may rebleed), normal PT, and markedly pro-
● Spontaneous or excessive internal or longed ACT and aPTT.
external bleeding in young male cats. ● In contrast to hemophilia A, prolonged aPTT in
hemophilia B is corrected by adding serum
(which contains factor IX but not factor VIII) to the
Pathogenesis sample. Prolonged aPTT in both hemophilia A and
B is corrected by adding plasma. This result is con-
Hemophilia B is caused by reduced synthesis, release
sistent with a deficiency of any of the non-consum-
or function of factor IX (Christmas factor).
● It is a heritable single-gene defect that is X-linked
able clotting factors, and its main value is to rule
out hemophilia A.
recessive. Newly arising cases probably represent
new mutations. Definitive diagnosis is based on quantification of
factor IX activity (FIX:C), similar to hemophilia A,
Factor IX is produced by vitamin K dependent synthe-
and ruling out acquired factor VIII deficiency (see
sis in the liver.
Circulating anti-coagulant, below).
Severity of clinical signs correlate with factor IX level
similar to hemophilia A. Differential diagnosis
● Most affected cats have levels < 10%.
● Carriers typically have levels ≈ 40–60%.
Differential diagnoses and differentiation for bleeding
for hemophilia B are similar to those for hemophilia A.
– Carriers may have up to ≈ 80% normal levels,
● Acquired factor IX deficiency has been reported
perhaps because factor IX levels increase with
in humans but not in cats.
stress.
Comparing hemophilia B to hemophilia A, with the
former:
Clinical signs ● Spontaneous bleeding is more common.
● Prolonged ACT and aPTT are corrected by adding
Clinical signs are usually noted in cats less than a year
serum to sample.
of age, but occasionally the diagnosis is made in an
older cat.
Treatment
Signs of spontaneous bleeding are mild to moderate.
Signs include hemothorax and hemoabdomen, shift- Transfusion with 10–20 ml/kg fresh or stored whole
ing lameness due to hemarthrosis, subcutaneous blood, fresh, fresh-frozen, refrigerated, or frozen
swellings, bruises, gingival bleeding. plasma. Factor IX is stable during normal refrigeration
time for red cell banking (up to 35 days) and in frozen Congenital hemophilia C has recently been described
plasma. If plasma products are used, 1–2 units of in a young female cat.
packed red cells may also be needed.
● Collect sufficient blood samples for hemostatic
testing prior to transfusion. Clinical signs
● A single transfusion may stop active bleeding in a
cat if there is no underlying injury or inflammatory Excessive bleeding following injury or procedures,
disorder. in this case neutering and declawing.
● Half-life of factor IX post-transfusion is proba-
bly only 24 hours, so repetitive transfusions every
24–48 hours may be necessary. Diagnosis
● Cats with absolute factor IX deficiency may theo-
Hemophilia C is rare.
retically become refractory to transfused factor IX
because of antibody formation. Hemostatic testing reveals normal platelet count and
BMBT (may rebleed), normal PT, and markedly pro-
Treatments in dogs and/or humans not evaluated in cats
longed ACT and aPTT.
include lyophilized factor IX, recombinant factor VIIa,
● In contrast to hemophilia A, as with hemophilia B,
inhibitors of fibrinolysis (e.g. aminocaproic acid), and
prolonged aPTT in hemophilia C is corrected by
gene therapy.
adding serum (which contains factor XI but not
factor VIII) to the sample. Prolonged aPTT in
Prognosis hemophilia A, B and C is corrected by adding
plasma. This result is consistent with a deficiency
Prognosis is good for cats kept in an environment that
of any of the non-consumable clotting factors, and
minimizes trauma and exuberant exercise, but bleeding
its main value is to rule out hemophilia A.
episodes requiring transfusion are likely to occur.
Definitive diagnosis is based on quantification of factor
IX activity (FXI:C), similar to hemophilia A, and ruling
Transmission
out acquired factor XI deficiency (see Circulating anti-
Factor IX deficiency is a heritable single-gene defect coagulant, below).
that is X-linked recessive. See Hemophilia A for inher-
itance patterns.
Prevention Differential diagnoses and differentiation for bleeding
As for hemophilia A, but testing for factor IX. for hemophilia C are similar to those for hemophilia A.
Acquired factor XI deficiency in a cat has been reported.
HEMOPHILIA C
Treatment
Classical signs Transfusion with 10–20 ml/kg fresh or stored whole
blood, fresh, fresh-frozen, refrigerated, or frozen
● Excessive bleeding in a young cat (single
plasma should be considered if there is critical hemor-
case).
rhage. Factor XI is stable during normal refrigeration
time for red cell banking (up to 35 days) and in frozen
plasma. If plasma products are used, 1–2 units of
Pathogenesis
packed red cells may also be needed.
Hemophilia C is caused by reduced synthesis, release ● Collect sufficient blood samples for hemostatic
or function of factor XI (plasma thromboplastin testing prior to transfusion.
antecedent). ● In the case reported, transfusion was not necessary.
● Half-life of factor XI post-transfusion is prob- Excessive bleeding after venepuncture, neutering

ably longer (2–3 days) than factor VIII or IX. and other surgical procedures.
● Cats with absolute factor XI deficiency may theo-
For cases with a defect not sufficiently severe to cause
retically become refractory to transfused factor IX
spontaneous hemorrhage, the age of detection will
because of antibody formation.
depend on the age when a procedure is performed.
Treatments in humans not evaluated in cats include Most cats are neutered at a young age, resulting in
lyophilized factor XI, recombinant factor VIIa, and detection of the defect at that time.
inhibitors of fibrinolysis (e.g. aminocaproic acid).
Signs due to anemia and local effects of hemorrhage
vary with severity of blood loss.
Prognosis
Some affected cats may not show spontaneous or
Prognosis is probably good for cats kept in an environ- excessive bleeding, also consistent with variable
ment that minimizes trauma and exuberant exercise. severity of the defect.
In one case a bleeding episode was suspected to have
Transmission been triggered by concurrent decreased platelet func-
tion associated with modified-live virus vaccination.
Transmission in cats is unknown. In humans, dogs and
cattle transmission is autosomal recessive.
Diagnosis
Prevention
Consistent signalment (young Devon Rex cats) and
As for hemophilia A, but testing for factor XI. signs of spontaneous or excessive bleeding are highly
suggestive.
VITAMIN-K RESPONSIVE COAGULOPATHY No evidence of other vitamin K related disorders.
IN THE DEVON REX ● No history of exposure to vitamin K antagonist poi-
sons.
Classical signs ● No clinical or laboratory evidence of liver disease.
● No diarrhea (exocrine pancreatic insufficiency and
● Spontaneous and excessive bleeding in
inflammatory bowel disease).
Devon Rex cats.
BMBT (may rebleed), and prolonged PT, ACT and
Pathogenesis aPTT. PIVKA time has not been reported but is pre-
sumably prolonged.
Vitamin K is essential for carboxylation of clotting fac-
tors II, VII, IX and X. The uncarboxylated clotting fac- Quantification of vitamin K dependent factor activ-
tors cannot bind calcium, a necessary step in clot ities, using techniques similar to factor VIII quantifica-
formation (see Vitamin K antagonist rodenticides and tion in hemophilia A.
drugs).
Normalization of PT, ACT, aPTT and factor activities
The enzyme responsible for carboxylation has reduced with vitamin K therapy.
affinity for vitamin K, impairing its function.
Clinical signs
Vitamin K antagonist rodenticide poisoning may be
Spontaneous bleeding in Devon Rex cats including ruled out in some cases on lack of exposure history.
hemothorax, intrapulmonary hemorrhage, hemarthrosis ● If exposure is possible, then the cat should be con-
and otic hemorrhages. Reported cases range from 5 fined in a rodenticide-free environment and treated
months to 2 almost years. with vitamin K for 6 weeks. After stopping
vitamin K therapy, PT ± aPTT should be monitored. Prevention

Clotting times will become abnormal again with the
genetic defect but remain normal if the cat had been Recommendations are tentative.
poisoned. Measure PT in parents and littermates to identify
● Toxicological analysis of blood can be used to affected cats.
identify presence of a rodenticide. ● If PT testing is cost-prohibitive, ACT should be
Other toxins and drugs significantly impairing vita- useful for initial screening (prolonged test result
min K function are rare and may be ruled out by history identifying affected cats); but if ACT is normal, PT
and improvement with drug withdrawal. should be performed.
Cats with coagulopathy secondary to liver failure Do not breed affected cats. Treat with vitamin K and
will have clinical and laboratory signs of liver disease, neuter.
e.g. subacute to chronic inappetence, jaundice, hepatic Consider not breeding related unaffected cats, in case
encephalopathy, and increased liver enzymes, respec- defect is autosomal recessive.
tively.
Exocrine pancreatic insufficiency and inflammatory
bowel disease severe enough to cause vitamin K defi- EXOCRINE PANCREATIC INSUFFICIENCY
ciency also cause diarrhea. (EPI)
Differential diagnoses for bleeding at a specific site Classical signs

include injury or inflammation at that site. These are
differentiated on the basis of other signs of injury or
● Chronic diarrhea, weight loss, polyphagia.
inflammation and normal hemostatic test results.
● Excessive bleeding may occur.
● Rare in cats.
Abnormal bleeding due to a platelet disorder is ruled
out on the basis of a normal platelet count and BMBT.
Pathogenesis
Thrombocytopenia is often present in DIC, in addition
to signs of a severe illness causing DIC. Dietary triglycerides are normally digested by pancre-
atic lipase to monoglycerides and fatty acids.
Treatment This process is needed for solubilization and subse-
quent absorption of fat-soluble vitamins, including
Vitamin K1 at an initial dose of 5 mg/day PO, and then
vitamin K.
tapered to a minimum dose required to keep PT normal.
In EPI, lipase deficiency can therefore result in vita-
Cats with life-threatening bleeding may require trans-
min K deficiency.
fusion (see Vitamin K antagonist rodenticides and
drugs). Vitamin K deficiency leads to coagulopathy due to
● Caution: There is a high-prevalence of type B deficiencies of factors II, VII, IX and X (see Vitamin K
blood type in this breed. Be sure to blood-type or antagonist rodenticides and drugs).
cross-match donor and recipient prior to transfusion.
Vitamin K deficiency is usually mild since there is not
complete absence of intestinal lipolysis.
Prognosis
Clinical signs
Excellent with vitamin K1 therapy.
Chronic diarrhea, weight loss, normal to increased
appetite (see The Cat With Signs of Chronic Small
Transmission Bowel Diarrhea, page 751).
Mode of inheritance is not known, but defect is likely Greasy soiling of the haircoat (especially perianal) may
to be autosomal. occur.
Clinical bleeding is rare and is most likely to be ment and improvement of diarrhea with pancreatic
excessive, e.g. following venepuncture, rather than enzyme supplementation.
spontaneous.
Concurrent supplementation with vitamin E (toco-
Prevalence of subclinical clotting factor deficiency is pherol) may increase vitamin K1 requirements.
not known.
Avoid unnecessary antibiotic therapy that may
reduce intestinal bacterial production of vitamin
Diagnosis K2.
● Antibiotic treatment may be necessary to treat
See The Cat With Signs of Chronic Small Bowel
small intestinal bacterial overgrowth.
Diarrhea (page 752) for diagnosis of EPI.
Hemostatic testing in the bleeding cat reveals normal
Prognosis
platelet count and BMBT (may rebleed), and pro-
longed PT, ACT and aPTT. The prognosis for normalization of hemostasis is excel-
lent.
Cats with EPI and clinically normal hemostasis may
have high normal range values or mild prolongation of
PT, ACT and aPTT. A sub-clinical effect may be better
INFLAMMATORY BOWEL DISEASE (IBD)
documented by measuring elevated PIVKA time and
quantification of factor VII using a technique similar to
Classical signs
factor VIII quantification in hemophilia A.
● Chronic diarrhea, weight loss, variable
appetite.
● Spontaneous or excessive bleeding may
Differential diagnoses for a cat with chronic diarrhea occur (uncommon).
and coagulopathy include:
● Inflammatory bowel disease. This is differenti- See main reference, The Cat With Signs of Chronic
ated from EPI by normal trypsin-like immunoreac- Small Bowel Diarrhea (page 769) for treatment of IBD.
tivity and intestinal biopsy showing inflammation.
● Primary intestinal disease and secondary cholan-
giohepatitis or hepatic lipidosis. These are identi- Pathogenesis
fied by routine laboratory work-up and biopsy.
Vitamin K deficiency leads to coagulopathy due to
Appetite is usually reduced with liver disease.
deficiencies of factors II, VII, IX and X (see Vitamin K
● Feline leukemia virus and feline immunodefi-
antagonist rodenticides and drugs).
ciency virus infections. Both viral diseases may be
associated with chronic diarrhea, but appetite is Vitamin K1 is the main source of vitamin K for
usually reduced. Coagulopathies may occur with mammals.
retroviral infections, but are usually subclinical. ● It is obtained from the diet (phylloquinone) and
Both viruses may cause thrombocytopenia. absorbed in the proximal small intestine.
● Unrelated causes of diarrhea and abnormal bleeding. ● Severe intestinal malabsorption may result in
vitamin K1 deficiency.
● The main causes of malabsorption in cats are IBD,
Treatment
hyperthyroidism and intestinal lymphoma Vitamin
See The Cat With Signs of Chronic Small Bowel K deficiency has been documented with IBD, and is
Diarrhea (page 752) for treatment of EPI. probably responsible for some of the increased
PIVKA times seen occasionally in hyperthyroidism,
Cats with EPI and clinical or laboratory evidence of
but has not been investigated in lymphoma.
coagulopathy should be given vitamin K1, 5 mg/kg SC
daily until normalization of PT. The need for further Vitamin K2 (menaquinone) is also an important
treatment will depend on response to vitamin K1 treat- source of vitamin K for mammals.
● It is produced by intestinal bacteria (especially ● Concurrent use of medium-chain triglyceride sup-

Escherichia coli and Bacteroides spp.) and absorbed plementation, 1–2 ml/kg/day PO will promote vita-
in the ileum and colon. min K absorption and promote weight gain, but the
● If IBD affects predominantly the proximal small product is unpalatable.
intestine, bacterial synthesis provides sufficient ● If oral vitamin K1 therapy is unsuccessful, vitamin
vitamin K2 to prevent coagulopathy. K3 therapy may be considered. Vitamin K3 is a
synthetic vitamin K that is less fat-soluble and is
absorbed in the colon. Unfortunately it causes a
Clinical signs
dose-dependent Heinz-body hemolytic anemia
Chronic diarrhea, chronic intermittent vomiting, and methemoglobinemia, and a safe but effective
weight loss, appetite varying from episodic inappetence dose in the cat has not been determined.
to polyphagia (see The Cat With Signs of Chronic
Avoid unnecessary antibiotic therapy that may reduce
Small Bowel Diarrhea, page 768).
intestinal bacterial production of vitamin K2.
Clinical bleeding is uncommon but spontaneous
bleeding diathesis has occurred.
Prognosis
Based on prolonged PIVKA time, prevalence of sub-
clinical factor deficiency in severe IBD is approxi- The prognosis for normalization of hemostasis is excel-
mately 30%. lent but ongoing vitamin K1 therapy may be needed
until the underlying disorder is resolved.
Diagnosis
Hemostatic testing in a bleeding cat reveals normal PANCREATITIS
platelet count and BMBT (may rebleed), and pro-
longed PT, ACT and aPTT. Classical signs
Cats with IBD and clinically normal hemostasis may ● Depression and anorexia.
have high normal range values or mild prolongation of
PT, ACT and aPTT. A sub-clinical effect may be better See main reference on page 272 (The Cat With
documented by measuring elevated PIVKA time and Depression, Anorexia or Dehydration).
quantification of factor VII using a technique similar to
factor VIII quantification in hemophilia A.
Clinical signs
The most common signs are non-specific.
Hypothermia, vomiting, abdominal pain and occa-
As for exocrine pancreatic insufficiency.
sionally a palpable cranial abdominal mass may be
present.
Treatment Icterus may be present from concurrent liver disease
or extra-hepatic bile duct obstruction.
Cats with IBD and clinical or laboratory evidence of
coagulopathy should be given vitamin K1, 5 mg/kg SC Hemostatic abnormalities may be present due to DIC of
daily until normalization of PT. The need for further varying severity or due to concurrent liver disease.
treatment will depend on response to vitamin K1 treat- ● Hemostatic abnormalities are usually subclinical.
ment and improvement of diarrhea with corticosteroid Clinical bleeding is unlikely unless there is severe
therapy and dietary manipulations. DIC or concurrent liver disease.
If intestinal malabsorption is not adequately controlled Cats with concurrent liver disease and pancreatitis are
and ongoing vitamin K supplementation is needed, oral more likely to have hemostatic defects and clinical
supplementation with vitamin K1 may be tried. bleeding than with either disease on its own.
Diagnosis CUTANEOUS ASTHENIA (EHLERS–DANLOS

See The Cat With Depression, Anorexia or SYNDROME)
Dehydration (page 273).
Classical signs
Hemostatic testing may reveal evidence of DIC (e.g.
thrombocytopenia, prolongation of clotting times), evi- ● Excessive wounding since birth.
dence of vitamin K deficiency (prolonged PT and ● Subcutaneous hematomas or seromas.
PIVKA time), and/or evidence of other hemostatic dis-
orders associated with concurrent liver disease (see
Liver disease, above). Clinical signs
Signs are present from birth, but may worsen with age.
Skin is hyperextensive and wounds easily with minor
See The Cat With Depression, Anorexia or trauma, and may feel softer. Scars from previous
Dehydration (page 275). Pancreatitis is difficult to wounds may be present. Signs result from abnormal
definitively diagnose without biopsy. Many diseases in collagen synthesis, and will vary in degree with the spe-
the cat cause non-specific signs and sub-clinical hemo- cific genetic defect.
static defects. Systematic elimination of diseases by ● The chief complaint may be bleeding from the
work-up helps narrow the list of differential diagnoses. skin, but bleeding is appropriate for the wound.
● Bleeding into the skin without a wound (petechia-
Treatment tion, ecchymoses) is not characteristic of the dis-

eases described to date in cats.
See The Cat With Depression, Anorexia or ● Subcutaneous hematomas and seromas may
Dehydration (page 277). occur because blood and lymphatic vessels are
If there is clinical bleeding, treat with vitamin K as for fragile or are injured when the skin stretches.
liver diseases and transfusions as for DIC. Concurrent signs include joint laxity, lens luxation
and cataracts.
Reported in domestic shorthaired, domestic longhaired,
STRANGULATION Himalayan and Burmese cats.
Classical signs
● Scleral hemorrhage. Diagnosis
Clinical signs are highly suggestive.
Clinical signs Skin extensibility index (SEI) > 19%. SEI = height of
Non-fatal strangulation may result in scleral edema and fold/body length × 100, where, with the cat standing, a
hemorrhage, and neurologic signs. Pulmonary edema fold of lumbosacral skin is pulled upwards and the
has also been seen in dogs. height from the top of the spine to the top of the fold is
measured, and body length is measured from the occipi-
tal crest to the base of the tail.
Diagnosis
Skin biopsy for histopathology and/or electron
History is diagnostic. Usually the collar or leash is microscopy of skin to document collagen abnormali-
caught in a tree. ties, special biochemical analyses, and measurement of
Skin lesions around neck. tensile strength.
Hemostatic testing is normal. Hemostatic testing is normal.

because of a platelet function defect. Spontaneous

bleeding and bleeding diathesis do not occur.
Classical signs
Diagnosis
● Polyuria, polydipsia, polyphagia.
● Abdominal distention, alopecia, fragile Clinical signs.
skin.
Routine blood smear reveals large pink cytoplasmic
inclusions in granulocytes and larger than normal
Clinical signs eosinophil granules.
Polyuria, polydipsia and polyphagia commonly Hemostatic testing reveals prolonged BMBT (9.33 →
occur because of insulin-resistant diabetes mellitus. 20 min) and decreased platelet aggregation.
Abdominal distention commonly occurs because of
muscle wasting and hepatomegaly. IDIOPATHIC THROMBOCYTOPATHIA
Cutaneous signs include patchy alopecia (most com-
Classical signs
mon), symmetrical alopecia and fragile skin.
● Spontaneous epistaxis and gingival
Fragile skin may bleed when it is torn, but bleeding is
bleeding.
typically slight.
Cats, unlike dogs, do not appear to bleed more easily
Clinical signs
from venepuncture sites.
Bleeding results from an abnormality in platelet
function affecting aggregation.
Diagnosis
Presumed to be a congenital defect since signs are
See The Cat With Polyuria and Polydipsia (page 251).
apparent at a young age.
Hemostatic testing is normal.
Recurrent epistaxis and gingival bleeding have been
seen.
CHEDIAK–HIGASHI SYNDROME
Diagnosis
Classical signs
Clinical signs.
● Persian cats with congenitally dilute
smoke-blue hair coat.
prolonged BMBT.
Abnormal platelet aggregation in vitro.
Clinical signs
ANTIPLATELET CARDIAC DRUGS
Signs are present from birth and are associated with an
autosomal recessive defect.
Classical signs
Affected Persian cats have a dilute smoke-blue hair
● None.
coat and yellow-green irises.
Ophthalmologic evaluation reveals epiphora and ble-
pharospasm in bright light and a red fundus. Clinical signs
Prolonged bleeding occurs at venepuncture sites, b-blockers and calcium-channel blockers inconsis-
surgical sites and following minor and major trauma, tently inhibit platelet aggregation in vivo.
Acepromazine, at one time extensively used in the protozoal infections, non-infectious inflammation and
management of arterial thromboembolism, inhibits immune-stimulation, and neoplastic infiltration.
platelet aggregation in humans, but does not in dogs Splenomegaly may also result from portal hypertension
and presumably has minimal effect in cats. and extra-medullary hematopoiesis. Most causes of
lymphadenopathy may also cause splenomegaly (see
Aspirin, n-3 fatty acids, and cyproheptadine variably
The Cat With Enlarged Lymph Nodes, page 393).
inhibit platelet aggregation in vitro but have a minimal
effect on BMBT when used as single agents. The most common cause of marked splenomegaly is
● These drugs have been given to cats in an attempt to neoplasia, especially mast cell tumor and lym-
prevent arterial thromboembolism due to cardiomy- phoma.
opathy.
Although the spleen of the cat is non-sinusoidal,
– Newer classes of antithrombotic drugs in
splenic sequestration of platelets does normally
humans inhibit platelet aggregation by pre-
occur. Splenomegaly could potentially contribute to
venting binding of fibrinogen or ADP to specific
thrombocytopenia, but it does not appear to be an
platelet receptors. These drugs have been shown
important mechanism and a bleeding tendency is
to impair platelet function in normal cats.
unlikely.
Clopidogrel currently shows the most promise
for clinical use.
The effect of the older drugs on bleeding in cats with a
Diagnosis
bleeding disorder is not known, but is unlikely to be
marked in most circumstances. Aspirin should probably Routine work-up to identify primary disease.
be avoided in cats with a moderate to marked hemostatic
Aspiration or surgical biopsy of spleen.
disorder. The effect of the newer platelet receptor block-
ing drugs on bleeding in cats with a bleeding disorder is Hemostatic testing may reveal thrombocytopenia
not known, but these drugs should likewise probably be and coagulopathy (e.g. DIC) secondary to the primary
avoided in cats with a moderate to marked hemostatic dis- disease.
order.
Diagnosis
VON WILLEBRAND’S DISEASE
History of drug therapy.
If a cat receiving one of these drugs has abnormal Classical signs
bleeding, another cause of the bleeding should be ruled ● Not known (rare disease).
out.
SPLENOMEGALY Clinical signs

There is a report of a 9-year-old male neutered cat with
Classical signs
persistent oral bleeding after tooth extraction.
● Enlarged spleen on abdominal palpation.
In dogs the most common signs are those of excessive
● Signs of a primary disease.
or prolonged bleeding following injury.
Clinical signs
Mild to markedly enlarged spleen on abdominal pal- Diagnosis
pation.
Hemostatic tests reveal prolonged BMBT, normal to
Other signs of a primary disease causing splenomegaly slightly prolonged ACT and aPTT, and decreased von
may be present. Diseases include bacterial, fungal and Willebrand’s factor (vWf:Ag).
FACTOR X DEFICIENCY Diagnosis

Hemostatic test results will vary with the coagulation
Classical signs factor inhibited and platelet abnormalities.
● Not known (rare disease). A circulating inhibitor is demonstrated by mixing
equal volumes of patient and normal plasma. If the
prolonged coagulation time in the patient plasma is
Clinical signs normalized, then it was due to a factor deficiency. (This
There is a report of a cat with mild excessive bleeding test works because PT and aPTT do not become pro-
after declawing and seizures attributed to intracranial longed until there is < 25% function, so the normal
hemorrhage at 3 years of age. plasma adds sufficient factors to the deficient plasma to
normalize the test). If the prolonged coagulation time
The defect appeared to be inherited. The mother and in the patient plasma is not normalized (i.e. the patient
one sibling were subclinically affected. plasma prolongs coagulation time in normal plasma),
then an inhibitor is present.
● If an inhibitor is demonstrated, more specific mix-
Diagnosis
ing studies may be performed using specific factor C
Hemostatic tests reveal normal platelet count and assays to identify the specific factor inhibitor.
BMBT, markedly prolonged PT, ACT, and aPTT and
normal TT.
Russell’s viper venom time (RVVT) is prolonged.
ANTI-COAGULANTS
Factor X:C is decreased. Classical signs

Rule out acquired factor X deficiency (reported in ● Spontaneous bleeding with excessive
humans but not cats). See Circulating anti-coagulant, anticoagulation.
below.
Clinical signs
CIRCULATING ANTI-COAGULANT
Heparin, low-molecular-weight heparin and war-
farin may be used as prophylaxis against thromboem-
Classical signs
bolism in cats with cardiomyopathy (see The Cat With
● Not known (rare disease). Signs of Heart Disease, page 130).
Heparin may be used in the treatment of pulmonary
Clinical signs thromboembolism and DIC (see above).
Primary or secondary autoimmune diseases may be There is a narrow therapeutic margin between effec-
associated with acquired circulating anti-coagulants tive and excessive anti-coagulant therapy. Excessive
(inhibitors), e.g. the lupus anti-coagulant in systemic therapy will result in spontaneous hemorrhage.
lupus erythematosus. The anti-coagulant may result in
spontaneous or excessive bleeding. Paradoxically, ani- Diagnosis
mals and humans with lupus anti-coagulants are also at
risk for thrombosis. History of anti-coagulant therapy.
Inhibitors to most coagulation factors have been Prolongation of ACT, aPTT, PT, PIVKA time and TT
reported in humans. There is a report of a 5-year-old cat with heparin and warfarin therapy. The ACT, aPTT and
with persistent epistaxis due to inhibition of factor XI TT are usually used to monitor heparin therapy, while
(plasma thromboplastin antecedent) causing a pro- PIVKA time and PT are used to monitor warfarin ther-
longed aPTT. apy. Routine coagulation tests are not affected by low-
molecular-weight heparin, where plasma anti-factor Xa occurs, hemostatic tests reveal prolonged PT ± pro-
activity is used to monitor therapy. longed ACT and aPTT.
VITAMIN K DEFICIENT DIET

ANTIBIOTICS
Classical signs
Classical signs
● Spontaneous bleeding with certain fish
diets. ● Abnormal bleeding associated with
antibiotic therapy.
Clinical signs
The cat has a relatively low dietary vitamin K Clinical signs
requirement and it is difficult to experimentally induce
Penicillins and some cephalosporins variably impair
vitamin K deficiency.
platelet function in humans, rabbits and dogs, and may
Some commercial fish-based diets caused a vitamin K exacerbate thrombocypenic bleeding. This is most
responsive bleeding diathesis during feeding trials, pos- important in humans with penicillins, when the platelet
sibly due to an anti-vitamin K factor in the diet. count is < 20 × 109/L (200,000/μl) or in the presence of
other hemostatic defects. Amoxicillin, cefalexin, and
cefazolin at standard doses do not impair platelet func-
Diagnosis tion in normal dogs and are unlikely to have any clini-
cally relevant hemostatic effects in cats.
The main cause of vitamin K deficiency is anorexia.
Other antibiotics that alter platelet aggregation in vitro
If no other explanation exists to account for a vitamin K
in humans, rabbits or dogs include tetracyclines, gen-
responsive coagulopathy, diet should be investigated.
tamicin and sulfonamides. The clinical effect, if any,
is less important than with the penicillins.
Fluoroquinolones do not appear to impair platelet
ANTI-CONVULSANTS function. Doxycyline and enrofloxacin at standard
doses do not impair platelet function. Doxycycline and
Classical signs enrofloxacin at standard doses do not impair platelet
function in normal dogs. These antibiotics are unlikely
● None (with respect to bleeding).
to have any clinically relevant hemostatic effects in
cats.
An idiosyncratic drug reaction may result in thrombo-
Clinical signs
cytopenia and platelet-type bleeding.
Phenobarbital and diphenylhydantoin (rarely used in
Antibiotic therapy may reduce bacterial synthesis of
cats) cause mild reduction in hepatic synthesis of vita-
vitamin K2 (menaquinone) by killing intestinal bacteria
min K dependent clotting factors. This is only a pro-
(especially Escherichia coli and Bacteroides spp.).
blem in a cat with another vitamin K related disorder.
Numerous antibiotics have been implicated in humans.
This is not usually a concern in the animal with other-
Diagnosis wise normal hemostasis, but may promote coagulopathy
in animals at risk for vitamin K deficiency.
Sub-clinical effect may be documented by PIVKA
time and/or quantification of vitamin K dependent fac- Moxalactam, cefamandole and cefoperazone may
tor activities using techniques similar to factor VIII directly impair vitamin K dependent factor synthe-
quantification in hemophilia A. If a clinical effect sis. These antibiotics are infrequently used in cats.
Sulfonamides, metronidazole and possibly fluoro- Presumably quantification of vitamin K dependent fac-
quinolones may exacerbate vitamim K antagonist tor activities could also demonstrate a deficiency.
rodenticide poisoning.
Actinomycin D, an anti-tumor antibiotic, may be a NON-STEROIDAL ANTI-INFLAMMATORY
vitamin K antagonist, but the clinical relevance of this DRUGS
in cats is not known.
Classical signs
Diagnosis
Abnormal bleeding associated with antibiotic ther-
Clinical signs
apy and improvement upon withdrawing therapy.
Non-steroidal anti-inflammatory drugs (NSAIDs) are
If vitamin K deficiency or antagonism is causing bleed-
being prescribed with increasing frequency for analge-
ing, hemostatic testing reveals prolonged PT ± prolonged
sia in cats.
ACT and aPTT, and improvement in coagulopathy
with vitamin K1 injection (assuming normal liver Similar to aspirin, non-selective NSAIDs impair
function). platelet function by inhibition of cyclooxygenase-1.
● Sub-clinical effect may be documented by PIVKA This may result in prolonged bleeding times and
time and quantification of vitamin K dependent fac- increased surgical hemorrhage in humans and dogs.
tor activities using techniques similar to factor VIII The effect on bleeding time in cats has not been well
quantification in hemophilia A. investigated, but, given that aspirin has minimal effects
on BMBT in the cat, NSAIDs are also likely to have
minimal effects.
ANTI-THYROID DRUGS
Diagnosis
Classical signs
History of drug therapy.
● Epistaxis, oral hemorrhages.
● Prolonged bleeding following procedures. If a cat receiving one of these drugs has abnormal
bleeding, another cause of the bleeding should be ruled
out.
Clinical signs
Spontaneous bleeding (e.g. epistaxis, oral hemor- MISCELLANEOUS DRUGS
rhages, melena) and excessive bleeding (e.g. following
venepuncture or surgery) due to anti-thyroid drugs Classical signs
(propylthiouracil, methimazole, carbimazole) is usually
due to thrombocytopenia caused by peripheral
destruction or megakaryocytic hypoplasia.
Methimazole and carbimazole may interfere with acti-
Clinical signs
vation of the vitamin K-dependent clotting factors II,
VII, IX and X. This effect in cats is minimal – PIVKA Numerous drugs inhibit platelet aggregation in various
time may be increased, but an increase in PT is unlikely. species in vitro. These include:
● Anesthetic and sedative agents: acepromazine,
diazepam, ketamine, propofol and halothane, but
Diagnosis
not barbiturates or isoflurane. Acepromazine and
Increased PIVKA time compared to baseline in a hyper- propofol do not inhibit platelet function in normal
thyroid cat being treated with an anti-thyroid drug. dogs.
● Anti-histamines: H1 and H2 blockers. H2 blockers ● Disturbances of platelet aggregation in vitro may

are frequently given to thrombocytopenic animals not have any clinical relevance in vivo.
with gastrointestinal hemorrhage because ulcera-
tion cannot be ruled out. Famotidine has less of an
Diagnosis
effect on platelets than either cimetidine or raniti-
dine. Sulcralfate will provide local gastrointestinal History of drug therapy.
protection without any effect on platelets.
If a cat receiving one of these drugs has abnormal
● The effect of these drugs on platelet function in cats
bleeding, another cause of the bleeding should be ruled
is not known, but they are unlikely to have any clin-
out.
ically relevant hemostatic effects.
RECOMMENDED READING
Bay JD, Scott MA, Hans JE. Reference values for activated coagulation time in cats. Am J Vet Res 2000; 63:
750–753.
Day M, Mackin A, Littlewood J (eds). Manual of Canine and Feline Haematology and Transfusion Medicine.
Quedgeley, Gloucester, British Small Animal Veterinary Association, 2000.
Evans RJ. The blood and haemopoietic system. In: Chandler EA, Gaskell CJ, Gaskell RM (eds) Feline Medicine and
Therapeutics, 2nd edn. Oxford, Blackwell Scientific Publications, 1994, pp. 192–226.
Jordan HL, Grindem CB, Breitschwert EB. Thrombocytopenia in cats: A retrospective study of 41 cases. J Vet Intern
Med 1993; 7: 261–265.
Kohn B, Weigart C, Giger U. Haemorrhage in seven cats with suspected anti-coagulant rodenticide intoxication.
J Feline Med Surg 2003; 5: 295–304.
Lisciandro SC, Hohenhaus A, Brooks M. Coagulation abnormalities in 22 cats with naturally occurring liver disease.
J Vet Intern Med 1998; 12: 71–75.
Peterson JL, Couto CG, Wellman ML. Hemostatic disorders in cats: A retrospective study and review of the litera-
ture. J Vet Intern Med 1995; 9: 298–303.
Tasker S, Cripps PJ, Mackin AJ. Evaluation of methods of platelet counting in the cat. J Small Anim Pract 2001; 42:
326–332.
Thomas JS, Green RA. Clotting times and antithrombin III activity in cats with naturally developing diseases: 85
cases (1984–1994). J Am Vet Med Assoc 1998; 213: 1290–1295.
PART 8
Cat with abnormal laboratory data
24 The anemic cat

Michael R. Lappin
KEY SIGNS
● Weakness, depression, lethargy.
● Increased heart and respiratory rates.
● ± Splenomegaly.
● ± Melena or hematochezia.
MECHANISM?
● Blood loss or red blood cell destruction (hemolysis) produces a regenerative anemia.
Failure of the bone marrow to produce adequate red blood cells produces a non-regenerative
anemia.
WHERE?
● Hemolytic anemia is intravascular or extravascular (liver, spleen), whereas blood loss anemia
can be into body spaces (abdomen, thorax) or out of the body (usually GIT).
● Non-regenerative anemia indicates a bone marrow problem.
WHAT?
● Hemoplasmosis (previously Hemobartonella felis) are the most common cause of regenera-
tive anemia.
● Non-regenerative anemia is most commonly the result of chronic disease, especially infec-
tious disease.
526
24 – THE ANEMIC CAT 527

Diseases causing an anemic cat
REGENERATIVE ANEMIA (> 60 000 RETICULOCYTES/ML) – HEMOLYSIS
ANOMALY
● Hereditary hemolytic anemia (pyruvate kinase deficiency, osmotic fragility, porphyria)
Rarely, diseases like pyruvate kinase deficiency in Abyssinian cats result in hemolysis. Hereditary
hemolytic anemias usually result in mild, intermittent regenerative anemia and weight loss.
Porphyria produces severe macrocytic, hypochromic anemia and brown discoloration of the teeth.
METABOLIC
● Hypophosphatemia* (p 534)
Extreme hypophosphatemia during treatment of ketoacidotic diabetic cats can result in increased
red blood cell fragility. Onset of anemia, muscle weakness or ataxia after intensive treatment of a
diabetic cat is suspicious.
● Microangiopathic hemolytic anemia* (p 534)
Red blood cells can be damaged when passing through abnormal vessels resulting in schistocytes.
Disseminated intravascular coagulation (fibrin strands), dirofilariasis, and splenic tumors or
hematomas can damage red blood cells. Lethargy, anorexia and depression may be present in addi-
tion to the signs of the underlying disease. Schistocytes are evident on thin blood smears but are
hard to detect in cats.
INFECTIOUS
● Hemoplasmosis*** (p 530)
In most parts of the world, the most common causes of hemolytic anemia are infectious, especially
from Mycoplasma haemofelis, and Candidatus M. haemominutum infection. Typically cats present
with pale mucous membranes, anorexia, mild to marked depression and sometimes fever.
● Cytauxzoonosis
Typically cats present with pale mucous membranes, anorexia, depression and fever. Dyspnea,
collapse and death occur commonly.
IMMUNE
● Immune-mediated hemolytic anemia** (p 532)
Primary immune-mediated hemolytic anemia in cats is unusual when compared to dogs but sec-
ondary immune-mediated red cell destruction can occur secondary to drugs, vaccines and infec-
tious agents. Anemia is usually regenerative but may be non-regenerative. Depression, and variable
fever, splenomegaly and icterus occur. Agglutination or a positive Coomb’s test are indicative of
an immune-mediated process.
TOXINS
● Drugs and toxins** (p 533)
Some drugs like acetaminophen and benzocaines and other toxins result in Heinz body anemia in
cats which is usually regenerative. Other drugs and toxins induce non-regenerative anemia (see
below). Lethargy, anorexia, weakness, pale mucous membranes and elevated heart and respiratory
rates are often present.
continued
528 PART 8 CAT WITH ABNORMAL LABORATORY DATA
continued
BLOOD LOSS
● Local diseases of blood vessels** (p 536)
Blood loss anemia can occur when blood vessels are damaged by trauma, erosive diseases like
tumors or fungal infections, and vasculitis-like systemic lupus erythrematosus. Signs include ane-
mia, and evidence of internal or external bleeding such as melena, hematochezia, hematuria, dysp-
nea, hemothorax or hemoabdomen.
● Platelet abnormalities (primary hemostatic defects)** (p 537)
Diseases of platelets including those resulting in thrombocytopenia or those resulting in decreased
platelet function. Anemia together with petechiae and ecchymoses at more than one site are typical
signs. Hemorrhage may involve the fundus of the eye, mucous membranes of the mouth, vulva,
and penis, and skin including ears.
● Factor abnormalities (secondary hemostatic defects)** (p 538)
Decreased amounts or function of coagulation factors. Typically there is anemia together with evi-
dence of hemorrhage at more than one site involving fundus of the eye, mucous membranes of the
mouth, vulva, and penis, and skin including ears. Dyspnea, coughing, hemothorax or hemo-
abdomen may also be evident.
● Hypertension* (p 539)
Systemic arterial hypertension rarely results in significant blood loss and anemia, except if epis-
taxis is involved. Retinal hemorrhage and epistaxis are most common sites of visible hemorrhage.
NON-REGENERATIVE ANEMIA (< 60 000 RETICULOCYTES/mL)
DEGENERATIVE
● Renal failure** (p 540)
Anemia occurs in many cats with chronic renal failure, but presenting complaints are usually those
of renal disease not anemia. Polyuria, polydipsia, inappetance and weight loss are typical.
METABOLIC
● Hypoadrenocorticism
While rare in cats, hypoadrenocorticism does occur and results in anemia. Depression, lethargy,
vomiting, diarrhea, anorexia and weakness occur.
● Hypothyroidism
Rarely, anemia may result from hypothyroidism following treatment of hyperthyroidism. Lethargy,
weight gain, seborrhea and delayed hair regrowth are typical.
● Iron deficiency
While rare in cats, chronic blood loss can result in microcytic anemia. Lethargy, anorexia, weight
loss and signs of chronic gastrointestinal disease resulting in chronic blood loss may be present.
Severe flea infestation in young kittens may result in anemia.
● Folic acid antagonism/deficiency
Chronic administration of pyrimethamine or sulfa drugs can result in macrocytic anemia. Dietary
insufficiency (tuna diet), malabsorption, and congenital defects may also cause folic acid defi-
ciency.
● Anemia of chronic disease*** (p 539)

Diseases associated with chronic inflammation, usually infectious or neoplastic, can result in ane-
mia of chronic disease. Chronic anorexia, lethargy and weight loss, with or without fever, are typi-
cally present.
NEOPLASTIC
●Myelophthitic diseases* (p 546)
Neoplasms of the bone marrow can crowd out red blood cell precursors. Lethargy, anorexia,
weight loss and pale mucous membranes are often present.
INFECTIOUS
● Feline leukemia virus** (p 540)
Lethargy, anorexia and weight loss are typical. Anemia may be a main presenting sign. Signs may
be referable to secondary infections or neoplasia.
● Feline infectious peritonitis (FIP), feline immunodeficiency virus (FIV)** (p 545)
Other classic viral diseases associated with non-regenerative anemia in cats include feline infec-
tious peritonitis and feline immunodeficiency virus. Lethargy, anorexia, weight loss and fever are
typical. Signs are referable to secondary infections (FIV) or effusion into body cavities and pyo-
granulomatous inflammation of the liver, kidney, eye or CNS (FIP).
● Ehrlichiosis and anaplasmosis
Uncommon diseases in cats compared to dogs. Lethargy, anorexia, depression and fever are the
most common signs. Other signs reported include hyperesthesia, lameness or joint pain, pale
mucous membranes, splenomegaly, dyspnea, diarrhea and uveitis.
IMMUNE
● Immune-mediated (pure red cell aplasia)
Immune-mediated reactions can be directed at precusor cells resulting in non-regenerative anemia.
Lethargy, anorexia, weight loss and pale mucous membranes are often present. Heart and respira-
tory rates may be elevated once anemia is severe.
TOXINS
● Drugs/toxins* (p 546)
Usually a history of exposure to substances like chloramphenicol, which damage the bone marrow.
Typically there is lethargy, anorexia and depression together with a history of administration of
drugs known to cause bone marrow damage. Vomiting and diarrhea may be evident.
INTRODUCTION
● Regenerative anemia is characterized by reticulo-
MECHANISM? cyte counts greater than 60 000/μl; non-regenera-
tive anemia has less than 60 000/μl.
Anemia is defined as a packed cell volume of less than ● By definition, it takes from 3–5 days after acute
27%. development of anemia to have maximal reticulo-
cytosis, and so acute anemia may initially appear as
Anemia is either regenerative or non-regenerative.
non-regenerative.
● If the anemia has been present for 3–5 days and the trauma, tumors or fungal infection, coagulopathies and
reticulocyte count is < 60 000 the anemia is non- thrombocytopenia.
regenerative.
Non-regenerative anemia is most commonly the result
The two primary differential diagnoses for regenera- of chronic disease (infectious, neoplastic or renal fail-
tive anemia are hemolysis (destruction of red blood ure). Infectious diseases include feline leukemia virus,
cells) and blood loss. feline infectious peritonitis, feline immunodeficiency
virus and ehrlichiosis.
Loss can occur out of the body through wounds, the
gastrointestinal tract, or the nose. Bleeding into body
cavities and parenchymal organs also occurs. DISEASES CAUSING ANEMIA:
● If the blood loss is out of the body, total protein REGENERATIVE ANEMIA DUE TO
concentrations are usually decreased, whereas HEMOLYSIS
blood loss into a body cavity and hemolytic anemias
usually has normal total protein concentrations.
HEMOPLASMOSIS***
Blood loss can result from local diseases of vessels like
trauma or erosion of the vessel due to diseases like Classical signs
neoplasia. Vasculitis, hypertension, factor abnormal-
● Previous history or presence of fleas.
ities and platelet abnormalities also can result in blood
loss anemia.
● +/- splenomegaly or icterus.
There are multiple mechanisms for hemolytic ● Lethargy, anorexia, depression.
anemia including infectious diseases, primary ● +/- fever.
immune-mediated diseases, microangiopathic dis-
eases, toxins, congenital diseases and metabolic
Transmission
diseases.
Mycoplasma haemofelis and Candidatus M. haemo-
Non-regenerative anemias generally imply bone
minutum and the causes of feline infectious anemia
marrow dysfunction, which can be caused by many
(previously hemobartonellosis).
things including infectious diseases, toxicities, neopla-
sia, chronic inflammation and metabolic diseases. Experimentally the organisms can be transmitted by
intramuscular, intraperitoneal or intravenous adminis-
tration of infected blood and transplacentally.
WHERE?
Transmission by the cat flea Ctenocephalides felis has
Hemolytic anemia is intravascular or extravascular, but
been shown for M. haemofelis, but not Candidatus
is usually extravascular (liver, spleen) in cats.
Mycoplasma haemomintum.
Blood loss in regenerative anemia can be into body
Cats with hemobartonellosis may have a history of
spaces (abdomen, thorax) or out of the body (usually
fighting.
GIT) as a result of local vascular damage, or systemic
coagulation or platelet problems.
Pathogenesis
Non-regenerative anemia indicates a bone marrow
problem. The organisms are epicellular parasites of red blood
cells (RBC).
WHAT? M. haemofelis (previously known as the large form) is
most pathogenic.
Hemotropic mycoplasmas (previously hemobar-
tonellosis) are the most common causes of regenerative Anemia is from immune-mediated reactions that are
anemia. Less common causes are immune-mediated, organism specific or directed at RBC membrane pro-
drug- or toxin-associated, vascular damage from teins that have been modified by the parasitism.
Antibody-coated red blood cells are removed by the tive cats suggesting it is more sensitive. Some healthy
reticuloendothelial system, and intravascular lysis is cats are PCR positive and so the predictive value for
unusual; Coomb’s positive test results are common. presence of disease is not 100%.
Level of parasitemia fluctuates rapidly making diagno- Macroscopic or microscopic agglutination, spherocyto-
sis difficult based on cytology. sis, or Coomb’s positive test results are suggestive.
The acute phase of disease usually develops within
3 weeks; spontaneous recovery followed by recurrence Differential diagnosis
from the chronic carrier state can occur.
Any infectious, immune-mediated, or neoplastic cause
Anemia associated with Candidatus Myco- of hemolytic anemia can look similar as a result of
plasma haemomintum is often detected in cats with signs associated with fever and anemia. Demonstration
current feline leukemia virus infection. of the organism by cytological assessment or PCR dif-
ferentiates mycoplasma-associated hemolytic anemia
In locations where feline leukemia virus is common,
from other causes.
approximately 50% of infected cats are co-infected
with the virus; co-infection with feline immunodefi-
ciency virus is rare. Treatment
Doxycycline at 10 mg/kg, PO, q 24 hours for the first
Clinical signs week and then continued q 24 hours for 2 weeks. If the
Infection is most common in male cats less than 3 cat will tolerate treatment, a total of 4 weeks of treat-
years of age, and occurs most often in the spring. ment may result in more cats becoming PCR negative.
Cats are usually presented for depression, lethargy While tetracycline at 22 mg/kg, PO q 8 hours can be
and anorexia. effective it is no longer recommended since doxy-
cycline is superior.
Pale mucous membranes are a common physical exami-
nation abnormality. Fever and icterus are also common. Enrofloxacin at 5–10 mg/kg, PO, q 12–24 hours for
2–3 weeks may be effective in cats that are intolerant of
Splenomegaly occurs in some from extramedullary tetracyclines. Doses over 5.5 mg/kg may be associated
hematopoiesis and immune stimulation. with retinal toxicity and blindness in a small percentage
Fleas or flea dirt may or may not be noted. of cats.
Chronic infection may lead to recurrent hemolytic For cats that do not tolerate or are resistant to tetracyclines
anemia or intermittent fever, depression and anorexia and enrofloxacin, imidocarb diproprionate at 5 mg/kg,
without hemolytic anemia. IM or SQ, q 2 weeks, for 2–4 injections can be used.
Chloramphenicol at 15 mg/kg, PO, q 12 hours for 3
Diagnosis weeks has been used but not studied experimentally;
this drug also has been associated with bone marrow
Diagnosis is based on cytological demonstration of
suppression.
the organism on the surface of RBC. However, the
organism may be difficult to find even though clinical Prednisolone at 1–2 mg/kg, PO, q 12 hours should be
signs are present, and at least 50% of cats are falsely used for at least the first week of therapy because of the
negative on cytological examination. immune-mediated pathogenesis.
The organism may dislodge from the surface of RBCs Treatment lessens clinical signs of disease but does not
placed in EDTA in cytologically negative suspect cats. resolve infection in many cats.
In suspect cats, repeat cytological assessment using
While there is no PCV that alone indicates when to
smears made from blood without anti-coagulants.
transfuse, whole blood transfusions are generally indi-
Polymerase chain reaction (PCR) is available com- cated if the PCV is dropping rapidly and heart and res-
mercially. PCR is positive in some cytologically nega- piration rates are elevated at rest.
Blood typing should be performed if possible in breeds RBC can be lysed in the bloodstream (intravascular) or
prone to the B type (British short hair, Devon Rex, removed by the reticuloendothelial system (extravascu-
Cornish Rex, Japanese bobtail, Scottish fold, Sphinx, lar), with the latter being most common.
Somoli).
Large concentrations of anti-RBC antibodies result in
Cross-match results may be hard to interpret due to cross-linking and macroscopic or microscopic aggluti-
spontaneous agglutination. nation.
Since M. haemofelis is the most common cause of Spherocytes are formed when fixed reticuloendothelial
hemolytic anemia in cats, treatment should be con- cells remove part of the antibody or complement-
sidered for all suspect cats, even if the organism can- coated RBC membrane.
not be found.
The immune reaction can be directed at RBC precur-
sors resulting in non-regenerative anemia.
Prognosis
Most treated cats survive. The prognosis is worse for
those with concurrent immunodeficiency-inducing dis- Clinical signs
eases. Depression, lethargy and anorexia are common pre-
Because treated cats are usually not cured, exacerba- senting complaints.
tions are common. History of recent vaccination (within 1 month) or
antibiotic administration may be present.
Prevention History of fleas is common in cats with hemotropic
Flea control and housing cats indoors lessen potential mycoplasmosis.
for exposure. Fading kitten syndrome occurs in kittens with a history
Cats used as blood donors should be tested for both of a type B queen mated to a type A tom (neonatal iso-
Mycoplasma haemofelis and Candidatus Myco- erythrolysis; see page 1134).
plasma haemomintum using PCR techniques. Donor Pale mucous membranes, tachycardia and tachypnea
cats exposed to fleas should be regularly retested. are common.
Splenomegaly and lymphadenopathy occur in some
IMMUNE-MEDIATED HEMOLYTIC cats.
ANEMIA**
Icterus is dependent on rapidity of anemia develop-
Classical signs ment. White blood cells are activated commonly result-
ing in fever.
● Lethargy, anorexia, depression, +/- fever.
● +/- splenomegaly or icterus.
Diagnosis
Presence of spherocytes is classic but difficult to
document in cats compared to dogs since normal RBC
Pathogenesis
of cats is relatively small, and they do not have central
Primary immune-mediated hemolytic anemia pallor.
(IMHA) is rare and the cause unknown.
Macroscopic or microscopic agglutination. If agglu-
Secondary IMHA occurs from hypersensitivity reac- tinating cells are noted, mix 1 drop of blood in EDTA
tions against drugs (like beta-lactam antibiotics), mod- with 1 drop 0.9% NaCl and repeat the thin blood smear.
ified-live vaccines, neoplasms, and infectious agents If cells are no longer clumped, massive roulette forma-
like M. haemofelis and feline leukemia virus. tion was occurring and not agglutination.
Direct Coomb’s testing can be used in cases without Chlorambucil at 0.2 mg/kg, PO, q 24 hours may be
spherocytes or autoagglutination to confirm presence of needed in some cats with glucocorticoid-induced side
IgG, IgM or complement on the surface of RBC. EDTA effects or incomplete control, and should be used in
blood is submitted to the laboratory for reaction with place of cyclophosphamide for long-term management.
Coomb’s reagent (anti-IgG, anti-IgM, anti-complement).
Azathiaprine at 0.3 mg/kg, PO, q 72 hours may be
Optimally, the laboratory should provide a titer, not the
needed in some cats with glucocorticoid-induced side
result of a single dilution. Feline-specific Coomb’s
effects or incomplete control, but extreme bone marrow
reagent must be used.
suppression can occur and chlorambucil is preferred.
Antinuclear antibody testing can be performed. Some
Whole blood transfusion may be indicated if the PCV
cats with systemic lupus erythematosus will be positive
is dropping rapidly, the cat is depressed, and if heart
and have primary immune-mediated hemolytic anemia.
and respiration rates are elevated at rest.
Erythrophagocytosis can be noted on bone marrow
examination; maturation arrest of RBC development
Prognosis
may be detected if immune response is directed at pre-
cursor cells. Prognosis with primary IMHA is unknown since it is
rare.
Differential diagnosis Theoretically, secondary IMHA should have a good
Any infectious or neoplastic cause of hemolytic or prognosis since the initiating antigen (M. haemofelis,
blood loss anemia can look similar because the signs of vaccines, antibiotics) can be removed.
fever and anemia are not specific, and immune destruc-
tion of RBC may be partly involved in the pathogene- Prevention
sis of the anemia. Diagnosis is often based on exclusion
of infectious and neoplastic causes, and demonstration Avoid over-stimulating cat immune systems with
of agglutination or a positive Coomb’s test. antibiotics and vaccines.
Cats with primary or secondary IMHA should be
Treatment housed indoors and no longer vaccinated.
Dexamethasone at 1 mg/kg, IV, once on day 1. Lessen exposure to fleas to potentially avoid infection
by M. haemofelis.
Prednisolone at 2–4 mg/kg, PO, q 12 hours initially
followed by decreasing doses every other week pro-
vided anemia is resolving. If maintenance treatment is
DRUGS/TOXINS**
required, the target dose is approximately 0.5 mg/kg,
PO, q 48 h.
Classical signs
Doxycycline at 5–10 mg/kg, PO, q 12 hours for at least
● Lethargy, anorexia, depression.
14 days in all cats with hemolytic anemia due to possi-
● Pale mucous membranes and elevated
ble hemobartonellosis.
heart and respiratory rate.
Dexamethasone administered at 0.1–0.2 mg/kg, PO, q ● History of exposure to oxidative toxin.
12 hours in cats resistant to prednisolone.
Cyclosporine at 1–5 mg/kg, PO, q 12–24 hours, for
Pathogenesis
7–14 days is indicated for acute treatment of cats that
are autoagglutinating or undergoing intravascular Oxidation of the globin in hemoglobin leads to for-
hemolysis. mation of Heinz bodies (precipitated hemoglobin).
Cyclophosphamide at 6.25–12 mg/cat, PO, 4 days Anemia results from cell lysis or framentation in cap-
weekly for 1–2 weeks has been used in some cats illaries because of fragility, or removal by the fixed
acutely but is not currently used by the author. reticuloendothelial system of the spleen and liver.

Lethargy, anorexia, weakness, pale mucous membranes Administer potassium phosphates at 0.03–0.12
and elevated heart and respiratory rates occur. mmol/kg/h until normophosphatemic.
History of exposure to oxidative toxins like acetamin- Alternately, prevent hypophosphatemia (and hypo-
ophen (iatrogenic), onions (foodstuffs like babyfood), kalemia) by giving calculated potassium require-
zinc (United States pennies, airline carrier hardware), ments as 30% potassium chloride and 50% potassium
propothiouracil (iatrogenic), methylene blue (iatro- dihydrophosphate.
genic), phenazopyridine (iatrogenic), vitamin K1 (iatro-
Phosphate concentrations are usually maintained
genic), propylene glycol (food stuffs; carrier in some
within normal concentrations by diet alone after reso-
medications), and benzocaine derivatives (iatrogenic).
lution of the ketoacidotic crisis.
Diagnosis MICROANGIOPATHIC HEMOLYTIC ANEMIA*

Heinz bodies (intracytoplasmic irregular retractile
Classical signs
granules) are seen cytologically on thin blood smears.
● Lethargy, anorexia, depression.
Methemoglobin levels can be elevated; blood has a
● Clinical signs of the primary disease.
brown color.

Remove the source of the oxidant injury. Diseases that involve small vessels like disseminated
intravascular coagulation (fibrin strands), dirofilari-
N-acetylcysteine at 140 mg/kg, PO, once followed by
asis, and splenic tumors or hematomas damage RBC
70 mg/kg, PO every 4–6 hours if severe methemoglo-
resulting in formation of schistocytes or fragments.
binemia is present.
History, physical examination, and laboratory assess-
Supportive care including whole blood transfusion if
ment support the primary disease.
needed.
Lethargy, depression, weakness and pale mucous mem-
branes may result if anemia is severe.
HYPOPHOSPHATEMIA*

● Anemia, muscle weakness in diabetic cat. Schistocytes are seen cytologically on thin blood
● Ataxia, seizures. smears.
Diagnostic work-up for the suspected primary cause
Clinical signs should be performed.
Extreme hypophosphatemia may occur during initial
treatment of ketoacidotic diabetes mellitus, and CYTAUXZOONOSIS
result in muscle weakness, ataxia, seizures and pale
mucous membranes. Classical signs
Liver disease may result in red blood cell fragility. ● Fever, depression, shock and death.
● Indoor/outdoor cats in the Gulf Coast
Diagnosis states.
● History of tick exposure.
Measurement of serum phosphorus concentrations.
Transmission The organism can be detected in infected macrophages

in bone marrow, spleen, liver, or lymph node aspirates
Bobcats are subclinically infected by Cytauxzoon felis stained with Wright’s or Giemsa stains.
and so are probably the natural host.
Serologic testing can be used to confirm exposure, but
Transmission occurs from infected bobcats to domestic is usually not needed clinically
cats by Dermacentor variabilis.
PCR assay has been studied experimentally and may
be available in the future.
Pathogenesis
Transmission of the organism results in clinical illness Differential diagnosis
in 5–20 days.
Any infectious, immune-mediated, or neoplastic cause
Schizonts and macroschizonts form in mononuclear of hemolytic anemia can look similar due to the signs
phagocytes, line the lumen of veins, and obstruct associated with fever and anemia. Identification of the
blood flow through tissues (tissue phase). organism is diagnostic.
Merozoites released from infected macrophages infect
erythrocytes causing hemolytic anemia (erythrocyte Treatment
phase). Fluid therapy and blood transfusion should be admin-
istered as indicated (see hemobartonellosis).
Clinical signs Imidocarb administered at 5.0 mg/kg, IM, every 14
Most infected cats are presented for depression. days for two doses or diminazene at 2.0 mg/kg, IM,
every 7 days for two doses are the drugs of choice but
Physical examination usually reveals fever, anorexia, no treatment is known to be effective.
dyspnea, depression, collapse, icterus, and pale
mucous membranes. Parvaquone, buparvaquone, thiacetarsamide and tetra-
cycline therapy have also been attempted.
Hypothermia develops in some cats preceeding death.
Death is a common sequel, but strains of C. felis that Zoonotic potential and prevention
spontaneously resolve have now been recognized.
Cytauxzoon felis is not known to infect people.
Most cases of cytauxzoonosis are in outdoor cats, but
ticks are generally not identified Tick control should be maintained, and cats in endemic
areas should be housed indoors.
The course of disease is generally 1 week or less in
cats infected with pathogenic strains.
HEREDITARY HEMOLYTIC ANEMIA
Cats infected with non-pathogenic strains may live for (PYRUVATE KINASE DEFICIENCY,
years. OSMOTIC FRAGILITY, PORPHYRIA)
Diagnosis Classical signs
Regenerative anemia, neutrophilic leukocytosis or

leukopenia, thrombocytopenia or thrombocytosis,
hemoglobinemia, hemoglobinuria, bilirubinemia and
● Young Abyssinian, Somalis, Siamese or
bilirubinuria are the most common laboratory abnor- DSH cat.
malities, but vary between patients.
Antemortem diagnosis is based on demonstrating the Clinical signs
ring-shaped erythrocytic phase on thin blood Congenital diseases resulting in hemolysis are rare in
smears which occurs in most cats with acute illness. cats.
Pyruvate kinase deficiency has been described in Classical signs—Cont’d

Abyssinian cats, Somalis and DSH with intermittent,
regenerative anemias. ● Evidence of trauma, neoplasia,
inflammatory or erosive disease.
Increased osmotic fragility of erythrocytes causing ● Melena, hematochezia, hematuria,
hemolytic crises with macrocytic regenerative anemia dyspnea, hemothorax or hemoabdomen.
and splenomegaly has also been documented in
Abyssinians and Somalis.
Cats with hereditary hemolytic anemias exhibit inter- Pathogenesis
mittent anemia and weight loss, and the clinical signs
Blood vessels are damaged by trauma (blunt trauma,
appear to be ameliorated by splenectomy.
foreign bodies, etc.), erosive diseases resulting from
Porphyria in a family of Siamese cats was associated tumors, chronic infections (fungal in particular), toxi-
with severe macrocytic, hypochromic anemia with cities (mainly gastrointestinal), or vasculitis like sys-
poikilocytosis, Howell–Jolly bodies, and nucleated red temic lupus erythematosus.
blood cells.
Porphyria in domestic shorthair cats is inherited as Clinical signs
an autosomal dominant trait, and is characterized by
Weakness and lethargy are common presenting com-
only a mild anemia.
plaints.
Porphyrins produce a brownish discoloration of teeth,
Blood usually is lost into tissues, spaces like the pleu-
bones (at necropsy), and urine, all of which fluoresce
ral space and peritoneal cavity, the gastrointestinal
bright pink-red with ultraviolet light.
tract (including palate of the cat), or any external dam-
aged tissue like the nose.
Diagnosis Bleeding may or may not be evident, depending on
where the blood is lost.
Measure pyruvate kinase activities.
Melena or hematochezia may be present in cases with
Measure blood porphyria concentrations. Demonstrate
gastrointestinal blood loss; exceptions include small
fluorescence of porphyrins in teeth or urine.
volume, chronic bleeding and acute loss.
Acute dyspnea or weakness associated with pale
Treatment mucous membranes and evidence of hemothorax or
hemoabdomen on centesis are typical findings.
Supportive care including transfusion if indicated.
In contrast to blood loss from coagulopathies or hyper-
Splenectomy for anemias caused by pyruvate kinase
tension, local diseases usually do not result in evidence
deficiency and increased osmotic fragility.
of bleeding at distant sites. The exception is vasculitis.
Fungal and neoplastic diseases of the nose that result in
REGENERATIVE ANEMIA DUE TO epistaxis usually have mucopurulent discharge prior to
BLOOD LOSS development of epistaxis.
Other clinical signs are associated with the primary dis-
LOCAL DISEASES OF BLOOD VESSELS** ease.
Classical signs
Diagnosis
● Anemia.
Diagnostic work-up and findings are dependent on the
● Bleeding internally or externally.
individual primary disease and site of bleeding.
Most bleeding disorders will have evidence of

PLATELET ABNORMALITIES (PRIMARY
hemorrhage in more than one site. The fundus of
HEMOSTATIC DEFECTS)**
the eye, mucous membranes of the mouth, vulva,
and penis, and the skin especially ear and ventral
Classical signs
abdomen are good places to evaluate for evidence of
● Anemia. hemorrhage.
● Petechiae and ecchymoses at more than
one site.
● Hemorrhage involving fundus of the eye,
Diagnosis
mucous membranes of the mouth, vulva,
and penis, and skin including ears. Platelet count should be made; spontaneous hemor-
rhage generally occurs with platelet counts of
< 50 000 platelets/μl.
Pathogenesis
Platelet estimates can be made; under oil immersion
Platelet diseases can be divided into those inducing
(1000×), every one platelet per field equates to
thrombocytopenia and those inducing platelet dys-
approximately 20 000 platelets/μl.
function.
When thrombocytopenia is suspected, scan the blood
The differential categories for thrombocytopenia
smear evaluating for clumps which may falsely lower
include consumption, destruction, decreased produc-
the count.
tion and sequestration.
If giant platelets are present, decreased production of
The most common causes of platelet consumption are
platelets is unlikely.
disseminated intravascular coagulation and con-
sumption at sites of inflammation. If persistent thrombocytopenia is present, a bone mar-
row examination is indicated to evaluate for myeloph-
The most common cause of platelet destruction is
thitic disease and latent feline leukemia virus
immune-mediated which can be either primary or sec-
infection (IFA or PCR; see FeLV section).
ondary to drugs and vaccines.
Platelet function deficits in cats are rare, however von
Platelets are produced by the bone marrow and so any
Willebrand’s disease does occur.
bone marrow disease can potentially result in thrombo-
cytopenia. Neoplasia and feline leukemia virus are Bleeding time assesses platelet function and should be
common examples. less than 5 minutes.
Sequestration of platelets usually occurs in the spleen Bleeding time should only be performed in cats with
or liver but is not a primary disease. normal platelet counts and factor tests (ACT, etc.).
Platelet function abnormalities can be iatrogenic
(aspirin), congential (rare in cats), or acquired
(hyperglobulinemia). Treatment
Treatment varies with the primary disease (see
appropriate section) but frequently includes administra-
Clinical signs
tion of fresh whole blood transfusion if life-threaten-
Diseases of platelets usually result in petechiae and ing hemorrhage is occurring.
ecchymoses.
Fresh plasma can be used if red blood cells are not
Ingestion of aspirin may be known. needed.
Clinical signs are usually consistent with where the pri- For suspected secondary immune-mediated thrombo-
mary bleeding is occurring and the primary disease cytopenia, remove the potential source if possible
resulting in hemorrhage. (antibiotic or vaccine).
Primary immune-mediated thrombocytopenia is rare in The fundus of the eye and mucous membranes of the
cats, but treatment is as discussed for hemolytic anemia mouth, vulva and penis are good places to evaluate for
(see appropriate section). evidence of hemorrhage.
Clinical signs are usually consistent with where the pri-
FACTOR ABNORMALITIES (SECONDARY mary bleeding is occurring and the primary disease
HEMOSTATIC DEFECTS)** resulting in hemorrhage.
Ingestion of vitamin K antagonistic rodenticides may
Classical signs
be known.
● Anemia.
Cats with hepatic insufficiency usually have other
● Evidence of hemorrhage at more than one
clinical signs like weight loss, anorexia, polyuria/poly-
site involving fundus of the eye, mucous
dipsia.
membranes of the mouth, vulva, and penis,
and skin including ears. Cats with cholestasis commonly have other clinical
● Dyspnea, coughing, hemothorax or findings like weight loss, anorexia and icterus.
hemoabdomen.
DIC is a syndrome induced by other diseases; clinical
findings are consistent with the primary disease.
Pathogenesis If severe enough to cause spontaneous hemorrhage,
hemophilia usually presents in younger cats.
Factor abnormalities can be divided into decreased
amounts (liver disease, DIC, hemophilia, cholestasis,
warfarin toxicity) or decreased function of coagula- Diagnosis
tion factors (circulating anti-coagulants like heparin).
Activated clotting time (ACT; normal < 65 seconds)
Hepatic insufficiency leads to decreased production can be used in clinical settings to assess the intrinsic
of procoagulants. and common coagulation pathways. Factor VII is the
only factor deficiency not screened by the activated
Hepatic cholestasis results in absence of vitamin K
clotting time (extrinsic pathway), but factor VII
and failure to convert factors II, VII, IX and X to
hemophilia is rare and so the ACT is an excellent
active coagulants.
clinical screening test for factor deficiencies.
DIC results in factor consumption Thrombocytopenia < 50 000 platelets/μl can prolong
the ACT by up to 10–15 seconds due to lack of
Hemophilia is the congenital lack of a factor or factors.
platelet phospholipid.
Warfarin toxicity results in vitamin K antagonism and
The activated partial thromoplastin time and pro-
the resultant failure to convert factors II, VII, IX and X
thrombin time as well as specific assessment of differ-
to active coagulants.
ent factors or proteins induced by vitamin K absence
Increased amounts of circulating anticoagulants are or antagonism are performed on citrated plasma; sam-
most common with mast cell tumors (heparin) or ples should be collected and stored prior to starting
DIC (fibrinogen degradation products). treatment.

Most bleeding disorders will have evidence of hemor- Treatment varies with the disease, but frequently
rhage in more than one site. includes administration of fresh whole blood transfu-
sion if life-threatening hemorrhage is occurring.
Decreased amounts or function of coagulation factors
usually results in bleeding into body cavities like the Frozen plasma can be used to supply coagulation fac-
chest and peritoneal cavity. tors if red blood cells or platelets are not needed.
If vitamin K antagonists are the cause of the hemor- ● Some normal cats will appear hypertensive due to
rhage, vitamin K1 should be given subcutaneously at epinephrine release from the stress of measuring the
1–5 mg/kg, q 12 hour for 24 hours. Dose is depend- blood pressure.
ent on the type of anti-coagulant ingested. Warfarin can
Renal and endocrine causes of hypertension should be
be treated with 1–3 mg/kg and long-acting products
excluded by bloodwork and urinalysis.
should be treated with 3–5 mg/kg. Oral administration
of vitamin K1 is initiated on day 2 at 1–5 mg/kg, q 12
Treatment
hours for 2 weeks (warfarin) to 6 weeks (long-acting
anti-coagulant) depending on the type of anti-coagulant ACE-inhibitors, calcium channel blockers, beta-blockers,
ingested. and sodium restriction are used to manage systemic
arterial hypertension in cats.
Vitamin K1 given intravenously can result in an ana-
phylactoid reaction. See appropriate sections for specific treatment recom-
mendations (page 134).
When vitamin K1 therapy is discontinued, the cat
should be returned in 72 hours for assessment of an
ACT or prothrombin time. If increased at that time, two
NON-REGENERATIVE ANEMIA
more weeks of therapy should be prescribed prior to the
(< 60 000 RETICULOCYTES/mL)
next evaluation.
HYPERTENSION*
ANEMIA OF CHRONIC DISEASE***
Classical signs
Classical signs
● Chronic lethargy, anorexia and depression.
● Sudden onset of blindness with dilated
pupils from retinal hemorrhage.
● Epistaxis.
Pathogenesis
● Evidence of diseases causing hypertension,
especially renal disease or Activation of leukocytes by the primary disease results
hyperthyroidism. in the production of cytokines like interleukin 1.
In the face of inflammatory cytokines, macrophages
Pathogenesis fail to release iron to be used for red blood cell pro-
duction.
Systemic arterial hypertension in cats is usually from
renal disease, hyperthyroidism, hyperadrenocorti- Red blood cell life span is slightly shortened.
cism and idiopathic (essential).
Response of the bone marrow to erythropoietin may be
blunted.
Clinical signs
Systemic arterial hypertension can result in hemor- Clinical signs
rhage; retinal hemorrhage and epistaxis are most
Diseases associated with chronic inflammation, usually
common.
infectious or neoplastic, can result in anemia of chronic
With the exception of epistaxis, volume of blood loss is disease.
usually small and so anemia is rare.
Clinical signs are those usually related to the primary
disease with minimal clinical findings associated with
Diagnosis the anemia.
Systolic blood pressure > 175 mmHg using a Doppler The anemia is generally mild compared to those asso-
system is abnormal. ciated with FeLV or immune-mediated diseases.
Diagnosis failure include shortened red cell survival, and the

effects of uremic toxins such as parathyroid hormone
Diagnosis is usually based on exclusion of other causes on erythropoiesis.
of non-regenerative anemia combined with documenta-
tion of a chronic neoplastic or inflammatory disease.
Diagnosis
Mild normocytic-normochromic, non-regenerative ane-
mia (PCV is generally 18–27%). Documentation of azotemia with suboptimal urine-
concentrating ability (see page 645).
Platelet counts are generally normal.
Exclude other causes of non-regenerative anemia.
Neutrophilia and monocytosis may be present due to
chronic inflammation induced by the primary disease. Mild to moderate normocytic, normochromic, non-
regenerative anemia (PCV = 15–27%).
Bone marrow cytology shows increased iron stores
in bone marrow macrophages. Neutrophil and platelet numbers are generally normal.
Any cause of non-regenerative anemia.
FeLV, myelophthtic disease, ehrlichiosis, anemia of
renal failure, hypoadrenocorticism.
Treatment
Treatment Human recombinant erythropoietin.

● 100 U/kg, SC, 3 days weekly for induction.
Remove the source of the chronic disease. ● Adjust dose and frequency to maintain PCV > 20
Whole blood transfusion if indicated. for maintenance.

● Antibodies may be generated against the human
Erythropoietin and other bone marrow stimulants are recombinant product inactivating it, which occurs
unlikely to be effective. in 20–30% of treated cats.
● Severe immune-mediated reactions rarely occur.
● Some clinicians use erythropoietin to induce remis-
RENAL FAILURE** sion of anemia and attempt to use anabolic steroids
to maintain remission.
Classical signs ● If iron deficiency is present, response to erythropoi-
● Weight loss, inappetence. etin can be blunted.

● Polyuria, polydipsia. If clinically indicated, administer a blood transfusion while
● ± Intermittent vomiting. waiting for an erythropoietin response. Indication is inap-
● Pale mucous membranes. petence, and increased heart and respiratory rates at rest.
Anabolic steroids (see page 1339).
Clinical signs
Polydipsia, polyuria, inappetence, weight loss, inter- FELINE LEUKEMIA VIRUS**
mittent vomiting, “rubber jaw”, small kidneys, and
other findings consistent with chronic renal failure (see Classical signs
page 234).
● Lethargy, anorexia, weight loss; usually in
The non-regenerative anemia is generally mild to cats < 6 years.
moderate (PCV ≥ 18) from erythropoietin lack, ● +/- clinical findings consistent with
unless accompanied by blood loss anemia from gas- lymphoma; masses, etc.
trointestinal hemorrhage or hemolysis from hypophos- ● +/- secondary infections of any organ system.
phatemia. Other factors contributing to anemia in renal
Pathogenesis ● Stage VI. Disseminated epithelial cell infection

Feline leukemia virus (FeLV) is a single-stranded with virus secretion in saliva and tears; 4–6 weeks
RNA virus that produces reverse transcriptase enzyme. PI; IFA positive; ELISA positive.
The envelope protein p15e is associated with the devel- Following exposure, cats either become persistently
opment of immunosuppression. infected, develop latent or sequestered infection,
become immune carriers or have self-limiting infec-
The core protein p27 is present in the cytoplasm of
tion.
infected cells as well as in the peripheral blood, saliva
and tears of infected cats; detection of p27 is the basis Whether or not infection occurs following natural
of the immunofluorescence and ELISA tests for exposure to FeLV is determined by the virus subtype or
FeLV. strain, the virus dose, the age of the cat when exposed,
and the cat’s immune responses.
The envelope glycoprotein 70 (gp70) contains sub-
group antigens A, B or C; these subgroups are associ- Approximately 30% of the cats with self-limiting
ated with the infectivity, virulence and disease caused infection will have provirus present (latent infec-
by individual strains of the virus. tion) which can be associated with p27-negative
lymphoma and possible reactivation to persistent
All cats carry subgroup A either alone or in combina-
viremia.
tion with B or C.
Some cats with latent infection also have evidence of
Subgroup A may cause malignancy by itself, but co-
immunosuppression.
infection with B or C may have a synergistic effect on
oncogenicity. Latent infection can be activated by the administra-
tion of glucocorticoids or other immunosuppressive
Exposure to gp70 results in the production of neutraliz-
drugs or pregnancy.
ing antibodies in some cats.
Atypical or sequestered (localized) infection
Feline coronavirus-associated cell membrane anti-
occurs in up to 26% of cats exposed to FeLV; the
gen is a FeLV-induced antigen expressed on the surface
bone marrow, spleen, lymph node and small intes-
of cells with virus-induced malignant transformation.
tine are the tissues most commonly involved. It is
Antibodies formed against this antigen can be detected
unknown what percentage of these cats develops
in some cats.
clinical disease but some cats will transmit the virus
Stages of infection after oral exposure and resultant to offspring.
immunofluorescent antibody (IFA) and enzyme-linked
In experimental studies, 100% of neonatal kittens,
immunosorbent assay (ELISA) test results:
70–85% of weanling kittens, and 15–30% of cats > 4
● Stage I. Replication in local lymphoid tissues;
months old were infected when exposed; adults may
2–12 days post-inoculation (PI); IFA negative;
be more difficult to infect than kittens due to the matu-
ELISA negative.
ration of macrophage function.
● Stage II. Dissemination in circulating lympho-
cytes and monocytes; 2–12 days PI; IFA negative; Subgroup C induces aplastic anemia from tropism for
ELISA positive. macrophages resulting in increased secretion of tumor
● Stage III. Replication in the spleen, distant necrosis factor-alpha.
lymph nodes and gut associated lymphoid tissue;
Immunodeficiency syndromes are likely to occur sec-
2–12 days PI, IFA negative, ELISA positive.
ondary to T lymphocyte depletion (both CD4+ and
● Stage IV. Replication in bone marrow cells and
CD8+ lymphocytes) or dysfunction, and either neu-
intestinal epithelial crypts; 2–6 weeks PI; IFA
tropenia or neutrophil function deficits.
negative; ELISA positive.
● Stage V. Peripheral viremia, dissemination via Myeloproliferative diseases likely develop from viral
infected bone marrow derived neutrophils and induction of bone marrow growth-promoting sub-
platelets; 4–6 weeks PI; IFA positive; ELISA positive. stances.
Transmission
Icterus.
The principal route of infection is prolonged contact ● Pre-hepatic icterus is related to immune-mediated
with infected cat saliva and nasal secretions; biting is destruction of red blood cells induced by FeLV or
not required but can transmit infection. secondary infection by M. haemofelis or Candidatus
Mycoplasma haemomintum (Haemobartonella
Fomite transmission and aerosol transmission are
felis).
unlikely due to poor survival of the organism in the
● Hepatic icterus is related to hepatic lymphoma,
environment.
hepatic lipidosis and focal liver necrosis.
Transplacental infection and transmission by milk ● Post-hepatic icterus may occur due to alimenteric
occur but more kittens are probably infected when lymphoma.
licked and groomed by the infected queen.
Respiratory abnormalities.
FeLV has been detected in semen and vaginal epithe- ● Sneezing, nasal discharge, pneumonia, bronchitis
lium and so venereal transmission is possible. and pyothorax occur in some FeLV-infected cats
from immunosuppression and secondary infections.
The role of blood-sucking arthropods in the transmis-
● Dyspnea and restrictive breathing pattern with muf-
sion of FeLV is largely unknown but considered of min-
fled heart or lung sounds are common in cats with
imal importance.
thymic lymphoma; these cats are generally < 3
years of age and may have decreased cranial chest
compliance on palpation.
Clinical signs
Lymphadenopathy due to lymphoma or hyperplasia
Any age, gender or breed of cat can develop signs of of lymphoid tissues occurs in FeLV-infected cats.
FeLV infection but the majority are male and between
Neoplasia.
1–6 years of age.
● Mediastinal (thymic), multicentric and ali-
Most FeLV-infected cats are evaluated for non-specific menteric lymphoma are common neoplasms asso-
signs such as anorexia, weight loss and depression or ciated with FeLV.
for evaluation of abnormalities associated with specific ● Fibrosarcomas occasionally develop in young cats
organ systems. co-infected with FeLV and feline sarcoma virus.
● Lymphocytic, myelogenous, erythroid and mega-
Of FeLV-infected cats evaluated at necropsy,
karyocytic leukemia all are reported secondary to
23% have evidence of neoplasia (96% – lymphoma/
FeLV infection; myelodysplasia and myelofibro-
leukemia complex) and the remainder die from
sis also occur.
non-neoplastic diseases including those from second-
ary infections due to immunosuppression. Urinary tract abnormalities.
● Urinary tract problems most frequently associated
Gastrointestinal abnormalities.
with FeLV-infected cats are urinary incontinence
● Stomatitis and halitosis may be secondary to
and renal failure.
overgrowth of normal bacterial flora or persist-
● Renal failure is generally secondary to renal lym-
ent calicivirus infection from immunosuppression.
phoma or glomerulonephritis.
● Vomiting and diarrhea occur in some FeLV-
● Urinary incontinence has been predominantly a
infected cats and may be due to opportunistic
small bladder, nocturnal incontinence that appears
infections such as salmonellosis, giardiasis or
to be caused by either sphincter incompetence or
cryptosporidiosis or lymphoma.
detrusor hyperactivity.
● A form of enteritis clinically and histopathologi-
cally resembling panleukopenia but apparently Ocular abnormalities.
related to FeLV infection has been described, and ● Intraocular lymphoma induces uveitis and glau-
is possibly secondary to enteric coronavirus coma in some cats; cats are generally presented for
infection. miosis, blepharospasm or cloudy eyes.
● Aqueous flare, mass lesions, keratic precipitates, Laboratory abnormalities.

lens luxations and glaucoma are often found on ● Anemia is common; non-regenerative anemia
ocular examination. occurs alone or in combination with decreases in
● If anterior uveitis is present, the abnormality is usu- lymphocytes, neutrophils and platelets.
ally because of co-infection with FIP, T. gondii, C. ● Evidence of abnormal red blood cell release from
neoformans or FIV. the bone marrow characterized by increased num-
bers of circulating nucleated red blood cells with-
Reproductive abnormalities.
out an appropriate reticulocytosis is common.
● FeLV-infected queens may be presented for abor-
● Examination of bone marrow often documents a
tion, stillbirth or infertility.
maturation arrest in the erythroid line.
● Kittens that are infected in utero but survive to par-
● Regenerative anemia is detected in some cats with
turition generally develop accelerated FeLV syn-
immune-mediated destruction of erythrocytes
dromes or die as a part of the kitten mortality
induced by FeLV or in some cats co-infected with
complex.
M. haemofelis.
Neurologic abnormalities. ● Microagglutination of erythrocytes or positive
● Nervous system disease is likely to develop due to direct Coomb’s testing occurs in some cats.
polyneuropathy or lymphoma. ● Neutropenia occurs in some due to bone marrow
● Neurologic abnormalities are occasionally second- suppression or immune-mediated destruction.
ary to other infectious agents like FIP or T. gondii. ● Renal azotemia occurs in cats with renal lym-
● Anisocoria, ataxia, weakness, behavioral change phoma.
and urinary incontinence are the most common ● Hyperbilirubinemia occurs due to pre-hepatic
neurologic signs. hemolytic anemia or hepatic disease associated
● Neurologic examination commonly reveals tetra- with lymphosarcoma.
paresis or paraparesis and decreased conscious ● Increased activities of liver enzymes develop second-
proprioception. ary to hepatic lipidosis or hepatic lymphosarcoma.
● Leukemic cells were detected in the bone marrow ● Proteinuria occurs in some FeLV-infected cats sec-
of 69% of a group of cats with spinal lymphoma. ondary to glomerulonephritis.
● Malignant lymphocytes characteristic of FeLV-
Secondary infections. induced lymphosarcoma are easily identified cyto-
● Concurrent infections by viral, bacterial, fungal,
logically, and occasionally are identified in
rickettsial and parasitic agents are commonly peripheral blood smears and in cerebrospinal fluid.
detected in FeLV seropositive cats; it is difficult ● Leukemias can be detected in peripheral blood
clinically to determine which are primary and smears and on bone marrow aspirates.
which are secondary to FeLV-induced immunosup-
pression.
● A strong association exists between FeLV and Diagnosis
infections with feline infectious peritonitis virus
Detection of FeLV antigens in neutrophils and
and hemotropic mycoplasmas (previously Haemo-
platelets by IFA or in whole blood, plasma, serum,
bartonella felis).
● Secondary infections may be more difficult to treat
saliva or tears by ELISA are most commonly used
clinically to document infection by FeLV.
in FeLV-infected cats that are immunosuppressed.
Antibody titers to FeLV envelope antigens (neutralizing
Musculoskeletal abnormalities.
antibody) and against virus-transformed tumor cells
● Multiple cartilaginous exostosis occur in some
(FOCMA antibody) are available in some research lab-
cats.
oratories but clinical use is limited due to poor prog-
● Polyarthritis with resultant stiffness and lame-
nostic value.
ness with or without swollen, hot and painful joints
occurs in some cats and has been attributed to Results of IFA and ELISA testing during the dissemi-
immune complex deposition. nation of FeLV are listed under Pathogenesis.
● The ELISA can detect p27 antigen prior to infec- due to false-positive ELISA results, false-negative
tion of bone marrow and release of infected neu- IFA results, or self-limiting infection.
trophils and platelets and so can be positive in some ● Cats that are ELISA-positive and IFA-negative
cats during early stages of infection or during self- are probably not contagious at that time, but should
limiting infection even though IFA results are neg- be isolated until retested 4–6 weeks later since
ative. progression to persistent viremia and epithelial cell
● Positive serum test results occur anywhere infection may be occurring.
between 2 and 30 weeks (generally 2–8 weeks) ● There is no reliable means of identifying local
after infection. or latent FeLV infections other than virus isola-
● Systemic epithelial tissue (including salivary glands tion and polymerase chain reaction on bone
and tear glands) infection occurs after bone marrow marrow cells.
infection. ● Positive ELISA or IFA results do not document
● There is generally a delay of 1–2 weeks after the immunodeficiency or disease induced by FeLV;
onset of viremia before ELISA tear and saliva tests many seropositive cats have disease manifestations
become positive. induced by secondary invaders.
● Since p27 can be detected by ELISA in cats that are
developing self-limiting infection, all cats positive
by serum ELISA should have the results con- Treatment
firmed immediately by IFA or should be isolated
Antiviral drugs.
and retested by ELISA in 4–6 weeks.
● Use of antiviral drugs is controversial.
● Some ELISA-positive cats that revert to negative
● Numbers of reported cats is minimal and so defini-
have become latently infected; the majority of
tive statements cannot be made for predicted
latently infected cats are negative by ELISA and
response. The primary goal of treatment is to
IFA but the virus can be isolated from the bone mar-
improve quality of life evidenced by attitude,
row.
appetite and physical appearance.
● False-positive ELISA results can develop second-
● If used, zidovudine (AZT) should be administered
ary to poor laboratory technique and are more com-
at 5 mg/kg bid. Cats should be monitored for devel-
mon with whole blood, tears or saliva than with
opment of anemia.
serum or plasma.
● 9-(2-phosphonoyl-methoxyethyl) adenine (PMEA)
● False-negative ELISA using tears or saliva occur
treated cats have greater therapeutic responses but
during early stages of infection.
more adverse effects than AZT-treated cats.
● Results of the IFA test are accurate 98% of the time.
● False-negative IFA results may occur when While nothing has been able to consistently clear
leukopenia or thrombocytopenia prevents evalua- viremia, immunotherapy may benefit some clinically
tion of an adequate number of cells. ill, persistently viremic cats. The practitioner should
● False-positive IFA results can occur if the blood realize that controlled studies for most are lacking and
smears submitted for evaluation are too thick. the following should be considered primarily anec-
● A positive IFA indicates that the cat is viremic and dotal.
contagious; viremia will be sustained for life in ● Interferon-alpha. Prevents release of budding
90–97% of cats with positive IFA results. virons. 30 units (1 ml) PO, once daily or once daily,
● Virtually all IFA-positive cats will also be ELISA every other week. 10 000 units/kg, SQ daily for
positive. several weeks if life threatened.
● The rare combination of IFA-positive and ELISA- ● Staphylococcus A. B lymphocyte and T lympho-
negative results suggests technique-related artifact. cyte activation, immune-complex binding, inter-
● Negative ELISA results correlate well with nega- feron induction, and immunoglobulin Fc binding.
tive IFA results and an inability to isolate FeLV. 1 ml/kg intraperitoneally, twice weekly for 10 weeks
● Cats that are ELISA-positive and IFA-negative are followed by 1 ml/kg intraperitoneally, twice weekly
termed discordant; discordant results are usually every fourth week for life.
● Propionibacterium acnes. Activation of macrophages ● Vaccination of cats not previously exposed to FeLV
and natural killer cells. Increased production of should be considered in cats at high risk (i.e. partic-
interferon, tumor necrosis factor, and interleukin ularly kittens less than 1 year old in contact with
1. 0.5 ml IV, twice weekly for 2 weeks followed by potentially infected cats).
0.5 ml IV, weekly for 20 weeks. ● Owners should be warned of the potential efficacy
● Acemannan. Enhanced release of tumor necrosis of less than 100%.
factor, prostaglandin E2, and interleukin 1-alpha by ● Cats should be tested for FeLV prior to vaccination.
macrophages. 2 mg/kg, IP, once weekly for 6 ● Vaccination is not indicated in seropositive cats.
weeks. ● Vaccination does not induce seropositivity.
● Pind-orf. Inactivated parapox ovis virus. ● Soft tissue sarcomas develop at the vaccination site
in 1:1000 to 1:10 000 cats given adjuvanted vac-
Antibiotics are often indicated for secondary infec-
cines.
tions and should be used at the high end of the dose
range for an extended duration.
Zoonotic aspects
Supportive care including fluid therapy, appetite stim-
While FeLV will grow in some human cell cultures
ulants and enteral nutrition supplied via force feeding
(with the exception of subgroup A), antigens of FeLV
or nasogastric, pharyngostomy, gastrostomy or jejunos-
have never been documented in the serum of humans
tomy tube placement may be indicated.
suggesting that this virus is species specific.
Blood transfusions, erythropoietin, hematinic agents,
Human complement lyses FeLV.
vitamin B12, folic acid and anabolic steroids generally
have been unsuccessful in the management of the non-
regenerative anemia. FELINE INFECTIOUS PERITONITIS VIRUS
(FIP), FELINE IMMUNODEFICIENCY VIRUS
Immunosuppressive therapy may be required in the
(FIV)**
management of hemolytic anemia but has the potential
for virus activation.
Classical signs
Prognosis ● +/- fever, pleural or abdominal effusion
(FIP).
The majority of cats (> 80%) with persistent viremia
● +/- CNS, hepatic, renal disease (FIP).
will die of an FeLV-related illness within 2–3 years.
● +/- secondary infections of any organ
Most cats with self-limiting infection will be subclini- system (FIV).
cally affected.
See main references page 339, The Thin, Inappetant Cat
(FIV), and page 372, The Pyrexic Cat (FIP).
Prevention
Clinical signs
Avoid exposure; house cats indoors.
Anemia is not usually a main presenting sign, and
Test and removal of seropositive cats can result in
occurs as a consequence of chronic disease. Signs of
virus-free catteries and multiple-cat households.
the agent predominate.
Multiple FeLV vaccines have been developed and
Typically FIP presents as fever, weight loss, anorexia
licensed in the last several years.
and lethargy. Highly proteinaceous pleural or abdomi-
● Due to variation in challenge study methodology and
nal effusions may be present, or there may be evidence
the difficulty of assessing preventable fraction of a
of hepatic, renal, ocular or CNS disease.
disease with a relatively low infection rate, long sub-
clinical phase, and multiple field strains, efficacy of Cats with signs from FIV often have lethargy,
individual vaccines continues to be in question. anorexia and weight loss associated with secondary
infections of the skin, and gastrointestinal or respira- Diagnosis

tory tracts.
Severe normocytic-normochromic, non-regenerative
anemia.
Diagnosis
Most drugs and toxins damage the bone marrow and
Diagnosis of FIV is based on the appropriate antibody so have concurrent thrombocytopenia and neutrope-
test, whereas pre-mortem diagnosis of FIP is usually nia.
presumptive, unless biopsy samples are available for
histological examination. Since bone marrow damage is present, anemia may be
severe.
Bone marrow hypoplasia can be documented by cyto-
DRUGS/TOXINS* logic examination of bone marrow aspirates or histol-
ogy of core biopsies but these techniques do not prove
Classical signs the cause of damage.
● Lethargy, anorexia and depression. Historical evidence of exposure to a drug or toxin is the
● Other specific signs of the toxin. best way to determine cause of anemia.
● Vomiting and diarrhea are common.
Clinical signs
FeLV, myelophthitic disease, ehrlichiosis.
Usually there is a history of exposure to the drug or
toxin; grizeofulvin, azathioprine, estrogens, chloram-
phenicol, some chemotherapeutic agents and non- Treatment
steroidal anti-inflammatory agents are most common.
Whole blood transfusions are given as needed.
Mechanism varies with the toxin. Bone marrow sup-
Recombinant erythropoietin can be administered as
pression (azathioprine, estrogens, chloramphenicol,
described for renal failure-associated non-regenerative
chemotherapeutic agents) is the mechanism for non-
anemia, but is unlikely to be effective since maximal
regenerative anemia. Any drug can be protein bound
erythropoietin responses are likely occurring.
and serve as a hapten for secondary immune-
mediated hemolytic anemia (see Regenerative ane- Antibiotics may be indicated if fever due to neutrope-
mia). Other drugs and toxins result in bleeding (see nia is occurring.
Regenerative anemia). Idiosyncratic reactions can
occur with most drugs or toxins, but each one listed
MYELOPHTHITIC DISEASES*
here also is an intrinsic toxin damaging the bone mar-
row if the toxic dose is exceeded.
Classical signs
Weakness, lethargy, pale mucous membranes,
● Lethargy, anorexia and depression.
tachycardia and tachypnea may be present due to
anemia.
Other clinical findings from the toxin inducing non- Clinical signs
regenerative anemia may be present.
Abnormalities result from neoplastic infiltration (lym-
Hemorrhage (thrombocytopenia) or evidence of phoma and myeloproliferative neoplasms most com-
infections (neutropenia) may be evident. mon) into the bone marrow inducing loss of normal
bone marrow cells.
Non-steroidal anti-inflammatory agents can cause clin-
ical findings consistent with gastrointestinal bleeding Findings may be consistent with the primary neoplasia;
or renal disease. i.e. masses.
Weakness, tachycardia and pale mucous membranes In dogs, infection may result in either a regenerative or
result from anemia. non-regenerative anemia.
Fever or other evidence of secondary infections Early in infection, acute aplastic anemia occurs
develop if neutropenia is present because of destruction of progenitor and proliferative
cells in the bone marrow. The resulting anemia is usu-
Bleeding results from thrombocytopenia.
ally mild or absent because of the long erythrocyte
lifespan.
Diagnosis
Secondary immune-mediated anemia may occur.
Pancytopenia (aplastic anemia) is most common;
In the chronic phase of the disease, hemopoietic stem
pure red cell aplasia is unusual.
cell injury results in moderate to severe non-regenera-
Lymphoma, myeloproliferative disease or multiple tive anemia.
myeloma are often detected on bone marrow cytology
Cats experimentally infected with Neorickettsia risticii
or biopsy.
develop morulae in mononuclear cells and occasion-
Circulating malignant cells may be detected. ally develop fever, depression, lymphadenopathy,
anorexia and diarrhea.
Differential diagnosis Cats experimentally infected with A. phagocytophilum
develop morulae in neutrophils and eosinophils.
FeLV, drugs or toxins, ehrlichiosis.
Cases proven by genetic sequencing were E. canis
(North America and France) or A. phagocytophilum
Treatment
(Sweden, Ireland, Denmark and North America).
Treat the neoplasm primarily.
Ehrlichia-like morula have been detected in mononu-
Supportive care. clear cells or neutrophils of naturally exposed cats in
the United States, Kenya, France, Sweden, Brazil and
Thailand.
EHRLICHIOSIS AND ANAPLASMOSIS
Other cases have been diagnosed based on the combin-
Classical signs ation of positive E. canis or A. phagocytophilum serol-
ogy, clinical or laboratory findings consistent with
● Lethargy, anorexia, depression and fever.
ehrlichial infection, exclusion of other causes, and
● Lameness from polyarthritis.
response to an anti-rickettsial drug. However, it is
unknown whether these cats were ill from the Ehrlichia
spp. infection.
Transmission
It is unknown how clinically ill, naturally exposed cats
are infected with an Ehrlichia canis-like organism. Clinical signs
Ixodes spp. ticks have been associated with several Cats are usually young and both males and females
cases with Anaplasma phagocytophilum (previously have been affected.
E. equi) infection. Cats infected by A. phagocytophilum have only been
Exposure to arthropods has been reported in about 30% diagnosed in areas with Ixodes ticks.
of the cases in the literature. Fever, inappetence, lethargy, weight loss, hyperes-
thesia or joint pain, and pale mucous membranes are
Pathogenesis the most common abnormalities. Splenomegaly, dysp-
Pathogenesis is unknown, but it is likely similar to dogs nea, uveitis, diarrhea and lymphadenomegaly are also
based on clinical and laboratory findings. detected in some.
Concurrent diseases are rarely reported but included Differential diagnosis

hemotropic Mycoplasma infection and lymphosar-
coma. Infectious, neoplastic, or immune-mediated diseases
resulting in fever, polyarthritis and anemia.
Anemia was reported for some cats; most are non-
regenerative and both cats with known regenerative
anemia were infected with a hemotropic Mycoplasma Treatment
spp.
Clinical improvement after therapy with tetracycline,
Leukopenia, leukocytosis characterized neutrophilia, doxycycline, or imidocarb dipropionate was reported
lymphocytosis, monocytosis, and intermittent thrombo- for most cats.
cytopenia can occur.
Doxycycline at 10 mg/kg, PO, q 24 h, for a minimum
Thromobocytopenia is the most common abnormality of 4 weeks.
in cats infected by A. phagocytophilum.
Imidocarb at 5 mg/kg, IM, q 14 days for 2 doses.
Hyperglobulinemia was reported for some cats; pro-
tein electrophoresis documented polyclonal gammopa-
thy in the cat assayed. Prognosis
Epidemiologic associations have been made with ocu- Good.
lar discharge, monoclonal gammopathy or pol-
yarthritis in E. canis seropositive cats and with outdoor
exposure and vomiting in N. risticii seropositive cats. Prevention and zoonotic aspects
Avoid exposure, house cats indoors.
Diagnosis
Ehrlichia canis and A. phagocytophilum infect people
Morulae appear as clusters of short rods in the cyto- as well as cats. However, transmission is from tick
plasm of leukocytes. exposure not contact with cats.
Determination of species by PCR or culture and elec- If indicated, use tick control on high-risk cats.
tron microscopy.
Presumptive diagnosis based on the combination of
positive serologic test results, clinical signs of disease
consistent with Ehrlichia infection, exclusion of other IMMUNE-MEDIATED (PURE RED CELL
causes of the disease syndrome, and response to anti- APLASIA)
rickettsial drugs.
Classical signs
Some cats with suspected clinical ehrlichiosis had anti-
bodies against E. canis and N. risticii and some had
antibodies against E. risticii alone or E. canis alone.
Positive serologic test results occur in healthy cats as
well as clinically ill cats, and so a diagnosis of clinical Clinical signs
ehrlichiosis should not be based on serologic test Most cases of pure red cell aplasia are thought to be due
results alone. to primary or secondary immune-mediated destruc-
Some cats proven by PCR assay to be infected by an tion of red blood cell precursors.
E. canis like organism were negative for E. canis anti- Lethargy or weakness, pale mucous membranes, and
bodies. elevated heart and respiration rates occur at rest.
All cats proven by PCR assay to be infected by Clinical course may be protracted due to the slow
A. phagocytophilum have also been seropositive. development of anemia.
Diagnosis tion defect. Mechanisms include folic acid antagonist

administration, dietary insufficiency, malabsorption
Feline leukemia virus infection, drugs and toxins and congenital defect.
should be excluded.
History of chronic (> 2 weeks) administration of folic
CBC generally reveals severe normocytic-normo- acid antagonists including pyrimethamine and sulfa
chromic, non-regenerative anemia with normal neu- drugs.
trophil and platelet numbers.
Clinical signs are associated with anemia and those of
Bone marrow examination reveals either maturation the disease the antibiotic was being used to treat.
arrest or lack of erythroblasts.
Diarrhea and weight loss may be associated with mal-
IFA or polymerase chain reaction for FeLV should be absorption syndromes.
performed on bone marrow cells.
The cat may have been fed a folic acid deficient diet
Spherocytes, positive direct Coomb’s test results and like tuna.
autoagglutination might be present in some affected
animals.
Diagnosis
Differential diagnosis Macrocytic-hypochromic, or macrocytic-normochromic
non-regenerative anemia with nuclear remnants.
FeLV, myelophthitic disease, ehrlichiosis, anemia of
chronic disease. Mean corpuscular volume >55 fl.
Neutropenia with hypersegmented neutrophils may be
Treatment present
Immunosuppressive therapy as described for regenera- History of drug administration.

tive hemolytic anemia (see page 533) should be pre- Bone marrow cytology shows erythroid hyperplasia
scribed. and megaloblastic changes.
Several blood transfusions may be required; since the Serum folate concentrations decreased (normal =
bone marrow is involved, response to therapy is more 13–38 μg/L) with normal cobalamin concentrations.
delayed.
Recombinant erythropoietin can be administered as Treatment
described for renal failure-associated non-regenerative
anemia (see page 540), but is unlikely to be effective Stop drug treatment.
since maximal erythropoietin responses are likely Folic acid supplementation at 0.004–0.01 mg/kg/day,
occurring. PO.
Signs resolve within 3 weeks of supplementation.
FOLIC ACID ANTAGONISM/DEFICIENCY

IRON DEFICIENCY
Classical signs
● Lethargy, anorexia and depression. Classical signs
Clinical signs
Folic acid is required for DNA synthesis, which is Clinical signs
important in red blood cell production; insufficient Most commonly develops from chronic loss of blood
folic acid results in macrocytic anemia as a matura- from the body.
The most common site of loss is the gastrointestinal

HYPOADRENOCORTICISM
tract.
Iron is required for the production of hemoglobin; lack Classical signs
of iron leads to microcytic, hypochromic anemia.
● Weakness, lethargy, anorexia.
Melena or hematochezia may or may not be present. ● Vomiting or diarrhea.
Clinical signs including vomiting, diarrhea and
weight loss that are associated with gastrointestinal
Clinical signs
diseases resulting in chronic blood loss.
Very rare in cats.
Gastrointestinal parasites (hookworms) and fleas
can result in iron deficiency anemia in kittens. Cats are usually presented for evaluation of depres-
sion, lethargy, vomiting, diarrhea and anorexia (see
Clinical signs of end-stage liver disease or portosys-
page 253).
temic shunts including failure to thrive and central
nervous system disease. Bradycardia in the face of shock may be present due
to hyperkalemia.
Melena or hematochezia may or may not be present.
Clinical signs of anemia are unusual, because the ane-
The primary disease generally is chronic and low
mia is mild.
grade; acute blood loss usually does not result in iron
deficiency and thus is usually regenerative.
Diagnosis
Diagnosis Normocytic-normochromic, non-regenerative anemia
Mild to severe microcytic-hypochromic, non-regenera- usually with a PCV of 15–27.
tive anemia. ACTH stimulation to document hypoadrenocorticism.
Mean corpuscular volume is generally < 39 fl.
Bone marrow iron stores subjectively are decreased. Treatment
Decreased serum iron concentrations and increased Treatment of shock and hyperkalemia acutely.
total iron binding capacity.
Glucocorticoid and mineralocorticoid supplementation
Thrombocytosis and occasionally neutrophilia are pres- (see page 254).
ent from non-specific bone marrow stimulation.
Serum bile acids, ultrasound, contrast studies, scinti-
HYPOTHYROIDISM
graphy and hepatic biopsy can be used to document
portosystemic shunts or end-stage liver disease.
Classical signs
● Lethargy, weight gain.
● Poor coat, seborrhea sicca, slow hair
Any cause of non-regenerative anemia. regrowth after clipping.

Control underlying disease. Extremely rare cause of anemia post-thyroidectomy or
I131 treatment.
Ferrous sulfate 50–100 mg/cat, PO, q 24 hours.
Most cats maintain enough thyroid function and never
It requires weeks to months to correct iron deficiency
become anemic.
since the gastrointestinal transferrin system can only
absorb small concentrations of iron daily. Obesity, lethargy and pale mucous membranes.
Poor coat, seborrhea sicca, slow hair regrowth after Decreased total and free T4 concentrations after treat-
clipping and thick skin. ment for hyperthyroidism.
Diagnosis Treatment
Normocytic-normochromic, non-regenerative anemia Levothyroxine supplementation (see page 1354).
usually with a PCV of 15–27.
RECOMMENDED READING
Breitschwert EB, Abrams-Ogg AC, Lappin MR, et al. Molecular evidence supporting Ehrlichia canis-like infection
in cats. J Vet Intern Med 2002; 16: 642–649.
Couto CG. Disorders of hemostatis. In: Couto G, Nelson R (eds) Small Animal Internal Medicine. Mosby, St. Louis,
MO, 1998, pp. 1192–1206.
Foley JE, Harrus S, Poland A, et al. Molecular, clinical, and pathologic comparison of two distinct strains of
Haemobartonella felis in domestic cats. Am J Vet Res 1998; 59: 1581–1588.
Jensen WA, Lappin MR, Kamkar S, Reagan, W. Use of a polymerase chain reaction assay to detect and differentiate
two strains of Haemobartonella felis in naturally infected cats. Am J Vet Res 2001; 62: 604–608.
Lappin MR. Infectious diseases section. In: Couto G, Nelson R (eds) Small Animal Internal Medicine. Mosby, St.
Louis, MO, 1998, pp. 1239–1337.
Neer TM, Breitschwerdt EB, Greene RT, et al. Consensus statement of ehrlichial disease of small animals from the
infectious disease study group of the ACVIM. J Vet Int Med 2002; 16: 309–315.
Stubbs CJ, Holland CJ, Reif JS, et al. Feline ehrlichiosis; literature review and serologic survey. Comp Cont Ed Pract
Vet 2000; 22: 307–317.
Tasker S, Lappin MR. Haemobartonella felis: recent developments in diagnosis and treatment. J Fel Med Surg 2002;
4: 3–11.
Tasker S, Binns SH, Day M J, et al. Use of a PCR assay to assess prevalence and risk factors for Mycoplasma
haemofelis and Candidatus Mycoplasma haemominutum in cats in the United Kingdom. Vet Record 2003; 152:
193–198.
25. The cat with polycythemia
Jacquie Rand and Annette Litster
KEY SIGNS
● Increased red cell concentration in peripheral blood.
● Injected mucous membranes.
MECHANISM?
● Dehydration resulting from disease of many organs may produce relative polycythemia.
Polycythemia may be an appropriate physiological response to hypoxia caused by pulmonary
or cardiac disease. Alternatively, inappropriate polycythemia may be associated with renal
space-occupying masses or other visceral tumors. Inappropriate primary polycythemia results
from a rare myeloproliferative disorder, polycythemia vera.
WHERE?
● Gastrointestinal tract, renal or skin (burns) disease causing excessive fluid loss.
● Cardiac or respiratory disease causing chronic hypoxia.
● Renal (space-occupying masses) or visceral (neoplastic conditions) conditions associated with
inappropriate erythropoietin secretion.
Bone marrow associated with myeloproliferative disease.
WHAT?
● The most common cause of polycythemia is dehydration. Hyperthyroidism produces mild
polycythemia in many cats. Appropriate polycythemia associated with hypoxia from chronic
respiratory or cardiac disease is less common. Primary or secondary inappropriate
polycythemia is very rare.

Diseases causing polycythemia
DEGENERATIVE
● Cardiac disease* (p 561)
Cardiac conditions such as cardiomyopathy which result in tissue hypoxia or cyanosis from
cardiac failure may stimulate increased erythropoietin production, resulting in increased red
552
25 – THE CAT WITH POLYCYTHEMIA 553
blood cell mass. Clinical signs may include dyspnea, lethargy, weakness, a gallop rhythm,
heart murmur and arrhythmia. Mucous membranes may be pale or cyanotic with prolonged
capillary refill time.
ANOMALY
● Congenital heart disease* (p 561)
Congenital cardiac anomalies associated with right to left shunting, e.g. tetralogy of Fallot,
reverse patent ductus arteriosus, and atrial or ventricular septal defects may cause secondary
polycythemia in young cats. There may be a history of lethargy and stunted growth, and on
clinical examination, dyspnea, cyanosis and a heart murmur may be noted. PCV is often
markedly elevated (> 60%).
● Renal space-occupying mass
Renal conditions such as renal cysts and hydronephrosis have been associated with inappropri-
ate erythrocytosis secondary to increased erythropoietin production, but these are very rare.
Kidneys are unilaterally or bilaterally enlarged on abdominal palpation, and there may be asso-
ciated clinical signs of renal disease such as polyuria and polydipsia.
NEOPLASTIC
● Polycythemia vera*(p 563)
Primary polycythemia is caused by a myeloproliferative disorder, similar to polycythemia vera in
humans. There may be a history of bleeding, seizures, polydipsia and polyuria, and physical exam-
ination reveals dark pink mucosa with a PCV often exceeding 60%. Circulating erythropoietin lev-
els are normal or low. This condition is very rare in cats.
Neoplasia of a wide variety of organs including the kidneys, liver, adrenal gland, female
reproductive tract and central nervous system have been associated with inappropriate poly-
cythemia. The condition is characterized by increased circulating erythropoietin levels without
a hypoxic stimulus. Impaired renal blood flow secondary to a space-occupying mass, or tumor
secretion of erythropoietin or erythropoietin-like substances have been hypothesized as possi-
ble causes of erythrocytosis. Clinical signs relate to the type of tumor involved and its anatomi-
cal location.
METABOLIC
● Dehydration*** (p 557)
Derangement of fluid balance from a variety of causes is the most common cause of poly-
cythemia in cats. Polycythemia occurs most commonly when excessive fluid loss through the
gastrointestinal tract (vomiting or diarrhea) or kidney (diabetes mellitus or renal
failure) is coupled with inadequate fluid intake. Typically there is depression and anorexia,
and signs that relate to the underlying condition such as polyuria, polydipsia, vomiting or diar-
rhea. Skin tents on pinching, mucous membranes are dry, and may have delayed refill.
Accompanying laboratory abnormalities include increased total protein, increased urine specific
gravity and pre-renal azotemia.
continued
continued
● Hyperthyroidism** (p 560)
Hyperthyroidism may be associated with a mild increase in PCV, possibly from a direct effect of
thyroxine on erythrocyte precursors. Affected cats are usually older (> 8 years), with a history of
weight loss despite a robust appetite. Associated clinical signs include irritable behavior, tachycar-
dia, sometimes with a gallop rhythm, polyuria, polydipsia and often chronic vomiting.
● Severe obesity (Pickwickian syndrome) (p 568)
Morbid obesity may predispose to tissue hypoxia from inadequate alveolar ventilation because of
fat accumulation in the thorax and compression of upper airways. Blood O2 saturation levels are
low (<92%) and there are slightly to markedly increased circulating levels of erythropoietin.
PHYSICAL
● High altitude (p 568)
Decreased O2 levels in the atmosphere at high altitudes may stimulate increased renal erythropoi-
etin production in response to tissue hypoxia. The cat is otherwise clinically normal, although
there may be mild dyspnea with a fast, shallow respiratory pattern. Circulating erythropoietin lev-
els are elevated.
PSYCHOLOGIC
● Stress-induced splenic contraction (p 567)
The stress response in cats may include splenic contraction, with a resultant infusion of stored
splenic erythrocytes into the circulation. Affected cats usually have an appropriate history and may
have other accompanying signs such as dilated pupils and behavioral changes. Hemoconcentration
caused by stress is usually mild and transient.
IATROGENIC
● Excessive blood transfusion or overdose of exogenous erythropoietin (p 564)
This is a potential, although previously unreported, cause of polycythemia. The diagnosis is made
with an appropriate history and clinical signs of erythrocytosis such as weakness, injected mucous
membranes and neurological signs.
IMMUNE
● Acute systemic anaphylaxis (p 566)
Acute systemic anaphylaxis results from an extremely rapid and overwhelming immune reaction to
a foreign antigen. It may cause hemoconcentration, most likely from a combination of fluid loss
caused by increased vascular permeability, and splenic contraction in response to acute shock.
There should be a history of exposure to a foreign antigen, usually protein. Anaphylaxis may occur
on the first exposure to the inciting antigen. Clinical signs include acute dyspnea, collapse, pale
mucus membranes and other signs of hypotensive shock.
INFLAMMATION
● Chronic pulmonary disease* (p 562)
Chronic pulmonary disease such as feline asthma/bronchitis complex may cause tissue hypoxia,
resulting in increased erythropoietin production and erythrocytosis. There is usually a history of
chronic coughing, with dyspnea and lethargy in more severe cases. Clinical signs include crackles
and wheezes on thoracic auscultation.
● Space-occupying renal masses including neopla-

INTRODUCTION sia, cysts or hydronephrosis may impair renal blood
flow and stimulate secretion of inappropriate con-
MECHANISM? centrations of erythropoietin.
– Polycythemia from a renal space-occupying
Increased red cell concentration may result from a rel- mass is sometimes accompanied by signs of
ative or absolute increase in erythrocytes. renal failure, such as polydipsia/polyuria,
reduced urine specific gravity and azotemia.
A relative increase in red blood cells is caused by
dehydration. In dehydration, a reduction in plasma Primary inappropriate polycythemia is called poly-
volume causes hemoconcentration, resulting in erythro- cythemia vera, and is a neoplastic proliferation of ery-
cytosis and increased total plasma protein concentra- throid cells, associated with low or undetectable
tion. Blood oxygen saturation levels are normal. erythropoietin concentrations. Typically PCV is
greater than 60–65%.
Transient absolute polycythemia may occur with
excitement when splenic contraction releases red cells Once the PCV exceeds 65%, the ensuing hypervis-
into circulation. cosity increases peripheral resistance, decreases
cardiac output and decreases oxygen transport to
Absolute polycythemia may be an appropriate physio-
the tissues. Increased blood volume distends vessels
logical response to chronic hypoxia from cardiac or
and together with sluggish flow, predisposes to
pulmonary disease, and is mediated by increased serum
thrombosis and vessel rupture. It is hypothesized
erythropoietin levels.
that erythrocytosis impairs renal tubular concentrating
● Signs relate to the underlying cardiac cause and
mechanisms, resulting in polyuria and polydipsia.
include a cardiac murmur and cyanosis consistent
with right to left shunting of blood causing hypoxia, Clinically, polycythemia causes injected mucous
e.g. tetralogy of Fallot, atrial or ventriclar septal membranes, torturous retinal blood vessels, and
defect (ASD or VSD). there may be a history of intermittent bleeding
● Clinical signs of chronic primary lung pathology diatheses.
include coughing, dyspnea, wheezes and crackles,
Insufficient vascular perfusion of the central nervous
which accompany generalized hypoxia in more
system may result in neurological signs such as
severe cases.
seizures, ataxia, abnormal behavior and/or
Alternatively, absolute polycythemia may be caused blindness.
by increased, but physiologically inappropriate,
erythropoietin secretion, associated with a variety of
neoplastic conditions or space-occupying renal
WHERE?
masses. In these cases, blood oxygen saturation lev-
els are normal. Relative polycythemia may result from gastrointesti-
● Secondary causes of inappropriate polycythemia nal or renal disease, and rarely from extensive skin
include visceral tumors involving the kidneys, burns which cause excessive fluid loss, or severe dis-
liver, adrenal gland, female reproductive tract and ease of any organ sufficient to cause marked lethargy
central nervous system. These occasionally secrete and inadequate fluid intake.
erythropoietin or an erythropoietin-like substance
Absolute polycythemia from a physiological increase
without a hypoxic stimulus. While these tumors
in erythropoietin concentration may result from car-
have been reported to cause polycythemia in
diac or pulmonary disease.
humans and dogs, they are yet to be reported as a
cause of polycythemia in the cat. Absolute polycythemia from a pathological increase in
– Clinical signs are expected to relate to the type erythropoietin concentration may result from space-
of tumor involved, its anatomical location, and occupying renal disease or neoplasia of a wide vari-
the polycythemia. ety of organs.
Primary absolute polycythemia is the result of a Secondary causes of inappropriate polycythemia

myelodysplastic condition of the bone marrow. include visceral tumors or a space-occupying renal
mass such as neoplasia, cyst or hydronephrosis. These
should be investigated using renal palpation, abdominal
WHAT? radiographs, abdominal ultrasonography and/or intra-
The most common cause of polycythemia is dehydra- venous pyelogram.
tion. Hyperthyroidism, acquired cardiac disease such Serum erythropoietin assay helps differentiate second-
as cardiomyopathy, and respiratory disease including ary from primary inappropriate polycythemia. However,
feline asthma/bronchitis complex are less common accurate measurement of feline erythropoietin is com-
causes of polycythemia. Renal cysts and hydronephro- promised by the lack of an assay technique validated
sis are rare causes of polycythemia in cats. All other for use in cats. A human ELISA assay technique has
causes of polycythemia are uncommon, with congeni- been successfully used to detect erythropoietin in cat
tal cardiac disease the most common cause of severe serum and is available through Dr Urs Giger at the
polycythemia. Polycythemia vera and neoplasia University of Pennsylvania.
secreting erythropoietin-like products are very rare
causes of severe polycythemia in cats. Serum erythropoietin concentrations are normal or
increased in most cases of secondary inappropriate
polycythemia.
DIAGNOSIS
Primary polycythemia (polycythemia vera) is likely
Relative polycythemia from dehydration should be sus- if PCV > 60–65% and there is no evidence of
pected if plasma protein is elevated and there is clin- dehydration, hypoxia, cardiac or pulmonary dis-
ical evidence of dehydration. ease, neoplasia or a space-occupying renal lesion.
● PCV is usually ≤ 60%. ● Erythropoietin is low or undetectable in primary
● Treatment with fluids normalizes PCV and plasma polycythemia.
protein concentration. ● Primary polycythemia may be accompanied by
leukocytosis and thrombocytosis.
Cats that are very stressed at the time blood is col-
● Bone marrow typically has increased cellularity,
lected may have transient polycythemia.
with erythroid hyperplasia or panhyperplasia, nor-
● PCV is usually ≤ 60 and polycythemia is mild and
mal maturation within the erythroid line, and nor-
transient.
mal morphology of cells.
Absolute polycythemia should be suspected if plasma
protein is normal and there is no evidence of dehy-
TREATMENT
dration, in an unstressed cat.
In relative polycythemia, intravenous or subcutaneous
Appropriate polycythemia (in response to hypoxia)
balanced electrolyte solutions should be administered
is differentiated from inappropriate polycythemia
to correct dehydration.
by measurement of oxygen saturation of arterial
blood. Primary polycythemia vera can be treated by a
● Appropriate polycythemia is likely if arterial oxy- combination of regular, intermittent phlebotomy
gen saturation is less than 92% (normal ≥ 97%). and fluid therapy. More severe cases may require
● Cardiac and pulmonary systems should be adjunct chemotherapy with hydroxyurea.
examined initially using auscultation and thoracic
In secondary polycythemia (appropriate or inappropri-
radiographs, and if indicated, by echocardiography
ate), the underlying disease must be diagnosed and
and electrocardiography.
treated, and symptomatic therapy with phlebotomy and
Inappropriate polycythemia should be suspected if fluid therapy should be provided to manage the erythro-
arterial oxygen saturation is normal. cytosis.
Accompanying clinical signs are attributable to the

DISEASES CAUSING POLYCYTHEMIA cause of the dehydration. Renal and gastrointestinal
tract fluid losses are common causes of dehydration,
DEHYDRATION*** and present with polyuria and polydipsia, or vomiting
and diarrhea, respectively, coupled with inadequate
Classical signs fluid intake.
● Skin tenting. Massive fluid deficits can occur after burns because of
● Tacky mucus membranes. fluid losses from the skin.
● Combination of increased PCV and plasma
Acute viral respiratory disease can cause dehydration
protein concentration.
because of losses from ocular and nasal discharges
● Signs attributable to underlying disease.
and hypersalivation.
Diagnosis
Pathogenesis
Characteristic clinical signs of dehydration are
A relative increase in red cells occurs as a result of accompanied by hemoconcentration, normal blood
dehydration. The increase in red cell concentration is oxygen saturation and increased total plasma pro-
secondary to decreased plasma volume from dehydra- tein concentration.
tion. Total red cell mass is normal, although red cell
mass can only be determined using radio-isotope-
tagged autologous red blood cells, a technique not gen-
erally available in practice. Since clinical signs of dehydration are characteristic, dif-
ferential diagnoses mainly refer to the condition caus-
Relative polycythemia occurs most commonly when
ing the dehydration, rather than to dehydration itself.
excessive fluid loss through the gastrointestinal tract
(vomiting or diarrhoea) or kidney (diabetes mellitus
or renal failure) is coupled with inadequate fluid Treatment
intake.
Fluid and electrolyte therapy is initially required to
restore intravascular volume because this is most
Clinical signs critical for survival, and then to replace fluid and elec-
trolytes in the extravascular compartments includ-
Clinical signs of dehydration include skin tenting,
ing both intracellular and interstitial fluid. Many
tacky mucus membranes and high plasma protein
patients that are dehydrated have adequate circulating
levels.
blood volume to maintain tissue perfusion, and do not
● Dehydration is assessed initially by examining skin
need rapid volume expansion.
turgor, usually by drawing the skin at the back of
the neck upward. Of total body water, 2/3 is intracellular and 1/3 is
– It is not until there is 5% dehydration that there extracellular. Only about 1/6 of body water is
is subtle loss of skin elasticity. intravascular.
– At 6–8% dehydration, there is a delay in ● Sodium and chloride are the major electrolytes in
return of the skin to its normal position, the the extracellular fluid.
capillary refill time may be slightly prolonged, ● Potassium and phosphates are the major elec-
and mucous membranes may be dry to touch. trolytes in intracellular fluid.
– At 10–12% dehydration, tented skin stands in
Type of fluid selected should be based on the elec-
place; mucus membranes are dry; the eyes are
trolyte and acid–base status of the cat, and whether it
sunken in the orbits; there is prolonged capillary
is being used for replacement or maintenance.
refill time; and there may be signs of shock.
– By 12–15% dehydration, signs of shock are Crystalloids are the most common types of fluids used,
present and death is imminent. and have sodium as their major osmotically active par-
ticle. Sodium and water rapidly traverse semipermeable ● Hypotonic fluids include 5% dextrose in water and
membranes such as the endothelium, and only 20–33% 0.45% sodium chloride with 2.5% dextrose. These
remains in the vascular space 30 min after adminis- fluids have similar osmolalities to plasma prior to
tration. administration, but once administered the dextrose
● Crystalloids may be balanced and have a similar is metabolized and the remaining fluid becomes
electrolyte composition and osmolality to normal hypotonic.
plasma (e.g. lactated Ringer’s solution, Plasma-lyte ● Five percent dextrose in water is useful as a carrier
A or Normisol-R), or unbalanced. Unbalanced fluid for administration of drugs and does not add
fluids (eg. 0.9% NaCl, 5% dextrose in water) are extra electrolytes to the cat. For example, it can be
used to correct specific deficits in plasma elec- used as a constant rate infusion (CRI). Drugs such
trolyte concentrations or water, and should be cho- as metoclopramide or morphine may be adminis-
sen only after serum electrolyte concentrations have tered as a constant rate infusion (CRI) in 5% dex-
been determined. trose in water.
● Fluids may also be classified as replacement flu-
Hypertonic fluids result in rapid volume expansion
ids, provided to correct electrolyte or pH imbal-
because the high sodium concentration (e.g. 7.5%
ances, or maintenance fluids, which are restricted
NaCl) or dextrose (10% dextrose) attracts water from
in sodium, contain additional potassium and are
the extravascular compartments, and small volumes
hypotonic when administered or after metabolism
(3–5 ml/kg) can be administered. However, the effect is
of dextrose, e.g. Plasma-Lyte 56, Normosol M,
short term (~30 min), and they should be administered
0.45% NaCl with added potassium, or 0.45% NaCl
with additional crystalloids, with or without colloids.
with 2.5% dextrose and added potassium, Plasma-
Administer the dose slowly IV over 5–10 minutes.
Lyte 56 with 5% dextrose, and Normisol-M with
Hypertonic saline is most useful in cats that require
5% dextrose.
small volume resuscitation, for example after head
Metabolic acidosis is the most common acid–base dis- trauma or pulmonary contusions. It can be combined
order, and is usually corrected with volume expansion, with colloids such as Hetastarch.
correcting the underlying disease, and using fluids with ● Hypertonic saline causes volume expansion equi-
an alkalizing effect. Where there is severe metabolic valent to colloids, but at 1/4 the volume adminis-
acidosis or hepatic failure, NaHCO3 may need to be tered.
added to the IV fluid infusion. ● Dose is 3–5 ml/kg of 7.5% NaCl administered
● Fluids containing lactate or buffers metabolized slowly IV over 5–10 minutes.

to lactate (acetate and gluconate) are alkalizing, Colloids contain osmotically active particles that are
because lactate is metabolized to bicarbonate by the too large to cross vessel walls, and most of the infused
liver, which makes it suitable for the treatment of volume remains in circulation. Colloids are indicated
metabolic acidosis. for rapid restoration of circulating fluid volume and
– Lactated Ringer’s solution is buffered by lactate. to slow loss of fluid from the intravascular space.
– Plasma-Lyte and Normosol are buffered by ● The addition of colloids to the fluid therapy regi-
acetate and gluconate. men may also be appropriate where losses are
Metabolic alkalosis is usually corrected once chloride ongoing from the intravascular space, such as with
deficits are corrected. Metabolic alkalosis occurs as a burns, acute shock, systemic inflammatory response
result of chloride depletion and dehydration, because syndrome (SIRS), sepsis or acute systemic anaphy-
to maintain intravascular volume, the renal tubules laxis. Commercially available hetastarch solution
reabsorb bicarbonate along with sodium instead of the may be used for up to 30% of the maintenance IV
depleted chloride. fluid requirements in severe cases while losses are
● Normal saline is unbuffered and has an acidifying
ongoing.
● In general, when administering colloids, divide the
effect.
dose into four aliquots and administer slowly IV
Hypotonic fluids should be used when there are free over 10–15 minutes. Recheck the cat after each
water deficits or when serum sodium is elevated. aliquot, carefully evaluating the lungs for signs of
pulmonary edema. Use a syringe pump or infu- ● Haemaccel® is a colloid solution available in
sion pump because cats are very sensitive to the Europe and Australasia that is comprised of 3.5%
volume expansion effects of colloids, and manual polygeline, a gelatin-based colloid.
administration increases the risk of adverse effects
To achieve a very rapid increase in intravascular vol-
such as pulmonary edema. Hypothermic cats are
ume using low volumes of infused fluids, colloids and
particularly sensitive to colloids, and administering
hypertonic saline can be combined. Replacement or
hypertonic saline or colloids to cats with undiag-
maintenance crystalloids are administered concurrently
nosed and asymptomatic hypertrophic cardio-
to maintain or replenish interstitial and intracellular
myopathy may precipitate pulmonary edema.
fluid levels, and are administered at 50% of the volume
Colloid solutions include dextran, hydroxyethyl that would be required if they were used alone.
starch (HES) and hemoglobin-based oxygen-carrying Examples of combinations used are:
solutions such as Oxyglobin®. They are contraindi- ● Combine 1.3 ml/kg of 23.4% NaCl with 2.7 ml/kg
cated for use in very dehydrated, oligouric patients of 6% hetastarch, and administer slowly over 10–15
because the possibility of renal damage is increased. minutes. Mixing the solutions together results in a
The fluid attracted intravascularly comes from within 7.5% NaCl solution.
cells, exacerbating intracellular dehydration. ● 20% NaCl at 1.5 ml/kg combined with Dextran 70
● Colloid osmostic pressure (COP) and volume- at 3 ml/kg and administer slowly over 10–15 min-
expanding capacity varies with the colloid as fol- utes. Mixing results in approximately 7% NaCl.
lows:
Plasma can be used as a colloid, but it is best used
● 6% hetastarch has a COP of 30 mmHg, and expands
when there is a specific indication such as pancreatitis
the volume by 1–1.3 ml per ml of colloid infused,
or a coagulation disturbance. It is not the preferred
and stays in the vascular space for 12–48 h.
method of replacing albumin or improving the oncotic
● 10% dextran 40 has a COP of 40 and expands the
pressure, because the volume of plasma required to
volume by 1–1.5 ml per ml of colloid infused, and
measurably increase serum albumin concentration is
stays in the vascular space for 4–8 h.
very large. However, it can be used as a component of
● 6% dextran 70 has a COP of 40 and expands the
fluid therapy to help increase plasma oncotic pressure
volume by 0.8 ml per ml of colloid infused, and
in a hypoproteinemic cat, and to decrease the tendency
stays in the vascular space for 4–8 h.
for loss of intravascular fluid. Plasma can be adminis-
● Dextran is made from high-molecular-weight lin-
tered at 20 ml/kg over 4 h in place of 1/3 of the calcu-
ear glucose polymers produced by bacteria, and is
lated crystalloid fluid volume to be administered.
available as Dextran 40 and 70, but Dextran 40 is
rarely used in veterinary medicine because of its The intravenous route of fluid administration is pre-
association with acute renal failure. The dose rate is ferred for correction of severe dehydration, major elec-
5–10 ml/kg, beginning with the lower dose. trolyte and acid–base imbalances, and shock. While the
● Hydroxyethyl starch is composed primarily of jugular, cephalic, femoral and saphenous veins are
amylopectin, and is a branched polysaccharide available for IV catheter placement, the cephalic vein is
closely resembling glycogen. It is available as the site of choice as the catheter is most readily secured
Hetastarch and Pentastarch. The standard dose rate at that site and less commonly soiled with urine and
is 10–15 ml/kg/day, but administer 2–5 ml/kg ini- feces than in caudal limb sites.
tially and re-evaluate the cat.
Fluid rates administered depend on the requirement of
● Oxyglobin® is used primarily for its oxygen-
the animal.
carrying capacity, but can be used for its colloidal
effect. However it is expensive to use solely for vol- If the cat has insufficient plasma volume to maintain
ume expansion. The COP of Oxyglobin is 37 mmHg, tissue perfusion, intravascular volume must be restored
thus, it has slightly more colloidal pull than rapidly.
Hetastarch, and retains oxygen-carrying capacity ● Inadequate tissue perfusion is indicated by:
for up to 40 h. The dose rate in cats is 1–2 ml/kg/h – Tachycardia and tachypnea, and sometimes
with a total dose of 15 ml/kg. bradycardia.
– Pale mucus membranes and increased capillary ● Replacement fluids include lactated Ringer’s,
refill time (> 2 s). Normosol-R or Plasma-Lyte A.
– Cold extremities.
If ongoing maintenance fluids are required over several
– Anuria or oliguria (<1 ml/kg/h urine produced).
days because fluid intake is inadequate or there are con-
– Decreased central venous pressure (< 5 cmH2O).
tinuing fluid losses, change to a maintenance fluid that
● Inadequate interstitial hydration is evident as tacky
resembles the amount of free water and electrolytes that
mucus membranes, skin tenting and sunken eyes.
would be consumed daily and are being lost.
Crystalloids can be used alone, but colloids and hyper- Maintenance solutions are hypotonic crystalloids that
tonic saline result in much more rapid restoration of are lower in sodium and chloride but higher in potas-
normal perfusion, because only small volumes need to sium concentration than plasma, such as Plasma-Lyte
be administered (3–5 ml/kg), and they act immediately 56, Normosol M, 0.45% NaCl with added potassium, or
to attract water into the vascular space. 0.45% NaCl with 2.5% dextrose and added potassium.
● When tissue perfusion is inadequate, for example ● Maintenance fluid rates are 70 ml/kg/day, but if
from severe dehydration or shock, crytalloids there are ongoing fluid losses from polyuria, diar-
administered alone can be infused at 40–55 rhea or vomiting, then calculate an additional
ml/kg/h for a total dose of 45–60 ml/kg to restore 5%/kg requirement (or 50 ml/kg/day), which is
circulating intravascular volume. This volume nearly equivalent to doubling the daily maintenance
should be reduced by 40–60% if colloids are rate. Fever can increase fluid requirements by
administered together with crytalloids. 15–20 ml/kg/day.
– In general, the patient should be reassessed after
Potassium is usually added to fluids at the following
1/4 to 1/3 is administered or after 15 min,
rates, and the infusion rate of the fluid is adjusted so the
because IV fluids administered too rapidly can
rate does not exceed 0.5 mmol (mEq)/kg/h.
cause pulmonary edema. Intravascular volume is
usually restored over the first 2 hours. Serum potassium Potassium
● If the electrolyte status of the patient is unknown, use concentration supplementation
a crystalloid most like plasma in sodium and potas- (mmol or mEq/L) to 1 L of IV fluids
sium content, pH and osmolality, such as lactated
>3.5 20 mEq
Ringer’s, Normosol-R or Plasma-Lyte A. These
30 mEq 3.0–3.5
have an alkalizing effect which is useful because
40 mEq 2.5–3.0
patients with reduced circulating blood volume are
60 mEq 2.0–2.5
usually acidotic. 0.9% NaCl can also be used.
80 mEq < 2.0
For hemodynamically stable patients with dehydra-
tion, fluid deficits are corrected over the first 12–24
Prognosis
hours, followed by maintenance fluid rates. Maintenance
rates of 70 ml/kg/day (3 ml/kg/h) are calculated, and The prognosis ultimately depends on the inciting con-
the dehydration fluid deficit is added to the mainten- dition, but acute dehydration treated with prompt and
ance figure. Dehydration fluid deficit is calculated by vigorous fluid therapy has an excellent prognosis.
the following formula: % dehydration × body weight
(kg) = fluid deficit (liters).
● For example, a 5 kg cat that is 10% dehydrated
HYPERTHYROIDISM**
requires 500 ml (0.1 × 5 L) to correct the fluid
deficit and 350 ml (70 × 5 ml) for maintenance, Classical signs
which is 850 ml in the first 24 h, or 35 ml/h or 0.59 ● Weight loss despite polyphagia.
ml/min. Using a microdrip set with 60 drops per ml, ● Polyuria/polydipsia.
the infusion rate is 35 drops per minute (0.59 ml × ● Tachycardia, sometimes with a gallop
60 drops/ml), or just over one every 2 seconds. This rhythm.
rate may be increased in the first 4–6 h to correct ● Mild erythrocytosis in some cases.
the fluid deficit more rapidly.
See main reference The thin cat (or cat with weight Hyperthyroidism is commonly treated with oral daily
loss) and a good appetite on page 304 for details. methimazole, which is generally continued for the life
of the cat.
Pathogenesis Surgical treatment by unilateral or bilateral thy-
Many hyperthyroid cats have mild increases in PCV, roidectomy may be recommended if the cat has accept-
which are thought to be a direct effect of thyroid hor- able anesthetic risk factors. Careful surgical technique
mone stimulating red cell precursors. Erythropoietin is necessary to avoid post-operative hypoparathy-
production may also be increased in hyperthyroidism, roidism and life threatening hypocalcemia.
because of the increased metabolic rate. Adjunctive treatment with beta-blockers or other
hypotensive agents may be necessary to manage the
Clinical signs cardiovascular complications of hyperthyroidism.
There is usually a history of weight loss despite
polyphagia.
Cats are often hyperexcitable and the coat is often Prognosis
unkempt from poor grooming. The prognosis for successful management of hyperthy-
Vomiting and polyuria/polydipsia occur in about one roidism is generally very good provided associated
third of cats. complicating factors such as thyrotoxic heart dis-
ease are well controlled.
On physical examination, there may be palpable thy-
roid nodules, and tachycardia or a heart murmur on
cardiac auscultation.
CARDIAC DISEASE INCLUDING
CONGENITAL DISEASE*
Diagnosis
Serum total thyroxine (T4) is usually increased, unless Classical signs
there is an accompanying medical condition that may ● Abnormal cardiac rhythm or rate, often
suppress total T4 to the upper half of the reference accompanied by a cardiac murmur.
range (“sick euthyroid syndrome”). In these cases, ● Blood O2 saturation is reduced (<92%).
a diagnosis of hyperthyroidism can be made by detec- ● Advanced cases may present with acute
tion of increased serum free T4 or by a triiodothyrox- dyspnea.
inine (T3) suppression test. ● Usually cardiomegaly on thoracic
radiography.
See main references The Cat With Abnormal Heart
Other causes of mild absolute erythrocytosis with Sounds and/or an Enlarged Heart and The Cat With
normal blood O2 saturation, such as stress-induced Tachycardia, Bradycardia, or an Irregular Rhythm on
splenic contraction, must be differentiated from ery- pages 140, 157 for details.
throcytosis associated with hyperthyroidism.
● Demonstration of increased thyroxine is diagnostic
for hyperthyroidism, although stress-induced Pathogenesis
splenic contraction could occur concurrently and
compound the mild polycythemia. Cardiac failure causes chronic hypoxia, stimulating
increased secretion of erythropoietin, resulting in
polycythemia.
Treatment
The most dramatic increases in PCV occur in young
The treatment of choice for hyperthyroidism is cats with congenital heart disease with right to left
radioactive I131 therapy where available. shunting (e.g. tetralogy of Fallot, reverse patent ductus
arteriosus, atrial or ventricular septal defects), but Medical therapy is instituted to treat the physiological
appropriate secondary polycythemia may also occur effects of cardiac failure. This may include treatment for
with left-sided or biventricular congestive heart fail- hypertension, cardiac rate disturbances, arrhythmia, pul-
ure, as occurs with cardiomyopathy. monary edema and/or pleural effusion. See The Cat With
Abnormal Heart Sounds and/or an Enlarged Heart and
The Cat With Tachycardia, Bradycardia, or an Irregular
Clinical signs Rhythm on pages 124, 157 for treatment details.
Feline cardiac disease usually presents at an Hypoxia in tetralogy of Fallot is decreased when the
advanced stage, with dyspnea and hypoxia (oxygen condition is treated by aortic banding, which reduces
saturation <92%). right-to-left blood flow.
There may be open-mouth breathing and cyanosis. Hematocrit should be reduced to 45% before sur-
Mucosae are dark pink, or purple if the poly- gery is performed to treat any underlying condi-
cythemia is caused by hypoxia from right to left shunt- tions, to decrease the risk of thromboembolism during
ing of blood in the heart or lungs. surgery. This is achieved by performing phlebotomy
and administering intravenous fluids.
Tachycardia and arrhythmia may be detected on car-
diac auscultation, with accompanying crackles and
wheezes on thoracic auscultation from pleural effusion Prognosis
and/or pulmonary edema.
The prognosis for feline cardiac disease is guarded and
Congenital cardiac disease often causes stunted may be poor if the disease is initially diagnosed at an
growth in comparison with littermates. advanced stage.
Diagnosis CHRONIC PULMONARY DISEASE*

Initial diagnosis may be made on auscultatory abnor-
malities, together with other signs of cardiac failure Classical signs
such as dyspnea and hypertension. ● ± History of chronic coughing.
Thoracic radiology reveals cardiomegaly with or ● Dyspnea may be acute, chronic or
without pulmonary edema and/or pleural effusion. intermittent.
● Cyanosis and open-mouth breathing in
Cardiac chamber abnormalities, abnormal wall thick- severe cases.
nesses and/or pressure or flow irregularities may be ● Crackles, wheezes and sometimes muffled
detected using echocardiology. cardiac sounds.
ECG abnormalities may be detected, although this is
not as common in cats as in dogs. See main references The Cat With Stridor (page 32),
The Dyspneic or Tachypneic Cat (page 47), The Cat
With Hydrothorax (page 71) and The Coughing Cat
Differential diagnosis (page 90) for details.
Other causes of chronic hypoxia, such as pulmonary
disease, should be differentiated from hypoxia from Pathogenesis
congenital or degenerative cardiac disease.
Respiratory disease causes chronic hypoxia, stimu-
lating increased secretion of erythropoietin and
Treatment resulting in polycythemia.
Treatment of cardiac conditions is dependent on cor- The most common cause of chronic pulmonary disease
rect diagnosis of the cause of cardiac failure. in cats is feline asthma/feline bronchitis complex,
which is an idiopathic inflammatory condition causing

Treatment
a combination of bronchoconstriction, chronic airway
inflammation and excessive mucus production. Treatment of respiratory conditions is dependent on the
Parasitic pulmonary disease such as lungworm or heart- correct diagnosis of the cause of the respiratory con-
worm may also cause chronic respiratory signs with dition, using a thorough diagnostic work-up proce-
intermittent hypoxia. dure.
Specific therapies are needed to treat respiratory
Clinical signs infections.
Coughing, intermittent dyspnea and hypoxia (oxy- Symptomatic medical therapy is recommended for
gen saturation <92%) are the most common clinical chronic inflammatory pulmonary disease such as
signs of chronic feline respiratory disease. Dyspnea feline asthma/bronchitis complex. Oral corticosteroid
may be acute, chronic or intermittent. therapy at anti-inflammatory dose rates and bron-
chodilators such as terbutaline or aminophylline may
There may be open-mouth breathing and cyanosis in
reduce the severity and frequency of dyspneic episodes.
severely affected cats.
Inhaled corticosteroid and/or bronchodilator therapy
Crackles and wheezes from bronchial disease and/or can be administered using pediatric asthma inhalers.
pleural effusion may be heard on thoracic auscultation.
Prognosis
Diagnosis
The prognosis for feline respiratory disease is good
Chronic pulmonary disease presents with auscultatory for most respiratory infections, although chronic
abnormalities, together with a history of intermittent infections may result in chronic inflammatory dis-
or continuous dyspnea and often chronic coughing. ease even after successful treatment of the infection.
Thoracic radiology reveals characteristic lung pat-
terns associated with bronchial, pleural or pul- POLYCYTHEMIA VERA*
monary disease.
Bronchoalveolar lavage cytology and microbiology Classical signs
is useful in the diagnosis of inflammatory or bacterial ● Injected dark pink mucous membranes.
(e.g. Mycoplasma felis) lung disease. ● ± History of intermittent bleeding
Fecal flotation and examination should be performed diatheses.
to check for parasites such as lungworm ● ± Systolic ejection (hemic) murmur.
(Aleurostrongylus abstrusus). ● ± Central nervous system signs, such as
seizures.
Serology should also be performed to detect heart- ● PCV > 60% with low serum erythropoietin
worm (Dirofilaria immitis) infection in endemic areas, concentration and normal blood O2
as clinical signs of feline heartworm disease are gener- saturation.
ally respiratory in nature.
Toxoplasma serology may be performed as the lungs
are a common site for the extra-intestinal (tissue) phase Pathogenesis
of the disease.
Polycythemia vera results from an absolute increase in
red cell mass because of a clonal proliferation of neo-
plastic erythroid stem cells in the bone marrow asso-
ciated with myeloproliferative disease.
Other causes of chronic hypoxia, such as congenital ● Erythroid precursors proliferate independent of
or degenerative cardiac disease, should be differenti- erythropoietin in a normal orderly pattern of matu-
ated from hypoxia caused by chronic pulmonary disease. ration.
Because normal feedback inhibition of erythrocytosis Treatment

does not occur, circulating erythropoietin levels are
usually very low. Primary polycythemia should be treated with phle-
botomy and intravenous fluids to reduce PCV to
Polycythemia vera is very rare in cats. below 60%.
There is often leukocytosis and thrombocythemia. Ten ml/kg/day of blood should be removed, and replaced
The erythrocytes produced in polycythemia vera are with an equivalent volume of fluid (0.9% NaCl or bal-
morphologically normal. anced electrolyte solution) or the cat’s own plasma.
● Regular phlebotomies may be adequate to maintain
PCV. If phlebotomies are required more than once
Clinical signs a month to maintain PCV < 60%, hydroxyurea ther-
Mucosae are dark pink. apy should be tried.
Bleeding may occur from numerous sites, e.g. nose, Bone marrow can be suppressed using hydroxyurea
gums, skin, gastrointestinal tract, urinary tract or in the indefinitely (15–30 mg/kg q 24 h with food, reduce
eye. dose to 15 mg/kg q 24–48 h after 7–14 days).
● Complete blood counts should be performed every
Central nervous system signs such as seizures, abnor- 7–14 days until PCV is normal, then every 3–4
mal behavior, ataxia and blindness often occur because months.
of reduced vascular perfusion of the central nervous ● When using hydroxyurea, serious bone marrow
system. depression resulting in anemia, thrombocytopenia
There may be a history of polydipsia and polyuria. and leukopenia may occur, so cats receiving the
drug need to be monitored carefully. If leukopenia,
Dilated tortuous retinal vessels and retinal hemor- thrombocytopenia or anemia develops, stop the
rhage may be observed on ophthalmic examination. drug until blood counts are normal, and then
A systolic ejection murmur (hemic murmur) may be resume at a lower dose.
present over the base of the heart secondary to abnor-
mal viscosity. Prognosis
The prognosis for polycythemia vera is guarded,
Diagnosis depending on the response to treatment and the inci-
dence of side effects of the therapies used.
Polycythemia vera is diagnosed when there is a combi-
nation of marked erythrocytosis (PCV > 60), low or
EXCESSIVE BLOOD TRANSFUSION
undetectable serum erythropoietin levels, normal
OR OVERDOSE OF EXOGENOUS
plasma protein concentration and normal blood O2
ERYTHROPOIETIN
saturation levels.
The bone marrow has increased cellularity with ery- Classical signs
throid hyperplasia or panhyperplasia. There is rela-
● Injected mucus membranes.
tively normal maturation of erythroid precursors and
● Weakness.
cells have normal morphology, with no evidence of
● CNS signs including seizures.
neoplasic features. Myeloid to erythroid ratio may be
normal, or reflect erythroid hyperplasia.
Clinical signs
Differential diagnosis This is a potential, although previously unreported,
cause of polycythemia.
Polycythemia vera needs to be differentiated from other
more common causes of erythrocytosis, such as dehy- Expected clinical signs are those of erythrocytosis, i.e.
dration, hyperthyroidism and chronic hypoxic car- weakness, injected mucus membranes and neurological
diac or pulmonary disease. signs.
Serum erythropoietin levels are normal or elevated,

Diagnosis
and blood O2 saturation levels are normal.
The diagnosis is made using a combination of an appro-
priate history and clinical signs.
NEOPLASIA Secondary inappropriate polycythemia must be differ-
entiated from relative polycythemia in dehydration,
Classical signs secondary polycythemia due to hypoxia, and from
primary polycythemia.
● Signs are referable to the causative space-
● In neoplastic conditions, there is a normal plasma
occupying mass.
protein concentration, normal blood O2 saturation
● Mucosae may be dark pink.
and normal or increased serum erythropoietin
● Signs of hyperviscosity, e.g. tortuous
concentration. This differentiates secondary inap-
retinal vessels, seizures, bleeding
propriate polycythemia associated with neoplasia
diatheses, polyuria, polydipisia.
from other conditions causing polycythemia.
Pathogenesis Treatment
It is hypothesized that renal and other visceral tumors Treatment should be directed at the tumor, which is the
may secrete erythropoietin or an erythropoietin-like underlying cause of the polycythemia.
substance, resulting in erythrocytosis. While these Polycythemia may reoccur if metastatic foci secrete
tumors have been reported to cause polycythemia in erythropoietin or an erythropoietin-like substance.
humans and dogs, they are yet to be reported as a cause
of polycythemia in the cat.
Prognosis
This kind of polycythemia is secondary to another
pathological condition and inappropriate, since The prognosis depends on the underlying cause of
blood O2 saturation levels are normal. the polycythemia. The prognosis with neoplasia varies
according to the tumor type.
Clinical signs
Clinical signs are referable to the underlying neoplasia RENAL SPACE-OCCUPYING MASS
and polycythemia.
Mucus membranes are dark pink. Classical signs
Signs of hyperviscosity include tortuous retinal vessels,

● Signs are referable to the causative space-
seizures and other CNS signs, and intermittent bleeding occupying mass.
diathesis.
● Dark pink mucosae.
● Signs of hyperviscosity, e.g. tortuous
retinal vessels, seizures, bleeding
Diagnosis diatheses, polyuria, polydipisia.
● ±Signs of renal insufficiency, such as
Erythrocytosis associated with neoplasia is diagnosed
azotemia, reduced urine specific gravity,
when there is a combination of marked erythrocytosis
polydipsia and polyuria.
(PCV > 60), normal or increased serum erythropoietin
levels, normal plasma protein concentration, and nor-
mal blood O2 saturation levels. Pathogenesis
Visceral tumors are diagnosed ideally by abdominal A space-occupying renal mass such as a cyst, hydro-
ultrasound, although intravenous pyelography may nephrotic disease or tumor may induce local tissue
also be a valuable imaging technique for renal masses. hypoxia, stimulating renal oxygen sensors, resulting in
increased erythropoietin production. These sensors are Treatment

thought to be located in the juxtaglomerular complex.
Treatment should be directed at the space-occupying
Some renal tumors may secrete erythropoietin or an mass, which is the underlying cause of the poly-
erythropoietin-like substance, resulting in erythrocy- cythemia.
tosis.
Nephrectomy may be considered in cases of second-
This kind of polycythemia is secondary to another ary inappropriate polycythemia from a renal space-
pathological condition and inappropriate, since occupying mass, but nephrectomy is considered a
blood O2 saturation levels are normal. last-resort treatment as the resultant reduction in func-
tional renal mass may precipitate renal insufficiency or
Clinical signs failure. Also, polycythemia may reoccur if metastatic foci
secrete erythropoietin or a functionally similar substance.
Clinical signs are referable to the inciting condition,
whether renal or neoplastic. Lethargy, weight loss and
inappetence are common.
Prognosis
The prognosis depends on the underlying cause of
Mucus membranes are dark pink.
the polycythemia. Polycystic renal disease is a
Signs of hyperviscosity may be present including tor- degenerative condition with a poor prognosis, and
tuous retinal vessels, seizures and other CNS signs, and most renal tumors have a guarded prognosis, at best.
intermittent bleeding diathesis. The prognosis with other kinds of neoplasia varies
according to the tumor type.
Signs of renal insufficiency, such as azotemia, reduced
urine specific gravity, polydipsia and polyuria may be
present. However, not all cases of polycythemia from ACUTE SYSTEMIC ANAPHYLAXIS
renal space-occupying masses will be accompanied by
signs of renal insufficiency, due to the relatively large Classical signs
functional reserve of the kidneys.
● Acute dyspnea.
● Hypotensive shock.
Diagnosis ● Collapse.
Renal space-occupying masses are best visualized using ● Pale mucous membranes.
abdominal ultrasound, although intravenous pyelog-
raphy may also be a valuable imaging technique. Pathogenesis
Serum erythropoietin levels are normal or elevated, Acute systemic anaphylaxis is caused by exposure to a
and blood O2 saturation levels are normal. foreign antigen, usually protein, and generally by the
intravenous route.
Differential diagnosis While prior exposure to the antigen is usually necessary
Secondary inappropriate polycythemia must be differ- for sensitization to occur, anaphylaxis may occur on
entiated from relative polycythemia caused by dehy- first exposure to the antigen. This is termed an ana-
dration, secondary polycythemia from hypoxia and phylactoid reaction.
primary polycythemia. Anaphylaxis causes increased vascular permeability,
● When a renal space-occupying mass is causing poly-
allowing potentially large amounts of plasma to escape
cythemia, plasma protein concentration and blood from the intravascular space, resulting in hemoconcen-
O2 saturation levels should be normal, while serum tration.
erythropoietin concentration is often inappropriately
high. These factors differentiate secondary inappro- It is also hypothesized that epinephrine is released
priate polycythemia due to a renal space-occupying during acute shock, causing splenic contraction and
mass from other conditions causing polycythemia. the infusion of large numbers of stored erythrocytes
into the circulation.
protocol), supplemental O2 and intravenous high-dose

Clinical signs
prednisolone sodium succinate (100 mg/cat IV). The
Clinical signs of acute systemic anaphylaxis vary rate of fluid administration should be as rapid as possi-
between species, as the major organs affected in the ble to restore circulating blood volume. In cats, 150 ml
reaction are species-specific. can be given rapidly in the first hour but additional flu-
ids should be administered more slowly to prevent pul-
Since the “shock organ” in the cat is the lung, pul-
monary edema. Fluid therapy may be evaluated by
monary signs such as severe acute dyspnea predominate.
monitoring blood pressure, packed cell volume and
Signs of hypotensive shock, such as pallor and col- urine output.
lapse, accompany the pulmonary signs.
Adjunctive therapy with bronchodilating agents
The onset of clinical signs occurs in seconds to min- (epinephrine 0.2 ml/cat of a 1:1000 dilution IV;
utes after exposure to the inciting antigen. terbutaline 0.1 mg/kg SC or IV) and antihistamines
(chlorpheniramine maleate 1 mg/kg SC) may also be
Occasionally, cutaneous swelling may be noted around
used.
the face and paws.
Prognosis
Diagnosis
Since acute systemic anaphylaxis is such an acute,
Polycythemia may be evident on hematological exam-
overwhelming and life-threatening condition, the prog-
ination. Typically, mucus membranes are pale and
nosis is guarded to poor, depending on how promptly
signs are peracute. This is in contrast to other causes of
and aggressively therapy is initiated, and perhaps on the
polycythemia where mucous membranes are dark pink
amount of inciting antigen to which the cat was
and there are often signs suggesting chronic disease
exposed and the rapidity of exposure.
such as weight loss. Diagnosis is made by a combina-
tion of appropriate history and characteristic clini-
cal signs. STRESS-INDUCED SPLENIC
No laboratory tests are currently available to make CONTRACTION
a definitive diagnosis of acute systemic anaphylaxis.
Classical signs
Blood O2 saturation is acutely and severely reduced.
● The stress response in cats may include
splenic contraction, with a resultant
Differential diagnosis infusion of stored splenic erythrocytes into
the circulation.
Polycythemia associated with anaphylaxis is usually
● Hemoconcentration caused by stress is
readily distinguishable from all other causes of poly-
usually mild and transient.
cythemia due to its peracute onset. Accompanying clin-
ical signs differentiate it from dehydration, which is
associated with more chronic signs including anorexia Diagnosis
and depression.
Affected cats often have an appropriate history of acute
Acute systemic anaphylaxis must be differentiated from stress. This may be stress associated with surgery or
other causes of acute shock such as major trauma. other treatment, as well as the flight-or-fight response
to acute stress.
Treatment There may be associated signs of acute stress such as
dilated pupils and behavioral changes.
Acute shock caused by anaphylaxis should be treated
by a combination of intravenous fluid therapy at Erythrocytosis should resolve promptly after the incit-
shock dose rates (perhaps including colloids in the ing incident.
SEVERE OBESITY (PICKWICKIAN HIGH ALTITUDE

SYNDROME)
Classical signs
Classical signs
● Mild polycythemia in an otherwise healthy
● Cats are morbidly obese (body condition cat living at altitude.
score 9/9), have chronic dyspnea and ● Decreased O2 levels in the atmosphere at
difficulty with normal ambulation. high altitudes stimulate increased renal
erythropoietin production in response to
tissue hypoxia.
Diagnosis
While the Pickwickian syndrome causing chronic

Diagnosis
hypoxia and resultant erythrocytosis has not been
reported in cats, it is logical to assume that this may Expected signs include mild polycythemia in an other-
occur. wise healthy cat.
Morbid obesity may predispose to tissue hypoxia from A presumptive diagnosis is based on finding mild poly-
inadequate alveolar ventilation because of fat accumu- cythemia in a cat living at high altitude (e.g. > 5000
lation in the thorax and compression of upper airways. feet/1500 m).
Blood O2 saturation levels are expected to be low
(<92%), and there should be slightly to markedly
increased circulating levels of erythropoietin.
RECOMMENDED READING
Giger U. Polycythemia: Is it p. vera? Proc 21st ACVIM Forum 2003: 742–744.
Nitchke EK. Erythrocytosis in dogs and cats: Diagnosis and management. Compend Contin Educ Pract Vet 2004; 26:
104–118.
Veterinary Information Network (VIN) at www.vin.com has many excellent board discussions and conference pro-
ceedings on use of fluids for dehydration and resuscitation including several by J Wohl, L Barton and TM Rieser.
26. The cat with hyperlipidemia
Boyd Robert Jones
KEY SIGNS
● Lipemia (lactescent appearance of plasma).
● Lipemia retinalis (lipemic appearance of retinal vessels with a pink or salmon
color).
● Cloudy cornea or anterior chamber.
● Cutaneous xanthomata (yellowish subcutaneous nodules or plaques).
MECHANISM?
● Hyperlipidemia is an increase in the plasma triglyceride and/or cholesterol
concentrations.
● Hyperlipidemia may result from a primary defect in triglyceride or cholesterol
metabolism.
● Hyperlipidemia may also occur when lipoprotein metabolism is altered by systemic
disease.
WHERE?
● Abnormalities occur in blood/plasma, eye, skin, peripheral nerves, spleen, kidney and liver.
● Hyperlipidemia should be suspected when there is a persistent fasting hyperlipidemia (> 12
hours after feeding) or when a cat has any of the following signs:
● Lipemia retinalis.
● Cloudy cornea or anterior chamber.
● Cutaneous xanthomata.
● Peripheral neuropathy.
● Splenomegaly.
WHAT?
● The most common causes of hyperlipidemia are idiopathic and secondary systemic diseases,
such as diabetes mellitus.
569

Diseases causing hyperlipidemia
ANOMALY
● Inherited hyperchylomicronemia (p 575)
Domestic shorthair cats. May have no clinical signs, or signs of hyperlipidemia such as lipemia retinalis,
xanthomata or peripheral neuropathy. Caused by a breed-related defect in lipoprotein lipase (LPL) acti-
vation due to a point mutation in the gene for LPL.
● Cholesterol ester storage disease (p 576)
Siamese < 1 year old, corneal clouding, intermittent diarrhea and vomiting, hepatomegaly.
Lysosomal acid lipase (cholesterol ester hydrolase) deficiency results in accumulation of choles-
terol esters in lysosomes.
METABOLIC
● Nephrotic syndrome (p 576)
Hypercholesterolemia occurs in the nephrotic syndrome as a sequel to protein-losing nephropathy.
Proteinuria with hypoalbuminemia are classical findings.
● Diabetes mellitus**(p 574)
Hypertrigylceridemia occurs in some cats with diabetes. LPL activity is reduced, but the cause of
the hypertriglyceridemia is likely multifactorial. Hypercholesterolemia may also occur and results
from increased hepatic synthesis of cholesterol.
● Idiopathic hyperlipidemia*** (p 573)
May have no clinical signs, or have signs of hyperlipidemia. Any breed may be affected but
Burmese kittens are over-represented and may present with severe anemia, lethargy and dyspnea.
The cause of many cases of hyperlipidemia will be unconfirmed. The cause in most of these cases
is due to a so far unidentified defect in lipid metabolism.
INTRODUCTION Lipid metabolism

Medium- and short-chain fatty acids are bound to albu-
MECHANISM min and transferred from the intestine directly to the
liver via the portal vein.
Definition of terms
Cholesterol and triglycerides are insoluble in plasma
Hyperlipidemia is an increase in the plasma trigly- and their transport through the bloodstream relies upon
ceride and/or cholesterol concentrations. their incorporation into specialized lipid–protein com-
plexes called lipoproteins.
Hyperlipidemia may result from a primary defect in
lipoprotein metabolism or from lipoprotein metabolism There are four classes of lipoproteins (chylomicrons,
being altered by systemic disease. VLDL, LDL and HDL), each with separate physical
and chemical characteristics.
Lipemia is the lactescent appearance of plasma and
indicates an increase in the plasma triglyceride concen- Each of the four lipoprotein classes have discrete roles
tration in chylomicrons and/or low-density lipoproteins. in plasma lipid transport.
26 – THE CAT WITH HYPERLIPIDEMIA 571
● Chylomicrons and VLDL are the primary trans- ● Triglycerides are released to adipose tissue, skeletal
porters of triglycerides. and cardiac muscle, and lactating mammary tissue
● LDL and HDL are the cholesterol transporters by lipoprotein lipase.
(LDL are the cholesterol suppliers; HDL are the ● The cholesterol-rich remnant particles are processed
cholesterol scavengers). by a second lipase, called hepatic lipase, to form
LDL.
All lipoproteins share a common structure.
● The hydrophobic components (triglycerides and Low-density lipoproteins (LDL) are formed from
cholesteryl esters) are carried in the core of the par- VLDL and deliver cholesterol to peripheral tissues such
ticle. as the adrenal and reproductive glands.
● These are surrounded by a polar coat of phospho- ● These lipoproteins migrate in the β-position on
lipids, special proteins called apolipoproteins, and electrophoresis.
a small amount of free cholesterol. ● Cholesterol delivery is facilitated by the interaction of
the structural protein of LDL (apolipoprotein B-100)
Chylomicrons are formed in the intestinal mucosa.
with specific receptors, called the LDL receptors.
They transport dietary triglycerides from the small
● LDL receptors are also found in high concentra-
intestine to adipose tissue for storage, to skeletal mus-
tions in the liver where they remove excess LDL.
cle for use as energy substrate, and to lactating mam-
mary tissue for milk fat synthesis. High-density lipoproteins (HDL) scavenge choles-
● Chylomicrons are the largest and lightest of the terol that is excess to tissue needs and transport it to the
lipoproteins, and remain at the origin on gel elec- liver. The HDL are the major carriers of cholesterol.
trophoresis. ● HDL are the smallest and most dense lipoproteins
● Triglycerides are removed from chylomicrons and migrate in the α-position on electrophoresis.
through the action of the enzyme lipoprotein ● In the liver, cholesterol is excreted as bile salts,
lipase. stored, or redistributed to other body tissues as
– Lipoprotein lipase is located on the luminal VLDL and LDL.
surface of capillary endothelium in adipose tis- ● HDL are secreted into the circulation from the
sue, skeletal and cardiac muscle, and lactating liver and intestine as small immature discoidal
mammary tissue. particles.
– Lipoprotein lipase is activated by apolipopro- ● The free cholesterol picked up from peripheral
tein C-II (apoC-II) on the surface of the chylo- tissues is esterified by the enzyme lecithin:choles-
micron, and releases the triglycerides as fatty terol acyl transferase (LCAT) to form cholesteryl
acids. esters, which enter the core of the particles.
– Chylomicrons are cleared from the blood – In humans, the cholesteryl esters are transferred
within 12 hours after eating, and therefore, are from HDL to chylomicrons, VLDL and LDL
not normally present in the fasted cat. and hence back to the liver.
– Removal of triglycerides from the chylomicron – Cats lack the enzyme responsible for this, cho-
leaves a smaller remnant particle that is rich in lesteryl ester transfer protein (CETP), so that
cholesterol. the HDL continue to pick up free cholesterol and
– The remnant particle is removed from the circu- expand under the action of LCAT.
lation by specific cell surface receptors in the – These large HDL particles then acquire apoE
liver that recognize apolipoprotein E (apoE) and are subsequently removed from the circula-
present on the surface of these particles. tion by the remnant and LDL receptors in the
liver.
Very-low-density lipoproteins (VLDL) export trigly-
cerides and cholesterol from the major site of endo-
Hyperlipidemia
genous synthesis in the liver, and deliver triglycerides
to peripheral tissues. Diagnosis of hyperlipidemia is based on history, physi-
● VLDL are also known as pre-β lipoprotein cal examination, examination of plasma and special
because of the electrophoretic mobility. laboratory tests.
Understanding the metabolic origins of hyperlipidemia

WHERE?
provides the basis for the investigation of patients and
for therapeutic management. Signs of hyperlipidemia cause problems in the follow-
ing organs: blood/plasma, eye, skin, peripheral nerves,
Fasting hypertriglyceridemia results from defects in
spleen, kidney, liver.
metabolism of chylomicrons and/or VLDL.
The most common signs include:
Hypercholesterolaemia results from defects in the
● Lipemia retinalis (lipemic appearance of retinal
metabolism of LDL and HDL.
vessels with a pink or salmon-colored appearance
Compositional changes in certain lipoproteins, for rather than red).
example cholesterol-enrichment of VLDL or trigly- ● Cloudy cornea or lipemic aqueous (cloudy ante-
ceride-enrichment of LDL, may also occur in certain rior chamber of eye).
disorders. ● Cutaneous xanthomata (well-circumscribed soft,
smooth, alopecic subcutaneous nodules or plaques,
which may have a yellowish appearance and may
Hypertriglyceridemia ulcerate in locations prone to trauma, often multiple
Plasma concentrations of triglycerides are raised when over the trunk and head, less frequently involve the
the amounts of chylomicrons and/or VLDL increase in limbs).
the circulation. ● Peripheral neuropathy resulting in paresis or
● Chylomicrons and VLDL are both catabolized by paralysis of cranial or spinal nerves (e.g. 3rd sym-
the enzyme lipoprotein lipase, which removes the pathetic producing Horner’s syndrome, trigeminal,
triglycerides from these particles. tibial or radial nerves).
● Defects in the activity of lipoprotein lipase, either ● Splenomegaly.
genetic or acquired, result in reduced clearance

of chylomicrons and VLDL and hypertriglyc-
WHAT?
eridemia.
The most common cause of hyperlipidemia is idio-
Persistence of chylomicrons in the circulation for > 12
pathic. The abnormality in lipid metabolism is uniden-
hours after ingestion of a fat-containing meal and in
tified.
fasting plasma are abnormal and suggest impaired
lipoprotein lipase activity. The most common metabolic cause is diabetes mel-
litus.
Chylomicrons rise to the surface and form a creamy
layer when plasma is refrigerated for 12–14 hours. The inherited diseases are uncommon but occur most
VLDL remain in suspension and produce a turbid or frequently in young kittens (weaning to 6 months age).
lactescent sample.
Diagnosis is based on history and physical examina-
tion, blood examination, special diagnostic tests and
Hypercholesterolemia histopathology.
Raised plasma cholesterol concentrations generally

result from deranged metabolism of LDL and HDL. LABORATORY REFERENCE RANGES
Raised HDL concentrations have been found in cer- Reference values (adult cats):
tain types of secondary hyperlipidemia in cats, but ● Cholesterol 1–4.5 mmol/L (40–170 mg/dl)
the precise metabolic origins of this change is ● Triglyceride 0.2–1.1 mmol/L (20–100 mg/dl)
unclear.
Clinical pathology laboratories have their own refer-
Hypercholesterolemia does not produce visible lipemia ence ranges for both cholesterol and triglycerides.
(opalescence) as HDL and LDL are too small to refract Always compare your results with your own labora-
light. tory’s reference ranges.
There are no significant breed or gender differences blood at 7, 12 and 24 hours post-prandially.
which affect plasma lipid values in cats. Measure triglyceride in each sample. Triglyceride
values should return to baseline by 7 hours and
Pregnancy is not a cause of secondary hyperlipidemia.
remain stable for 24 hours. Cats with altered
During lactation, the concentration of cholesterol triglyceride metabolism will show elevated triglyc-
decreases owing to a reduction in VLDL cholesterol eride values which fail to return to baseline by 24
and LDL cholesterol concentrations and suppression of hours.
HDL cholesterol production. ● Quantification of the individual lipoprotein
classes by qualitative methods (gel electrophore-
The plasma cholesterol concentration in suckling kit-
sis). Electrophoresis confirms the relative abun-
tens up to 8–12 weeks of age is significantly higher
dance of a lipoprotein class: chylomicrons (origin),
than the adult reference range reflecting the fat content
VLDL (pre-Beta), LDL (beta) and HDL (alpha 1).
of the queen’s milk.
● Lipoprotein separation and quantification#.
● Assay of lipoprotein lipase activity. The Heparin
The cat with hyperlipidemia – what to do response test. Collect a basal blood sample.
Administer 100 IU heparin intravenously and col-
Is the hyperlipidemia from a recent meal?
lect a second blood sample after 10 minutes.
● Fast overnight and resample. Plasma should be
Measure triglyceride in each sample. A reduction in
cleared of lipid in 7–8 hours in a healthy cat.
triglyceride indicates LPL activity. Special lipid
● The presence of hypercholesterolemia in the
laboratories can complete more specialized LPL
absence of triglyceridemia does not give visibly
assays# on each sample. This procedure is advised.
lipemic plasma.
● Assay of LCAT activity#.
● If hyperlipidemic, measure the plasma cholesterol
● PCR analysis for a specific genetic disease#.
and triglyceride. If triglyceride is elevated there is
– The tests marked # are available in a small num-
a defect in chylomicron or VLDL metabolism. If
ber of research laboratories and are not available
the cholesterol is elevated there is more likely a
to most veterinarians.
defect in LDL and/or HDL metabolism.
● Is the hyperlipidemia secondary to other diseases?
Eliminate other diseases including: DISEASES CAUSING
– Diabetes mellitus (polyuria, polydipsia, weight HYPERLIPIDEMIA
loss, persistent hyperglycemia, glycosuria).
– Nephrotic syndrome (proteinuria, hypoalbu-
minemia, hypercholesterolemia). IDIOPATHIC HYPERLIPIDEMIA***
If no secondary disease is identified, the problem is Classical signs
probably a primary disorder of lipid metabolism.
● None.
Specialized tests are available and can be applied in the ● Lipemia retinalis.
investigation. They are useful in lipidemic cats to deter- ● Cutaneous xanthomata.
mine the metabolic basis for the hyperlipidemia, which ● Anemia.
helps determine therapy. ● Lipemic aqueous or cornea.
These tests include:
● Hypertriglyceridemia and/or
● Chylomicron refrigeration test: Harvest serum or
hypercholesterolemia.
plasma and refrigerate at −4˚C overnight. Chylo-
microns, if present will rise to form a “cream” layer
Pathogenesis
(the supranatant). If the infranatant is lactescent this
indicates elevated triglyceride in VLDL. Idiopathic hyperlipidemia includes all cats with hyper-
● Tests of chylomicron clearance: Fast for 24 hours. triglyceridemia and/or hypercholesterolemia for which
Collect a basal blood sample. Feed a small meal of the defect in lipid metabolism is unidentified. Currently
a high-fat tinned cat food (4–5 g per cat). Collect most cats with hyperlipidemia are classified as idiopathic.
Burmese kittens are over-represented, but any breed Once hypertriglyceridemia resolves, many kittens can
may be involved. tolerate normal cat food.
Pathogenesis is unknown, but it is probably due to a Gemfibrozil (Lopid, Parke Davis, 7.5–10 mg/kg daily)
primary defect of lipid metabolism, if secondary causes may help reduce triglyceride values if dietary therapy
(diabetes nephrotic syndrome) have been eliminated. alone fails.
There is probably one phenotypic expression for many Marine (fish) oils which are rich in n-3 fatty acids may
different genetic mutations, which may involve the reduce plasma triglycerides by decreasing the synthesis
enzyme lipoprotein lipase or other essential molecules of VLDL. Dose at 10–30 mg/kg PO daily for cats that
in lipoprotein metabolism, e.g. apolipoproteins. are unresponsive to dietary fat restriction.
The pathogenesis of the concurrent clinical signs and Always check body weight at regular intervals if cats
anemia is unknown. are on a calorie-restricted or reducing diet to ensure
normal weight is maintained.
Clinical signs
There may be no clinical signs, just hyperlipidemia. DIABETES MELLITUS**
Alternatively, a variety of clinical signs may occur
Classical signs
including:
● Lipemia retinalis. ● Polyuria, polydipsia.
● Cutaneous xanthomata. ● Polyphagia or inappetance.
● Lipemic aqueous. ● Weight loss.
● Frequently associated with severe anemia (PCV ● Persistent hyperglycemia, glycosuria.
< 11%) in kittens around the time of weaning.
Kittens may present with acute lethargy, dyspnea See main references on page 236 for details (The Cat
and death within 48 h. Usually the entire litter has With Polyuria and Polydipsia).
severe fasting hypertriglyceridemia. Reported in
purebred (including Siamese, Persian, Burmese,
Pathogenesis
Oriental) and domestic shorthair breeds.
Hyperlipidemia occurs in some cats with diabetes
Diagnosis mellitus.
Confirmation of hypertriglyceridemia and/or hyper- Rarely, cats with diabetes have concurrent hyper-
cholesterolemia. adrenocorticism or acromegaly, conditions which result
in insulin-resistant diabetes mellitus.
Other diagnostic tests may indicate where the abnor-
mality of lipid metabolism is located by the relative dis- The hypertriglyceridemia results from a combination
tribution of the lipoproteins. of reduced lipoprotein lipase activity as insulin is
required for normal activity of this enzyme, increased
Treatment synthesis of VLDL due to poor regulation of hormone-
sensitive lipase, increased flux of non-esterified fatty
Severely anemic kittens need emergency treatment
acids to the liver and increased triglyceride synthesis.
with supplemental oxygen and a blood transfusion
to survive. The raised cholesterol concentrations reflect increased
hepatic synthesis, which leads to down-regulation of
The plasma triglyceride should be reduced to less
LDL receptor activity and increased LDL.
than 5.5 mmol/L (500 mg/dl), which minimizes the
risk of hyperlipidemia-associated signs.
Clinical signs
Feed either a homemade or commercial diet low in sat-
urated fats, calorie restricted, and high in fiber to Signs of diabetes mellitus (polyuria, polydipsia, weight
reduce lipid values. Wean kittens onto a low-fat diet. loss).
Lipemic plasma. Clinical signs

Lipemia retinalis. No clinical signs other than hyperlipidemia may be evi-
Cutaneous xanthomata (very rare finding in diabetic dent.
cats). Alternatively, a variety of clinical signs may occur
including:
● Lipemia retinalis.
Diagnosis
Increased plasma or serum glucose and glycosuria, ● Peripheral nerve paralysis involving:
together with signs of diabetes (see Diabetes mellitus in – 3rd sympathetic cranial nerve (Horner’s syn-
The Cat With Polyuria and Polydipsia, page 237). drome with protrusion of 3rd eyelid, miosis, nar-
rowed palpebral fissure).
Treatment – Tibial nerve.
– Radial nerve.
Insulin or oral hypoglycemic drugs. See Diabetes mel- – Trigeminal nerve.
litus for treatment details, page 237. ● Splenomegaly.
● Xanthomata in other organs including:
Feeding a low-fat diet is essential.
– Intestine.
– Heart.
INHERITED HYPERCHYLOMICRONEMIA – Liver.
Classical signs In kittens there is increased still-birth rate, reduced

body mass and reduced growth rates.
● Domestic short-haired cats.
● Hyperchylomicronemia and
Diagnosis
hypertriglyceridemia.
● Lipemia retinalis (if triglyceride > 15 Gross lipemia of fasting blood samples. Blood looks
mmol/L). like “cream of tomato soup”.
Massive hyperchylomicronemia and elevated VLDL.
● Peripheral neuropathies.
Cream layer and lactescent serum or plasma are present
● Reduced appetite and lethargy.
after refrigeration.
● or NO CLINICAL SIGNS other than
hyperlipidemia. Raised triglycerides (15–150 mmol/L, 1300–13 000
mg/dl).
Raised triglyceride and cholesterol in chylomicrons
Pathogenesis
and VLDL.
Absent lipoprotein lipase (LPL) activity.
Lowered LDL cholesterol.
Inherited as an autosomal recessive mode of inheritance.
Reduced fat tolerance. Post-prandial plasma lipid val-
Heterozygotes have intermediate LPL activity consis- ues are significantly elevated for > 48 hours after fat
tent with an autosomal recessive trait. ingestion in homozygous cats.
Molecular basis for the LPL deficiency is a single base- There is no difference in lipoprotein composition
pair change in the lipoprotein lipase gene. An arginine between normal and affected genotypes except for an
for glycine transposition is present at amino acid increase in the ratio of apoC to apoE in chylomicrons
residue 412 in exon 8. and VLDL.
This mutation results in the expression of catalytically Pre- and post-heparin plasma contains increased LPL
inactive enzyme, which fails to be activated or to bind mass, but no enzymic activity, that is, triglyceride does
appropriately. not decrease after heparin.
PCR mismatch analysis can detect normal cats, homozy- Diagnosis

gotes and heterozygotes for this genetic defect.
History of vomiting and diarrhea with corneal
clouding.
Treatment
Plasma cholesterol values are in the reference ranges.
A low-fat diet either homemade or commercial will
Plasma triglyceride and low-density lipoprotein are
reduce blood lipid values and clinical signs will regress
increased.
after 4–12 weeks.
Plasma and serum are grossly normal.
Siblings and parents should be tested, and affected
homozygotes and heterozygotes neutered and not bred. Heparin response test indicates normal lipoprotein
lipase activity.
The prevalence of this mutation in cat populations is
very low. Cytoplasmic vacuolation containing cholesterol esters
is present in a proportion of neutrophils (16%), lym-
phocytes (56%), and monocytes (60%), stained by
CHOLESTEROL ESTER STORAGE DISEASE
Wright-Giemsa.
Classical signs Acid lipase activity in cultivated fibroblasts and hepa-
tocytes is markedly decreased compared with controls.
● Siamese cats.
● Corneal clouding.
● Hepatomegaly. Differential diagnosis
● Intermittent vomiting and diarrhea.
Other inherited metabolic and lysosomal storage diseases.
Pathogenesis Treatment
Lysosomal lipase (cholesterol ester hydrolase) In theory, a reduced-fat diet and treatment with one of
hydrolyzes cholesterol esters in various lipoproteins as the HMG CoA-reductase inhibitors (statins) should
they are removed from plasma and enter the cellular reduce cholesterol synthesis, and up-regulate LDL-
compartment. receptor activity thus reducing plasma cholesterol,
Deficiency of this enzyme results in cholesterol ester triglyceride and the LDL cholesterol concentrations.
accumulation within lysosomes which may result in This treatment was not attempted in the reported cases.
organ failure and death.
The condition is transmitted as an autosomal recessive NEPHROTIC SYNDROME
mode of inheritance in the Siamese.
Classical signs
Homozygous recessive cats are more severely affected
than the heterozygotes. ● Proteinuria.
● Hypoalbuminemia.
● Peripheral edema.
Clinical signs ● Ascites.
Siamese breed.
● ± polydipsia, polyuria.
Onset of signs before 1 year of age.

Pathogenesis
Corneal clouding.
Rare disease in cats.
Intermittent vomiting and diarrhea.
Hypercholesterolemia is a common sequel to protein-
Hepatomegaly. losing glomerulopathy.
LDL and HDL cholesterol concentrations are both Diagnosis

increased.
Proteinuria.
The exact pathogenesis of the cholesterol elevation is
unknown. Hypoalbuminemia.
Concurrent hypercholesterolemia.
Clinical signs
Peripheral edema.
Ascites.
± polydipsia and polyuria.
RECOMMENDED READING
Ginzinger DE, Lewis MES, Yuanhong MA, et al. A mutation in the lipoprotein lipase gene is the molecular basics
of Chylomicronemia in a colony of domestic cats. J Clin Invest 1997; 97: 1257–1266.
PART 9
Cat with signs of gastrointestinal
tract disease
27. The cat with salivation

Victor Hans Menrath
KEY SIGNS
● Drooling.
● Excessive salivation.
MECHANISM?
● Ptyalism (drooling) occurs as a result of either: excessive saliva production or normal
production of saliva but inability to swallow or retain saliva in the mouth.
WHERE?
● Oral causes – mouth (including pharynx) and tongue.
● Extra-oral causes – includes central nervous system and gastrointestinal tract causes.
WHAT?
● Fear or stress is the most common cause of non-pathological ptyalism in the clinic situation.
Careful examination of the oral cavity is essential to distinguish oral from extra-oral
causes.
● Recurrent, intermittent, non-stress-induced ptyalism in young cats (usually less than 1 year) is
likely to be caused by portosystemic shunt.
● Other causes of recurrent, intermittent ptyalism (usually in cats more than 1 year old) include
hiatal hernia, gastroesophageal intussusception and diaphragmatic hernia.
● Most other causes of ptyalism are likely to be acute in onset and produce continuous drooling.
Pain is a major cause of ptyalism in cats.
578
27 – THE CAT WITH SALIVATION 579

Diseases causing salivation
ANOMALY
● Portosystemic shunt (PSS)* (p 588)
Congenital liver abnormality causing intermittent central nervous system (CNS) signs with ptyal-
ism. Usually in young cats (< 1 year). Often associated with eating. Affected cats are often very
stunted in size.
MECHANICAL
● Esophageal foreign body* (p 590)
Repeated swallowing attempts with neck outstretched/retching, regurgitating white or blood
stained foam.
● Oral foreign body** (p 586)
Acute onset of salivation, gagging and pawing at the mouth. Dysphagia, halitosis and inappetence
may be evident. Most commonly associated with a bone lodged laterally between the 4th upper
premolars.
NEOPLASTIC
● Oral neoplasia* (p 587)
Squamous cell carcinoma most common. Often under tongue or associated with a canine tooth or
in tonsillar region. Ulcerated and/or proliferative.
PSYCHOLOGICAL
● Psychogenic causes*** (p 582)
Ptyalism can be caused by stress, fear, pleasure and pain.
INFECTIOUS
● Rabies (p 599)
Progressive central nervous system signs of muscle fasciculation, weakness, ataxia com-
bined with behavioral changes, low-grade fever and ptyalism in unvaccinated cats. Serious
zoonosis.
● Feline herpes virus** (p 583)
Pronounced ptyalism can occur in the very early stage of the disease. Invariably followed by
the normal classical signs of viral upper respiratory disease – i.e. sneezing, naso-ocular
discharge, etc.
● Feline calicivirus** (p 582)
Ptyalism as a result of tongue laceration due to virus, usually in young kittens. Often associated
with other upper respiratory signs – e.g. chemosis, sneezing, coughing.
● Feline spongioform encephalopathy (FSE) (p 600)
Progressive central nervous signs including hindlimb ataxia, behavioral changes, hyperesthesia,
head tremor and muscle fasciculation. Ptyalism.
continued
580 PART 9 CAT WITH SIGNS OF GASTROINTESTINAL TRACT DISEASE
continued
● Feline panleukopenia (parvo virus) (p 600)

Continuous ptyalism has been recorded in a 3-month-old kitten suffering from feline panleukope-
nia caused by feline parvovirus.
INFLAMMATORY
● Esophagitis* (p 591)
Characterized by repeated attempts at swallowing, ptyalism, “neck stretching” and regurgitation of
ingested food, often with mucoid foam. Early treatment essential to prevent secondary esophageal
stricture.
● Periodontal disease/periodontitis*** (p 582)
Saliva-stained perilabial fur, often reluctance to pick up food, quidding and pawing at mouth.
IMMUNE
● Feline oral inflammatory disease (plasmacytic-lymphocytic stomatitis)** (p 585)
Mild to severe granulomatous inflammation in fauces. Often extremely painful and refractory to
treatment. Cats resent mouth examination.
● Eosinophilic granuloma complex (EGC)** (p 586)
Orange-white lesions on tongue surface, soft and hard palate. Usually associated excessive groom-
ing due to skin allergy. Lesions often painful.
TOXIC
●Household cleaners and disinfectants* (p 587)
Common cause of chemical burns on tongue. Especially shower recess cleaners.
● Acetaminophen (paracetamol) toxicity (p 595)
Facial edema, cyanosis and chocolate urine. Prompt treatment is essential.
● Organophosphate and carbamate toxicity (p 594)
Carbamate toxicity is most common. Miosis, muscular twitching and hypersalivation.
● Pyrethrin and pyrethroid toxicity (p 595)
Salivation, tremors, seizures. No definitive test for diagnosis.
● Spider envenomation (p 597)
Severe pain, vocalization, hyperexcitability and ataxia early, progressing to muscular weakness and
collapse. Severe, prolonged ptyalism, possibly due to pain.
● Dieffenbachia (dumb cane) poisoning (p 598)
Sudden onset of salivation immediately after chewing plant. Tongue paralysis is characteristic.
● D-limonene, linalool and crude citrus oil extracts (p 598)
Used in insecticidal sprays and shampoos. Ptyalism may be the only clinical sign. Muscular
tremors and ataxia can occur in more severely affected cases.
● Lead poisoning (p 596)
Gastrointestinal signs (inappetance, diarrhea) and/or CNS signs (behavioral changes, seizures,
blindness).
● Oral medication** (p 584)

Can be unpleasant tasting or irritant to the oral mucous membranes. Some drugs can cause a
delayed hypersalivation (e.g. trimethoprim-sulfa combinations).
TRAUMA
● Tongue laceration** (p 584)
Sudden onset, inability to eat, rapid secondary bacterial infection.
● Jaw fracture/dislocation** (p 584)
Inability to chew, slack jaw, asymmetry of jaw.
●Hiatal hernia/gastroesophageal intussusception (p 592)
Uncommon, intermittent salivation, age of cats. Intussusception can be rapidly fatal.
● Diaphragmatic hernia with incarcerated stomach (p 598)
Very uncommon, intermittent salivation, often associated with feeding and dyspnea.
INTRODUCTION
Medication or attempted medication with unpleasant-
MECHANISM? tasting oral medication.
Ptyalism (hypersalivation, drooling, hypersialosis) Pleasure is a common non-pathological cause of

occurs as a result of ptyalism at home. This often occurs in older cats and is
usually associated with other signs of pleasure, e.g.
Either: excessive saliva production due to stimulation
purring and kneading of paws.
of the salivary nuclei located in the brainstem via local
receptors (taste and tactile) in the mouth and on the Ptyalism at home unassociated with pleasure and
tongue, or via higher centers in the central nervous ptyalism in the clinic, unassociated with fear or stress
system (CNS). suggests a pathological cause.
Or: normal or increased saliva production but with an Careful history-taking will help differentiate patho-
inability to swallow or retain the excessive saliva in the logical from non-pathological causes of ptyalism.
mouth due to an anatomical problem.
Careful examination of the oral cavity will help differ-
entiate oral from extra-oral causes of ptyalism.
WHERE? Recurrent, intermittent (non-stress-induced) ptyalism
Oral causes mouth (including pharynx) and tongue. in young cats (<1 year old) is likely to be caused by
portosystemic shunt.
Extra-oral causes including CNS and gastrointestinal
tract (especially esophagus and stomach). Other causes of recurrent, intermittent ptyalism include
hiatal hernia, gastroesophageal intussusception and
diaphragmatic hernia.
WHAT?
Most other causes are likely to be acute in onset and
The most common non-pathological cause of ptyalism in
produce continuous drooling.
the clinic situation is fear or stress and occurs especially
in very nervous cats. These cats do not have ptyalism at Pain is a major cause of ptyalism in the cat – usually
home. combined with dilated pupils.
DISEASES CAUSING SALIVATION PERIDONTAL DISEASE/PERIODONTITIS***
Classical signs
PSYCHOGENIC CAUSES***
● Dysphagia.
Classical signs ● Pawing at mouth.
● Halitosis.
● Ptyalism. ● Ptyalism.
● Dilated pupils.
With Bad Breath or Oral Lesions).
Pathogenesis
Fear, anxiety, pleasure, nausea. Clinical signs
May be exacerbated by underlying or concomitant Severe peridontal disease will result in tooth loss, deep
hyperthyroidism. pockets with heavy anaerobic infections and strong hal-
itosis.
Anticipation of unpleasant experience (e.g. tableting or
painful injection). Cat may show signs of attempting to pick up food,
dropping it and pawing at mouth.
Especially in “highly-strung” cats, e.g. Siamese.
Peri-labial fur may be saliva stained.
Makes oral medication virtually impossible.
Feline odontoclastic resorptive lesions (“neck lesions”)
Probably the most common cause of ptyalism in the cat
can also be very painful and show similar signs.
in the clinic situation.
Diagnosis
Clinical signs Probing to identify periodontal pockets. Tapping affected
Drooling, ptyalism. teeth will cause jaw “chattering”.
Usually during traveling or at veterinary clinic.

Often triggered by cat recognizing unpleasant event FELINE CALICIVIRUS**
to come.
Classical signs
Pupils dilated when due to stress or fear.
● Sneezing, coughing, oculonasal discharge.
Repeated lip smacking and swallowing ● Oral ulceration, especially tongue.
● Ptyalism.
See main reference on page 11 for details.

Treatment
0.01 mg/kg PO or SC atropine 1/2 hour before traveling/-
event. Clinical signs
Diazepam 0.5 mg/kg PO or SC 1/2 hour before traveling/- Sudden onset of acute conjunctivitis (usually one eye
event. first).
Above drugs can be combined. Rapidly followed by sneezing, coughing, pyrexia.
Tongue ulceration is common – ulcer is usually large, Severe clinical signs are usually associated with a
in the central tongue it is often butterfly-shaped. very short incubation period (1–4 days) (i.e. severity
Ulceration of the nose philtrum, dorsal surface hard of signs is virus dose-responsive).
palate, footpads can also occur.
Salivation is followed by varying degrees of pharyngi-
Most commonly in kittens 8–12 weeks of age. tis, laryngitis, tracheitis and esophagitis and classical
signs of viral upper respiratory tract infection, i.e.
Salivation due to ulceration and pain in the tongue.
coughing, sneezing, runny eyes and nose.
Occasional viral pneumonia, lameness (“limping kit-
May have concurrent FeLV, FIV, calicivirus, bordetella
ten syndrome”).
or mycoplasma infection.
Growth rate of kittens is often temporarily delayed.
Diarrhea can occur and be protracted. Clinical signs
Hypersalivation syndrome usually occurs in adult
Diagnosis unvaccinated or poorly vaccinated cats, with novel
exposure.
Clinical signs.
Severe drooling salivation with depression and rapid
Response to antibiotics.
dehydration precedes classical signs of viral upper res-
PCR, viral isolation. piratory tract disease.
Pyrexia usually lasts for period of hypersalivation
Treatment (24–48 h).
Supportive nursing and broad-spectrum antibiotics, e.g. Often followed by severe pharyngitis, laryngitis, tra-
doxycycline (2.5 mg/kg PO q 24 h), cephalexin (30 cheitis, esophagitis (retching, choking cough, vomit-
mg/kg PO q 12 h). ing) and requires long periods of intensive care if signs
are severe.
Maintain hydration.
Diagnosis
FELINE HERPES VIRUS** PCR, viral isolation.
Classical signs of viral upper respiratory tract infection
Classical signs
(i.e. sneezing, coughing etc.) follow salivation within
● Sudden onset of severe ptyalism. 24–48 h.
● Depression, inanition, dehydration.
● Pyrexia followed by sneezing, coughing
Treatment
naso-ocular discharge.
Rapid dehydration can occur – IV fluid support, steam
See main reference on page 7 for details (The Cat With inhalation therapy.
Acute Sneezing or Nasal Discharge).
Place feeding tube (esophagostomy, gastrostomy).
Be prepared for 2–4 weeks intensive nursing if signs
Pathogenesis
are severe.
Caused by feline herpes virus I.
Prevent secondary bacterial rhinitis and sinusitis with
Viral replication in oral mucosa and/or perhaps salivary broad-spectrum antibiotics, e.g. cephalexin (30
glands causes massive production of saliva in the very mg/kg PO; 15 mg/kg q 12 h) or amoxycillin/clavulanic
early stages of the course of the disease. Viral paro- acid (12.5 mg/kg PO q 12 h) which should be contin-
tiditis could be involved in the cause of salivation. ued for 4 weeks minimum.
Prognosis Reluctance to groom.
Good with good intensive care. Paws and chest are sticky with foul-smelling saliva.
Cat will almost always become a herpes virus carrier. Rapid secondary bacterial infection.
ORAL MEDICATION** Diagnosis

Obviously lacerated tongue.
Classical signs
● Ptyalism, excessive salivation.
Treatment
● Usually immediately following oral
medication. Surgical debridement and repair with absorbable
● Sometimes ptyalism delayed. sutures (e.g. 4/0 plain gut).
Antibiotics. Parenteral or paste-form best, e.g. cephalexin
Clinical signs (15 mg/kg IM q 12 h), amoxycillin/clavulanic acid
(8.5 mg/kg SC or IM q 24 h).
Acute ptyalism following attempted or successful oral
medication.
Often associated with rapid tongue movements in an JAW FRACTURE/DISLOCATION**
attempt to remove drug or taste from mouth.
Classical signs
Ptyalism is often delayed for 5–10 minutes after the
successful administration of trimethoprim-sulfa tablets. ● Ptyalism.
● Mouth held open (“slack-jawed”).
Ptyalism is self-limiting and usually short duration (e.g.
● Jaw asymmetry.
5–10 minutes).
Clinical signs
Treatment
Excessive salivation.
Treatment is not necessary.
Unable to close jaw.
Reassure owner that it is self-limiting.
Jaw dislocation without fracture is uncommon – temporo-
mandibular dislocation can be rostrodorsal (most
TONGUE LACERATION**
common) or caudo-ventral. Dislocation is almost
invariably bilateral.
Classical signs
Mandibular symphyseal separation is most common
● Ptyalism.
and is often associated with temporo-mandibular dislo-
● Dysphagia.
cation and/or fracture of the mandible, causing jaw
● Halitosis.
asymmetry.
Trauma from cat’s own teeth biting on tongue (e.g. Symphyseal separation is usually obvious on examina-
car accident, falling from height). tion.
Trauma from cat fight – claw slicing tongue. Careful palpation of both horizontal and vertical sec-
tions of mandibles from inside mouth under anesthesia
Clinical signs will help to identify fractures.
Hemorrhage may be significant if acute. Careful radiography.
Treatment granulomatous tissue may partially occlude pharynx

in severe cases.
Rostral tempero-mandibular joint (TMJ) disloca-
tion can be reduced by placing a ballpoint pen or pen- Dysphagia, excessive salivation and weight loss occur
cil horizontally across the mouth behind the lower in severe cases.
molars and forcibly closing mouth until joints relo- Severe faucitis is often associated with FIV or FeLV
cated. infection.
Caudal TMJ dislocations are reduced in a similar
fashion but the mandible is forced rostrally.
Surgical repair of symphyseal separation by using cir- Treatment
clage stainless steel wire. Thorough dental prophylaxis and complete extraction
of all teeth showing resorptive lesions. Severe faucitis
FELINE ORAL INFLAMMATORY DISEASE** often responds to extraction of all molars and premolars
(PLASMACYTIC-LYMPHOCYTIC and any retained root tips.
STOMATITIS/FAUCITIS) (PLASMA CELL Antibiotic therapy using amoxycillin (10 mg/kg PO q
GINGIVITIS AND PHARYNGITIS) 12 h), metronidazole (10 mg/kg PO q 12 h) or clin-
damycin (5.5 mg/kg PO q 12 h) often results in
Classical signs improvement, but rarely complete resolution of inflam-
● Ptyalism. mation. Doxycycline (25 mg/kg PO q 24h) has anti
● Difficult prehension. infammatory effects.
● Halitosis. In most cases, antibiotic therapy will need to be combined
● Pain, reluctance to open mouth. with immunosuppresive therapy. Many cases will not
● Severe faucitis, gingivitis. be able to be medicated orally and will require par-
enteral therapy, e.g. methylprednisolone acetate (2–4
Pathogenesis mg/kg IM).
Etiology unknown. Suggested causes are viral (espe- If the cat can be medicated orally, prednisolone (2
cially calicivirus), bacterial and immunological (pos- mg/kg PO q 12 h) for 10 days, then taper.
sibly hypersensitivity to plaque proteins). For very refractive cases, may have to use azathioprine
The condition appears to be the result of a chronic- (0.3 mg/kg PO q 72 h), or cyclophosphamide
immune-mediated process because lymphocytes and (6.25–12.5 mg/cat once daily, 4 days PO per week) or
plasma cells predominate, and lesions respond to chlorambucil (0.1–0.2 mg/kg q 24 h PO initially, then
immunosuppressive drugs. q 48 h) or aurothioglucose (0.5–1 mg IM every 7
days). Cyclosporine (5 mg/kg PO q 12–24h) can be
Moderate to severe calicivirus-induced gingivitis very effective.
occurs commonly in young (8–12 weeks) kittens with
or without concomitant tongue ulceration. Gingivitis A topical gel (Bonjela ®, choline salicylate, cetalko-
often persists as chronic gingival hyperplasia through nium chloride, Reckitt & Coleman Pharmaceuticals,
adulthood, predisposing to excessive plaque, periodon- UK) applied with or without sedation/anesthetic has
tal disease and early loss of teeth. A small percentage been reported to ameliorate the faucitis and gingivitis
of these cats develop plasmacytic-lymphocytic faucitis in affected cats. The gel is rubbed into the lesions in
later in life, usually middle age. the mouth over a period of about 2 minutes once
a week until signs regress. Note that this is an off-
label use of this product designed as an oral analgesic
Clinical signs gel in humans and contains salicylate. To date there
Intense oral pain and resentment to oral examination have been no reported adverse reactions with its use
occurs with severe faucitis. Bright red proliferate in cats.
Prognosis Pathogenesis
This condition, in its severe form remains one of the Immune-mediated process resulting in granuloma
most difficult and frustrating to treat in feline prac- formation (eosinophilic granuloma) in the oral cavity,
tice. Thorough oral debridement is essential. especially the dorsum of the tongue and hard palate,
but can occur in other areas, e.g. soft palate.
Most cases eventually end up requiring chronic medica-
tion with immunosuppressants for the rest of their lives. Histopathology shows typical granuloma formation
with collagen degeneration.
ORAL FOREIGN BODY**
Usually associated with a concurrent pruritic skin dis-
ease and excessive grooming.
Classical signs
The cause of this association is unknown. Oral
● Ptyalism, acute onset.
mucous membrane trauma from excessive grooming
● Gagging, pawing at mouth.
could cause the lesions, or both the oral and skin
● Halitosis.
lesions may be a reaction to antigens, such as flea anti-
● Dysphagia.
gen, on the coat.
Pathogenesis
Clinical signs
Usually sliver of bone jammed laterally between 4th
upper premolars. Salivation and dysphagia usually only occurs in
severe cases of eosinophilic granuloma complex with
Linear foreign body (string, cotton) around base of
associated glossitis.
tongue.
Oral exam reveals single or multiple raised, firm 1–2
Clinical signs mm white-yellow nodules, scattered throughout mouth,
but especially on dorsum tongue surface causing the
Salivating, pawing at mouth – sometimes bleeding
surface of the tongue to have “cobble-stone” appear-
laceration around mouth from self-trauma.
ance. Associated glossitis may occur causing difficulty
Dysphagia, halitosis. in prehension and swallowing.
Evidence of over-grooming and itchy skin disease is
Diagnosis
usually present.
Self evident on oral examination.
Halitosis may occur with secondary bacterial infection.
Examine roof of mouth and under tongue.
Diagnosis
Treatment
Lesions have a very characteristic appearance.
Remove foreign body.
Histopathology confirms diagnosis.
Antibiotics if secondary infection from self-trauma or
foreign body damage.
EOSINOPHILIC GRANULOMA COMPLEX Oral neoplasia. Squamous cell carcinoma usually occurs
(EGC)** on the ventral surface of the tongue in the region of
frenulum and has an ulcerated, red appearance.
Classical signs
● Ptyalism. Treatment
● Dysphagia.
Treatment can be difficult and frustrating.
Treat concurrent skin allergy and ectoparasites to Differential diagnosis

achieve control.
Inflammatory polyps – usually have stalk.
Change to a novel protein diet.
Intra-oral abscess and granulation tissue can have a
Regular manual grooming and bathing. similar appearance – differentiate by biopsy or trial
Prednisolone (2 mg/kg PO q 12 h for 5–10 days, then antibiotics.
taper). Eosinophilic granuloma complex (linear granu-
Megestrol acetate (2.5–5 mg/cat PO for 4 days, then loma) has characteristic white-yellow nodules – dif-
2.5–5 mg q 5–7 days until lesions regress). ferentiate by biopsy or trial corticosteroids.
NB This drug, although very effective, has numerous side
effects especially in the Burmese breed (diabetes melli- Treatment
tus, pyometra, obesity, iatrogenic Cushings disease).
Treatment of lingual squamous cell carcinoma in the
Cyclosporine (5 mg/kg PO q 12–24h). cat has not proved successful, however some of the
Doxycycline (2.5 mg/kg PO q 24h). newer chemotherapic agents may be more effective
combined with tumor excision.
Mandibular masses can be treated by partial
ORAL NEOPLASIA * mandibulectomy.
Classical signs
Prognosis
● Ptyalism, often blood stained.
● Halitosis. Grave for squamous cell carcinoma of the tongue.
● Dysphagia. For other tumors, the prognosis will depend on the
tumor type and suitability for treatment.
Pathogenesis
Squamous cell carcinoma is the most common neo-
plasm. Usually on the ventral surface of the tongue HOUSEHOLD CLEANERS AND
causing immobility of the tongue but sometimes tonsil- DISINFECTANTS*
lar crypt or under the canine tooth.
Classical signs
Usually in older cats (> 10 years).
● Ptyalism, acute onset.
Other tumors include epulis, fibroscarcoma and lym- ● Dysphagia.
phoscarcoma. ● Depression, saliva-stained front feet.
Clinical signs
Excessive salivation, often blood stained. Signs usually Pathogenesis
present longer than 1 week.
Most common household cleaning products and disin-
Dysphagia, difficulty in prehension. fectants are extremely toxic to cats.
Facial distortion, halitosis. These include chlorine (sodium hypochlorite), strong
alkalis, strong acids, pine oils, phenolic compounds,
Weight loss due to inability to eat or metastatic disease.
hydrocarbons and quaternary ammonium com-
pounds.
Diagnosis
Most cause contact necrosis of skin and mucous
Biopsy and histologic examination.
membranes especially if undiluted or incorrectly
Radiography to assess extent of tumor invasion. diluted.
Most toxicities occur when the cat licks water con- Pain control in the early stages, e.g. buprenorphine
taining cleaner residues (e.g. shower recess cleaners) (0.005–0.01 mg/kg IV, IM q 4–8 h).
or by licking paws after walking through the chemical.
This causes corrosive damage of the tongue surface, PORTOSYSTEMIC SHUNT*
mucous membranes of the mouth and occasionally,
esophagus. Classical signs
● Ptyalism, excessive salivation.
Clinical signs
● Repeated swallowing and lip smacking.
Acute onset of hypersalivation, depression, dysphagia. ● Behavioral and neurological signs
including seizures.
Front legs are often wet and stained with saliva.
● Signs are intermittent, progressive and
Rapid secondary bacterial infection occurs in the often associated with eating.
mouth causing halitosis. ● Usually in young cats (< 1 year).
Tongue slightly swollen, partially immobile, and the
dorsal surface initially appears very pale and dull
Pathogenesis
(early necrosis).
Portosystemic shunts (portocaval shunt, portovascular
Sloughing may occur to variable extent of the sur-
anastomosis) are vascular communications between
face of the tongue leaving raw, ulcerated surface –
portal and systemic venous systems.
usually within 36–48 hours.
Clinical signs are the result of gut-produced neuro-
There is rapid onset of dehydration due to saliva loss
toxins bypassing normal detoxification in the liver,
and inability to lap water.
entering the systemic circulation and affecting the
Neurological signs (muscle weakness, fasciculations, CNS.
seizures) may occur with quaternary ammonium and
These gut-produced neurotoxins include ammonia,
pine oil/phenolic compound toxicities.
mercaptans, GABA agonists, benzodiazepam ligands
Esophageal corrosion may occur with choking, gag- and tryptophan.
ging and retching and regurgitation of white foam.
Portosystemic shunts can be congenital or acquired,
Other areas of body may be affected, e.g. pads of feet. intrahepatic or extrahepatic.
Most feline portosystemic shunts are congenital, single
Diagnosis
and extrahepatic.
History of exposure.
Reduced blood supply to the liver often results in a
Occasionally characteristic smell of toxic agent, e.g. small liver.
chlorine.
High urinary excretion of ammonia and uric acid may
Methemoglobinemia indicates toxicity involves pheno- result in urate urolithasis and/or ammonium biurate
lic compound. crystals in urine.
Treatment
Clinical signs
Wash corrosive material off cat.
CNS disturbances associated with hepatic
Supportive fluids, nutrition, and broad-spectrum encephalopathy are most frequent, occurring in 95% of
antibiotics, e.g. cephalexin (15 mg/kg IM q 12 h). cases of feline portosystemic shunting.
Corticosteroids in the early stages, especially if Neurological signs vary considerably and include mild
esophagitis is suspected, e.g. dexamethasone (0.1–0.2 behavioral changes (aggressive behavior, staring into
mg/kg IV, IM q 12–24 h). space, head-pressing), ataxia, weakness, stupor,
blindness, dilated pupils, tremors, seizures, coma Biochemistry – normal to decreased BUN, hypocho-
and death. lesterolemia, mild increase in ALT and AST.
The hallmark of the CNS signs is that they are inter- Ultrasonography – can be useful to visualize shunt
mittent, progressive in severity and often precipi- vessel especially with intrahepatic shunts.
tated by a high-protein meal.
Portography – contrast portogram via mesenteric vein
Hypersalivation is an especially prominent clinical provides definitive diagnosis and location of shunt vessel.
sign (78%).
Urinalysis – may reveal ammonium biurate crystals or
Signs wax and wane with episodes lasting minutes to urate uroliths.
hours and may or may not be associated with feeding.
Liver biopsy – histology shows periportal fibrosis, bile
Signs related to hepatic dysfunction include stunted duct hyperplasia.
growth, delayed anesthesia recovery, diarrhea, poly-
Transcolonic portal scintigraphy – availability likely
dipsia/polyuria and lethargy.
to be restricted.
Signs of urinary tract disease as a result of urate urolithi-
asis include hematuria, dysuria and pollakiuria. Differential diagnosis
Signs often abate with antibiotic administration (i.e. The combination of intermittent, recurrent ptyalism
reduced production of toxic metabolites by enteric bac- and neurological signs associated with eating in a
teria). young cat is almost pathognomonic for portosystemic
shunt.
In cats, clinical signs of hepatic encephalopathy most
commonly become apparent at about 6 months of Viral encephalitides such as rabies and feline spon-
age. gioform encephalopathy can present with severe CNS
disturbances combined with ptyalism but these diseases
Diagnosis are always progressive and signs are continuous.
Serum bile acids – 2 hours post-prandial always ele- Lead poisoning can occasionally present with clinical
vated with portosystemic shunts (>100 μmol/L). signs of intermittent neurological disturbances and
● Serum bile acids are specific indicators of hepato- hypersalivation in the cat. Blood lead levels will con-
biliary disease in the cat. Fasting bile acids are nor- firm or rule out diagnosis.
mally less than 5 μmol/L and 2 hour post-feeding
Pyrethrin and pyrethroid toxicity produces signs of
bile acids usually less than 20 μmol/L. Cats with
hypersalivation and neurological signs. Signs are con-
portosystemic shunt usually have elevated (>100
tinuous and history of recent exposure generally con-
μmol/L) bile acids 2 hours after feeding. Serum bile
firms diagnosis.
acids concentration cannot however differentiate
between hepatocellular, vascular or cholestatic liver Organochlorine (chlorinated hydrocarbon) and
disease. organophosphate toxicity is characterized by hyper-
salivation and neuromuscular disturbances including
Ammonia tolerance test: more specific than bile
muscular disturbances such as muscular twitching,
acids, but not practical unless in-house ammonia test-
weakness and seizures. History of exposure and serum
ing available as ammonia is very labile. Cats with por-
cholinesterase levels (OP) will confirm diagnosis.
tosystemic shunt may have normal fasting blood
ammonia levels. Blood is taken 30 minutes after a chal-
Treatment
lenge with 100 mg/kg ammonium chloride. This
ammonia-loading test, although very specific, has a The medical management of portosystemic shunt
propensity for inducing vomiting and excessively high encephalopathy plays a vital role in both pre- and
serum ammonia levels causing severe CNS signs. post-surgical treatment.
Hematology – RBC microcytosis may occur (MCV Medical management on its own, however, is palliative
< 39 fl). at best.
Medical management consists of:

ESOPHAGEAL FOREIGN BODY*
● Minimize formation and absorption of ammonia
and other toxic substances by the administration
Classical signs
of oral antibiotics (ampicillin (20–40 mg/kg PO
q 8 h), metronidazole (10–25 mg/kg PO 24 h), ● Hypersalivation, dysphagia.
and oral lactulose 2.5–5 ml q 8 h). The dose of ● Gagging, retching, swallowing,
lactulose (a palatable syrup) should be increased outstretched neck.
or reduced to produce soft stools 2–3 times daily. ● Regurgitating white or blood-tinged foam.
● Retention enemas can be used to treat hepatic
coma. The enema consists of neomycin (15
mg/kg) plus lactulose (diluted 1:2 with warm
Pathogenesis
water) and is given in doses of 40–200 ml and
repeated until colon is completely empty and then Caudal-pointing papillary spines on the tongue and the
given every 6–8 hours as long as the coma persists. playful nature of cats make linear foreign body (string,
● Determine blood glucose, fluid, electrolyte and cotton thread) ingestion common. These are often
acid–base status of patient and normalize bal- wrapped around the base of the tongue.
ances using lactated Ringers solution supple-
Other foreign bodies include sewing needles, fish
mented with 2.5–5% dextrose and potassium
hooks, hair balls, V-shaped cooked avian bones (e.g.
chloride depending on laboratory results.
wish-bone) and string attached to the end of continen-
Control seizures with diazepam (0.25–0.5 mg/kg IV q tal sausages. These usually lodge at thoracic inlet,
6–8 h). base of the heart or at diaphragm hiatus.
Dietary therapy – the ideal diet should contain the Complications include secondary aspiration pneumo-
minimum amount of high-biological-value pro- nia, esophageal perforations, regional esophagitis with
tein, highly available carbohydrates as the primary or without secondary stricture and bronchoesophageal
source of energy, adequate levels of arginine and fistula.
minerals, and be palatable. Diets designed for renal-
failure cats generally meet these requirements
although, in severe cases, even more protein restric- Clinical signs
tion may be required.
Acute onset of gagging, retching, ptyalism, often with
Surgery is ultimately the treatment of choice as it offers neck stretched forward.
the possibility of cure.
Regurgitation of white foam often stained with fresh
● Surgery involves isolating the shunting vessels
blood.
and partial (using ameroid constrictor band) or
complete ligation depending on measured por- Signs of depression, anorexia, fever, cough and dysp-
tal venous pressure. nea can suggest esophageal perforation or aspiration
● Rapidly fatal portal hypertension and gastroin- pneumonia.
testinal venous stasis may occur with complete
Signs are generally continuous and persistent.
ligation of the shunting vessel and close obser-
vation is required for 48 hours in case repeat
surgery is required to relax the ligature.
Diagnosis
● Clinical signs of hepatic encephalopathy may
recur months after surgery, necessitating repeat History of playing with or eating a potential foreign
surgery to re-ligate the shunting vessel. body.
Plain and/or contrast radiography to demonstrate for-
Prognosis
eign body.
Good if surgery successful.
Endoscopy is useful to confirm the presence of a for-
Often difficult to manage medically without surgery. eign body and to assess damage to the esophagus.
Check under tongue for linear foreign body (e.g. cotton Pathogenesis
or string).
Most commonly due to gastric reflux during and after
anesthesia.
Pre-anesthetic and anesthetic agents suppress normal
Pharyngeal foreign body or acute pharyngitis. esophageal motility and can cause the lower esophageal
Examine pharynx under general anesthetic. sphincter to relax allowing gastric reflux.
Acute viral esophagitis/pharyngitis/laryngitis. Usually Refluxed in hydrochloric acid can reduce esophageal
other viral signs predominate (i.e. sneezing, running pH to 2.0 and cause protein denaturation of the
eyes, etc.). Both calici and herpes virus possible. esophageal mucosa.
Acute gastroesophageal intussusception or hiatal Once esophagitis exists, the lower esophageal sphinc-
hernia – usually intermittent signs. ter becomes incompetent, perpetuating reflux.
Caustic chemical pharyngitis/esophagitis (rare) is Tilting of the surgery table and poor patient prepa-
always associated with chemical burning of the dor- ration (food-filled stomach) before surgery predis-
sum of the tongue. poses cats to reflux esophagitis.
Esophagitis can occur secondary to esophageal for-
Treatment eign bodies or persistent vomiting.
Retrieval of the foreign body by endoscopy. Rarely, esophagitis can result from ingestion of caustic
Perforating foreign bodies require thoracotomy and agents.
esophagotomy. Pooling of gastric fluids and resultant esophagitis char-
Sewing needles and fish hooks on string can often by acteristically occurs in the region of the base of the
retrieved by passing a plastic tube down the string to heart.
dislodge and guard the foreign body during retrieval. Young animals with congenital esophageal hernia are
Broad-spectrum antibiotics (amoxicillin 20 mg/kg SC likely to have a higher risk for reflux esophagitis.
or IM q 12 h). Occasionally, esophagitis associated with severe feline
Withhold food and water for 24–48 hours. herpes virus or calicivirus infection occurs.
Intravenous or subcutaneous fluid support will be Pain and inability to swallow probably plays a major
required first 24–48 hours. role in pathogenesis of ptyalism.
Some foreign bodies can be pushed into the stomach If untreated, esophagitis often leads to secondary
and retrieved by gastrotomy. esophageal stricture.
Prognosis Clinical signs

Good unless esophageal perforation has occurred. Dysphagia, excessive salivation, repeated swallow-
ing attempts with out-stretched neck occurs in the
ESOPHAGITIS* early, acute phase of the disease syndrome.
Regurgitation of white froth, often blood stained
Classical signs occurs in the early stages of acute, severe esophagitis.
● Excessive salivation. Signs generally occur within 24–48 hours of anesthetic
● Repeated attempts at swallowing. if post-anesthetic esophagitis.
● Anorexia, dysphagia.
● Regurgitation. Intense pain associated with swallowing attempts may
cause the cat to cry out.
Concomitant oral ulceration and stomatitis may indi- Treatment

cate caustic chemical ingestion.
Acute reflux or chemical esophagitis must be
Regurgitation of food and/or vomiting can occur in treated aggressively in the early stage in an attempt
milder cases of esophagitis, hiatal hernia or to prevent fibrous esophageal stricture.
healing/stricture phase of severe acute esophagitis.
Preferably, all medication should be given parenter-
ally for the first 5–6 days.
Diagnosis
Broad-spectrum antibiotics to control secondary bacter-
History of chemical exposure, ingestion of a foreign ial infections (amoxicillin/clavulanic acid).
body or a recent anesthetic.
Corticosteroids to prevent stricture (dexamethasone
Survey radiographs of the esophagus are often unre- 0.2 mg/kg IM or IV q 12–24 h).
markable.
Sucralfate suspension to protect mucosa per os if not
Endoscopy reveals variable hyperemia, bleeding, vomiting (0.25 g PO q 8–12 h).
ulceration and pseudomembranes of the esophageal
mucosa, or a foreign body. Cimetidine (10 mg/kg IV, IM PO q 6–8 h) or raniti-
dine (2.5 mg/kg IV q 12 h; 3.5 mg/kg PO q 12 h) to
Post-anesthetic reflux esophagitis lesions are character- reduce gastric acidity.
istically in the region over the base of the heart.
Metoclopramide (0.2 mg/kg IV, IM, PO q 6–8 h) or
Reflux due to severe vomiting or hiatal hernia char- cisapride (5 mg/cat q 8–12 h) to promote gastric emp-
acteristically causes esophagitis in the distal esopha- tying.
gus.
Narcotics for pain control e.g. methadone 0.1–0.5
Endoscopy can differentiate a functional esophageal mg/kg IV or IM q 4–6 h
stricture due to severe mucosal and sub-mucosal
inflammation and edema from a fibrous stricture Placement of gastrotomy or esophagotomy tube for
(forming subsequent to severe esophagitis). nutrition while “resting esophagus” – leave in place
5–7 days.
Differential diagnosis Surgical repair of hiatal hernia, gastroesophageal her-

nia or diaphragmatic hernia.
Hiatal hernia usually causes intermittent signs of
vomiting, ptyalism, regurgitation and dyspnea. Plain Prognosis
radiography shows a soft tissue density dorsal to the
vena cava in the caudal thorax. Contrast radiography Esophageal stricture due to fibrosis and scarring sec-
reveals the gastric fundus in the region of the terminal ondary to esophagitis is common and is characterized
esophagus. by repeated regurgitation after eating.
Gastroesophageal intussusception – may cause inter- This can be treated with gradual dilatation of stricture
mittent signs but often causes persistent and severe by balloon dilation catheter or bouginage. Often
clinical signs of vomiting and salivation leading to requires repeated dilation over weeks or months to
rapid onset of vascular shock and death. Plain or con- achieve resolution of signs.
trast radiography or endoscopy to confirm.
Diaphragmatic hernia involving the stomach – rapid HIATAL HERNIA/GASTROESOPHAGEAL
expansion of incarcerated stomach after eating due to INTUSSUSCEPTION
accumulating gases causes rapid onset of dyspnea, sali-
vation and attempts to vomit. Plain or contrast radiog- Classical signs
raphy to confirm presence of stomach in the chest. ● Ptyalism.
Often history of feeding immediately prior to onset ● Vomiting/regurgitation.
of signs.
Classical signs—Cont’d Diagnosis

● May or may not be related to eating. Gastroesophageal intussusception:
● Dyspnea, hematemesis, collapse, shock, ● Plain thoracic radiographs show the presence
death with large intussusceptions. of a soft tissue mass in the esophagus cranial to
● Signs often intermittent the diaphragm. The gastric gas bubble in the cra-
nial abdomen is often missing indicating that the
stomach has prolapsed into the esophagus.
● The diagnosis can be confirmed with a barium
Pathogenesis swallow in which the barium will not pass

beyond the intussusception.
Hiatal hernia denotes herniation of the distal esopha- ● Endoscopy will reveal.
gus and proximal stomach into the thoracic cavity.
Hiatial hernia:
Hiatal hernias tend to be intermittent in nature but can ● The hernial sac is formed by the stretched
be persistent. phreno-esophageal ligament and sliding hernias
Gastroesophageal intussusception occurs when the are frequently associated with gastric reflux and
stomach (and occasionally duodenum, spleen, etc.) pro- esophagitis.
lapses (invaginates) into the distal esophagus with ● Plain radiographs may or may not reveal herni-
resultant compromise of blood supply to the prolapsed ation of the stomach and diagnosis is usually
segment. Gastroesophageal intussusception is usu- confirmed by barium swallow under fluo-
ally acute and persistent but can be chronic with inter- roscopy or by endoscopy.
mittent signs. ● Applying abdominal pressure during radiog-
raphy may help induce hernia.
Congenital or acquired laxity of the hiatus is sus- ● Endoscopy is also valuable in assessing the
pected to predispose to both hiatal hernias and gastroe- degree of esophagitis due to gastroesophageal
sophageal intussusception. reflux.
Diaphragmatic hernia may predispose to post-surgi-
cal gastroesophageal intussusception.
Reflux esophagitis occurs with both gastroesophageal
intussusception and hiatal hernias. Megaesophagus is often associated with hiatal hernia
and gastroesophageal intussusception. Regurgitation
is a predominant sign. Confirm that the megaesophagus
is unassociated with hiatal hernia or gastroesophageal
Clinical signs intussusception by esophagram.
Although uncommon, both gastroesophageal intussus- Esophageal foreign body. Signs of gagging, retching,
ception and hiatal hernias are a significant rule-out in salivation, repeated attempts at swallowing generally
ptyalism. acute onset and continuous. History of eating or play-
Chronic intermittent vomiting is characteristic for ing with foreign body. LOOK UNDER TONGUE!
both hiatal hernia and chronic gastroesophageal Confirm with plain and/or contrast radiographs or
intussusception. endoscopy.
Chronic, intermittent ptyalism can occur with or with- Porto-systemic shunt. Severe pain associated with
out vomiting and weight loss. gastroesophageal intussusception may induce signs that
may be confused with portosystemic shunt.
Acute bouts of respiratory distress may occur. Portosystemic shunt can be confirmed with serum bile
Large, acute gastroesophageal intussusception can acids.
cause rapid onset of shock associated with hemateme- Diaphragmatic hernia with incarcerated stomach.
sis, dyspnea, collapse and sudden death. Confirm with X-rays/contrast.
Treatment Cats are more susceptible to OP toxicity than dogs.

Poisoning often occurs following use of canine flea
Medical treatment: products on cats.
● Control of esophagitis and clinical signs with
ranitidine (3.5 mg/kg PO q 12 h) or cimetidine Most cat poison cases are due to carbamates.
(5–10 mg/kg PO q12 h).
● Feed low-fat diet. Fat delays gastric emptying
Clinical signs
time and it is therefore desirable to feed low-fat
diets. Elevated feedings may help some cats Early signs include apprehension, increased swallow-
and should be trialled especially if megaesopha- ing, ptyalism, muscular twitching around the face
gus is present. and eyes. Miosis and bradycardia occur.
● If no response to medical therapy surgical
Muscular twitching progresses to whole-body muscle
repair is warranted. fasciculations and generalized tetany causing a stiff-
Surgical repair involves anatomical replacement of legged gait progressing to a sawhorse stance (i.e. all
herniated organs, reduction in size of esophageal hia- four legs stiff and apart).
tus, phrenicoesophageal plexy and left-sided fundic Abdominal pain, cramping diarrhea, vomiting and
gastropexy. frequent urination occurs commonly and eventually
progresses to muscular weakness and paralysis.
Death can occur due to respiratory failure.
ORGANOPHOSPHATE AND CARBAMATE
TOXICITY Delayed neuropathy: certain OPs (e.g. fenthion) can
cause a delayed (usually 7–10 days) neuropathy caus-
Classical signs ing hindlimb weakness and characteristic ven-
troflexion of the neck. All the other signs of acute OP
● Ptyalism, lacrimation, vomiting, diarrhea, poisoning are absent when delayed signs occur.
pollakiuria. Delayed neuropathy may occur after minimal exposure
● Miosis, muscular tremors, seizures. and there may be no history of acute signs in the pre-
● Dyspnea, respiratory failure. ceding 7–10 days.
● Bradycardia, depression, death.
● Rapid onset of clinical signs.
Diagnosis
History of recent application of OP or carbamate and
Pathogenesis characteristic signs.
Organophosphates (OPs) and carbamates cause inhibi- Cholinesterase assay – whole blood, serum or plasma.
tion of acetylcholinesterase (AChE) and pseudo- Results should be interpreted in light of clinical signs
cholinesterase, which allows accumulation of and time of onset of signs.
acetylcholine (ACh) in RBCs and the post-synaptic
receptors of nervous tissue and muscle. Differential diagnosis
Accumulation of ACh results in marked excitation of Pyrethrin toxicity – history of exposure.
all effector organs.
Quaternary ammonium toxicity – history of exposure
OPs are generally considered irreversible inhibitors of and ptyalism with mouth ulcers rather than general-
AChE activity, while carbamates are slowly ized parasympathetic signs as occur with OPs.
reversible inhibitors.
OPs are stored in fat and slowly released into the cir- Treatment
culation. Lean, long-haired breeds of cats are more
severely affected. Establish IV fluid line and (oxygen/ventilation if needed).
Atropine IV (0.25–0.5 mg/kg) repeated to effect can be Diagnosis

given S/C once stabilized. Do not over-atropinize.
History of exposure, clinical signs.
Diazepam (1 mg/kg IV) repeated to effect to control
seizures. No definitive diagnostic clinical test available to
date.
Muscle fasciculations can be controlled with diphenhy-
dramine (2–4 mg/kg PO q 8 h).
2-PAM (20 mg/kg IM or IV) is effective against con-
firmed OP toxicity if given in the first 24 hours. Organophosphate/carbamate toxicity – blood choline-
Repeat 8 hourly until stable. Can be given with sterase level low.
atropine. Do not use in carbamate toxicity.
Prevent further absorption – wash cat with hair sham- Treatment
poo, and give activated charcoal PO. Diazepam (0.2 mg/kg IV) to effect to control tremors
Diphenhydramine is used to treat delayed neuropathy or seizures.
(2–4 mg/kg PO q 8 h). Phenobarbital IV if not controlled with phenobarbital
add pentobarbital IV. NB Phenobarbital is an anticon-
Prognosis vulsant where pentobarbital stops muscular activity.
Pentobarbital is associated with paddling on recovery,
Generally good with treatment. which can be difficult to distinguish from seizure activ-
ity, and makes it less suitable for acute seizure control.
PYRETHRIN AND PYRETHROID TOXICITY Wash cat to reduce further absorption.
Classical signs Recovery usually in 1–4 days.
● Ptyalism. Small doses of atropine (0.01–0.02 mg/kg IV, IM, SC

● Tremors, ataxia, seizures. q 6–8 h) can be used to control salivation. (Do not
● Depression or hyperexcitability. over-atropinise.)
● Vomiting, diarrhea. IV fluids, O2, ventilation in severely affected cases.
Pathogenesis ACETAMINOPHEN (PARACETAMOL)

TOXICITY
Popular insecticide for use on cats.
Slows the closing of the sodium ion gate in nerve cells Classical signs
resulting in repetitive discharges or membrane depolar-
● Ptyalism.
ization.
● Pale, blue-tinged mucous membranes.
Extremely bitter taste of topically-applied pyrethroids. ● Facial edema, respiratory distress.
● Anorexia, vomiting.
● Hemoglobinuria.
Clinical signs
Ptyalism, tremors, ataxia, seizures.
Occasionally dyspnea and coma occurs. Pathogenesis
Hyperthermia, vomiting and diarrhea can occur. Acetaminophen is widely used as an antipyretic and
analgesic in human medicine.
Rapid onset of signs post exposure (within a few
hours). Most common drug-induced toxicosis in the cat.
Metabolized in the liver to glucuronide and sulfate Treatment

conjugates.
Prompt and early treatment is essential.
Cats are deficient in glucuronyltransferase and the
glucuronidation and sulfation biotransformation routes Gastric lavage within 4–6 hours of ingestion.
are rapidly saturated, causing acute toxicity. Activated charcoal per os.
Hepatic necrosis and methemoglobinemia results. N-acetylcysteine (Mucomyst) 140 mg/kg as a 5% solu-
Fatal methemoglobinemia usually occurs before signs tion PO or IV as a loading dose, then 70 mg/kg PO or
of hepatic necrosis develops. IV q 4 h for 3–5 additional treatments.
Cats are poisoned by as little as 50–60 mg/kg: that is, Ascorbic acid 125 mg PO q 6 h.
one adult tablet. Electrolyte and fluid therapy.
Handle patient with least stress.
Clinical signs
A rough estimate of the methemoglobin content of
Cyanosis and tachypnea. blood can be made by comparing the color of the
Salivation and abdominal pain. patient’s drop of blood against that of a drop of
blood from a normal cat against a white background
Facial edema and often edema of the paws. (e.g. white absorbent paper). A noticeable brown
Heinz body anemia. coloration compared with normal blood indicates a
methemoglobin content of more than 10%. This sub-
Chocolate-colored urine (hemaglobinuria, hematuria). jective test can be used to monitor the effectiveness
Jaundice. of treatment and should be performed every 2–3
hours.
Rapid onset of clinical signs (within a few hours of
ingestion). Good nursing and maintain body temperature.
Death ensues 18–36 hours after ingestion, if Whole blood transfusion if necessary to treat
untreated. hemolytic anemia.
Recovery usually within 48 h.
Diagnosis
History of drug administration.
Prognosis
Characteristic combination of facial edema and
chocolate-colored urine. Guarded to poor if severe methemaglobinuria
(>50%) or hemolysis.
Heinz bodies on RBCs.
Good with very early and aggressive treatment.
Methemoglobinemia.
Progressive rise in liver enzymes.
Low blood glutathione levels. LEAD POISONING
Serum acetaminophen concentration maximally ele- Classical signs

vated within 1–3 h after ingestion.
● Gastrointestinal – diarrhea, vomiting,
inappetance.
Differential diagnosis ● CNS signs – behavioral changes,
Phenolic and phenolic compound toxicity. depression, seizures.
● Occasionally, intermittent ptyalism.
Nitrite poisoning.
Clinical signs of acetylcholine and norepinephrine resulting in sus-

tained muscle spasm.
Usually in young cats.
The mechanism of severe pain at the bite site and
Vague, chronic gastrointestinal signs most common – regions remote from the actual bitten area is not well
e.g. inanition, inappetance, poor growth, occasionally understood.
diarrhea and vomiting.
CNS signs can occur in more severe cases and include Clinical signs
behavioral changes (depression, aggression, lethargy)
seizures and blindness. Initially, severe pain characterized by crying out.
Occasionally, intermittent ptyalism. Hyperexcitability, ataxia, muscle rigidity and spasm,

progressing to muscle weakness and collapse.
Prolonged, severe ptyalism, possibly due to pain.
Diagnosis
Death can occur from respiratory failure.
History of access to lead, e.g. old house renovation
(lead-based paint, dust from sanding).
Diagnosis
Blood lead greater than 0.4 ppm.
Clinical signs.
Treatment History of contact with latrodectus spider.
Chelation of lead with calcium disodium ethylene Laboratory evaluation not helpful.
diamine tetra-acetate (CaEDTA) 100 mg/kg SC daily in
four divided doses. Dilute CaEDTA to a concentration
Treatment
of about 10 mg CaEDTA/ml with 5% dextrose solution
for 5 days. In severe cases, a further 5-day course can Latrodectus antivenine results in dramatic improve-
be given after a rest period of 5 days. ment of clinical signs if given in the acute phase of the
disease and good results can be achieved even if given
Relapses of clinical signs of lead poisoning are com-
24 hours after envenomation.
mon and are treated as they arise.
● Premedicate with antihistamine (chlorpheni-
ramine 2.5–5 mg IM or SC) and have epinephrine
SPIDER ENVENOMATION (2.5–5 μg/kg IV) on hand. Latrodectus antivenine is
prepared from the hyperimmune serum of horses.
Classical signs ● Dose of antivenine is 1 vial (500 units) given by
intramuscular injection.
● Ptyalism.
● In life-threatening situations the intravenous route
● Hyperexcitability.
can be used but the risk of anaphylaxis is greater.
● Ataxia, paralysis.
Muscle spasm can be controlled with small doses of
intravenous diazepam (0.2–0.5 mg/kg q 6 h), but
Pathogenesis
avoid respiratory depression.
Latrodectus spp. spiders include black widow (USA),
Supportive care includes intravenous fluids, corti-
red back spider (Australia) and katipo (New
sone and atropine (to control salivation).
Zealand).
Venom contains alpha-latroxin, a potent neuro-toxin.
Prognosis
The toxin opens cation-selective channels at the presy-
naptic nerve terminals, causing release of large amount Good with use of antivenine; guarded without.
DIEFFENBACHIA (“DUMB CANE”) DIAPHRAGMATIC HERNIA WITH

POISONING INCARCERATED STOMACH

● Ptyalism. ● Uncommon.
● Tongue paralysis. ● Intermittent bouts of ptyalism often
● Dysphagia. associated with dyspnea.
● Anxious expression, often after eating.
Pathophysiology
Pathogenesis
Dieffenbachia is a popular decorative indoor plant. The
leaves contain irritant calcium oxalate crystals, which Stomach, with or without other abdominal organs, is
the plant can propel into the tissues of the mouth of cats chronically incarcerated in pleural cavity by constricting
chewing on the plant by means of special contractile cells. diaphragm subsequent to traumatic diaphragmatic
hernia.
Plant extract also contains protealytic enzymes, which
trigger the release of histamines and kinins and con- Sudden expansion of the stomach due to a large meal,
tribute to clinical signs. with or without associated gas production causes acute
onset of hypersalivation with anxious expression.
Plant is also known as “dumb cane” because it pro-
duces paralysis of the tongue. Rapid expansion of stomach volume after eating causes
sudden onset nausea, which in turn, causes ptyalism.
Clinical signs
Clinical signs
Sudden onset of signs. There is immediate pain on
chewing plant. Sudden onset of salivation with intent, anxious
expression and varying degrees of dyspnea.
Immediate salivation. Often head shaking.
Usually signs occur immediately after eating.
Sometimes change in voice.
Examination of mouth reveals mild to moderate Differential diagnosis
mucosal edema and tongue paralysis and swelling.
Portosystemic shunt is associated with elevated post-
prandial bile acids and CNS signs.
Diagnosis
History of plant chewing. Diagnosis
Plain and/or contrast radiography.
Treatment
Treatment
Symptomatic – rinse mouth with water or milk to pre-
cipitate soluble oxalates. Surgical repair of hernia.
Antihistamines (diphenhydramine 2–4 mg/kg IV, IM,
D-LIMONENE, LINAPOOL, AND CRUDE
PO q 6–8 h), and corticosteroids (dexamethasone
CITRUS OIL EXTRACTS
0.1–0.2 mg/kg IV, IM, PO q 12–24 h) to relieve pain
and swelling.
Classical signs
● Moderate to severe ptyalism.
Prognosis
● Muscular tremors (shivering).
Prognosis is very good as clinical signs regress after ● Ataxia.
24–48 hours.
Clinical signs Viral replication occurs in myocytes and spreads to

neuromuscular junctions and neurotendinal spindles.
Used as insecticidal sprays or shampoos.
Virus spreads to CNS via intra-axonal fluid within
Immediate sign of toxicosis is hypersalivation which peripheral nerves, then to peripheral sensory and motor
lasts 15 minutes to 1 hour. neurons.
More severely affected cats develop muscular tremors Salivary glands contain large amounts of virus
and ataxia. Hypothermia occurs. which is shed in saliva.
Clinical signs generally abate within 4 hours. Infection through contact with infected reservoir ani-
mals (bats, skunks, raccoons and foxes) or infected
Treatment dogs and cats.
Wash cat in unmedicated shampoo.

Clinical signs
Maintain body temperature.
Initial clinical signs are present for only 24 hours and
include low-grade fever and behavioral changes (e.g.
DIBUTYL PHTHALATE irritability, hiding or increased affection).
Classical Signs The excitatory stage (“furious rabies”) may last 2–4
days and is not always exhibited.
● Profuse salivation and foaming.
● Occasional retching and/or vomiting. Signs include muscle fasciculations, ptyalism, weak-
ness, ataxia and increased aggressiveness and irri-
tability.
Clinical Signs The final stage (“dumb” rabies) lasts 1–4 days and
general paralysis and convulsions precede death.
Used luminescent agent in “Glo-Jewellary” and as
insect repellent Diagnosis
Has extremely bitter taste and causes immediate hyper- History of no vaccination with approved killed vaccine.
salivation when cat bites into toy.
History of exposure to bite or scratch wounds from
Signs of hypersalivation generally self limiting once infected dogs or cats.
taste removed from mouth.
History of exposure to reservoir animals including
foxes, skunks, raccoons and bats.
RABIES
Typical clinical signs with progression almost invari-
Classical signs ably to death within 7–10 days.
● CNS signs, behavioral changes. EXTREME ZOONOTIC POTENTIAL.

● Ptyalism, frothing. Immediately notify authorities when rabies is sus-
● Fever. pected. Follow official policy for handling suspected
rabies cases, including tissue or fluid samples.
Pathogenesis Minimal changes in CSF analysis and routine blood
analysis.
Single-stranded RNA Lyssavirus.
Histological confirmation with finding Negri bodies
Virus inoculation via bite wound from rabid animal or
within the CNS on post-mortem.
via mucous membrane contact with infected body flu-
ids, e.g. saliva. Immunofluorescent antibody test on CNS tissue.
Differential diagnosis Prognosis

Portosystemic shunt – intermittent, often associated Grave.
with eating. Lack of rapid progression of signs over
7–10 days resulting in death. Confirm with post-pran-
FELINE PANLEUKOPENIA (PARVO VIRUS,
dial serum bile acids.
FELINE ENTERITIS, FELINE DISTEMPER)
Pyrethrin and pyrethroid toxicity – no behavior
changes and history of exposure and serum Classical signs
cholinesterase levels (OP) will confirm diagnosis.
● Vomiting, diarrhea.
Feline spongioform encephalopathy also has combi- ● Lethargy.
nation of neurological signs and hypersalivation. ● Severe dehydration.
Histopathology differentiates. ● High mortality.
Treatment
Clinical signs
No treatment should be attempted. Almost uniformly
fatal. Usually in young (2–6 months) kittens.
Follow official guides for management of suspected Acute-onset vomiting, often severe diarrhea.
rabies case. Fever in early stages of disease.
Rapid dehydration.
Prognosis
Severe depression.
Always grave.
Although not generally a feature of feline panleukope-
nia, continuous ptyalism has been recorded as the pre-
FELINE SPONGIOFORM dominate clinical sign in kitten with confirmed
ENCEPHALOPATHY (FSE) panleukopenia at post-mortem examination.
Classical signs
Diagnosis
● CNS signs, progressive.
● Hypersalivation. No vaccination history, recent exposure to virus.
Panleukopenia is the most consistent clinical finding.
Clinical signs Complete blood counts show leukocyte counts between
500 and 3000 cells per microliter during the acute
Progressive neurological signs including ataxia (espe- phase of the disease.
cially pelvic limbs), behavioral changes, hyperesthesia,
head tremor, muscle fasciculations. Canine parvovirus antigen fecal immunoassay will
detect feline parvovirus antigen in feces of affected
Ptyalism. cats.
Viral isolation from feces or affected tissues.
Diagnosis
Histopathology.
Histopathology shows discrete vacuolation of gray
matter throughout CNS.
Treatment
Treatment Rehydration, intravenous fluids.
Supportive only. Re-establishment of electrolyte balance.
Prognosis
Broad-spectrum antibiotics (amoxicillin/clavulonic
acid 62.5 mg/cat PO q 12 h). Guarded to poor in young kittens.
Whole blood transfusion in severely affected cats. If cat survives 5 days, prognosis improved markedly.
RECOMMENDED READING
Sherding RD (ed). The Cat: Diseases and Clinical Management, 2nd edn. WB Saunders Company, Philadelphia,
1994.
The Veterinary Clinics of North America, Small Animal Practice, Toxicology for the Small Animal Practitioner
1975; 5: 4623–4652.
The Veterinary Clinics of North America, Small Animal Practice, Non-cardiac Surgical Diseases of the Thorax 1987;
17: 2333–2358.
The Veterinary Clinics of North America, Small Animal Practice, Liver Disease 1995; 25: 2337–2355.
Tilley, Smith. The 5 Minute Veterinary Consult – Canine and Feline, 3rd edn. Lippincott, Williams and Wilkins,
1997.
28. The cat with bad breath or oral
lesions
Gary John Wilson
KEY SIGNS
● Bad breath.
● Oral mass, ulceration or inflammation.
● Calculus.
MECHANISM?
● Bad breath occurs from the production of volatile sulfur-containing compounds. Hydrogen sul-
fide and methyl mercaptan account for approximately 90% of these. Gram-negative bacteria
are primarily responsible for malodor production.
WHERE?
● Oral cavity, nasal cavity, nasopharynx and respiratory tract.
WHAT?
● Most cats with bad breath have periodontal disease.

Diseases causing bad breath or oral lesions
ORAL CAVITY
ANOMALY
● Congenital anomaly of hard palate (cleft palate) (p 610)
Cleft palate results in rhinitis and secondary bacterial infection and nasal discharge in young kit-
tens.
MECHANICAL
● Oral foreign body* (p 609)
Foreign bodies include grass seed, bone fragments and hair. They are usually acute onset associ-
ated with sneezing, rubbing the face, pawing at the mouth, coughing or gagging.
602
28 – THE CAT WITH BAD BREATH OR ORAL LESIONS 603
NEOPLASTIC
● Oral neoplasia** (p 607)
Visible tumors often with secondary bacterial infection and periodontal disease. Signs may include
rubbing face, pawing at mouth or facial distortion.
INFECTIOUS (BACTERIAL)
●Periodontal disease*** (p 604)
Chronic disease with halitosis, inflamed gums and calculus on teeth.
●Oronasal fistula (p 610)
Chronic occasional sneezing and nasal discharge associated with dental disease or trauma.
●Bacterial infection of tongue lacerations* (p 609)
Halitosis with purulent open wound on or under tongue.
● Oral ulcerations associated with viral causes (herpesvirus and calicivirus)* (p 607)
Oral lesions are more common with calicivirus infection and the vesicles rupture to form oral
ulcers, which allows secondary bacterial invasion.
IMMUNE/IDIOPATHIC
● Feline oral inflammatory disease (plasmacytic-lymphocytic gingivopharyngitis
complex, plasmacytic-lymphocytic stomatitis/faucitis)** (p 606)
Chronic severe inflammation of gingiva and fauces.
● Eosinophilic granuloma complex (p 611)
Lip ulcer or raised firm lesions especially on the tongue or hard palate. Oral lesions postulated to
be secondary to chronic licking.
TRAUMA
● Mandibular and maxillary fractures (p 610)
Inability to chew, salivation and rapid secondary infection of traumatized tissue.
● Tooth fracture with periapical abscessation (p 610)
Fractured teeth often go unnoticed in cats and will progress to pulp death and periapical abscessa-
tion and possible external discharge.
TOXIC
● Oral ulcerations associated with uremic or toxic causes (p 607)
Oral ulceration may occur with uremia or associated with concentrated cleaning agents, allowing
secondary bacterial invasion.
EXTRA-ORAL CAUSES OF BAD BREATH (NASAL CAVITY, ESOPHAGUS, LOWER
AIRWAY)
INFECTIOUS
Bacterial:
● Bacterial rhinitis secondary to viral upper respiratory tract disease* (p 608)
Chronic mucopurulent or hemorrhagic nasal discharge and sneezing.
continued
continued
● Infections associated with esophageal or lower airway disease (p 609)

Infections secondary to primary disease of the esophagus or lower respiratory tract.
Fungal:
Chronic mucopurulent or hemorrhagic nasal discharge, sneezing and occasional facial distortion
with associated halitosis.
Diagnosis is made after examination under general

INTRODUCTION anesthesia, radiography, laboratory tests or a combina-
tion of these.
MECHANISM?
Volatile sulfur-containing compounds are the major DISEASES CAUSING BAD BREATH
contributors to malodor (bad breath). OR ORAL LESIONS
Hydrogen sulfide and methyl mercaptan account for
approximately 90% of the total sulfur content of mouth PERIODONTAL DISEASE***
air.
Anaerobic Gram-negative bacteria utilize sulfur- Classical signs
containing amino acids for the generation of volatile ● Halitosis (bad breath).
sulfur-containing compounds. ● Calculus on teeth.
● Inflamed gums.
WHERE?
Diseases of the oral cavity, nasal cavity, nasopharynx Pathogenesis
and the respiratory tract may cause bad breath and oral Plaque is a matrix of bacteria, salivary glycoproteins,
lesions. food particles, epithelial cells and leukocytes, which
Any malodor from the oral cavity indicates disease. adheres to the tooth surface.
History and detailed physical examination (often under Plaque can only be removed mechanically; it cannot
anesthesia) are essential for diagnosis. be rinsed off.
Oral lesions should be expected if the cat is reluctant to Supragingival plaque occurs above the gum line and
allow oral examination (or shows any other signs of subgingival plaque below.
oral pain). Subgingival plaque bacteria are responsible for the
pathology found in periodontal disease.
Initially edema and inflammation of the gum mar-
WHAT? gins (gingivitis) is seen, which is followed by loss of
The most common diseases causing bad breath and oral epithelial attachment at the base of the gingival sul-
lesions are: cus with subsequent periodontal pocket formation.
● Periodontal disease. Destructive processes continue with eventual loss of
● Feline oral inflammatory disease (plasmacytic- the periodontal ligament and alveolar bone (peri-
lymphocytic gingivopharyngitis complex). odontitis).
If allowed to progress untreated, eventually the tooth Evaluate radiographically to assess loss of crestal bone
will be lost. (bone between teeth) and loss of bone around the tooth
roots.
As periodontal disease progresses, the bacteria change
initially from anaerobic Gram-positive bacteria to
Gram negative to anaerobes, and finally to fusiforms Differential diagnosis
and spirochetes.
Feline oral inflammatory disease (or plasmacytic-
The halitosis is due to the production of volatile sul- lymphocytic gingivopharyngitis complex) has similar
fur compounds by the plaque bacteria (especially by signs in the early stages to early periodontal disease
the anaerobes). but cats rapidly develop a severe inflammation of
the whole gingiva and often a concurrent faucitis
Chronic low-grade bacteremia from periodontal dis-
(compared to inflammation of the gum margin only
ease can have systemic effects on other organs (espe-
with periodontal disease). The tissues are grossly
cially kidney, myocardium and liver).
inflamed and are friable, bleed easily and are
extremely painful.
Clinical signs
Feline odontoclastic resorptive lesions may appear
Healthy gingiva is shiny with a sharp margin, which similar to localized areas of periodontal disease with
appears almost transparent under magnification and has gingival hyperplasia covering the resorptive lesion.
a sulcus depth which is less than 0.5 mm. Probing under general anesthesia will reveal the
lesion. These lesions are also extremely painful and
With gingivitis the margins are edematous and
cats will often avoid using these teeth.
inflamed (red line around edge of marginal gingiva)
and may bleed on probing. Halitosis will be present
and supragingival calculus may be present. Treatment
As disease progresses, pocket formation begins with Dental prophylaxis to eliminate the bacteria causing
associated subgingival plaque. Halitosis and supragin- odor and to remove diseased tissue so as to allow the
gival calculus will be present and subgingival calculus reattachment of the gingiva.
may also be present. ● This is done under general anesthesia to ensure that
subgingival plaque is removed.
Further deterioration leads to bone loss, deep pocket
● The steps involved are supragingival scaling, sub-
formation, furcation exposure (loss of bone between
gingival scaling, polishing and flushing (irriga-
tooth roots of multi-rooted teeth) and tooth mobility.
tion) of the sulcus.
Severe periodontal disease will result in tooth loss,
For the more severe cases treatment may also involve
deep pockets with heavy anaerobic infections and
periodontal surgery to expose affected tissue and to
strong halitosis. The cat may show signs of systemic
allow complete subgingival cleaning and extraction.
disease and refuse to eat or attempt to swallow food
without chewing. Antibiotics are usually not required.
Diagnosis Prognosis
History of halitosis and, in severe cases, there may be a Good if secondary organ damage has not occurred.
reluctance to chew food and occasional pawing at
mouth.
Prevention
Clinical signs are diagnostic.
Daily brushing is recommended but does require
In the anesthetized cat, determine the severity of dis-
owner and cat compliance.
ease by a thorough oral examination. This will include
palpation of loose teeth and the use of a periodontal Chewing raw meaty bones such as chicken wings will
probe to check for the presence of periodontal pockets. help to mechanically remove the plaque.
Calculus control diets, which are designed to remove Most frequently involves the gingiva caudal to the
the adhered plaque as they are chewed, due to their canine teeth and the fauces but can occur associated
abrasive nature or to compete with plaque for salivary with the incisors as well.
calcium ions.
In severe cases the entire gingiva (not just the gingival
Dental chews will help in mechanically removing margin) as well as the fauces becomes grossly inflamed.
plaque.
More prevalent in purebred cats.
FELINE ORAL INFLAMMATORY DISEASE**

(OR PLASMACYTIC-LYMPHOCYTIC Diagnosis
GINGIVOPHARYNGITIS COMPLEX,
Clinical signs are diagnostic in severe cases.
PLAMACYTIC-LYMPHOCYTIC
STOMATITIS/FAUCITIS) In early cases, the severe inflammatory reaction of the
gingival margin (which bleeds easily on palpation) is
Classical signs suggestive.
● Halitosis. The diagnosis can be confirmed by biopsy if necessary.
● Grossly inflamed gums especially in
premolar and molar areas.
● Gums bleed easily. Differential diagnosis
● Very painful and cats often bad tempered.
Periodontal disease. The inflammation is less acute,
less severe and restricted to the gingival margin.
Pathogenesis Chronic calicivirus faucitis and gingivitis. The
The etiology of this condition is unknown. Suggested inflammatory response is less severe with calicivirus.
causes have been bacterial, viral (especially calicivirus) Acute herpesvirus and calicivirus infections. This is
and immunological (possible hypersensitivity to plaque associated with lingual and palatal ulcerations and
proteins). other signs of respiratory tract infection such as sneez-
The condition may be the result of chronic immune- ing and oculonasal discharge.
mediated processes.
Lymphocytes, plasma cells and neutrophils are the
Treatment
predominate cells found at biopsy.
Initially, a careful and thorough dental prophylaxis
and appropriate antibiotic therapy (must be effective
Clinical signs
against anaerobes such as Actinomyces sp.,
Intense oral pain (and often bad-tempered cats which Peptostreptococcus sp. and the black pigmented bac-
resent oral examination). teroides) will give relief although only temporary in
most instances.
When eating, affected cats often attempt to swallow the
food without chewing due to the oral pain. The Corticosteroid therapy will produce improvement
appetite appears reduced due to the cat’s reluctance to whilst used.
prehend food.
Permanent resolution is common following extraction
Halitosis. of all teeth caudal to the canines (but these teeth must
be extracted completely including all of the roots).
Dysphagia, excess salivation and weight loss in severe
cases. In cases that suffer recurrence following extraction
(less than 5%), acupuncture may result in resolution.
Proliferation of gingiva with extensive inflammation.
The tissue is friable and bleeds readily on palpation. Acupuncture alone will produce short-term relief.

The prognosis is guarded for those treated without Intra-oral abscess and granulation tissue can have a
extraction. similar appearance to neoplasia but will be differenti-
ated by biopsy.
With complete extraction, the prognosis is fair to good.
Eosinophilic granuloma complex is often smaller and
can be differentiated by biopsy.
Prevention
Until the etiology is understood, no prevention is possible. Treatment
Treatment of lingual squamous cell carcinoma in the
ORAL NEOPLASIA** cat has not proved successful.
Classical signs Mandibular masses can be treated by partial

mandibulectomy (the complete hemimandible can be
● Presence of oral mass. removed if necessary).
● Dysphagia, excessive salivation, hemorrhage.
● Halitosis.
Prognosis
The prognosis for squamous cell carcinoma of the
Pathogenesis tongue is grave.
Neoplasia may involve gingiva, tongue, oral mucosa or For other tumors, the prognosis will depend on the
tonsils. tumor type and suitability for treatment.
Squamous cell carcinoma is the most common neo-
plasm in cats and is most often found on the ventral ORAL ULCERATIONS FROM VIRAL, UREMIC
tongue. OR TOXIC CAUSES*
Other types of oral tumor are infrequent in the cat.
Classical signs
Neoplasia usually occurs in older cats (> 10 years).
● Excessive salivation.
● Tongue and pharyngeal ulceration.
● Anorexia.
Clinical signs
Oral mass. See main reference on page 578 for details (The Cat
With Salivation).
Excessive salivation, dysphagia or oral hemorrhage.
Facial distortion.
Pathogenesis
Halitosis.
Feline herpesvirus and feline calicivirus can cause an
Poor body condition due to inability to eat or metasta- ulcerative stomatitis in association with upper respira-
tic disease. tory tract disease.
● Calicivirus infection most commonly causes oral
lesions especially on the tongue and hard palate.
Diagnosis ● The lesions begin as vesicles, which coalesce and
rupture, forming ulcers.
Biopsy and histologic examination.
● Lesions caused by herpesvirus occur less frequently
Radiography to assess the extent of hard tissue tumors. but are usually more severe.
Cats with uremia produce increased ammonia in the Treatment

saliva. Uremia also causes damage to blood vessels
resulting in vasculitis. Ulceration of the oral mucosa Antibiotics to control secondary bacterial infections.
may be caused by the combination. Fluid therapy, soft foods and adjunct therapy (for the
Toxic causes of oral ulceration in the cat are most fre- primary disease) until lesions are healed.
quently associated with household cleaning agents. Pain control.
● These toxic agents include sodium hypochlorite
and sodium hydroxide that are used for cleaning
showers and bathrooms, and quaternary ammo- BACTERIAL RHINITIS SECONDARY
nium compounds. TO VIRAL UPPER RESPIRATORY TRACT
● The cat damages the oral mucosa whilst licking the
DISEASE*
walls or floor or from licking it off their feet.
● These cats may also have lesions on their feet if
Classical signs
exposure was from walking in the chemical. ● Chronic sneezing and snuffling.
● Mucopurulent nasal discharge.
Clinical signs ● Stertorous respiration.
Excessive salivation and oral pain. See main reference on page 21 for details (The Cat
Oral ulceration associated with concurrent upper res- With Signs of Chronic Nasal Disease).
piratory tract disease.
Fever is often present associated with herpesvirus and Clinical signs
calicivirus ulceration but not with uremic or toxic ulcers. Chronic mucopurulent nasal discharge.
Sudden onset of salivation, dysphagia and depression Chronic sneezing and snuffling.
with toxic ulceration.
Stertorous respiration.
Loss of sense of smell, fever and oral pain results in
anorexia. Halitosis may be present.
Halitosis.
Diagnosis
Diagnosis History of clinical signs after an acute upper respira-

tory tract infection.
Presence of oral ulcers.
Radiography demonstrating fluid densities in nasal
Virus identification using PCR if ulcers are associ- cavity and sinuses with loss of turbinates.
ated with upper respiratory tract disease.
Cytology showing many neutrophils with intra- and
Blood tests for uremia. extracellular bacteria and no evidence of Cryptococcus
History of exposure to toxins liable to produce oral sp. or neoplastic cells.
ulceration.
Differential diagnosis Neoplasia. Usually older cats and radiographic signs
are more often unilateral. Biopsy will differentiate.
Electrical or heat burns to the tongue and oral mucosa
are rare in the cat. Lack of fever and history of poten- Cryptococcosis. Often has nasal distortion or visible
tial for exposure help to differentiate these from infec- polyp protruding through nares. Differentiate with
tious causes. cytology or serology.

Long-term broad-spectrum antibiotic therapy. Hemorrhage may be significant if acute.
Surgery (rhinotomy) to curette sinuses may be tried as Sudden onset of reluctance to groom, excessive saliva-
a salvage procedure. tion and reluctance to eat.
Halitosis develops as tissue becomes infected.
ORAL FOREIGN BODY*
Laceration may be on the dorsal surface or sublingual
(more often).
Classical signs
● Gagging, pawing at mouth. Diagnosis
● Halitosis.
● Dysphagia. Visualize the laceration.
Clinical signs Differential diagnosis

Sudden onset of gagging and pawing at the mouth. Foreign bodies can usually be seen.
Dysphagia. The cat will often appear very hungry but Ulcerations secondary to trauma.
has difficulty swallowing.
Rapid jaw and tongue movements. Treatment
Surgical debridement and repair.
Diagnosis
Evidence of foreign body or trauma caused by the for- INFECTIONS ASSOCIATED WITH
eign body in the oral cavity or pharynx. ESOPHAGEAL AND LOWER AIRWAY
Most commonly the tongue or pharynx are involved DISEASE
especially with string or cotton.
Classical signs
Differential diagnosis ● Dysphagia, regurgitation (esophageal
Oral tumors. These can be differentiated visually from disease).
a foreign body. ● Dyspnea, coughing (lower airway disease).
Traumatic lacerations. These are usually associated

with hemorrhage and no foreign body will be found on Clinical signs
examination. Halitosis.
Treatment Dysphagia, regurgitation and possible reluctance to eat

with esophageal disease. Esophageal tumors and for-
Removal of the foreign body. eign bodies are most often associated with halitosis.
Dyspnea, coughing with lower airway disease. Foreign
BACTERIAL INFECTION OF TONGUE bodies, airway tumors and purulent bacterial infec-
LACERATIONS* tions are most frequently associated with halitosis.

● Hemorrhage. Radiography to demonstrate lesions.
● Reluctance to groom and excessive salivation.
Auscultation and ultrasonography.
Asymmetry of jaw.
ORONASAL FISTULA
Hemorrhage in acute stages.
Classical signs
Excessive salivation.
● Occasional sneezing.
Halitosis associated with secondary bacterial infection
● Unilateral nasal discharge.
of traumatized tissue.
● Excessive licking of nose.
See main reference on page 27 for details (The Cat Diagnosis

Palpation and radiographic demonstration of fracture.
Clinical signs
Most often associated with dental disease; occasion- TOOTH FRACTURE WITH PERIAPICAL
ally occurs after trauma, with formation of a fistula in ABSCESSATION
the hard palate.
Classical signs
Occasional sneezing.
● Presence of fractured tooth.
Unilateral nasal discharge (usually mucopurulent but
may be hemorrhagic). If associated with dental disease
or unilateral traumatic fistula.
Clinical signs
Excessive licking of nose.
Fractured tooth.
Oronasal fistula visible if tooth is absent.
Oral pain in acute phase (< 48 hours) then no pain until
Advanced periodontal disease.
periapical abscess forms.
Halitosis.
Calculus build-up on teeth on affected side of mouth
due to reluctance to chew with affected tooth.
Diagnosis
Halitosis may be present if the periapical abscess is
Presence of oronasal fistula on periodontal probing draining intra-orally.
(vigorous movement of probe results in blood from
nostril).
Diagnosis
Presence of fractured crown.
MANDIBULAR AND MAXILLARY
FRACTURES
CONGENITAL ANOMALY OF THE HARD
Classical signs PALATE (CLEFT PALATE)
● Mouth held open (often with tongue
Classical signs
protruding).
● Jaw asymmetry. ● Snuffling and nasal discharge.
● Excessive salivation. ● Visible evidence of cleft.
Clinical signs
Clinical signs
Unwilling (or unable) to close mouth and tongue pro-
truding. Snuffling and nasal discharge, which is usually bilateral.
In young kitten with congenital cleft, milk is visible Diagnosis

coming from the nose during feeding.
Serology for cryptococcus antibody.
In traumatic cleft, dried blood around the nose and
mouth and facial injuries. Cytology for identification of the organism.
Halitosis is associated with rhinitis and secondary

infection from food in the nasal passages. EOSINOPHILIC GRANULOMA COMPLEX
Classical signs
Diagnosis
● Ulcerated lesion near the midline of the
Evidence of cleft. upper lip.
● Raised firm lesions in the oral cavity
CRYPTOCOCCOSIS (especially tongue and hard palate).
Classical signs See main reference on page 1088 for details (The Cat
With Non-Healing Wounds).
● Chronic nasal discharge.
● Facial distortion (nasal bones).
Clinical signs
See main reference on page 25 for details (The Cat Ulcerated lesion on the upper lip near the midline.
Raised firm lesions (with yellow-white spots through-
out) in the oral cavity especially on the tongue and
Clinical signs hard palate.
Chronic nasal discharge and snuffling.
Distortion of bridge of nose or nasal polyp is present Diagnosis
in most cases. Biopsy.
Depression and anorexia.
Other organs may be affected.
RECOMMENDED READING
DeBowes LJ, Mosier D, Logan E et al. Association of periodontal disease and histologic lesions in multiple organs
from 45 dogs. J Vet Dent 1996; 13: 57–60.
Harvey CE, Emily PP. Small Animal Dentistry. St. Louis, Mosby, 1993, pp. 89–143, 150–155.
Hennet P. Chronic gingivo-stomatitis in cats: long-term follow-up of 30 cases treated by dental extractions. J Vet Dent
1997; 14: 15–21.
Tonzetich J. Production and origin of oral malodor: a review of mechanisms and methods of analysis. J Periodontol
1977; 48: 13–20.
Wilson GJ. Feline Dentistry and Oral Cavity Diseases. Sydney, University of Sydney Post Graduate Foundation in
Veterinary Science, 2002.
29. The cat with signs of regurgitation
(acute or chronic)
Debra L Zoran
KEY SIGNS
● Passive elimination via the mouth of swallowed food.
● Food is typically undigested.
● Gagging or retching may occur concurrently.
MECHANISM?
● Regurgitation is a passive act that may involve several anatomic regions of the alimentary
tract: oral cavity, oropharynx, esophagus or occasionally the stomach.
● Oral or pharyngeal disease is more often associated with dysphagia (difficulty swallowing).
● Regurgitation is a more typical presenting sign of esophageal disease.
● Regurgitation is not associated with prodromal signs (no anxiety, nausea or hypersalivation),
there will be no abdominal muscular activity, and is often composed of recently swallowed
food (undigested, whole).
● In cases of chronic megaesophagus, where food may sit undisturbed for hours in the distal
esophagus, the food may have a more liquid, unformed character.
● The pH of the material may be neutral, slightly basic (oral) or slightly acidic (stomach), but
is typically in a range of pH 4–7.
WHERE?
● Regurgitation is usually associated with disease of the esophagus:
● Megaesophagus (acquired or congenital).
● Associated with esophageal anomalies, e.g. diverticular structures, vascular ring anomalies.
● Esophagitis, esophageal strictures or foreign bodies.
● Associated with oropharyngeal disease, e.g. stomatitis-pharyngitis complex.
● Parasitic diseases of the esophagus.
Signs of gagging or retching are often associated with regurgitation (or vomiting) in cats
and include many oral, dental and pharyngeal infectious, inflammatory, neoplastic or toxic
disorders.
WHAT?
● The most common causes of regurgitation in cats are esophagitis (due to a variety of infectious
or inflammatory causes), esophageal stricture, esophageal foreign bodies, and more rarely pha-
ryngeal or esophageal neoplasia.
612
29 – THE CAT WITH SIGNS OF REGURGITATION 613

Diseases causing signs of regurgitation
ANOMALY
● Vascular ring anomalies (persistent right aortic arch – PRAA) (p 623)
Vascular ring anomalies cause regurgitation soon after the kitten is weaned onto solid food.
● Esophageal diverticular structures (p 624)
These may be clinically silent or associated with regurgitation, painful swallowing, lethargy and
decreased appetite, depending on the size of the diverticular structure.
MECHANICAL
● Esophageal foreign body** (p 616)
Foreign bodies may cause gagging, retching or regurgitation, depending on what they are, how
long they have been present in the esophagus, and whether or not they are caustic.
● Esophageal stricture* (p 618)
This is a complication of esophagitis that results in regurgitation due to narrowing or nearly com-
plete obstruction of the esophageal lumen.
● Eating too fast (food gulping) (p 628)
Regurgitation of undigested food may be caused by eating too fast or food gulping.
● Hiatal hernia (gastroesophageal intussusception) (p 625)
This is a rare disorder associated with intermittent regurgitation or vomiting due to herniation of
the stomach through the esophageal hiatus.
● Esophageal fistula (p 625)
This is an abnormal communication between the esophagus and respiratory system that usually
results from foreign body penetration or a ruptured diverticulum. Clinical signs will include regur-
gitation as well as respiratory signs (e.g. coughing, dyspnea, etc.).
IDIOPATHIC
● Esophageal hypomotility/idiopathic megaesophagus (acquired or congenital)* (p 621)
Regurgitation may or may not be associated with eating. Aspiration pneumonia is a common com-
plication resulting from the frequent regurgitation.
Regurgitation occurs due to the development of megaesophagus secondary to abnormal function-
ing of the autonomic nervous system. This rare disorder is also associated with abnormal colonic
and ocular muscle functions, among other things.
IMMUNOLOGIC
● Myasthenia gravis (acquired or congenital)* (p 622)
Myasthenia gravis can be acquired or congenital and results in megaesophagus (regurgitation) sec-
ondary to the presence of antibodies to the acetylcholine receptor in the neuro-muscular junction,
with the end result being smooth muscle dysfunction.
continued
continued
INFLAMMATORY
● Esophagitis*** (p 615)
Esophagitis is an inflammatory disease of the esophagus that has multiple causes such as reflux
disease, post-anesthesia, chronic vomiting, caustic or irritant ingestion and results in regurgitation
and may progress to esophageal strictures if left untreated or if severe.
INHERITED
● Hereditary myopathy of Devon Rex cats (p 626)
This is an inherited myopathy in young Devon cats that presents as generalized appendicular
weakness. Ventroflexion of the head and neck, dorsal protrusion of the scapulae and megaesopha-
gus with regurgitation are the main clinical features of hereditary myopathy.
NEOPLASTIC
● Esophageal neoplasia (squamous cell carcinoma, metastatic neoplasia)* (p 619)
This is a rare tumor in cats, but is the most common tumor of the esophagus. The tumor creates an
obstructive lesion that results in regurgitation, weight loss and anorexia.
● Mediastinal neoplasia* (p 628)
Thymic lymphoma and thymoma commonly result in extraesophageal obstruction and
regurgitation.
TOXIC
● Lead poisoning* (p 619)
Lead poisoning is usually marked in the early phases with vomiting and GI signs. Neurologic
signs develop late or with chronic exposure and may lead to the development of smooth muscle
dysfunction (megaesophagus) and regurgitation.
● Plant ingestion* (p 620)
Regurgitation secondary to plant consumption is usually due to their irritant or caustic properties
that result in the development of esophagitis.
rial is typically composed of recently swallowed food

INTRODUCTION (undigested, may still be whole) with saliva.
In cases of chronic megaesophagus, where food may
MECHANISM? sit undisturbed for hours in the distal esophagus, the
Regurgitation is the passive removal of ingesta, food may have a more liquid, unformed character.
saliva, and other material from the upper GI tract (oral
The pH of the material may be neutral, slightly
cavity, oropharynx and esophagus).
basic (oral) or slightly acidic (stomach), but is typi-
Regurgitation of stomach contents can occur but is cally in a range of pH 4–7.
much less common than vomiting.
Diseases of the esophagus rarely cause hematologic
Regurgitation is not associated with abdominal mus- or biochemical abnormalities, and their diagnosis
cle contraction, has no prodromal signs (no anxiety, often requires contrast radiography, endoscopy or
nausea or hypersalivation preceeding it), and the mate- other sophisticated imaging techniques.
● Drugs (primarily due to direct injury if retained in

WHERE?
the esophagus, e.g. doxycycline, potassium glu-
Classically, regurgitation is considered to be the hall- conate, propranolol).
mark of esophageal disease. ● Secondary to trauma from esophageal foreign
bodies.
Gagging or retching, painful swallowing or dysphagia
can all be signs of esophageal disease, however, most of Other than traumatically induced esophagitis, the most
the time these signs are associated with oral or oropha- common cause of esophageal inflammation in cats is
ryngeal disease (see page 602, The Cat With Bad Breath reflux of acid, pepsin and stomach contents into esopha-
or Oral Lesions). gus as a result of anesthesia or chronic vomiting.
The esophagus does not have the mucosal protection
WHAT? mechanisms that are present in the stomach, and
thus, acid and chemical mucosal injury from reflux will
Esophageal diseases that may be associated with
set into motion a localized inflammatory response
regurgitation include esophagitis, cardiac anomalies
that, if uncorrected, can result in esophageal stricture
(e.g. persistent right aortic arch), mechanical problems
formation or perforation.
(e.g. strictures, foreign bodies or fistula), metabolic dis-
orders (megaesophagus – acquired, congenital or idio-
pathic), or toxic (plant ingestion, etc.). Clinical signs
Many diseases of the esophagus may be difficult, if Regurgitation following eating is the predominant
not impossible to treat. clinical sign in cats with esophagitis, but vomiting,
Megaesophagus, strictures, diverticuli, hiatal hernias, anorexia, weight loss, lethargy and gagging may also
fistulae and esophageal neoplasia are all very difficult be observed.
to manage or cure. Onset of regurgitation following an anesthetic pro-
Esophagitis is the most common and potentially cedure or foreign body retrieval is highly suspicious
most treatable esophageal disease of cats other than of esophagitis.
foreign bodies and ingestion of plant material.
Diagnosis
DISEASES CAUSING SIGNS
OF REGURGITATION A history of a recent onset of regurgitation after an
anesthetic procedure should immediately suggest
esophagitis.
ESOPHAGITIS***
Concurrent oral ulceration suggests chemical, ther-
Classical signs mal, calicivirus or uremic ulceration.
● Regurgitation is the most common sign. History (chemical, thermal, anaesthesia, drugs, foreign
● Vomiting, gagging, retching, anorexia, bodies) usually identifies the problem.
weight loss and lethargy. Esophagitis in cats due to consumption of a chemical
or thermal agent may be associated with completely
Pathogenesis normal baseline blood work.
Esophagitis can be caused by a wide variety of insults, Survey radiography may be helpful if the esophageal
including infectious (e.g. calicivirus). inflammatory process is also causing motility dis-
● Gastroesophageal reflux disease (persistent vomit- turbances that can be seen as esophageal dilatation
ing, anesthesia, lower esophageal sphincter abnor- radiographically. Rarely, contrast radiography may be
malities, hiatal hernias). useful in identifying areas of mucosal irregularity
● Chemical (caustic agents) or thermal injury. suggestive of esophagitis. Contrast radiographs are
most helpful in identification of esophageal stricture Prophylactic antibiotics that are effective against
formation. pathogens present in the oral mucosa are only indicated
(amoxicillin, clavamox, cephalexin, clindamycin) in
Definitive diagnosis of esophagitis, and any complica-
severe esophagitis cases where mucosal damage is so
tions associated with it, is achieved by endoscopic
severe that normal mucosal defenses are compromised.
examination of the esophagus and biopsy.
Reduction of gastric acidity with histamine-2 blockers
Note: a normal-appearing mucosa does not rule out
(famotidine 0.5–1.0 mg/kg PO q 24 h) or protein pump
esophagitis. However, in most cases, mucosal ery-
inhibitors (omeprazole 1 mg/kg PO q 24 h) is also indi-
thema, hemorrhage and increased friability are
cated, especially if gastroesophageal reflux disease is
common findings.
suspected.
Mucosal cytoprotectants, such as sucralfate
(250–500 mg PO q 8–12 h made into a slurry) have also
Essentially any cause of regurgitation or chronic vom- been recommended to reduce further mucosal injury,
iting should be considered as a differential because the however their effectiveness is questioned.
signs are so non-specific and many overlap with other
Drugs that increase lower esophageal sphincter
diseases.
tone, metoclopramide (0.1–0.2 mg/kg PO q 12 h) and
cisapride (5 mg/kg PO q 12 h), are indicated when
Treatment acid reflux is suspected and may be required long-
Treatment of esophagitis is first aimed at correcting term to prevent disease recurrence in cats with this
the underlying cause. If the cause cannot be identified disease.
and corrected, management of the esophagitis will be In all cases, the treatment should be continued for at
extremely difficult. least 2–3 weeks beyond the resolution of clinical
Symptomatic therapy then is used to control the signs to prevent recurrence and allow complete healing
inflammatory process that is ongoing in the of the tissue.
esophageal mucosa. This type of approach will require
both “resting” the esophagus and pharmacologic Prognosis
therapy.
The prognosis is good in cats with mild esophagitis or
In cats with mild esophagitis, simply withdrawing when severe esophagitis is managed aggressively and
food for 24–48 hours is often sufficient to allow does not result in stricture formation.
mucosal healing. Upon re-feeding, the diet should be a
soft, low-fat, non-abrasive food that will not re-injure In cases of esophagitis that develop strictures, the
the tissue. prognosis is guarded to fair. See section on stricture
management for details.
When severe esophagitis is present, feeding should be
administered via alternative feeding methods.
ESOPHAGEAL FOREIGN BODY**
Provide enteral nutrition via a gastrostomy or
jejunostomy tube (pharyngostomy or nasogastric Classical signs
tubes will continue to irritate the esophagus and may
allow continued gastroesophageal reflux) or use total ● Acute onset of regurgitation is the most
parenteral nutrition if the cat is also vomiting. common sign.
● Gagging or retching are also observed,
Corticosteroids (0.5–1.0 mg/kg PO q 12 h) are indi- especially when the object is in the cranial
cated if stricture formation is expected to occur, but esophagus.
will not help in cases where a stricture has already ● Rarely, acute respiratory distress may also
occurred and may reduce healing in severe cases, so occur.
must be used with caution.
Pathogenesis Endoscopy may be required in some cases to identify

small or radiolucent objects, and is very useful in
Esophageal foreign bodies are relatively common in retrieving some objects.
cats because of their curious nature, propensity to chew
on or ingest string or like objects, and their consump- In some cases, contrast radiographs may be required
tion of hair (or bones) from prey or grooming. to identify radiolucent objects or fistula.
String foreign bodies will usually pass through the GI Because of the acute onset of clinical signs in cats
tract if they are not anchored. with esophageal foreign bodies, a routine database is
usually completely normal.
Common reasons for string foreign bodies to become
anchored include, attachment around the base of the Cats that develop a small esophageal perforation may
tongue or if the string is attached to a needle that have an inflammatory leukogram.
becomes lodged in the wall of the esophagus or GI tract.
The greatest dangers from esophageal foreign bodies Differential diagnosis
are perforation and esophagitis. Primary differentials include ingestion of a caustic,
Esophageal perforation is a life-threatening condition irritating or noxious substance that causes acute
because it leads to fulminant (tension) pneumotho- esophagitis.
rax and pneumomediastinum. Extremely small per- Oral ulceration is usually present following ingestion
forations (needle punctures) may not result in tension of caustic or irritating substances.
pneumothorax but instead cause mediastinitis and
pleuritis or even fistula formation. Other causes of regurgitation are typically associated
with clinical signs of a chronic nature (esophageal
Esophagitis is important because it can lead to hypomotility, gastroesophageal reflux esophagitis, neo-
esophageal stricture if the inflammatory response is plasia) and thus are less likely.
severe or chronic.
An acute onset of regurgitation or anorexia are the The initial goal is the immediate removal of the for-
most common presenting signs, and these may be eign object from the esophagus. This must be done
associated with hypersalivation, gagging, retching or carefully to minimize further esophageal damage
anxiety. and complications (e.g. vagal tone induced brad-
yarrhythmias, further mucosal trauma or development
If the foreign body causes an esophageal perforation, of a perforation).
the cat may present in extreme respiratory distress.
Endoscopic retrieval should be attempted first
The severity of the signs observed often relate to because of the difficulties associated with esophageal
what the object is (e.g. string, hair, bones, needles, surgery, unless there is radiographic evidence of a
wire), whether the object is causing a partial or com- perforation.
plete obstruction, and the duration that it has been
present (e.g. presence of esophagitis, stricture, etc.). Use of both a rigid proctoscope and a flexible endo-
scope has been very successful. The flexible scope is
used to manipulate the object free with grasping tools,
Diagnosis
and the proctoscope to protect the esophagus from fur-
The acute onset of hypersalivation and regurgitation ther damage as the object is moved orad.
is often suggestive of an esophageal foreign body,
If the object cannot be safely removed in an oral
and the diagnosis is frequently confirmed by visualiz-
direction, but can be propelled into the stomach, this
ing string entrapped around the base of the tongue.
is the next best option. The object may be allowed to
Survey radiographs will often reveal a radio-opaque pass (bony material) through the GI tract on its own or
foreign object. can be removed by gastrostomy.
Thoracotomy to remove an esophageal foreign body Pathogenesis

is only used as a last resort, when all other efforts
have failed, or when an esophageal perforation is Esophageal strictures are a complication of severe
eminent or has occurred. esophagitis, and are most commonly associated
with gastroesophageal reflux esophagitis which
Following removal of the object by endoscopy, close occurs most commonly as a complication of per-
inspection of the esophagus to determine the extent sistent vomiting or can occur as a result of reflux
of injury is important. during general anesthesia. There is usually a lag
If there is severe esophagitis or a small perforation of 2–3 weeks between anesthesia and stricture for-
(needle), medical management of these conditions mation.
should include placement of a nasogastric or gastros- Less frequent causes of esophageal strictures are
tomy tube for feeding and medical management of reflux esophagitis as a result of gastroesophageal reflux
esophagitis (gastric acid blockers, motility modifiers, or hiatal hernia.
mucosal protectants, and possibly antibiotics will be
required). Therapy should be continued for 2–3 weeks Strictures form when the esophageal mucosa is
beyond cessation of clinical signs. severely damaged and the inflammatory process
extends down into the submucosa and muscular
Prognosis and prevention layers.
Prevention is clearly aimed at reducing the opportu-

nity for cats to ingest these objects by “cat-proofing” Clinical signs
the home and preventing prey-catching and consump- Regurgitation following eating is the most common
tion. However, it is impossible to foresee all possible presenting complaint. Liquid may be able to pass
problems, so early recognition is also important to a depending on the severity of the strictured area.
successful outcome.
If the stricture is caused by severe esophagitis second-
The prognosis is good to excellent if the object can ary to chronic vomiting, other signs may include
be immediately retrieved and the damage to the weight loss, lethargy and anorexia.
esophagus is minimal.
In cases of a chronic esophageal foreign body, pres- Diagnosis
ence of severe esophagitis, perforation or great diffi-
culty in removing the object, the prognosis is The diagnosis may be suspected on survey radiogra-
guarded to poor. phy, but can be confirmed with contrast films or
endoscopy.
Cats that develop esophageal strictures resulting
from severe esophagitis may require repeated bougi- Endoscopy should be used to evaluate esophageal
nage to allow passage of ingesta. strictures and to obtain biopsies to rule out esophageal
neoplasia, if indicated.
Cats requiring thoracotomy and esophageal surgery
to remove a foreign object will have a very guarded Routine blood work will typically be normal, unless
prognosis to survive the procedure, let alone return to the cat is also chronically vomiting, or the regurgitation
normal function. has been present long enough to affect serum protein
levels or hydration status.
ESOPHAGEAL STRICTURE*
Classical signs All causes of regurgitation should be considered in the
● Regurgitation is most common sign. initial approach, but the finding of a narrowed lumen
● Vomiting, anorexia, weight loss and on contrast radiographs narrows the primary differ-
lethargy. entials to neoplasia, peri-esophageal masses, foreign
bodies and stricture.

Esophageal strictures can be corrected one of two ways: Early clinical signs include gastrointestinal tract signs
by balloon or bougie dilation or surgical removal. such as inappetance, salivation, vomiting and weight
loss.
Every effort to correct the problem by stretching the
strictured area with balloon catheterization or Other less common signs of lead toxicity include diar-
bougienage should be made, because of the difficulty rhea, and abnormalities of the hemogram are less com-
of the surgical procedure and the numerous complica- mon in cats than dogs (basophilic stippling, nucleated
tions associated with it. RBCs).
In most cases, multiple dilation procedures are In the late stages, other central nervous system signs
required to slowly stretch out the stricture site to an such as ataxia and seizures may occur.
approximately normal size.
Regurgitation secondary to megaesophagus is very
Balloon catheters dilate the stricture site with radial rare in cats.
forces and can be used endoscopically or fluoroscopi-
cally, thus providing better visualization of the site and
better control over the force exerted. Diagnosis
Bougies dilate with longitudinal shearing and may Serum blood lead levels are the definitive means of
require multiple procedures. Bougies are associated diagnosis of lead poisoning.
with a greater risk of tearing or perforation and thus The diagnosis is helped by a history of exposure to
balloon dilation is preferred. lead-containing paints usually associated with home
Corticosteroid therapy (1.0–2.0 mg/kg/day) to prevent renovation or other objects such as batteries.
further fibrosis has been recommended but is controver- Signs of inappetence, weight loss and behavioral
sial and has not been proven effective in this regard. changes should prompt consideration of lead poisoning
In many cases of stricture, the inciting cause is long as a differential.
resolved, but if esophagitis is ongoing due to gastric Hematologic findings are often absent.
reflux, this should be managed as well (see section
under esophagitis). Survey radiographs in cats that have a history of regur-
gitation will reveal esophageal dilation or megaesoph-
Prognosis agus, and in long-standing cases, may reveal aspiration
pneumonia as well.
The prognosis is guarded for cats with esophageal stric-
tures. Many cats can be helped temporarily with dilation
procedures, but the stricture recurs or requires repeated ESOPHAGEAL NEOPLASIA* (SQUAMOUS
procedures to maintain an open esophageal passageway. CELL CARCINOMA, METASTATIC
NEOPLASIA)
LEAD POISONING*
Classical signs
Classical signs ● Regurgitation secondary to obstruction,
● Inappetance, weight loss. esophagitis or motility disturbances.
● Behavior changes (irritable, aggressive). ● Weight loss, inappetance and respiratory
● Regurgitation secondary to megaesophagus signs are also common.
is rare.
● Vomiting or diarrhea.
Clinical signs
● Seizures or other central nervous system
signs. Esophageal neoplasia creates an obstructive lesion that
is associated with regurgitation, especially after inges-
See main reference on page 596 for details. tion of food, and is typically seen in older cats.
Other signs may include weight loss, anorexia and Signs may be intermittent or chronic in nature
respiratory signs if aspiration pneumonia occurs. depending on the availability of the plants.
The most common neoplasm is squamous cell carci- Other signs include dysphagia, gagging or repeated
noma, although esophageal tumors in general are rare swallowing efforts.
in cats, and the tumor will metastasize early to regional
lymph nodes and lung.
Diagnosis
Diagnosis Plants that are associated with esophageal or gastric
irritation include: Poinsettia (Euphorbia spp.),
The presence of regurgitation as the predominant
Mistletoe (Phoradendron spp.), Aloe vera, Crown of
clinical sign will lead the clinician to suspect
Thorns (Euphorbia spp.), Snow on the Mountain
esophageal disease.
(Euphorbia spp.), Azalea (Rhododenderon), Castor
Because many of these cats are older, a variety of bean (Ricinus spp), Rosary pea (Abrus), English ivy
hematological and biochemical abnormalities may be (Hedera), Daphne (Daphne), Christmas rose
present, but there are no typical changes associated (Helleborus), Holly (Ilex), Privet (Ligustrum), Iris (Iris),
with esophageal disease on the blood work. Narcissus (Narcissus), Phildendron (Philodendron),
Wisteria (Wisteria).
The diagnosis may be suggested by finding an intralu-
minal or mass lesion obstructing the esophageal Diagnosis is based upon historical exposure or evi-
lumen on contrast radiography. dence of exposure in the regurgitated material.
Endoscopic evaluation and biopsy are the least inva- In some cats, endoscopy should be performed to rule
sive and most efficient means of obtaining a definitive out esophagitis due to other causes and determine
diagnosis of esophageal neoplasia, although surgical the extent of the lesions.
approaches will also give diagnostic information as
well.
Surgical resection of most esophageal neoplasms is
difficult if not impossible due to the fact that most Other causes of esophagitis, especially gastro-
tumors are well advanced at the time of diagnosis. esophageal reflux disease and other causes of chronic
Surgical excision of thymonas is often rewarding as vomiting should be considered.
the mass is usually benign and discrete.
PLANT INGESTION* Treatment

Most cases are not associated with severe esophagi-
Classical signs
tis that requires alternative alimentation routes or
● Intermittent or persistent regurgitation or aggressive medical therapy.
vomiting of plant material.
Reduction of hyperacidity with histamine-2 blockers
(famotidine 0.5–1.0 mg/kg PO q 24 h), administration
of anti-emetics (primarily for the prokinetic action of
metoclopramide) as needed and feeding a bland diet is
Clinical signs all that will be required in most cats.
Regurgitation or vomiting after ingestion of plants In cats with severe esophagitis, more aggressive
containing materials that are irritating, caustic or therapy will be required to prevent formation of stric-
abrasive. tures or fistula. See section on esophagitis.
Cats with aspiration pneumonia may have hemato-

ESOPHAGEAL HYPOMOTILITY/IDIOPATHIC
logic or biochemical profile abnormalities, but these
MEGAESOPHAGUS (ACQUIRED OR
will be non-specific.
CONGENITAL)*
● Contrast radiographs are rarely indicated but
will confirm the diagnosis in cases with minimal
Classical signs
dilation.
● Regurgitation, often not associated directly
Other diagnostics are used to determine if the disease
with eating.
is congenital, acquired or idiopathic.
● Cats may develop aspiration pneumonia
● Fluoroscopy (to evaluate motility).
resulting in:
● Endoscopy (for esophagitis or obstructive disor-
respiratory distress, coughing, wheezing,
ders).
lethargy, anorexia.
● Neuromuscular examination (muscle or nerve
biopsies, electrodiagnostics, e.g. EMG, nerve con-
Pathogenesis duction testing).
● Measurement of antibodies to acetylcholine
Esophageal hypomotility disorders may be idio-
receptors (myasthenia gravis).
pathic in origin or occur secondary to a known disease
● Blood lead levels.
entity (acquired or secondary megaesophagus).
● Creatine kinase measurement is of little value as the
Idiopathic megaesophagus appears to be caused by a polymyopathies in cats that cause megaoesophagus,
defect in peristalsis due to abnormal neural signal path- i.e. Devon Rex myopathy and myasthenia, are not
ways and increasing evidence suggests that the disease associated with increased creatine kinase levels.
is inherited (Siamese cats have the greatest prevalence). ● Testing of endocrine and autonomic (e.g. dysauto-
nomia) function.
The secondary causes of megaesophagus are numerous
and include: Idiopathic megaesophagus is a diagnosis made by
● Neuromuscular disorders (dysautonomia, myas- exclusion of all other possible causes.
thenia gravis, polymyopathies and polyneu-
ropathies, e.g. tetanus may cause regurgitation
secondary to hiatal hernia).
● Inflammatory disorders (e.g. esophagitis). There are numerous differentials for regurgitation
● Obstructive disorders (foreign objects, peri- or intra- (esophageal hypomotility, inflammatory, obstructive,
esophageal masses, ring structures, hiatal hernia). neoplastic, toxic or chemical irritants, or due to gastro-
● Stomach or pyloric dysfunction resulting in esophageal reflux), but once megaesophagus is found
chronic regurgitation or reflux. on survey radiographs, the list of differentials
● Toxicity (e.g. lead). is reduced to the idiopathic, congenital or acquired
forms of megaesophagus.
The secondary causes of megaesophagus that have
major importance clinically are discussed separately
Treatment
in this chapter.
Treatment of esophageal hypomotility disorders in cats
is symptomatic, unless a reversible cause for the
Diagnosis
megaesophagus is identified and corrected before the
The history and signalment of chronic regurgitation esophagus is permanently damaged.
will be suggestive of esophageal disease.
Other supportive measures include managing dehy-
Survey radiographs are usually all that is required dration with fluid therapy as needed, elevated feeding
to confirm the presence of megaesophagus. Survey of multiple, small, liquid meals (note: although some
radiographs also are important in determining the pres- cats will respond better to foods that are solid or
ence of aspiration pneumonia, the most common semi-solid) to facilitate gravitation of food into the
complication of megaesophagus. stomach, and management of aspiration pneumonia
if it occurs (bronchodilators, antibiotics if needed, oxy- Diagnosis

gen supplementation, and coupage).
The definitive diagnosis is made by the demonstration of
If oral feeding is unsuccessful, despite trying different antibodies (Ab) to the acetylcholine receptor (AchR),
food types and consistencies, gastrostomy tube feed- either in serum or neuromuscular junction biopsies.
ing may be required for long-term management.
Nasogastric and esophagostomy tubes are generally not The EMG in cats with myasthenia will show the classic
good long-term options for feeding management. decremental response (each successive spike will have
a lower magnitude, corresponding to the fatigue of the
muscle.
Prognosis Acquired myasthenia gravis is believed to be an
The prognosis depends upon several factors but immunologic disease resulting in the destruction of
especially upon the cause. If an underlying disorder AchR by immunoglobin produced against the recep-
can be identified and corrected (e.g. dilation due to tor, but thymoma and other diseases are also seen in
PRAA), the prognosis may be favorable. conjunction with acquired myasthenia.
Idiopathic megaesophagus and megaesophagus due Congenital myasthenia is due to lack of AchR, rather
to neuromuscular function disorders (dysautonomia than immune-mediated destruction of receptors. This
or myasthenia gravis) is guarded to poor. form of myasthenia is rare in cats.
An intravenous ednophonium chloride test may be
performed on cats with generalized muscle weakness.
MYASTHENIA GRAVIS* (CONGENITAL OR This short-acting cholinesterase-inhibiting drug results
ACQUIRED) in alleviation of weakness in about half of affected cats.
Muscle biopsy may show histopathologic signs of
Classical signs myositis.
● Regurgitation due to megaesophagus, and
generalized muscle weakness. Differential diagnosis
● Dysphonia and cervial ventroflexion are
more common in cats. Other causes of megaesophagus, including idiopathic
ME, PRAA, chronic esophagitis, metabolic or toxic
See main reference on page 896 for details. causes.
Treatment
Clinical signs
Supportive care for acquired myasthenia and associ-
Regurgitation is reported due to megaesophagus.
ated megaesophagus includes:
Generalized muscle weakness is seen in the general-
ized and acute fulminating forms of the condition, but Elevated feedings.
not in focal myasthenia.
Tube (NG, gastrostomy) feeding.
Dysphonia and cervial ventroflexion are more common
Management of aspiration pneumonia as required
in cats than in dogs.
with antibiotics and bronchodilators.
Congenital myasthenia is more common in Siamese
Immunosuppressive therapy (prednisolone 2–6
and DSH cats, while acquired myasthenia appears to
mg/kg/day or azathioprine).
be more common in Somalis and Abbysinians and
occurs in slightly older kittens (4–6 months). Acetycholinesterase antagonists (pyridostigmine bro-
mide 0.2–2.0 mg/kg q 8–12 h PO).
Acquired myasthenia has a bimodal age distribution,
with most affected cats being young adults (2–3 years) If available, plasmapheresis may be used in some cats
or older (9–10 years). with acquired megaesophagus.
Thymectomy is indicated in cats with a thymoma and Other signs include respiratory distress, coughing or
associated megaesophagus. lethargy associated with aspiration pneumonia that
occurs secondary to regurgitation.
Congenital myasthenia does not respond well to
immunosuppressive therapy and thus supportive care
is essential. Diagnosis
Some cats with severe megaesophagus succumb to A presumptive diagnosis is often made based on the
aspiration pneumonia. history and signalment, however, survey radiographs
followed by introduction of contrast media are
required to make the definitive diagnosis and differen-
VASCULAR RING ANOMALIES
tiate megaesophagus due to a vascular ring struc-
(PERSISTENT RIGHT AORTIC ARCH –
ture from other causes.
PRAA)
Routine hematology and serum biochemistry values
Classical signs will be normal unless the kitten has developed an aspi-
ration pneumonia or secondary bacterial pneumonia as
● Regurgitation when kitten is weaned onto
sequelae to the anomaly.
solid foods.
Echocardiography can be used to determine which
type of vascular ring structure is involved, but is not
Pathogenesis
necessary to make the diagnosis.
The vascular ring anomalies are congenital malforma-
tions of the aortic arches which result in a ring around
the esophagus that results in an esophageal obstruction. Differential diagnosis
In cats, a persistent right aortic arch is the most com- The primary differential for this disease is congeni-
mon anomaly causing esophageal obstruction and tal megaesophagus, but the presence of the con-
regurgitation. stricted area at the base of the heart, along with onset
Other rare, but reported anomalies include the double of signs at the time that the kitten begins to consume
aortic arch and the left aortic arch with right ligamen- solid food will help differentiate the two diseases.
tum arteriosum. Other causes of regurgitation will be readily ruled out
The obstruction of the esophagus with persistent right by the survey radiographs.
aortic arch anomaly is created because the esophagus is
trapped by the aorta on the right, the heart base ven-
trally, and the ligamentum arteriosum dorsolaterally on Treatment
the left.
The only treatment is surgical removal of the con-
stricting band to release the entrapped esophagus.
Clinical signs
In kittens with long-standing esophageal dilatation
The classical sign associated with a vascular ring due to the vascular ring, esophageal hypomotility cra-
anomaly is the acute onset of regurgitation in a kit- nial to the stricture may be permanent and require
ten that has just been weaned onto solid food. life-long management (see Management of mega-
In most kittens, regurgitation will occur immedi- esophagus).
ately after eating, but later in the course of the dis- Treatment of aspiration pneumonia is supportive:
ease, as the esophagus becomes more dilated and oxygen supplementation, fluids, antibiotics if a bac-
non-functional, regurgitation may occur at any time terial component is present, and respiratory therapy
with no relationship to food intake. (bronchodilators, expectorants, coupage) as needed.
Prognosis Diagnosis
The prognosis is guarded to good. If esophageal func- There is no classic history or signalment that will lead
tion returns after the removal of the constricting band, to a presumptive diagnosis, however, the signs will be
the prognosis is very good, but in those kittens with suggestive of esophageal disease in most cases.
residual esophageal dilatation and hypomotility, the
Hematologic and serum biochemical profiles are typ-
long-term prognosis is guarded to poor.
ically normal.
Survey radiographs may be suggestive if there is a
ESOPHAGEAL DIVERTICULAR
large diverticulum, but in most cases contrast studies
STRUCTURES
are necessary to confirm the presence of the sac-like
structure.
Classical signs
Endoscopic examination of the esophagus is also
● Regurgitation, pain when swallowing,
diagnostic and also may provide information about the
lethargy, and decreased appetite.
cause or any associated complications. In cats that have
very small diverticula, endoscopy will be a more
Pathogenesis helpful diagnostic procedure than contrast radi-
ographs which could miss the lesion.
Esophageal diverticula are sac-like dilations of the
esophageal wall that can be congenital or acquired.
Acquired diverticula are secondary to one of two
scenarios: Any cause of regurgitation should initially be consid-
ered a differential. But blood work and radiographs
Trauma or an obstruction (e.g. foreign body) that
(survey and contrast) will help to rule out some of the
causes increased intraluminal pressure resulting in a
more common causes of regurgitation, which include
dilation or diverticulum developing cranial to the
megaesophagus, esophageal foreign bodies, esophageal
injury site.
masses and peri-esophageal masses.
Esophageal fibrosis secondary to an inflammatory
Endoscopic examination will be required to rule out
process (either in the esophagus or in the surrounding
esophagitis and other inflammatory causes of regur-
tissues) that causes a contraction of esophageal tissue
gitation.
and the formation of a diverticular sac.
Congenital diverticula are rare in cats. Treatment
Diverticula should be managed as conservatively as
Clinical signs possible, due to the difficulties and complications asso-
Clinical signs are usually only observed with a large ciated with esophageal surgery.
diverticula. If an underlying cause can be identified and cor-
Signs that may occur include: rected, this greatly improves the chances for treatment
● Regurgitation.
success.
● Inappetence and weight loss. Conservative management of diverticula includes
● Pain when swallowing or thoracic pain. preventing food accumulation in the sac, either by
● Respiratory signs. elevated feedings of gruel or liquid diets or by place-
● Fever. ment of a gastromy tube to by-pass the esophagus.
Respiratory signs can be secondary to aspiration If the conservative management fails, either due to the
pneumonia or can be associated with an inflammatory cause or size of the diverticulum, surgical excision and
process in the lungs that is the cause of esophageal reconstruction are options, but esophageal dysfunc-
fibrosis and diverticulum formation. tion and stricture are common sequelae to surgery.
Prognosis Diagnosis
The prognosis for cats with an esophageal diverticulum Survey radiographs of the thorax may reveal a soft
depends on its cause and size. tissue density and gas in the region of the caudal
dorsal mediastinum, but contrast radiography will
In cats that have a small diverticulum for which the
confirm the presence of the hernia (unless it is a sliding
cause has been identified and removed, the prognosis is
hernia that is in the normal position at the time of radi-
guarded to good.
ographs) or untussusception.
If the diverticulum is large, the cause is uncor-
In some cases fluoroscopy will assist in identifying a
rectable, or there is no response to conservative
sliding hernia.
management, the prognosis is poor.
HIATAL HERNIA/GASTROESOPHAGEAL Differential diagnosis

INTUSSUSCEPTION
Diagnosis may be difficult if the hernia is sliding or
Classical signs the intussusception is intermittent and the signs are
intermittent in nature. All the major esophageal disor-
● Intermittent or persistent regurgitation or ders (esophagitis, hypomotility, stricture, etc) should be
vomiting. considered and ruled out by appropriate testing.
Pathogenesis
Treatment
Hiatal hernia is the protrusion of any abdominal con-
If the cat is symptomatic, treatment is as for reflux
tents through the esophageal hiatus of the diaphragm
esophagitis (histamine-2 blockers, metoclopramide
into the thorax. With gastroesophageal intussusception,
and sucralfate as needed).
the stomach is prolapsed into the lumen of the distal
esophagus. In cats with persistent clinical signs that do not
improve with conservative medical therapy, surgical
Hiatal hernia is an uncommon problem in cats, but
intervention is indicated.
occurs due to enlargement of the hiatal membrane
(may occur from trauma) or as a result of laxity in
the phrenoesophageal membrane. Hiatal hernias Prognosis
have been reported in association with generalized
Fair to good, especially since cats with hiatal hernias
tetanus.
or gastroesophageal intussusceptions tend to have inter-
Cats more commonly have sliding hiatal hernias, with mittent clinical signs.
cranial displacement of the abdominal esophagus and
part of the stomach through the esophageal hiatus.
ESOPHAGEAL FISTULA
Gastroesophageal intussusception can cause both
esophagitis and esophageal obstruction. Classical signs
● Regurgitation or dysphagia occurring in
Clinical signs
conjunction with coughing or respiratory
Intermittent or persistent regurgitation or vomiting distress.
are the most common signs.
Some cats may show abdominal pain on palpation of Pathogenesis
the anterior abdomen.
Fistula development is the result of esophageal
Respiratory distress may be seen with large hiatal her- ischemia and necrosis that ultimately leads to a small
nias or gastroesophageal intussusceptions. perforation. The process of healing leads to develop-
ment of a fibrous tract and a communication devel- Treatment

ops between the esophagus and the respiratory system.
The only treatment is surgical closure of the fistula
The most common pathway in cats is between the and correction of the underlying cause if it is still
left caudal lung lobe or the accessory lung lobe and present (e.g. diverticulum, neoplasia).
the esophagus.
In some cats, lobectomy may be necessary as well.
The most common cause of fistula development is an
esophageal foreign body that penetrates (e.g. needle) Symptomatic therapy for the pneumonia and
but other causes include diverticular structures and esophageal disease includes: esophageal rest (nasogas-
neoplasia. tric or gastrostomy tube), antibiotic and bronchodila-
tor therapy as needed, and drugs to control esophagitis
if it is present (e.g. ranitidine, metoclopramide, sucral-
Clinical signs fate, etc).
Signs are referrable to both the esophagus and lower
respiratory tract. Prognosis
Signs of esophageal disease include regurgitation, Guarded. Any esophageal disease that requires surgi-
painful swallowing or repeated swallowing attempts. cal correction must be regarded as having a guarded
The majority of signs are respiratory, and include prognosis because of the high rate of complications that
dyspnea, coughing, tachypnea, anorexia, fever and occur following surgery (e.g. stricture).
weight loss, associated with the accumulation of
esophageal contents in the affected lung lobe. Prevention
The smaller the fistula, the fewer the clinical signs Rapid identification and correction (removal) of
and the more difficult it is to diagnose. esophageal foreign bodies, diverticular structures or
neoplasia (if possible).
Diagnosis
A large fistula may be visualized on survey radio-
graphs, as well as the pulmonary changes associ- HEREDITARY MYOPATHY OF DEVON REX
ated with pneumonia (increased alveolar and interstitial CATS
pattern).
Classical signs
In cats with a very small fistula, contrast radi-
ographs may be required to identify the structure. In ● Young Devon Rex cats.
some cases, these may be so small that endoscopy is ● Appendicular weakness and fatigability.
not a means of definitive diagnosis either. ● Passive ventroflexion of the head and neck.
● Dorsal protrusion of the scapulae.
Endoscopic examination should be performed to
● Megaesophagus is common, and
obtain biopsies to determine if the lesion is neoplas-
choking and laryngospasm may occur
tic or not.
when eating.
If there is significant pulmonary disease, the cat may
have an inflammatory leukogram. See main reference on page 900 (The Cat With Neck
Ventroflexion) for details.
Pathogenesis
Diverticular structures, esophageal strictures, radiolucent
esophageal foreign objects, and aspiration pneumonia The disease is inherited in an autosomal recessive
secondary to esophageal hypomotility, should all be con- fashion. The pathological defect causing the muscle
sidered when a differential list is being formulated. weakness has not been determined.
Clinical signs 0.5–1.0 mg/kg PO q 24 h), drugs that increase

esophageal sphincter tone (cisapride 5 mg/kg PO q 12
Affected cats have ventroflexion of the head and neck h), and mucosal cytoprotectants (sucralfate 250–500 mg
because weakness of the dorsal cervical muscles leads PO q 8–12 h).
to an inability to support the head. Ventroflexion is
accentuated during locomotion, micturition and Other supportive measures include elevated feeding
defecation. of small, liquid meals, or even gastrostomy tube
feeding.
A high-stepping forelimb gait, head bobbing and
progressive dorsal protrusion of the scapulae may
also be seen, particularly following exertion, stress or Prognosis
excitement. Guarded to poor. Most of these cats suffer from
Cats often have problems prehending and swallowing chronic reflux esophagitis with megaesophagus and
food, partly because of their abnormal head position many die suddenly of laryngospasm after choking on
and partly because of oropharyngeal weakness. food.
Acute upper airway obstruction may develop due to

accumulation of ingesta in the vicinity of the larynx, Prevention
and this may lead to fatal laryngospasm. Because the condition is associated with an autosomal
recessive gene, the parents of any affected kittens
Diagnosis should no longer be used for breeding.
Diagnosis is made on a combination of history, breed

and clinical signs. DYSAUTONOMIA
Routine bloodwork including serum K+, creatine kinase Classical signs
and aspartate transaminase shows no abnormalities.
● Regurgitation secondary to
Muscle tone, and spinal reflexes are all within nor- megaesophagus.
mal limits. ● Constipation.
Sparse fibrillation potentials and positive sharp ● Mydriasis.
waves are present on EMG. ● Dry mucous membranes of mouth and eye.
Muscle biopsy reveals highly variable muscle fiber See main reference on page 792 for details.
sizes, with increased numbers of nuclei, internal nucle-
ation and split or degenerating fibers.
Pathogenesis
Survey or contrast radiographs may reveal mega-
esophagus with a U-shaped diverticulum at the thoracic Generalized degeneration of the autonomic ganglia
inlet. results in loss of GI tract motility, and loss of auto-
nomic control to the eye and heart.
Clinical signs
Other myopathies such as X-linked muscular dystro-
phy, nemaline myopathy and hypokalaemic polymyopa- Clinical signs usually develop over 48 hours and depres-
thy should be considered, as well as myasthenia gravis. sion and anorexia are present in nearly all cats.
Regurgitation occurs secondary to megaesophagus.
Treatment Vomiting often occurs and regurgitation may be
reported as vomiting.
Symptomatic treatment for reflux esophagitis may be
given, including histamine-2 blockers (famotidine Constipation is commonly reported.
Mydriasis is present with normal vision and third eye- There are no other abnormal clinical findings other
lids are commonly prolapsed. than the cat appears to gulp or swallow its food without
chewing it.
Keratoconjunctivitis sicca and dry oral mucous
membranes may be present.
Other signs include bradycardia (60–120 bpm) and Diagnosis
hypotension All clinical, biochemical, radiographic and endo-
Anal areflexia has been reported. scopic studies (if performed) will be normal.
Dysuria in association with a distended urinary This is a diagnosis of clinical presumption based on
bladder also occurs. history, physical exam and the ability to control the
signs by feeding smaller meals more frequently or
The disease is rare in the US (some regional areas reducing the competition for food that may create food
especially in the central mid-west have more cases) but gulping.
was more common in Europe in the 1980s.
It is usually seen in young (< 3 years) cats. Differential diagnosis
Hiatal hernia, mild gastroesophageal reflux, mild
Diagnosis esophageal hypomotility or lower esophageal sphincter
The constellation of clinical signs is suggestive of disease.
autonomic nervous system dysfunction. Food intolerance and food allergy may cause vomiting
There is no definitive diagnostic test for dysauto- very soon after eating which could be mistaken for
nomia, but the following tests of autonomic function regurgitation.
are supportive:
● Intraocular physostigmine fails to provoke a
Treatment
response, but pilocarpine causes immediate miosis.
● Intradermal skin testing – There is no response to Feed the cat smaller meals more frequently or change
histamine (no wheal or flare). feeding location or time to reduce competition for
● Epinephrine should not be given to cats with food or the tendency to eat rapidly.
dysautonomia because fatal arrhythmias may
develop.
MEDIASTINAL NEOPLASIA
● Cats will respond to atropine (increased heart rate),
which proves that the post-ganglionic receptors are
Classical signs
still able to appropriately respond to stimulus.
● Anorexia.
● Regurgitation.
EATING TOO FAST (FOOD GULPING)
● Other systemic signs if paraneoplastic
disease occurs.
Classical signs
● Thymic lymphoma/thymoma is a
● Intermittent regurgitation of food mostly benign anterior mediastinal
immediately after ingestion, often in mass, usually found in older cats. Most
tubular form. affected cats are FeLV negative and the
tumor may be associated with para-
neoplastic syndromes, such as
Clinical signs
myasthenia gravis, polymyositis,
Intermittent regurgitation of whole food, often in myocarditis or dermatitis.
tubular form, immediately after it is consumed.
RECOMMENDED READING
August JR (ed). Consultations in Feline Internal Medicine. WB Saunders, Philadelphia, PA. 2001; 4.
Mears EA, Jenkins CC. Canine and feline megaesophagus. Comp Cont Ed 1997; 19(3): 313–326.
Sellon RK, Willard MD. Esophagitis and strictures. Vet Clin North Am Small Anim Pract 2003; 33: 945–967.
Guilford WG, Center SA, Strombeck DR, Williams DA (eds). Strombeck’s Small Animal Gastroenterology, 3rd edn.
WB Saunders, Philadelphia, PA. 2000.
Tams TR. Esophagoscopy. Small Animal Endoscopy. WB Saunders, Philadelphia, PA. 1999; 2.
30. The cat with signs of acute vomiting
Debra L Zoran
KEY SIGNS
● Active elimination of stomach contents through the mouth.
● ± Preceded by nausea, pacing, and salivation.
● Usually digested food or liquid with acidic or neutral pH.
● ± 1 week’s duration.
MECHANISM?
● Vomiting is an active process that must be distinguished from regurgitation.
● Vomiting in cats is associated with abdominal muscle contraction, and signs of considerable
muscular effort and anxiety prior to the event.
● Vomitus may consist of undigested food material (if swallowed whole), partly digested or even
liquid, and may be clear, yellow (bile stained) or brown (food colored).
WHERE?
● Vomiting may result from gastrointestinal disease or extra-intestinal tract diseases.
● Vomiting is rarely associated with colonic disease, except when toxins associated with fecal
retention affect the vomiting center and chemoreceptor trigger zone.
WHAT?
● The most common causes of acute vomiting are:
● Mechanical obstructions (including foreign bodies).
● Extra-intestinal tract diseases such as hepatitis.
● Renal failure or pancreatitis, dietary (indiscretion).
● Inflammatory diseases (e.g. IBD).

Diseases causing signs of acute vomiting
DEGENERATIVE
Dysfunction of the autonomic nervous system resulting in dilated pupils, dry mucous membranes,
regurgitation, vomiting, constipation, bradycardia and dysuria.
630
30 – THE CAT WITH SIGNS OF ACUTE VOMITING 631
MECHANICAL
● Gastrointestinal foreign bodies (obstruction)** (p 636)
Acute onset of vomiting that may be projectile if the obstruction is at the pylorus. Vomiting may
be intermittent if object is not causing a complete obstruction. Linear foreign bodies (e.g. string)
may be evident wrapped around the base of the tongue.
●Intussusception* (p 643)
Acute onset of vomiting, anorexia and lethargy and occurs more often in kittens. The obstruction
may be palpated in some cats.
● Motility disturbances (ileus, gastroesophageal reflux)* (p 647)
Vomiting is not associated with eating and usually is bile stained due to presence of duodenal
content.
● Antral pyloric hypertrophy/stenosis (p 660)
Vomiting of partially or completely digested food usually several hours after eating, and may be
projectile in nature. Siamese cats may be predisposed. Vomiting may appear to be acute in onset in
the congenital form, as the vomiting occurs when the kitten begins to eat solid food.
METABOLIC
● Hepatopathies (hepatic lipidosis, cholangitis, drug-induced hepatopathy)** (p 638)
Anorexia, lethargy and vomiting are persistent. Cat may or may not be icteric.
● Diabetes mellitus* (p 643)
Acute onset of vomiting, lethargy, anorexia associated with uncontrolled diabetes mellitus. Cats
are usually older, in poor body condition and may be severely dehydrated or in shock if owner
does not recognize the condition until late.
● Acute renal failure/pyelonephritis* (p 645)
Acute renal failure is associated with an acute onset of vomiting and depression (may be primary,
e.g. ischemic, hypovolemic, or secondary, e.g. post renal obstruction). Other signs include tachyp-
nea, oliguria or anuria, hypothermia. Pyelonephritis causes intermittent vomiting, pain over the
sublumbar region, decreased appetite, occasionally fever and polyuria.
● Hypercalcemia (p 652)
There are many causes of hypercalcemia, but the clinical signs most commonly seen are anorexia,
vomiting, weight loss and lethargy or weakness.
NEOPLASTIC
● Gastric or small intestinal neoplasia* (p 641)
The most common tumor of the feline digestive system is alimentary lymphoma. Other tumors that
occur in the stomach and small intestine are adenocarcinomas (second), and mast cell tumors
(third), with fibrosarcomas, leiomyosarcomas and carcinoids occurring rarely. The primary site of
gastric tumors is the pylorus. With the exception of lymphoma, which can occur at any age, most
tumors occur in old cats. The clinical signs most often observed are anorexia, weight loss and vom-
iting, which may occur as acute vomiting when the tumor causes a GI obstruction.
continued
continued
NUTRITIONAL
● Food intolerance or dietary indiscretion** (p 635)
Indiscretion is associated with an acute vomiting due to over-eating, eating too quickly or ingest-
ing a foreign substance (food or non-food), e.g. lizards, beetles, plants. Food intolerance causes
intermittent vomiting or loose stools, with no pattern or association with eating, and resolves when
food source is changed to omit offending substance from diet.
INFLAMMATORY
● Acute pancreatitis** (p 639)
Anorexia and lethargy are the most common signs, with abdominal pain and vomiting being
observed much less frequently.
● Gastritis/gastric ulcer disease** (p 637)
Acute onset of vomiting, anorexia and lethargy. May be associated with hematemesis if there are
deep erosions or ulcers.
● Septicemia/bacteremia/endotoxemic shock (p 655)
Vomiting is only one of the signs that may occur, others include hypothermia, weakness or col-
lapse, depression, weak or thready pulses, tachypnea and pale to gray mucous membrane color.
● Peritonitis (p 655)
Abdominal pain, distention, fever, decreased appetite and lethargy are the most common presenting
signs. Vomiting may occur, but is not a consistent problem.
● Encephalitis/meningitis (p 659)
Vomiting, when it occurs, is due to inflammatory effects on the CRTZ or results from systemic
effects of the disease that is causing the encephalitis, e.g. histoplasmosis, toxoplasmosis, crypto-
coccosis, etc. Most cats with inflammatory CNS disease either have seizures, neurologic deficits,
ataxia or dysmetria, or cervical pain.
● Vestibular disease (p 656)
Vomiting is more commonly associated with peripheral vestibular disease. In addition to vomiting,
other clinical signs may include head tilt, ataxia, nystagmus and circling.
INFECTIOUS
Viral:
● Feline panleukopenia virus* (p 650)
Infectious viral enteritis of young cats that is often fatal in unvaccinated populations due to the
severity of the clinical signs and systemic septicemia. Clinical signs include an acute onset of
anorexia and depression, followed by vomiting. Diarrhea may not occur, or is delayed for
24–48 hours. The disease is a relatively rare problem in well, vaccinated cats due to the efficacy
of the vaccine.
Bacterial:
● Helicobacter spp.* (p 646)
The true importance of Helicobacter in feline gastritis is still unknown, but increasing evidence
points to them having a role in inflammatory diseases of the stomach, liver and pancreas.
● Salmonellosis* (p 648)
Primarily a problem in young or debilitated cats, as most cats are asymptomatic carriers. In adult
cats, vomiting, diarrhea, anorexia and weight loss are more common, while in kittens, systemic
signs of infection, including fever or hypothermia, weakness or collapse due to septicemia and
endotoxemia.
PARASITIC
● Physaloptera (p 653)
Intermittent vomiting episodes in young, outdoor cats that hunt. Occasionally the small worms are
observed in the vomitus.
● Ollulanus tricuspis (p 654)
Acute onset of vomiting in free-roaming or colony cats associated with infection with this gastric
nematode, which has a direct life cycle.
● Ascarids (p 654)
Intermittent vomiting in young kittens is sometimes observed with large worm burdens due to the
mass of worms obstructing normal passage of ingesta. More common signs include unthriftiness,
diarrhea and pot-bellied appearance.
TOXIC
● Plant ingestion/toxicity* (p 646)
Many plants do not produce severe toxicity (Philodendron, Diffenbachia, Euphorbia, Caladium,
etc,), but a few are nephrotoxic (Lilium e.g. lilies, rheum, e.g. rhubarb, oxalis e.g. sorrel) and cause
vomiting in addition to signs of renal failure. Other plants that cause vomiting are ricinus
(castor bean), robinia (black locust), and solanum (nightshade) to name a few of the more com-
mon species.
● Pharmacologic/antibiotic induced* (p 642)
Acute onset of vomiting after initiating antibiotic therapy. Antibiotics associated with vomiting:
ampicillin, cephalosporins, tetracycline, erythromycin.
● Ethylene glycol* (p 648)
Vomiting occurs in two stages, one is associated with the initial ingestion of the toxin and is due to
alcohol intoxication and metabolic acidosis. Other signs that occur during this time are salivation,
depression, ataxia and polydipsia. The second stage occurs 2–3 days later and vomiting, depres-
sion and oral ulcers develop secondary to the acute, anuric renal failure, which is the end stage of
this toxicity.
● Pyrethrins\pyrethroids\permethrins\organophosphates* (p 644)
Vomiting, diarrhea, hypersalivation, contact dermatitis, ataxia, excitation, seizures and dyspnea are
all reported signs of toxicity to these insecticides.
● Anesthetic agents (Xylazine) (p 658)
Xylazine-induced emesis is a well-known side effect of its administration and is often used thera-
peutically.
● Chemotherapy drug-induced vomiting (p 658)
Those drugs associated with vomiting include: actinomycin-D, cyclophosphamide, cytosine arabinoside,
dacarbazine, doxyrubricin, methotrexate, mitoxantrone, vinblastine.
continued
continued
● Non-steroidal anti-inflammatory drug (NSAID) toxicity (p 656)

Vomiting associated with non-steroidal anti-inflammatory drugs (aspirin, ibuprofen) is usually
associated with acute gastritis and erosions that occur secondary to the anti-prostaglandin effects
on the stomach. Ibuprofen will also cause acute renal failure. Acetaminophen does not induce gas-
tritis but vomiting has been observed in cats due to the hepatotoxicity. Other clinical signs that
occur more frequently and are more important include facial edema, pruritus, salivation, tachyp-
nea, depression and cyanosis (due to methemoglobinemia).
● Arsenic poisoning (p 659)
Arsenic is found in herbicides, insecticides, wood preservatives and blood parasiticides. Initial
clinical signs include vomiting, diarrhea, anorexia and depression. This is followed by hepatic and
renal failure.
INTRODUCTION WHERE?
Vomiting may result from gastrointestinal disease or
MECHANISM? extra-intestinal tract diseases.
Vomiting occurs when the vomiting center in the Acute vomiting associated with extra-intestinal dis-
medulla is stimulated, which can occur by several eases may be due to:
mechanisms: ● CNS disease (e.g. encephalitis or vestibular disease).
● Effect of blood-borne toxins or drugs. ● Pancreatitis.
● Afferent impulses from the cerebral cortex, ● Hepatobiliary disease.
chemoreceptor trigger zone (CRTZ), the ● Renal disease causing acute or chronic renal failure.
vestibular apparatus, or receptors in the phar- ● Metabolic or endocrine diseases including
ynx or abdominal viscera. ketoacidotic diabetes mellitus and hypercalcemia.
● Systemic illness or infection, e.g. septicemia,
The chemoreceptor trigger zone (CRTZ) is stimulated
pyometra.
by:
● Blood-borne toxins, including uremic toxins or Primary gastrointestinal diseases that cause acute
drugs. vomiting involve the stomach or small intestine:
● Parasites, e.g. Physaloptera, Ollulanus, etc.
Vomiting is an active process that must be distin- ● Infectious diseases, e.g. Salmonella, Helicobacter.
guished from regurgitation. ● Inflammatory diseases, e.g. IBD.
Vomiting in cats is associated with abdominal muscle ● Neoplasia.
contraction, and signs of considerable muscular ● Mechanical, e.g. foreign body obstruction, intus-
effort and anxiety prior to the event. susception, motility disturbances.
● Dietary disturbances, e.g. indiscretion or food
Vomitus may consist of undigested food material (if
intolerance.
swallowed whole), partly digested or even liquid, and
may be clear, yellow (bile stained) or brown (food col- Vomiting is rarely associated with colonic disease,
ored). except when toxins associated with fecal retention affect
the vomiting center and chemoreceptor trigger zone.
Vomitus is not typically tubular in form, nor does it
contain large amounts of white frothy material.
WHAT?
The pH of vomitus is usually acidic (pH < 4), but may
be neutral (pH 7) if duodenal content is present (bile The most common causes of acute vomiting are:
reflux). mechanical obstructions (including foreign bodies),
extra-intestinal tract diseases (such as hepatitis, renal Food intolerance is usually a cause of chronic, inter-
failure or pancreatitis, dietary indiscretion), and mittent vomiting, but kittens may present acutely with
inflammatory diseases (e.g. IBD). diarrhea when they are first introduced to new foods.
Diarrhea may result when a rapid change in food over-
Many cats vomit intermittently, and these episodes
whelms the digestive capacity. Changes in food com-
are attributed to trichobezoars (hairballs). However,
position require changes in digestive enzymes.
some of these cats may be vomiting due to dietary
indiscretion or food intolerance, gastric parasites, Ingesting a foreign substance (dietary indiscretion)
motility disturbances, pancreatitis or other acute such as lizards, beetles, moths or plants may cause
inflammatory disorders. acute vomiting. Over-eating or eating too quickly is
poorly documented as a cause of vomiting in cats.
Acute, persistent vomiting episodes that occur along
with other clinical signs such as lethargy, anorexia or
diarrhea, usually signal a more serious problem that
Clinical signs
should be investigated more thoroughly. Examples of
problems fitting this category include intussusception, Intermittent but persistent vomiting or mucoid, soft
erosions/ulcers, acute renal failure, neoplasia or inflam- feces are common signs. Poor hair coat or failure to
matory bowel disease. thrive may also be noted but this is less common.
DISEASES CAUSING SIGNS OF ACUTE Diagnosis

VOMITING There is no definitive diagnostic test for this problem
other than to observe a response to changing the diet.
FOOD INTOLERANCE OR DIETARY
INDISCRETION**
Classical signs Intermittent but unrelenting vomiting in an otherwise
● Intermittent vomiting. healthy cat suggests possible motility disturbances,
● Large bowel diarrhea or soft, mucoid feces. antral pyloric hypertrophy, gastric parasites or early
IBD.
Pathogenesis
Treatment
Food intolerance is a non-immunologic, adverse reac-
Changing the diet to a diet that does not contain the
tion to a substance(s) present in food. This reaction
offending substance. This may be as simple as chang-
may be to a food component such as the type of protein
ing from a grocery store brand to a premium brand food
or carbohydrate, or it may be to the colorings, preserv-
(or vice versa), but also may require changing to a
atives, flavorings, etc. that are present in pet foods.
hypoallergenic food product (IVD’s Limited diets,
Natural chemicals in foods such as amines, salicylates
Hill’s d/d, Eukanuba Response formula, Waltham,
and monosodium glutamate may stimulate nerve end-
etc.). Kittens often respond to being fed exactly the
ings and have also been associated with food intoler-
same food as a sole diet for at least 3 days.
ance. Highly flavored or “rich” food has more of these
chemicals. Cats may be sensitive to more than one
food. Signs may require a “binge” or several days of Prognosis
exposure before they are evident.
Good if the appropriate food can be found, which is
The actual mechanism associated with vomiting or usually not a difficult problem. However, the cat may
diarrhea due to food intolerance is unknown. have to remain on the diet indefinitely.
With gastric or upper small intestinal obstructions,

GASTROINTESTINAL FOREIGN BODIES
acute onset of frequent vomiting or gagging is
(OBSTRUCTION)**
common.
Classical signs Dehydration, lethargy and anorexia are common in
these cats, and they may show evidence of abdominal
● Frequent, severe vomiting episodes with
discomfort (either on palpation or by posture).
upper GI obstruction.
● Intermittent vomiting with lower intestinal In cats with a lower intestinal obstruction, diarrhea
obstruction. will probably be more likely, vomiting less frequent
● Anorexia. and severe, and dehydration and abdominal pain more
● Dehydration. variable.
● Diarrhea is more prevalent with lower
If the foreign body is of significant size or if intestinal
intestinal obstructions.
plication from a linear foreign body is present, these
● Abdominal pain.
abnormalities may be palpable.
Cats that develop an intestinal perforation as a result
Pathogenesis
of the foreign body deteriorate rapidly and develop
GI foreign bodies occur more commonly in young depression and fever, hypovolemia/shock.
cats, because of their curious nature, tendency to ingest
non-food substances (string, rubber bands) and prey
(hair, fur, bones). Diagnosis
Linear foreign bodies (e.g. string, yarn, thread, etc.) History and physical examination findings are very
are the most common foreign body in cats and create important in pointing to the diagnosis (always examine
problems from the motility disturbances that are cre- under the tongue of vomiting cats).
ated resulting in intestinal plication or intussuscep-
Hemogram and serum biochemistry profile findings
tion, and from the intestinal perforation due to string
will likely be normal if the condition is acute.
migration through the intestinal wall. Thread, with or
without a needle, and string are the most common Long-standing or severe linear foreign bodies or GI
causes, and in some countries, the string from the end perforation will show an inflammatory response, evi-
of a sausage is a common culprit. dence of dehydration (hemoconcentration or elevated
proteins) and electrolyte abnormalities consistent
Linear foreign bodies may first be caught under the
with vomiting (hypokalemia is most common).
base of the tongue, creating not only an oral lesion, but
also preventing the possible passage of the string The diagnosis is obtained by imaging studies, includ-
through the GI tract. Alternatively, they may become ing radiography (plain or contrast), ultrasonography
trapped at the pylorus, with the rest of the string pass- or upper GI endoscopy. Radiographs may reveal evi-
ing into the small intestine. dence of intestinal plication (wash board appearance)
which is the classic presentation for string foreign
Many foreign objects (especially hair, but including
bodies. In some cases, endoscopy will allow retrieval
string) will pass through the GI tract, so if an obstruc-
of the foreign object, and is a useful means of assess-
tion occurs, it may be due to a disturbance in motility,
ing other damage (e.g. erosions, ulcers, or tears in the
narrowing of lumen or other pathology that prevents
mucosa).
the normal passage of the object.
Clinical signs
The signs depend upon the location of the foreign The acute onset, age of occurrence and history or
object and will help in many cases to localize the physical examination findings usually point to a for-
lesion. eign body.
However, some cats with linear foreign bodies have a Pathogenesis

waxing/waning course of vomiting and anorexia that
may not suggest the diagnosis immediately. Gastritis results from hyperacidity, loss of mucosal
protection (mucus, bicarbonate), reduced mucosal
Other differentials in those cases would include infec- blood flow, or mucosal damage from direct trauma, irri-
tious, dietary or inflammatory gastrointestinal diseases. tation or chemical erosion.
Treatment Continued damage leads to development of a gastric

erosion (lesion in mucosa only) or ulcer (lesion affect-
In cases where the object is still in the stomach, it is ing the deeper tissue layers of the stomach wall).
sometimes possible to safely retrieve the object (nee-
dle, small toy, etc.) via an endoscopic procedure. Non-steroidal anti-inflammatory drugs (NSAIDs)
reduce the synthesis of prostaglandins which are nec-
Most GI foreign bodies however, will require surgical essary for gastric mucus secretion. Gastric mucus is
removal, and some may be a surgical emergency when the primary means of surface protection against acid,
GI perforation has occurred. irritants and trauma.
Cats that are severely dehydrated from persistent vomit- Hyperacidity can occur secondary to liver failure
ing, or have suspected intestinal perforation and leakage (hypersecretion of gastrin and reduced mucosal blood
should be stabilized as much as possible with aggressive flow), renal failure (hypergastrinemia) or mastocytosis
fluid therapy and broad-spectrum antibiotics prior to (increased release of histamine), or can result from
surgery (e.g. combination of ampicillin/amoxicillin or long-term use of gastric acid-suppressing drugs (e.g.
cefazolin and enrofloxacin, amikacin or cefoxitin). Some proton pump inhibitors), or a gastrinoma (gastrin-secret-
cats with a protracted history of vomiting will benefit ing tumor) which is a very rare endocrine tumor in cats.
from histamine-2 blockers or GI protectants if gastritis
or gastric erosions are suspected. A decrease in bicarbonate delivery to the gastric
mucosa occurs in metabolic acidosis (e.g. renal failure)
Motility-modifying agents, such as metoclopramide, and in states of reduced blood flow (e.g. shock), thus
should not be used until the obstruction is relieved. resulting in mucosal injury.
Prognosis
Clinical signs
The prognosis is good unless large portions of bowel
must be resected which potentially leads to short bowel Vomiting occurs with or without hematemesis.
syndrome. Vomiting may be acute in onset with drug-induced
gastritis or ulcers, but for most other causes is
Prevention chronic due to the development of hyperacidity from
The key is to prevent ingestion of string, rubber bands, metabolic or inflammatory diseases.
needle and thread, string, etc., to not allow cats to Anorexia or decreased appetite and lethargy occur
ingest prey, and to use caution in the type of pet toys in cats with severe erosions or ulcers.
that the cat is allowed to play with.
Anterior abdominal pain is more common with ulcer
GASTRITIS/GASTRIC ULCER DISEASE** disease.

● Acute or chronic vomiting, with or without History of acute onset, exposure to NSAIDs, ingestion
hemoptysis. of chemical or toxin irritating to gastric mucosa, or
● Anorexia or reduced appetite. episode of ischemia (shock).
● Lethargy.
● Anterior abdominal pain. Radiographic findings are usually non-diagnostic, but
may identify a deep erosion/ulcer with contrast.
A deep erosion or ulcer may be identified via ultra- chronic renal failure), long-term therapy with histamine
sound, but simple gastritis or superficial mucosal ero- blockade will be necessary to help reduce the develop-
sions will only be diagnosed by endoscopy examination ment of new erosions or ulcers.
or biopsy.
In severe or deep ulcers, surgical intervention may
Endoscopy is the definitive way to diagnose mucosal be necessary but this is unusual. Emergency surgical
erosions and ulcers, and also may help identify a intervention will be necessary in cats that have perfo-
cause via histopathologic examination of the tissue. rating ulcers. Many deep or perforating ulcers are
caused by an invasive neoplasm, or by fungal disease
in geographic areas where systemic fungal infections
are prevalent.
Acute gastritis due to erosions/ulcers will mimic many
Cats with severe disease that are unable or unwilling to
causes of acute vomiting, including dietary indiscre-
eat for more than 3 days should have nutritional sup-
tion, mechanical or obstructive disorders, infectious
port provided, either through placement of a feeding
causes, toxin-induced (especially plant ingestion), pan-
tube for enteral feeding, or by parenteral nutrition.
creatitis, and metabolic or endocrine diseases such as
hepatitis, renal failure or neoplasia.
Prognosis
Treatment The majority of cats will recover completely from the
insult if the cause can be identified and corrected, and
Treatment is aimed at identification and correction of
in most other cases the disease can be successfully
the underlying cause of the primary lesion, reduction
managed. In cats with ulcers due to neoplasia, the
of acid secretion and protection of the gastric
prognosis is guarded to poor.
mucosa to allow it to heal. This is accomplished by:
● Administration of histamine-2 receptor antagonist
(H2RA) (e.g. cimetidine 5 mg/kg PO q 8 h, ranitidine Prevention
0.5–1.0 mg/kg PO q 12 h, or famotidine 0.5–1.0
Reduce opportunities for ingestion of toxic or irritating
mg/kg PO q 12–24 h).
substances.
– Famotidine is the most potent and only H2RA to
effectively reduce acid in dogs. No studies have Management of diseases causing hypergastrinemia
been completed in cats. (renal failure, hepatic disease) should always include
– Proton pump inhibiting drugs (omeprazole therapy for gastritis.
1 mg/kg PO q 24 h) are the most effective in
Prevent ischemia and shock-induced gastric erosions
reducing acid secretion but can be difficult to
by rapid replacement of fluids following shock, and
dose.
maintenance of hydration during surgical procedures,
– Sucralfate (250–500 mg PO q 8–12 h) is also a
etc.
useful adjunct therapy for cats with significant
gastric erosions or ulcers, as it will act as a surface
protectant. Sucralfate must be given in an acidic
environment to be effective, so it should be HAPATOPATHIES** (HEPATIC LIPIDOSIS,
administered at least 1 hour prior to giving hista- CHOLANGITIS, DRUG-INDUCED
mine-blocking or proton pump-inhibiting drugs. HEPATOPATHY)
– Feeding nothing per os for the first 24 hours,
then feeding a highly digestible, bland, low- Classical signs
residue diet, either commercial or homemade
● Weight loss, anorexia, vomiting, icterus
(e.g. small amounts of low-fat beef, chicken or
and depression are the most common
turkey), will be beneficial.
signs.
In cases where treatment of the underlying cause is not
possible or where management is the only option (e.g. See main reference on page 421 for details.
Clinical signs ACUTE PANCREATITIS**

Weight loss (often dramatic), anorexia, vomiting,
icterus and depression are the most common signs. Classical signs
Other signs may include ascites (this is rare with ● Anorexia, lethargy and depression are the
hepatic lipidosis, but may occur with end-stage most common signs.
hepatopathies or cholangitis). ● Vomiting is seen in less than 50% of cats
Most hepatopathies are associated with chronic with pancreatitis.
vomiting, but drug-induced hepatopathies (e.g. glipi-
zide) are associated with acute vomiting.
Pathogenesis
Diagnosis The cause of acute pancreatitis in cats is unknown,
but it has been associated with trauma, some infectious
The presence of icterus helps to narrow the differentials diseases (herpes virus, toxoplasmosis, feline infectious
list to hepatic, pre-hepatic and post-hepatic diseases. peritonitis, etc.), hepatic lipidosis, drugs, and extension
The hemogram in cats with hepatic disease is often of inflammation from the small intestine. Recently pan-
abnormal (e.g. mild, non-regenerative anemia, with creatitis has been observed to occur in association
RBC morphology having schistocytes, leptocytes or with inflammatory bowel disease and cholangitis,
target cells present), but the changes are not specific but whether it is due to a common inflammatory reac-
for liver disease. However, it does help rule out pre- tion or innocent bystander situation is unknown.
hepatic causes of icterus. The destructive process in the pancreas is initiated by
Serum chemistry abnormalities may include elevated activation of trypsinogen, which leads to the activa-
liver enzyme activities (mild to marked increases), tion of other proteases, lipases and inflammatory medi-
hyperbilirubinemia, hypocholesterolemia, hypoal- ators such as kininogens and free radical species.
buminemia, decreased BUN, and electrolyte alter- Activation of these processes leads to activation of
ations (consistent with vomiting or dehydration, e.g. complement, induction of coagulation disorders such as
hypokalemia, hypernatremia). DIC and hypovolemic shock.
The urinalysis will have bilirubinuria, and occasion- Acute necrotizing pancreatitis is a common finding in
ally may have urate crystalluria if the liver failure is cats with diabetes mellitus that die within the first week
severe or end-stage. of diagnosis despite treatment. Histologic evidence of
pancreatitis is found in approximately 50% of cats with
Ultrasonography is the most useful imaging modal- diabetes mellitus.
ity, because it can also be used to obtain fine-needle
aspirates or biopsies (note: check for a possible coagu- In dogs, hyperlipoproteinemia, high-fat/low-protein
lopathy before performing a blind biopsy). In cats with diets, obesity, some drugs (furosemide, azathioprine,
hepatic lipidosis the liver is enlarged and hepatocytes L-asparaginase, sulfonamides, tetracyclines, cortico-
are crowded out by lipid, but cats with cholangitis may steroids) and metabolic states (hypercalcemia, uremia)
have a normal, large or small liver. are implicated as risk factors for pancreatitis, but no
such association has been reported for cats.
Liver biopsies taken via surgical exploratory
laparotomy have greater accuracy, and will also
allow placement of a gastrostomy or jejunostomy
Clinical signs
tube (which is essential for cats with hepatic lipi-
dosis and important for any cat that doesn’t eat for Anorexia, lethargy and dehydration are the most
longer than 3–5 days). Again, the cat should be common presenting signs in cats, unlike the classic
checked for a possible coagulopathy before surgery is signs of vomiting and abdominal pain that are exhibited
performed. in dogs.
Fewer than a third of cats with pancreatitis will present An elevated serum trypsin-like immunoreactivity (TLI)
with vomiting, abdominal pain, diarrhea, tachypnea or assay (the feline-specific assay must be used) cannot
dyspnea, or a palpable anterior abdominal mass. accurately predict pancreatitis in cats, however, a value
of greater than 100 μg/L has been reported to have an
Cats tend to have a more variable clinical course
80% specificity and 33% sensitivity for pancreatitis.
than the disease in dogs, with some cats having a
course of anorexia, lethargy and weight loss that A feline pancreatic lipase immunoreactivity (fPLI)
does not suggest acute illness, while other cats will assay has been recently developed and validated. This
present with acute deterioration, severe shock and assay is very specific (90%), and highly sensitive
collapse. (100%), for acute pancreatitis but only 65% specific for
chronic pancreatitis.
A critically ill diabetic cat that does not respond to
appropriate therapy within the first 24–48 hours of A recent study showed that the combined use of fPLI
therapy should be suspected of having acute necrotiz- and abdominal ultrasound was nearly 100% specific
ing pancreatitis. and sensitive for acute pancreatitis.

Diagnosis of pancreatitis in cats is very difficult, The vague and non-specific clinical signs make it
primarily because of the vague clinical presentation. impossible to rule out other causes of extra-intestinal
and intestinal disease until a complete work-up has
Hematologic changes, if they occur, are non-specific:
been performed.
neutrophilia, hemoconcentration, thrombocytopenia
(late), and anemia (late). In very ill cats, the other major differentials include
peritonitis, septicemia and endotoxic shock.
Serum biochemical abnormalities are common, but
also non-specific: hyper- or hypoglycemia, elevated
alanine aminotransferase, elevated serum alkaline phos- Treatment
phatase, hyperbilirubinemia, hypercholesterolemia,
Oral alimentation should be withheld for 1–3 days if
hypokalemia, hypophosphatemia, hypocalcemia. Serum
vomiting is present in cats with pancreatitis to reduce
amylase and lipase values are unreliable and unin-
pancreatic secretions. Return to full feed gradually and
terpretable (pancreatitis in cats has been associated
feed cats a highly palatable, but highly digestible, diet
with elevations, decreases and normal values of both
(Hills feline i/d, Iam’s low residue diet, etc.). In cats
enzymes).
that are not vomiting, and especially those that have
Hypocalcemia, when present, is suggestive of acute been anorectic for more than 3 days, oral alimentation
necrotizing pancreatitis and a poorer prognosis. should not be withheld and feeding tubes should be
placed, if needed.
Radiographic abnormalities are highly variable but
those that may be observed include decreased contrast Eliminate, if possible, any predisposing factors that are
in the right, cranial abdomen; dilated and gas-filled present.
small intestines; or a mass effect in the area of the pan-
Aggressive fluid therapy is the cornerstone of treat-
creas with transposition of duodenum, stomach and
ment, not only to correct the dehydration that occurs
transverse colon.
from vomiting, but also to reduce the effects of
Ultrasonography is a very useful diagnostic tool for microvascular stasis on the pancreas and other vascular
evaluating pancreatic pathology. Changes in pancreas beds (pulmonary, renal, hepatic). In some cases colloid
size, echogenicity and the presence of masses can often therapy in addition to crystalloids is very beneficial.
be detected. However, pancreatic abnormalities Attention to the need for potassium supplementation,
found via ultrasound may persist for months after phosphorus, and other electrolytes, such as magnesium,
the condition has resolved. sodium and chloride are essential.
In cats with concurrent hepatic lipidosis or those that prognosis. These cases are more difficult to manage
must be held off food for greater than 5 days, enteral (require TPN or jejunostomy feeding) and have more
nutrition via a jejunostomy tube or total parenteral complications (coagulation abnormalities and tendency
nutrition will be a necessary component of the treat- toward development of pulmonary thromboembolism).
ment plan. J-tubes must be surgically placed, which may
increase the risk of complications due to pancreatitis.
GASTRIC OR SMALL INTESTINAL
Total parenteral nutrition requires strict attention to
NEOPLASIA*
sterility and close monitoring of electrolytes and is more
suited to referral institutions than general practice.
Classical signs
Vomiting should be controlled with antiemetic ther-
● Chronic, progressive vomiting that may
apy. Either metoclopramide (0.1–0.2 mg/kg IV q 8 h)
include hematemesis.
or chlorpromazine (0.01–0.025 mg/kg IV) are effective,
● Weight loss.
but it is important when using any phenothiazine
● Anorexia.
antiemetics that you ensure adequate volume expansion
● Lethargy or depression.
so that hypotension is avoided. If gastritis is suspected
● Diarrhea may occur if the location of the
histamine-2 blockers such as ranitidine or famotidine
lesion is in the small intestine.
should also be considered.
Corticosteroids are indicated in cats that are in shock See main reference on page 675 for details (The Cat
and may be helpful in cats with chronic pancreatitis With Chronic Vomiting).
from concurrent IBD or cholangitis.
Abdominal pain should be controlled with butor- Clinical signs
phanol (0.1–0.8 mg/kg IV q 4–6 h), buprenorphine (0.03
Acute vomiting may occur occasionally or the signs
mg/kg q 6–8 h) or meperidine (2–4 mg/kg IM q 6–8 h).
occur acutely, while the disease itself is chronic.
Antibiotics should not be routinely used in pancreatitis.
Typically chronic, progressive vomiting that may
Indications for use of antibiotics include evidence of
include hematemesis is observed.
toxic changes in the neutrophils, the cat is febrile, or
other signs of sepsis or septicemia are present. In Weight loss, anorexia, lethargy or depression are also
cases where a pancreatic abscess is suspected or a con- common.
cern, parenteral cephalosporins (cefazolin, 20–30
Diarrhea may occur if the location of the lesion is in the
mg/kg IV, cephalothin 20–35 mg/kg IV) combined with
small intestine.
fluorinated quinolones are recommended.
Signs occur in older cats, however, lymphoma occurs in
The major complications of pancreatitis include:
cats of all ages and may be associated with FeLV infection.
development of pancreatic abscesses, pancreatic fibro-
sis resulting in obstruction of the common bile duct or
development of diabetes mellitus, peritonitis, pul- Diagnosis
monary thromboembolism, acute renal failure, and dis-
Palpation of the abdomen may reveal a mass or thick-
seminated intravascular coagulation. In those cases,
ened intestinal loops in some cases.
surgical intervention may be required (abscess, peri-
tonitis, stricture), but in cases where respiratory, car- Hematology and serum chemistry profiles are usu-
diovascular, renal or coagulation abnormalities develop ally non-specific, but help to rule out other causes of
the prognosis is guarded to poor. vomiting. The most frequent hematologic abnormality is
anemia of chronic disease (normocytic, nor-
mochromic), but blood loss anemia is also observed.
Prognosis
The abnormalities found in the chemistry profile
Cats with concurrent hepatic lipidosis or cholangitis depend on the extent of the disease and severity of
and acute necrotizing pancreatitis have a worse vomiting, and are non-specific.
The most helpful diagnostic procedures are imaging erythromycin, lincomycin, sulfasoxazole, tetra-
techniques: radiography, ultrasonography or possibly cycline, trimethoprim-sulfadiazine.
endoscopy. Depending on the location and size of the
The mechanism for induction of nausea or vomiting
mass, ultrasonography will not only allow visualiza-
varies for each drug. For example, erythromycin is a
tion of the lesion, but may also allow diagnosis via fine-
prokinetic and is highly acidic, causing a direct irritant
needle aspiration or biopsy.
effect on the gastric epithelium.
Ultimately, histopathologic examination of the tissue
Some drugs can be given without inducing vomiting if
is necessary for a definitive diagnosis, and in many
they are given with food, while others may induce vom-
cases, surgical exploratory for both biopsy and resec-
iting whether or not food is present because the effect
tion is the best approach.
is not directly on the stomach.

Inflammatory bowel disease – This is usually not asso- Anorexia or a decrease in appetite is the most com-
ciated with hematemesis or severe weight loss, and mon sign of drug-associated discomfort, followed by
occurs in young to middle-aged cats. vomiting or regurgitation.
Metabolic diseases, e.g. hyperthyroidism, chronic renal Diarrhea may occur following antibiotic use, but is
or liver diseases. usually associated with a disruption in microflora of the
colon resulting in colitis or large bowel diarrhea.
Chronic pancreatitis.
Diagnosis
Treatment
The diagnosis may be straightforward if the cat was
For adenocarcinoma, mast cell tumors and other previously not vomiting and started vomiting after the
tumors that tend to occur as solitary mass lesions, sur- drug was administered. However, if drugs are being
gical removal via intestinal resection is the primary given to treat a disease for which vomiting or diarrhea
approach. Biopsies should be obtained of liver, are already present, differentiating the drug effect from
regional lymph nodes and mesenteric tissues to the disease will be quite difficult.
determine if metastasis has occurred or its extent.
An especially important example of this is in cats with
Chemotherapy has not been proven effective for adeno-
cholangitis that have signs of vomiting due to their
carcinoma or intestinal mast cell tumors.
disease, and have to be on long-term antibiotic ther-
Lymphoma is generally an infiltrative neoplasm and apy to treat their disease. It is sometimes very difficult
chemotherapy using the COP protocol is the treatment to determine whether a worsening of clinical signs is
of choice. See main reference on page 676 for details. due to the therapy or a worsening of the disease. In
those cases, careful assessment of the physical findings
and blood work changes will be necessary to separate
PHARMACOLOGIC (ANTIBIOTIC-INDUCED)
the two problems.
Classical signs
Treatment
● Anorexia.
The best approach is to stop use of the antibiotic in
● Vomiting.
question, and if antibiotic therapy is still required,
● Diarrhea.
switch to an appropriate antibiotic of another class.
Pathogenesis Prognosis and prevention

Vomiting associated with antibiotics is a common Some antibiotics are best given with food (e.g. beta lac-
occurrence and can occur with almost all of the popu- tams), and in those cases, adverse effects are sometimes
lar antibiotics, including: amoxicillin, cephalexin, avoided by using the drug as it is recommended.
The vomiting is easily controlled by changing to

INTUSSUSCEPTION*
another antibiotic, so the prognosis is excellent.
Classical signs
KETOACIDOTIC DIABETES MELLITUS*
● Acute vomiting, anorexia and lethargy,
usually in kittens.
Classical signs
● Abdominal discomfort.
● Vomiting. ● Endotoxemia or shock may ensue if the
● Lethargy or depression. intussusception is complete.
● Anorexia and weight loss.
● Polyuria/polydipsia.
Pathogenesis
See main reference on page 236 for details (The Cat The exact pathophysiology of the development of
With Polyuria and Polydipsia). intussusception is unknown.
Uncoordinated peristalsis resulting in vigorous con-
Clinical signs traction of a segment of bowel into an adjacent quies-
cent segment that occurs due to any variety of causes is
At the time of diagnosis, one third of diabetic cats have
involved, and a common predisposing cause in cats is a
a history of vomiting, and with ketoacidosis, an acute
string foreign body.
onset of vomiting may occur.
The end result is that a segment of intestine telescopes
Vomiting, lethargy or depression, anorexia,
or invaginates into the adjoining, distal segment of
polyuria/polydipsia and weight loss are the classical
bowel, causing an intraluminal obstruction, vascular
signs of ketoacidotic diabetes mellitus in cats.
compromise of the affected bowel segments and ulti-
Diabetic cats may also present without weight loss or mately the development of entoxemia and shock.
depression, and polyphagia and polydipsia are still
Bowel regions that undergo changes in diameter
prominent signs.
(gastroesophageal junction and iliocolic junction) seem
Cats with severe, long-standing ketoacidotic diabetes to be at the greatest risk, but intussusceptions occur at
mellitus may have neurologic signs such as stupor, any location, and are classified according to their loca-
obtundation and coma. tion within the gastrointestinal tract.
Intussusceptions cranial to the jejunum are termed high
Diagnosis intussusceptions and generally are more severe (signs
are more acute and have more rapid clinical deteriora-
Typical hemogram and serum chemistry abnormalities
tion) than distal intussusceptions.
include mild non-regenerative anemia (chronic disease),
leukocytosis, lymphopenia, hyperglycemia, elevated Siamese and Burmese cats appear to have a predilec-
liver enzyme activities, hypokalemia, hypo-magnesemia, tion for development of intussusceptions.
hypophosphatemia, and metabolic acidosis.
Most intussusceptions occur in young animals (< 1
The urinalysis, in conjunction with the presence of year of age).
hyperglycemia, is diagnostic and shows glucosuria
Intussusceptions are rare in cats compared to dogs.
and ketonuria. Cats may be ketonemic and have ace-
tone breath before ketonuria is detected on the dip-
stick. Clinical signs
Many cats will also have concurrent bacteriuria, with An acute onset of vomiting and lethargy, with diarrhea
elevated protein, blood or white cells. occurring occasionally, is typical in kittens.
With high intussusceptions, vomiting, abdominal dis- be prepared for surgery by correcting fluid and elec-
comfort, anorexia, lethargy, dehydration and hypo- trolyte imbalances, administration of broad-
volemia leading to shock are the most common clinical spectrum, parenteral antibiotics (combinations such
signs. as ampicillin/amoxicillin or cefazolin and enrofloxain,
amikacin, cefoxitin or imipenam), and use of hista-
Low intussusceptions (at the iliocolic junction) typi-
mine-2 blockers (ranitidine or famotidine) or protec-
cally present with bloody, mucoid diarrhea, tenesmus,
tants (e.g. sucralfate) if gastric erosions or ulceration is
intermittent vomiting and weight loss. In many of these
suspected.
cases, the intussusception can be palpated.
Motility-enhancing drugs, such as metoclopramide,
are contraindicated in patients with GI obstruction
Diagnosis
and should not be used.
Hemogram and serum biochemistry profiles will be
After surgical correction, which is most commonly
variable depending on the severity and location of
surgical resection and anastomosis, if gastric ulcera-
the intussusception, however, dehydration, electrolyte
tion is not a complicating factor, oral alimentation
abnormalities, anemia and leukocyte changes have all
should be instituted in the first 24 hours, to enhance
been observed depending on the cause of the intussus-
the return of normal motility and reduce the possibility
ception.
of post-operative ileus.
Radiographs and/or ultrasound examination of the
gastrointestinal tract are the best means of confirming
Prognosis and prevention
the diagnosis. A gas- or fluid-filled, dilated loop of
bowel is present immediately cranial to the intussus- The key point is that correction of the intussusception
ception, which may not be visualized without using a does not necessarily alleviate the problem unless the
contrast agent. If there is not too much gas to obstruct underlying cause can be identified and corrected.
adequate images, intestinal intussusceptions are usually Otherwise recurrences are possible and even likely.
readily identified using ultrasound, and are character-
Surgical procedures, such as multiple enteroplexy, are
ized by visualizing the folds of intestine layered on top
recommended to reduce the risk of recurrence.
of one another.
Prognosis is guarded to good if the anesthesia and surgi-
Contrast studies may be used but should not be done at
cal procedure is uncomplicated.
the expense of delaying treatment in severely ill cases.
Endoscopic examination or colonoscopy can also be
PYRETHRINS/PYRETHROIDS/-
used to obtain a diagnosis, especially with low intussus-
PERMETHRINS /ORGANOPHOSPHATES*
ceptions, but this is rarely needed and may be very dif-
ficult in kittens.
Classical signs
Differential diagnosis ● Vomiting, diarrhea.
● Hypersalivation, agitation.
Many diseases that can precipitate an intussuscep-
● Contact dermatitis.
tion (viral enteritis, foreign bodies, gastroenteritis,
● Tremors, ataxia, and possibly seizures.
intestinal parasitism, etc.) also have clinical signs that
mimic it.
A thorough physical examination, diagnostic evalua- With Salivation).
tion, and close patient monitoring are essential.
Clinical signs
Treatment
Signs associated with contact exposure or ingestion of
Intussusception must be considered a surgical emer- pyrethrin/pyrethroid-containing pesticides are gener-
gency. Cats with signs of shock or endotoxemia should ally mild.
Vomiting, diarrhea, hypersalivation and agitation Renal failure is a rare cause of acute vomiting in the
are the most common signs seen with exposure to per- cat.
methrins in cats. This is currently the most commonly
In cats that do vomit, the signs are generally chronic
reported toxicity in cats in the United States due to the
and associated with the effects of increased uremic tox-
accidental or inadvertent exposure of cats to the over-
ins causing nausea by their effects on the CRTZ and
the-counter flea products available for dogs.
also by associated hypergastrinemia and the direct
Severely affected cats may develop muscle tremors, effects on the stomach.
ataxia, excitation or seizures.
Cats with pyelonephritis may only have vague signs of
Organophosphate insecticides cause a combination of inappetence, fever or abdominal discomfort.
signs that include salivation, lacrimation, increased
defecation and urination due to the stimulation of
the parasympathetic nervous system. Other clinical Diagnosis
signs that may occur are vomiting, tremors, ataxia,
hyperthermia, dyspnea and seizures. Severely poisoned Palpation of the abdomen may reveal enlarged or
cats may die from the systemic effects of the toxin. painful kidneys (acute renal disease, pyelonephritis,
FIP, renal neoplasia or polycystic kidney disease), or
Diagnosis small, misshapen kidneys (chronic renal disease).
History of exposure to or ingestion of products con- Marked azotemia (elevated BUN and creatinine),
taining permethrin (most common) or pyrethroids. hyperphosphatemia, hyperkalemia and metabolic aci-
dosis in conjunction with isosthenuria (or impaired
There is generally no need for further diagnostic testing urine-concentrating ability, e.g. urine specific gravity
since signs will abate with removal of pyrethrins or per- < 1.030) and oliguria/anuria are classically associated
methrins from the skin or GI tract and supportive care. with acute renal failure, while mild azotemia, hypo-
With organophosphates, if there is no known expo- kalemia, hyperphosphatemia, and metabolic acidosis
sure, but the toxicity is suspected based on clinical with isosthenuria and polyuria/polydipsia are found
signs, measurement of serum cholinesterase activity with chronic renal diseases.
levels may aid diagnosis. Levels less than 25% of nor- Pyelonephritis and other inflammatory diseases of
mal are highly suggestive of OP toxicity. the kidneys have fewer hematologic or biochemical
changes. Some cats may have an inflammatory leuko-
ACUTE RENAL gram (neutrophilia with or without a left shift), but
FAILURE/PYELONEPHRITIS* azotemia does not occur until late (renal failure
develops).
Classical signs
Urinalysis is very helpful in distinguishing infectious,
● Anorexia or decreased appetite. or inflammatory, renal diseases from other problems.
● Polyuria/polydipsia, and weight loss.
Pyelonephritis is difficult to diagnose definitively and
Occasional chronic vomiting, in advanced
is only confirmed by culture of organisms directly from
cats.
the kidney, either via ultrasound-guided pyelocentesis
● Cats with pyelonephritis may only have
or during a surgical exploratory.
vague signs of inappetence, fever or
abdominal discomfort. Other tests of renal function include intravenous pyelo-
grams or scintigraphic assessment of GFR, but these
See main reference on page 278 for details. are not universally available.
Ultrasound is also a useful tool for assessing renal
Clinical signs
size and infrastructure, and is helping to assess the
Anorexia or decreased appetite, polyuria/polydipsia, patency of the ureters, presence of calculi, neoplasms,
and weight loss are the classic signs of renal disease. cysts or other abnormalities.
Differential diagnosis Typically, the hemogram and serum chemistry pro-

file is completely normal, especially since the vomit-
The wide range of clinical signs resulting from various ing episodes are not frequent enough to cause
renal diseases can mimic many different diseases, and electrolyte imbalances or dehydration.
so the initial history and physical examination are
extremely important. The most useful diagnostic test is endoscopic exami-
nation and biopsy. The organisms will be visualized
Most of the more common extra-intestinal, systemic best via histopathologic examination, but cytology or
diseases that can cause vomiting should be considered culture of the gastric contents has also yielded the
in the initial differentials, but the history, physical organisms in some cases. However, culture of
exam, minimum database, and urinalysis (with culture Helicobacter pylori requires special media and cul-
if bacteria or WBC are present) will rule out most of the ture conditions to be successful, but is the best means
diseases of concern (e.g. diabetes mellitus, hepatopathies, of finding this pathogenic species.
hyperthyroidism, etc.).
Clo-tests, which are enzymatic tests of the presence of
Imaging studies will help rule in or out the other major urease used in humans to screen for Helicobacter spp.
differentials: neoplasia, pancreatitis and mechanical organisms in gastric content, have not been adequately
disturbances. evaluated in cats; however, because cats have some
Inflammatory bowel disease requires histopathologic Helicobacter spp. as normal flora, this test is not likely
confirmation, which can be obtained by endoscopic to be helpful.
biopsies or via a surgical exploratory.
Treatment PLANT INGESTION/TOXICITY*

The treatment of each individual renal disease is differ- Classical signs
ent, and the reader is referred to the primary reference
for details. ● Most plants do not cause severe toxicity,
but may cause drooling, vomiting or
diarrhea due to their irritant effects on
HELICOBACTER SPP.* mucous membranes.
● Severe toxicity may result in hepatic or
Classical signs renal failure, with vomiting, diarrhea,
depression, anorexia occurring secondary
● Anorexia. to these effects.
● Vomiting.
● Usually associated with chronic vomiting,
but may have acute onset of signs. Pathogenesis
Most plants do not cause severe toxicity, but may cause
See main reference on page 682 for details drooling, vomiting or diarrhea due to their irritant
effects on mucous membranes.
Clinical signs Severe toxicity may result in hepatic or renal failure,
The predominant clinical sign continues to be chronic, with vomiting, diarrhea, depression, anorexia occurring
intermittent vomiting. secondary to these effects.
Plants associated with an acute onset of vomiting fol-
lowing ingestion include mistletoe, azalea, black
Diagnosis
nightshade, Christmas cherry, Christmas rose, daffodil,
The disease mimics so many other causes of vomiting glory lily, jessamines, lantana, larkspur, poinsettia, rhodo-
that a thorough diagnostic evaluation is required to dendron, tulip, wild rosemary, youpon holly (to name a
make the diagnosis. few).
The specific cause of vomiting or other signs of toxi- Once signs of nephrotoxicity are observed following
city is very plant-dependent and quite variable in lily plant ingestion, progression to anuric renal fail-
severity. ure and death is unavoidable. Supportive care with
fluid therapy may slow the onset of signs, but there is
no effective treatment.
Clinical signs
Vomiting is the most common sign following ingestion
MOTILITY DISTURBANCES*
of plant material, whether or not it is poisonous/toxic to
(GASTROESOPHAGEAL REFLUX, ILEUS)
the gastrointestinal tract or not. Other signs may
include anorexia, drooling, dysphagia or diarrhea.
Classical signs
● Vomiting or regurgitation (esophagitis).
Diagnosis
● Abdominal distention or abdominal pain
History of exposure or ingestion is essential in many due to accumulation of gas in the bowel.
cases, because there is so much variability in presentation. ● Anorexia.
Plants that cause vomiting due to irritation or direct
GI upset: Philodendron (sweetheart vine), Diffenbachia
(dumb cane), Euphorbia (poinsettia), Caladium (ele-
phants ear), Ricinus (castor bean), Robinia (false aca-
Clinical signs
cia) and Solanum (potato, Christmas cherry) spp. to
name a few of the more common plants. Vomiting or regurgitation (due to esophagitis) or diar-
rhea may all be observed, depending on the segment of
Plants that cause vomiting secondary to nephrotoxic-
bowel affected.
ity: Lilium (lily), Rheum (rhubarb) and oxalis spp.
Anorexia and dysphagia are more common with
esophagitis.
Mild abdominal distention or abdominal pain due to
Acute onset of vomiting in an otherwise healthy cat:
accumulation of gas in the bowel can occur.
consider dietary indiscretion, foreign body or ingestion
of other toxins. Epigastric pain and hypersalivation are due to
esophagitis.
Cats ingesting plants that are nephrotoxic will have
signs that are indistinguishable from other causes of
vomiting due to systemic metabolic, infectious or
Diagnosis
inflammatory diseases.
Ileus may be suspected by palpation of flaccid,
dilated loops of bowel. Gut sounds are decreased or
Treatment absent.
In most cases, the vomiting is self-limiting after the
Survey abdominal radiographs may show dilated, gas-
offending plant is removed from the GI tract.
and fluid-filled loops of bowel.
Gastric protectants or histamine-2 antagonists may
Adynamic ileus can be confirmed by a contrast
be indicated if severe gastritis develops.
study using barium-impregnated polyethylene spheres
Gastric lavage may be helpful if large amounts of irri- (BIPS), scinitigraphy or fluoroscopy to assess motility.
tant plants are consumed and will reduce further Contrast radiographs or endoscopy will be required to
absorption of more toxic metabolites from other plants. identify esophagitis.
Other treatments that may be necessary include fluid Esophagitis may be clinically silent but if regurgitation,
therapy, antiemetics and offering food that is bland hypersalivation and anorexia are present should be
or highly digestible. considered.
Definitive diagnosis depends on the isolation of

SALMONELLOSIS*
Salmonella spp. from properly cultured fecal samples
or from blood cultures in cats with bacteremia.
Classical signs
● Most cats have asymptomatic infections.
● In young kittens watery or hemorrhagic
ETHYLENE GLYCOL*
diarrhea is the most common sign.
● Vomiting, lethargy and anorexia may also
Classical signs
occur, but are uncommon and usually
associated with septicemia. ● Vomiting occurs after ingestion due to the
direct toxicity of ethylene glycol to the GI
See main reference on page 719 for details (The Cat tract.
With Signs of Acute Small Bowel Diarrhea). ● 24–36 h later, lethargy, vomiting, anorexia
and depression occur secondary to renal
failure.
Clinical signs
Cats may develop one of three possible clinical syn-
dromes: (1) asymptomatic carrier state, (2) gastro-
Pathogenesis
enteritis, or (3) fulminant septicemia/bacteremia.
Automobile antifreeze is the most common source of
Gastroenteritis is typically characterized by diar-
this toxin for small animal poisoning.
rhea that may be watery, mucoid, bloody or all
three. Typically, fever, depression and anorexia are Other sources of ethylene glycol include household
first observed, followed by vomiting, abdominal pain cleaning products, lacquers and cosmetics.
and diarrhea.
Ethylene glycol itself is not nephrotoxic, but is an alco-
Cats with septicemia or bacteremia may not have hol that results in signs of stupor, vomiting and weak-
any GI signs, and instead are febrile, lethargic, anorec- ness. It is the metabolism of ethylene glycol to
tic and may show signs of septic shock (e.g. hypo- glycoaldehyde, glyoxylic acid, glycolate and oxalic
volemia, weakness, poor capillary refill time, acute acid that result in the development of acute, oliguric
renal failure). to anuric renal failure and ultimately death due to
direct toxic effects on the nephron.
The disease may persist for 3–4 weeks in severely ill
cats, and shedding may occur for up to 6 weeks. Renal injury is also a result of deposition of calcium
oxalate crystals in the tubular lumen that lead to
tubular obstruction and back leak, however, this is less
Diagnosis
a cause of death than the other mechanisms.
History and physical examination will be important
suggestive factors but there are numerous causes of
acute diarrhea in young cats.
Clinical signs
Routine hematology and serum biochemistry pro-
Initial signs occur within the first few hours following
files are typically unremarkable in the early phases,
ingestion and include vomiting, hypersalivation,
but will show evidence of dehydration, electrolyte
ataxia and depression, which are associated with
imbalance and leukocyte abnormalities in the later
alcohol intoxication.
stages. Cats with bacteremia/septicemia will have a
left shift (greater than 500 band neutrophils found on If the cat is not treated at this stage, metabolism of
hemogram) or degenerative neutropenia (neutropenia the ethylene glycol leads to formation of severe
in the presence of toxic changes and without evidence metabolic acidosis, oxalate crystalluria and renal
of band cells) and may have hepatic or renal compro- shutdown (acute anuric renal failure) within 24–48
mise as a result of the endotoxemia. hours.
Signs of ethylene glycol poisoning at this stage mimic Intussusception or foreign body obstruction should
those of all causes of acute, anuric renal failure and be considered in young cats.
include vomiting, depression to obtundation, severe
dehydration and hypovolemia due to vomiting, and lack
of urine production once dehydration is corrected. Treatment
In the end stage of anuric renal failure, cats often Immediately evacuate the stomach by inducing eme-
become over-hydrated, with the development of pul- sis to prevent further absorption of the toxin.
monary edema, peripheral edema and ascites.
If the ingestion just occurred, administer activated
Once the development of anuric renal failure has charcoal to reduce additional absorption of the
begun, the prognosis is grave, and only dialysis and ingested material from the GI tract. However, absorp-
renal transplantation will save the cat. tion of ethylene glycol is within minutes, so once clin-
ical signs are present, this is not indicated.
If the cat has signs of acute toxicity and exposure is
Diagnosis > 2–3 hours prior to presentation, administration of
20% ethanol (5 ml/kg IV q 4 h) is recommended to
The diagnosis is often made based upon a history of
compete with the alcohol dehydrogenase and slow
known or suspected exposure to/ingestion of ethylene
metabolism of the ethylene glycol to its nephrotoxic
glycol (antifreeze). In cats, amounts of less than a tea-
metabolites.
spoon can be potentially fatal.
In acute toxicity, give 4-methypyrazole (4-MP), an
When there is no known exposure to ethylene glycol
ethylene glycol antagonist, which, if administered
and the animal is presented in acute renal failure, an
within 4 hours of ingestion, will prevent metabolism of
index of suspicion is required to make the diagnosis.
the drug to its toxic metabolites. Between 4–12 hours
Presence of oxalate or hippurate crystals in the urine
after ingestion, 4-MP will be less effective, but still
of a cat in acute renal failure is highly suggestive of
may help reduce the severity. After 12 hours, the prog-
ethylene glycol ingestion.
nosis is grave. In general, 4-MP is less effective in cats
Definitive diagnosis can be made by toxicologic than in dogs.
analysis of serum for presence of metabolites of ethyl-
Management of acute renal failure is essential, and
ene glycol in the blood or by using a commercially
includes correction of fluid deficits using isotonic flu-
available blood test kit for use in clinical practice set-
ids, correction of electrolyte disturbances and correc-
tings that detects the presence of ethylene glycol in
tion of metabolic acidosis with cautious use of sodium
blood. This test is most effective when used within
bicarbonate therapy.
12–24 hours of ingestion.
Close assessment of urine output is essential to pre-
Cats with ethylene glycol toxicity will have markedly
vent fluid overload. An indwelling urinary catheter
increased serum osmolality, a profound metabolic
should be placed to measure output, and furosemide
acidosis (with increased anion gap) and calcium
and mannitol should be administered to promote
oxalate crystalluria to support the diagnosis.
increased diuresis and urine flow.
In cats with oliguric or anuric renal failure, hemodialysis
may ultimately be required to manage the renal failure.
Exposure to poisonous plants, especially the lily fam-
ily which cause acute renal failure.
Prognosis
Ketoacidotic diabetes mellitus, acute renal failure
The prognosis is guarded if the intoxication is imme-
due to infectious or other causes, hepatic disease/fail-
diately discovered, the material removed from the GI
ure are important extra-intestinal differentials.
tract and preventative measures instituted to control
In older cats, neoplasia should be considered. metabolism of the poison.
In cats that are presented greater than 4–6 hours cats properly vaccinated against panleukopenia virus
after ingestion the prognosis is very guarded to poor, are probably immune for life.
and in cats already showing signs of anuric renal fail-
ure the prognosis is grave. Clinical signs
Anorexia, depression and extreme lethargy are very
FELINE PANLEUKOPENIA VIRUS* common clinical signs initially. These are followed by
vomiting, diarrhea and dehyration that can be quite
Classical signs severe. Typically, persistent vomiting, which may be
bile-stained, occurs as an early sign in most cats, and
● Anorexia, vomiting, depression, weakness
can be associated with acute dehydration.
and dehydration are commonly observed
signs. Diarrhea occurs later in the course of the disease and
● Disease is most severe in kittens, and has is not present in all cats.
a high mortality rate.
In the acute form, most kittens are febrile, and may
● Diarrhea is less frequent and occurs later
become septicemic. In the late stages of the disease, the
in the course.
cat will almost always become hypothermic.
Kittens affected with cerebellar hypoplasia will be
Pathogenesis
ataxic, hypermetric, dysmetric, incoordinated and
The disease is caused by a feline parvovirus which have a base-wide stance. These kittens will be other-
only infects rapidly replicating cells (e.g. intestinal wise normal both neurologically and physically at
epithelium, granulocytes, and if infected early in life, birth, and clinical signs will not be apparent until 3–4
granular cells of the cerebellum and developing retina). weeks post-partum when they begin to walk.
In rapidly dividing cells, the virus causes cell cytoly- Most affected animals will be kittens that have come
sis thus destroying the affected cell populations. from an unvaccinated queen or from a premise with
● In the bone marrow, cells of the white cell series many unvaccinated cats in close proximity. The highest
are affected, and lymphoid tissue throughout the morbidity and mortality is in kittens 3–5 months of age.
body undergoes necrosis, resulting in a rapid and
Sudden death may be observed in kittens anywhere
severe decrease in white cell numbers that eventu-
from 4 weeks to 12 months of age.
ally results in panleukopenia.
● In the GI tract, the crypt cells are destroyed
resulting ultimately in the destruction of the intes- Diagnosis
tinal epithelium. This leads to malabsorption,
The history, signalment and physical examination
vomiting and diarrhea, and secondary bac-
findings are all suggestive of the disease.
teremia. The colon is less affected because of the
slower mitotic rate of colonocytes. However, in its milder forms, the disease can be
difficult to differentiate from many gastrointestinal
If the queen is infected while the kittens are in utero,
diseases, including salmonellosis.
the kittens will be stillborn, aborted, or fetal death
will result in resorption, depending upon the stage of The most consistent hematologic abnormality is pan-
the pregnancy. Young kittens infected during the leukopenia, with leukocyte counts typically ranging
neonatal period (< 10 days after birth) will have between 500–3000 cells/μl. The nadir in the white cell
cerebellar hypoplasia (ataxia, hypermetria) and count occurs 4–6 days after infection. Because the
retinal dysplasia (blindness). disease is so acute, serum biochemistry values are usu-
ally within normal limits. There is a correlation between
In unvaccinated feline populations, the disease is
the degree of leukopenia and severity of the illness.
associated with very high morbidity and mortality,
and is highly infectious. However, vaccination is There is no licensed ELISA test kit for the feline par-
extremely effective in preventing the disease, and vovirus, however, the canine test kit will detect the
feline parvovirus in feces as well. The test is very sen- tenance of fluid and electrolyte balance and preven-
sitive and specific (> 90%) for parvoviruses. False pos- tion of secondary bacterial infection until the body is
itives may occur following vaccination with able to neutralize the virus with antibody.
modified live virus vaccines, and false negatives may
Aggressive fluid therapy is the cornerstone of
occur early in the course of disease (days 1–3 post-
treatment, to correct the dehydration that occurs from
infection) before viral shedding is actively occurring.
vomiting. Attention to the need for potassium supple-
Serologic testing is still an important diagnostic test mentation, phophorus, and other electrolytes, such as
for feline panleukopenia, but it requires paired sam- magnesium, sodium and chloride are essential.
ples (acute and convalescent) that show a rise in titer
In cats that are unable to eat for 3–5 days, enteral
to be definitive, and therefore is the most useful in cat-
nutrition via a feeding tube or total parenteral nutri-
tery situations to help plan preventative management
tion may be a necessary component of the treatment
programs.
plan. Once the vomiting is controlled, oral alimentation
Other tests that can be performed include virus isola- (via nasoesophageal, esophageal or gastrostomy tubes)
tion on feces or tissues and electron microscopy for can be instituted. It is important to begin nutritional
detection of virus particles in the feces. support as soon as possible, as the GI tract requires
this protein to repair the injured epithelium. In addition,
further immunosuppression will occur if protein mal-
nutrition occurs in addition to the leukopenia resulting
In its severe form, few diseases mimic feline pan- from the viral attack.
leukopenia. However, milder clinical forms of the dis-
Vomiting should be controlled with antiemetic ther-
ease must be differentiated from all other infectious
apy. Either metoclopramide (0.1–0.2 mg/kg IV q 8 h)
causes of gastrointestinal disease.
or chlorpromazine (0.01–0.025 mg/kg IV) are effective,
In particular, feline leukemia virus can present in but it is important when using any phenothiazine
some cats with a panleukopenia-like syndrome. The antiemetics that you ensure adequate volume expansion
diagnosis is made when the cat is tested for feline so that hypotension is avoided. If gastritis is suspected
leukemia virus and found to be positive. Most FeLV histamine-2 blockers should also be considered.
cats are also anemic, which helps in differentiation of
Antibiotic therapy is very important in these kittens,
the two viruses.
as they are at great risk of development of systemic sep-
Salmonella infections in cats are usually subclinical, ticemia due to the loss of intestinal epithelium and
but when they are severe, can present with a fulminant leukopenia that ensues as a result of the viral infection.
gastroenteritis. Non-regenerative hypochromic anemia, Four-quadrant therapy (Gram positive, Gram nega-
lymphopenia, thrombocytopenia, neutropenia with a tive, anaerobes and aerobes) is important. Combination
left shift, and toxic leukocytes are found in cats with therapy using ampicillin (10–20 mg/kg q 8 h)/amoxi-
systemic disease and endotoxemia. A mature neutro- cillin (5–10 mg/kg q 12 h) and either amikacin (6–8
philic leukocytosis is more characteristic of chronic or mg/kg q 24 h) or enrofloxacin (2.5 mg/kg q 12 h) are
localized disease. good choices.
Rarely, cats with griseofulvin toxicity develop a severe
leukopenia and GI signs that resemble panleukopenia. In Prognosis
contrast to the viral disease, the leukopenia caused by
Guarded. The older the kitten is when it is infected, the
griseofulvin toxicity is persistent. Griseofulvin toxicity
more likely it is to survive the disease. However, in
is more likely to occur in FIV-positive cats.
young kittens, mortality will be very high, despite
aggressive therapy.
Treatment
The more severe the leukopenia, the poorer the
Treatment is supportive, but must be aggressively prognosis, with white cell counts below 500 cells/μl
administered if it is to be successful. The key is main- having a grave prognosis.
Kittens with mild cerebellar hypoplasia may make suit- 3 hours of ingestion. Within 2–3 days of ingestion,
able pets, as the condition is not progressive. diarrhea and acute renal failure occur.
Hypercalcemia occurs in a minority of cats with
Prevention
chronic renal failure. Acute decompensation of renal
Vaccination is the key to prevention. Current vac- function may lead to acute onset of vomiting.
cines are very effective in preventing the disease and
Hypercalcemia of malignancy, hypercalcemia second-
have been responsible for reducing the incidence of the
ary to hyperparathyroidism and idiopathic hypocal-
disease in cats to a very low level. Further, once a cat
cemia cause vague clinical signs of greater than
has been appropriately vaccinated for this disease, the
1 week duration. These signs include anorexia, vomit-
immunity is likely to be life-long.
ing, lethargy or muscle weakness and weight loss as the
Maternal antibodies derived from the queen will be most common signs observed.
protective, but by 12 weeks of age are waning.
Idiopathic hypercalcemia has been reported in cats
Kittens should be vaccinated every 2–3 weeks from 6–7
where acidifying diets were implicated. Idiopathic
weeks of age until they are 12 weeks of age.
hypercalcemia was associated with chronic vomiting,
The virus is extremely hardy, and will persist in the weight loss, dysuria, inappropriate urination, anoxeria,
environment for years, unless it is killed by appropriate pollakiuria and lethargy.
disinfectants (clorox). Before presenting any new cats
to a household that has had a cat with panleukopenia in
Diagnosis
it, the new cat should be vaccinated appropriately (kit-
tens > 12 weeks should have had two vaccinations 2–3 Primary hyperparathyroidism (HPT) is much rarer in
weeks apart). cats than hypercalcemia of malignancy and hypercal-
cemia of malignancy is rare in cats compared to dogs.
In catteries where there are panleukopenia outbreaks,
control is achieved by vaccination, isolation of suscep- A history of potential exposure to rodenticides contain-
tible cats from infected cats, and good hygiene meas- ing cholecalciferol is valuable if hypercalcemia is asso-
ures to prevent further spread. ciated with acute vomiting and depression.
The most common neoplasms associated with hyper-
calcemia are hematopoietic (lymphoma, multiple
HYPERCALCEMIA (HYPERCALCEMIA OF
myeloma), solid tumors with bony metastasis, e.g. squa-
MALIGNANCY, HYPERPARATHYROIDISM/
mous cell carcinoma, and apocrine cell adenocarci-
CHOLECALCIFEROL POISONING,
noma of the anal sac, which is rare in cats.
IDIOPATHIC)
Hematologic abnormalities in HPT and cholecalciferol
Classical signs poisoning are uncommon, but non-regenerative anemia
is commonly associated with chronic renal failure.
● Anorexia, vomiting, lethargy or muscle
weakness and weight loss may be the only The serum chemistry abnormalities include hyper-
outward signs. calcemia (serum total and ionized), hyperphos-
● Other signs include polyuria/polydipsia, phatemia (cholecalciferol), renal failure and elevated
muscle wasting and shivering/tremors. liver enzyme activities (hypercalcemia of malignancy,
cholecalciferol).
See main references on page 245 (The Cat With
Phosphorus is elevated in renal failure and cholecalci-
Polyuria and Polydipsia for details).
ferol toxicity but normal or decreased for all other
causes of hypercalcemia.
Clinical signs
Azotemia is also common with hypercalcemia due to
Cholecalciferol poisoning (e.g. Rampage, Quintox) the development of nephrocalcinosis or other renal
results in vomiting, lethargy and depression within damage.
Imaging studies are very important in ruling out mittent, and rarely associated with severe bouts of vom-
occult neoplastic disease as the source of the hyper- iting, dehydration or illness.
calcemia.
Serum PTH is elevated with HPT and chronic renal Diagnosis
failure, but low with neoplastic diseases, idiopathic
Hematology and serum biochemistry profile are within
hypercalcaemia and cholecalciferol toxicosis.
normal limits.
PTH-related protein (PTHrP) is decreased with HPT
Fecal examination may expose the ovoid to ellip-
and cholecalciferol toxicity, but increased with neopla-
soidal, thick-shelled, larvated eggs (30–40 × 20 μm),
sia and chronic renal failure. PTHrP is usually unde-
but this is not a reliable means of making the diag-
tectable in idiopathic hypercalcemia.
nosis.
Ionized calcium levels may be helpful in ruling out
Radiographs will be unremarkable, but endoscopic
renal failure as a cause of hypercalcemia (e.g. ionized
examination will allow visualization of the worms.
calcium is low in renal failure and elevated in all other
hypercalcemic diseases). Oftentimes, the diagnosis, if not confirmed by direct
visualization of worms in stomach via endoscopy, is
Idiopathic hypercalcemia is associated with an increased
made by response to appropriate treatment.
serum total calcium or serum ionized calcium concentra-
tion, or both. Serum phosphorus, albumin and 25-hydroxy-
cholecalciferol (vitamin D3) concentrations are normal in Differential diagnosis
cats with idiopathic hypercalcaemia.
Other infections with spirurid worms, e.g. Spiroceri,
will produce similar eggs and occasionally cause vom-
PHYSALOPTERA iting.
Classical signs Gastritis, gastric trichobezoars and dietary indis-

cretion or food intolerance should all be considered,
● Vomiting. because the signs are similar (mild, intermittent).
● Worms may be present in vomitus.
Treatment
Pathogenesis
Anthelmintics such as fenbendazole (25–50 mg/kg PO
Physaloptera spp. are spirurid worms that are trans-
q 24 h for 3–5 days) or pyrantel which are effective in
mitted to cats by ingestion of infective larvae present
the stomach will be curative.
in coprophagous beetles, bugs or in transport hosts
such as birds, rodents or frogs. They are most preva- Cats that are on monthly heartworm preventative-
lent in the southern United States, where conditions containing ivermectin plus pyrantel (Heartguard) will
are favorable for the intermediate/transport hosts of have effective control of any infection or re-infection. It
these parasites to persist. is not known whether selemectin or milbemycin are
effective (at the heartworm-preventative dose) in pre-
Physaloptera spp. are small (2.5–5.0 cm) worms with
venting or treating physaloptera.
cuticular collars and spiraled tails that cause acute gas-
tritis even when they are present in very small Consider histamine-2 blockers (e.g. ranitidine or
numbers. famotidine) or sucralfate to reduce gastritis, if the
signs are severe.
Clinical signs
Prognosis
Vomiting is typically the only clinical sign, and
worms may be present in vomitus. In most cases, cats Good. Response to treatment is excellent and because
are otherwise completely healthy, vomiting is inter- there is no migration of parasites beyond the stomach
wall, re-treatment is unnecessary unless the cat is re- must be given to all cats/kittens that are housed
infected. together.
Pyrantel is not absorbed from the GI tract to any
Prevention appreciable amount and thus is the safest to use in kit-
tens under 4–6 weeks of age.
Prevent ingestion of the carrier beetles, bugs or trans-
port hosts (birds, rodents). Repeat treatment in 3–4 weeks to effectively kill
prepatent stages.
ASCARIDS Reinfection is prevented by good sanitation.
Roundworms have zoonotic potential (visceral or ocu-
Classical signs
lar larval migrans), although this is not as great a prob-
● Abdominal distention, colicky abdominal lem as the canine roundworm.
pain.
● Poor body condition, not nursing or eating.
● Diarrhea or abnormal feces.
OLLULANUS TRICUSPIS
Classical signs
● Vomiting.
Clinical signs
The most common signs of roundworm infection in kit- Pathogenesis
tens are abdominal distention, colicky abdominal
Ollulanus tricuspis is a nematode parasite infecting the
pain, poor body condition/hair coat and diarrhea or
gastric glands of cats resulting in acute gastritis and
soft feces.
vomiting. The life cycle of the parasite is direct.
Vomiting worms or vomiting due to masses of worms
The life cycle is completed in the cat with infection of
obstructing passage of ingesta is very uncommon in
other cats occurring via ingestion of parasite-
cats (compared to dogs), as is the clinical sign of
containing vomitus.
coughing due to larval migration.
The parasite is found worldwide, but there have only
Adult cats develop innate immunity and thus, unless
been sporadic reports of infection in the United States.
they are immunocompromised, rarely have clinical
Free-roaming and colony cats are more likely to be
signs of intestinal roundworm infection.
exposed and infected than are household cats.
Diagnosis
Fecal flotation will reveal spherical egg (Toxocara cati)
Clinical signs
with pitted outer shell membrane containing a single
zygote, and approximately 75 μm in size. Toxascaris is Vomiting is the most common clinical sign, and occa-
also an ovoid egg of similar size but has a smooth shell. sionally the worms may be found in the vomitus.
Some cats may have a peripheral eosinophilia, sugges- Anorexia and weight loss may be observed in severely
tive of parasite infestation, but this is not a consistent parasitized cats.
finding nor one that is specific for roundworm infection.
Infection occurs primarily in adult cats in colonies or
high-density environments (catteries, shelters or
Treatment
homes with many cats living together) that have the
Anthelmintics such as pyrantel (5–10 mg/kg PO once) opportunity for close intimate contact necessary for
or fenbendazole (25–50 mg/kg PO q 24 h for 3 days) parasite transmission.
Diagnosis Vomiting or diarrhea are not common signs, but

when they occur they are often associated with severe
Detection of the parasites can be difficult because no disease.
ova are released and the larvae and adults are
digested during normal passage through the gas- Fever and abdominal distention/effusion may also be
trointestinal tract. Gastric lavage, examination of present.
vomitus or endoscopic examination are the recom-
mended procedures for diagnosis of these parasites.
Diagnosis
Abdominal radiographs (plain, contrast) and ultra-
Differential diagnosis sonography will suggest peritonitis and may pinpoint
The major differentials are Physaloptera spp. and larval location or cause (ruptured gallbladder, pancreatitis,
forms of Aelurostrongylus spp. (the lung worm), which bowel rupture). Radiographic findings consistent with
may be coughed up and swallowed. peritonitis include loss of abdominal detail that is
often focal, but may include the entire abdomen.
Ultrasound can readily detect any fluid accumula-
Treatment and prognosis. tion in the peritoneal space that is occurring as a
Little is reported about treatment regimes for Ollulanus result of the inflammatory process.
spp. but it is likely that fenbendazole (25–50 mg/kg PO
Definitive diagnosis confirming the presence of peri-
q 24 h for 3–5 days) would be effective against these
tonitis can be obtained by abdominocentesis or diag-
nematodes.
nostic peritoneal lavage and cytologic/bacteriologic
examination of fluid.
Prevention Cytology of periotoneal fluids consistent with peri-
Keeping cats from contacting/ingesting infected vomi- tonitis is characterized by increased cellularity (pri-
tus by housing cats indoors, or by isolating cats that are marily neutrophils, with or without intracellular
known to be infected, is an effective means of preven- bacteria if the process is septic), and protein and is
tion. often described as an exudate. The key to differentiat-
ing peritonitis from FIP or neoplastic causes of
abdominal effusion is examination of cell types, as
PERITONITIS FIP is typically pyogranulomatous, but with a low to
moderate cell count, and neoplastic infiltrates will most
Classical signs commonly be lymphocytes or carcinomatous.
● Abdominal pain, lethargy, ascites, anorexia Hematology is non-specific, and usually shows an
and fever are common signs. inflammatory leukogram, stress leukogram or
● Vomiting or diarrhea are less frequent, but sequestration of neutrophils (neutropenia).
often observed in more severe cases.
See main reference on page 467 for details. SEPTICEMIA/BACTEREMIA/ENDOTOXIC

SHOCK
Clinical signs
Classical signs
Abdominal discomfort/pain, lethargy and anorexia
are common signs and must be differentiated from FIP ● Generalized depression, fever or
or other causes of abdominal effusion. hypothermia.
● Tachycardia/tachypnea and signs of shock.
This is a rare clinical problem in cats, and occurs ● Vomiting is not consistently present but
most often secondary to intestinal perforation (e.g. does occur.
string foreign body).
Clinical signs side with peripheral vestibular disease and towards the
affected side with central vestibular disease), circling,
This is a rare clinical problem in cats. falling, ataxia, and horizontal (more typical for peripheral
Cats with septicemia are severely depressed, may be disease) or rotary (more typical of central disease) nys-
febrile or hypothermic (although this is often a poor tagmus are much more prominent than GI signs.
prognostic sign), and will have systemic signs of shock Vomiting or anorexia occur due to disequilibrium
(tachycardia, tachypnea, decreased capillary refill). effects, but are not common clinical signs of cats
Other signs, especially in cats with septic shock, may with vestibular disease. Vomiting is usually only seen
include vomiting or bloody diarrhea and anorexia. in the first 1–2 days after onset and is infrequent (1–2
single episodes in the first 48 hours).
There is no particular age, breed or sex predilection
to development of septicemia or endotoxemia, but Vomiting is more common with peripheral vestibu-
cats with severe infections, immunocompromise (e.g. lar disease or idiopathic vestibular syndrome, and is
FeLV or FIV+) or stress may be prediposed. rarely associated with central vestibular disease.
Altered consciousness, postural deficits or other cranial
Diagnosis nerve deficits are not typically seen.
Hemogram may reveal neutrophilia progressing to Diagnosis

neutropenia and thrombocytopenia. There may be
hyperglycemia early, progressing to hypoglycemia History and physical examination findings are highly
later. Hyperkalemia, elevated liver enzymes and suggestive of vestibular disease.
azotemia are common, and bacteriuria may be present. Evaluation of cats with vestibular disease should
Blood culture is indicated in patients with suspected include a minimum data base (hematology, serum chem-
bacteremia to confirm the infection exists. Blood cul- istry profile and urinalysis), otoscopic examination, radi-
tures should be obtained in a sterile manner from multi- ographs of the tympanic bulla. CT of the bulla and area
ple venipuncture sites (if possible), and, ideally, samples of the 8th nerve are also important diagnostic tests.
should be obtained over several hours (every 2–4 hours Major causes of vestibular signs include: idiopathic
collect a new sample) to maximize the opportunity to vestibular syndrome (diagnosis of exclusion), otitis
obtain a positive sample. Urine culture is also helpful media/interna (diagnosis by myingotomy, culture, radio-
in cases with renal seeding of the infection. graphs or CT), middle ear polyps (CT), trauma, neo-
Imaging studies are important in further evaluating the plasia (radiographs or CT), endocrine diseases causing
extent of illness and may help identify a focus of infec- neuropathies (diabetes mellitus and hyperadrenocorti-
tion (radiographs of chest, abdominal ultrasound). cism) and toxic insults (aminoglycoside antibiotics,
topical chlorhexidine or iodophor compounds).
VESTIBULAR DISEASE A minor cause of vomiting is motion sickness from the

vestibular dysfunction during car rides.
Classical signs
PHARMACOLOGIC TOXICITY (NON-
● Head tilt, circling, falling. STEROIDAL ANTI-INFLAMMATORY DRUG
● Infrequent vomiting and anorexia may (NSAID) TOXICITY)
occur.
Classical signs
● Anorexia.
Clinical signs ● Vomiting, with or without hematemesis.
● Abdominal pain.
Occasionally cats with an acute onset of vestibular dis- ● Diarrhea, with or without melena.
ease vomit, but signs of head tilt (away from the affected
Pathogenesis Typically, the hematology and serum chemistry profile

will be normal with NSAIDs other than acetamino-
Cats are much more sensitive to the effects of phen, unless the cat has severe erosions or ulcers that
NSAIDs because they have a reduced capacity to have been bleeding. In those cases, anemia of blood loss
metabolize these drugs in their liver (poor glucuronyl will be present, and in some cases can be quite dramatic.
transferase activity).
Cats may present in acute, oliguric or anuric renal
The adverse consequences of NSAID ingestion on the failure, and in these cats, severe azotemia, hyperphos-
gastrointestinal tract are due to multifactorial effects on phatemia, hyperkalemia and severe metabolic acidosis
the tissue, including direct toxicity to the epithelium, may be present.
increased back diffusion of acid, decreased synthesis of
prostaglandins, mucus and bicarbonate, decreased Confirmation of gastritis, gastric erosions or ulcers
mucosal blood flow and microvascular injury. requires imaging studies. The most definitive means
of diagnosis is via endoscopy whereby through both
Acetaminophen (paracetamol), which is an analgesic, visualization and histopathology the diagnosis can be
antipyretic drug sometimes included in the NSAID confirmed. Severe ulcers can also be visualized on
group, does not have the same toxic effects on the gas- contrast radiographs or via ultrasound.
trointestinal tract. In fact, the toxicity of acetamino-
phen in cats is very high, but the toxic effect is due to Differential diagnosis
the oxidant effects on red cells causing methemoglo-
binemia, hemolysis, Heinz body anemia and hepato- Other differentials to consider are acute pancreatitis,
toxicity. mechanical obstructions, infectious agents such as
Helicobacter that cause acute gastritis and acute gastri-
tis/gastric disease of other causes.
Clinical signs
Treatment
Cats that have ingested aspirin, ibuprofen or related
NSAIDs are likely to show acute signs of GI upset Stop further ingestion of NSAIDs, and remove as
which may include anorexia, vomiting (with or without much of the drug from the GI tract as possible
hematemesis), or abdominal pain. (lavage, induce vomiting, administer activated char-
coal). This is especially important if the ingestion was
Chronic ingestion of these drugs may result in inap- an accidental overdose and has occurred within the past
petence, vomiting or diarrhea (with or without 2–4 hours, although gastric lavage is most useful if per-
melena). formed within 1 hour of ingestion.
Acute overdoses of NSAIDs, especially ibuprofen, In cases where the signs of acute gastritis or gastric
naproxen, etc., may result in acute oliguric or anuric ulceration are associated with blood loss, a transfu-
renal failure. sion may be necessary. This is especially true if perfo-
Cats that have ingested acetaminophen (paracetamol) ration has occurred and immediate surgical intervention
will have hypersalivation and vomiting early, fol- is necessary.
lowed by development of cyanosis (methemoglobine- Treatment is non-specific, as with any gastritis or ulcer
mia) and facial pruritus within a few hours. Later, patient: administer histamine-2 blockers (ranitidine or
untreated cats may develop edema of the face and famotidine), mucosal cytoprotectants (sucralfate), and
paws, and will ultimately develop liver failure if they antiemetics (metoclopramide) if indicated. If the cat is
survive the initial toxicity. dehydrated from the vomiting episodes, fluid therapy
and possibly potassium supplementation will also be
indicated.
Diagnosis
Prognosis
History of ingestion and appropriate clinical signs
are usually enough to support NSAID-induced gastritis Good with appropriate therapy and aggressive manage-
or ulceration as the cause of the GI signs. ment unless there is gastric or duodenal perforation, or
acute renal failure has developed before the cat presents Diagnosis
to the hospital.
A history of cancer chemotherapy and appropriate clin-
ical signs are often sufficient to make a presumptive
Prevention diagnosis. However, it is always important to bear in
NSAIDs should be used cautiously in cats and cats that mind that the vomiting could be unrelated to the
receive these drugs require frequent careful evaluation. drugs, and represent an additional problem associated
with the disease or a new problem that is unrelated to
Accidental exposure to medications not intended for the disease.
cats should be prevented.
Misoprostil (a prostaglandin agonist) has not been eval-
uated in cats as a gastric protectant. Differential diagnosis
Vomiting may be due to the neoplastic disease itself.
TOXICITY (CHEMOTHERAPY DRUG-

INDUCED VOMITING) Treatment
Vomiting associated with cancer chemotherapy can be
Classical signs difficult to manage in some situations. The most effec-
● Anorexia. tive anti-emetic drugs for this purpose are the drugs
● Vomiting, with or without hematemesis. that block the effects on the CRTZ, such as metoclo-
● Abdominal pain. pramide. In very severe cases, ondansetron or
● Diarrhea, with or without melena. dolasetron are other alternatives.
In animals that have uncontrollable vomiting, the treat-
ment regimen may have to be altered to allow the cat to
Pathogenesis have reasonable quality of life.
Nausea and vomiting are frequent complications of

cancer chemotherapy drugs. There are many different Prognosis
chemotherapeutic agents and they all vary in their Guarded, primarily because of the presence of cancer
effects; however, cisplatin, doxorubricin, vincristine requiring chemotherapy for treatment or control.
and methotrexate commonly cause gastrointestinal
side effects.
The cause of the vomiting may be due to direct stimu- ANESTHETIC AGENT (XYLAZINE)
lation of the CRTZ or toxicity to the gastrointestinal
tract by inhibiting the rapidly dividing stem cells that Classical signs
populate the GI epithelium. Vincristine does not have
direct cellular toxicity, but may induce ileus, which can
● Lethargy, sedation.
result in vomiting, diarrhea or both.
● Vomiting.
● Bradycardia.
● Hypotension.
Clinical signs
The most common GI signs observed with cancer
Pathogenesis
chemotherapy drugs are non-specific, and include
anorexia, vomiting, with or without hematemesis, Xylazine is an alpha-2 adrenergic antagonist seda-
abdominal pain due to bloating from ileus, diarrhea, tive-anesthetic that will induce emesis in cats within
pyrexia due to development of secondary infections, or minutes of administration due to direct effects on the
lethargy. CRTZ.
Clinical signs Some cats with only central nervous system disease
will have a normal physical examination, with only
Clinical signs associated with xylazine administration neurologic deficits or abnormalities found with careful
are either associated with the sedation effects (which assessment.
also include some profound cardiovascular effects such
as bradycardia and hypotension) or vomiting.
Diagnosis
Diagnosis Hematology and serum biochemistry profiles help
Vomiting is such a common side effect following define systemic or infectious causes (e.g. viral, bacte-
administration of xylazine that the drug is used fre- rial or fungal causes).
quently to induce vomiting. Radiographs of cervical, thoracic and lumbar spine are
used to rule out diskospondylitis or evidence of neo-
Treatment plasia.
There is no need to treat vomiting associated with Cerebrospinal spinal fluid analysis (cytology and
xylazine administration since it is self-limiting. culture) may be essential for the diagnosis, but caution
should be exercised during CSF collection due to pos-
sible elevated intracranial pressure which could cause
ENCEPHALITIS/MENINGITIS tentorial herniation.
Classical signs Imaging studies (MRI and CT scanning) are impor-

tant means of lesion localization and identification, but
● Neurologic signs predominate and depend are not universally available.
on the location.
● Ataxia, dementia, nerve deficits, or cervical ARSENIC POISONING
pain may be evident.
● Vomiting is often associated secondary to Classical signs
the systemic illness (fungal, bacterial,
protozoal or viral) that is causing the ● Vomiting, diarrhea, anorexia and
disease. depression occur early.
● Arsenic toxicity eventually results in
See main reference on pages 829, 859 for details (The hepatic and renal failure (depression,
Cat With Seizures, Circling and/or Changed Behavior anorexia, vomiting and diarrhea along with
and The Cat With Tremor or Twitching). oliguria or anuria, or icterus and ascites.
Clinical signs Pathogenesis

Neurologic signs predominate and depend on the Arsenic may be present in herbicides, insecticides,
location in the brain that is affected. If the rostral fossa wood preservatives and treatments used for blood par-
is affected, seizures, circling, pacing, personality asites (including heartworm).
change, and decreased responsiveness are common. If
the caudal fossa is affected, depression, head tilt, facial Cats appear to be more commonly poisoned than dogs,
paralysis, incoordination and other brainstem abnor- possibly due to consumption of prey or insects killed by
malities are noted. the toxin.
Vomiting is uncommon, but is often associated with Toxicity may be acute, resulting in immediate and life-
the presence of systemic illness (fungal, bacterial, pro- threatening illness, or chronic, and more insidious.
tozoal or viral) that has also affected the CNS.
Clinical signs
Other clinical signs, such as fever, depression, weak-
ness, hypotension or shock may be observed with cats Acute arsenic toxicity is associated with vomiting,
that are systemically ill. diarrhea or hematochezia, abdominal pain, weakness
and shock-like signs (e.g. rapid, weak pulses, prostra- days. BAL toxicity may occur (e.g. vomiting, tremors
tion, subnormal body temperature and collapse). or convulsions), which will require cessation of the
drug.
Chronic, low-grade exposure to arsenic may be
impossible to detect clinically, as anorexia is the only DMSA (dimercepto succinic acid) is often used in chil-
consistent sign. dren, because it is less toxic than BAL, but its effec-
tiveness in cats has not been evaluated.
Diagnosis If the cat is in acute, oliguric or anuric renal failure,
dialysis may be necessary.
Historical information of exposure to heavy metals is
a very important means of getting the diagnosis, how-
ever, such information is not always known.
ANTRAL PYLORIC
The hemogram and serum chemistry profile will be HYPERTROPHY/STENOSIS
unremarkable when the cat presents with signs of gas-
trointestinal disturbance. Classical signs
Arsenic poisoning also causes hepatocellular necro- ● Vomiting is the primary sign, and usually is
sis, which will be evidenced by elevations in serum ala- observed several hours after eating.
nine aminotransferase and alkaline phosphatase ● Projectile vomiting will be observed if the
enzymes. Other abnormalities may include elevations pylorus is obstructed.
in bilirubin, bile acid values and decreases in albumin
(end stage). See main reference on page 694 for details of The Cat
With Signs of Chronic Vomiting.
Nephrotoxicity associated with arsenic poisoning is
also associated with isosthenuria, azotemia and eventu-
ally oliguria/anuria. Clinical signs
Definitive diagnosis is made by measurement of Vomiting is the most common sign. In adult cats, the
arsenic concentrations in urine (acute), kidney, liver, vomiting occurs as a chronic problem, but in kittens
vomitus or hair (chronic). may occur as acute vomiting in a kitten that is just
beginning to consume solid foods.
Differential diagnosis In congenital pyloric stenosis, the kittens begin to
vomit shortly after they are started on solid food.
Other heavy metal toxicoses (e.g. lead), ingestion of
caustic agents, or ingestion of poisonous plants should Acquired pyloric hypertrophy in adult cats has a
be considered. more variable presentation, but is usually associated
with intermittent vomiting of digested food several
Acute renal failure due to other infectious or metabolic
hours after consumption.
causes may mimic arsenical nephrotoxicity.
If the pylorus is completely obstructed the vomiting
may be projectile.
Treatment
Chronic intermittent vomiting and gastric distention
The first step is to remove the source of arsenic if pos-
may lead to gastroesophageal reflux or esophagitis
sible. If the toxin has been ingested, lavage the stom-
which may be associated with regurgitation or inappe-
ach and administer activated charcoal to minimize
tence and the resulting weight loss.
further absorption of the agent from the GI tract.
Promote excretion of the toxin from the body by
Diagnosis
starting fluid diuresis and administration of BAL
(British anti-Lewisite, dimercaptol) at a dose of 2.5–5 History and signalment are suggestive of a gastric emp-
mg/kg in oil, IM, q 4 h for 2 days, then q 12 h up to 10 tying disturbance.
Hemogram, serum chemistries and urinalysis are typi- Clinical signs

cally unremarkable.
Dysautonomia is generally seen as an acute onset of
Survey radiographs of the abdomen may be normal or depression, anorexia, constipation, dry external
show gastric distension. Contrast radiographs may nares and mouth, reduced tear production or dry
identify hypertrophic gastric mucosa or a narrow eye, bradycardia, regurgitation (due to megaesopha-
gastric outflow pathway (“beak sign”). gus) and dilated pupils.
Ultrasonography may be able to detect a thickened Other clinical signs that may be present, but are less
pyloric antrum. common, include anal areflexia, fecal incontinence,
Fluoroscopy or scintigraphy can be used to evaluate and dysuria or urinary incontinence.
gastric peristalsis and emptying, but are not universally The disease occurs primarily in Great Britain, but
available. sporadic cases have been reported in the United States
Gastric endoscopy may be normal or may reveal and elsewhere.
thickened folds of mucosa, the pyloric antrum may Most affected cats are young (< 3 years old) and have
not insufflate normally, or the pylorus may be too no breed or sex predisposition.
stenotic to allow passage of the endoscope through the
orifice.
Diagnosis
Definitive diagnosis requires an exploratory laparo-
tomy and histopathologic examination of tissue. In general, routine hemogram, biochemistry tests and
urinalysis are within normal limits.
Megaesophagus may be observed on routine thoracic
DYSAUTONOMIA radiographs.
Constipation or obstipation may also be detected on
Classical signs abdominal radiographs.
● Vomiting or regurgitation, diarrhea, Schirmer tear tests will be abnormal (< 5 mm) in
anorexia and constipation are the primary most animals.
GI signs.
● Dry eyes, mucous membranes and nose Ophthalmic pharmacology testing may be helpful, but
may be observed. is not 100% reliable in detecting dysautonomia.
● Bradycardia. However, in dysautonomic cats phospholine iodide will
● Dilated pupils. have no miotic effect, and pilocarpine will have an
exaggerated miotic effect.
See main reference on page 792 for details (The Low plasma or urinary catecholamine concentrations
Constipated or Straining Cat). also confirms sympathetic insufficiency.
RECOMMENDED READING
August JR. Consultations in Feline Internal Medicine. WB Saunders, Philadelphia, PA. 2001, 4.
Ettinger SW, Feldman EC. Textbook of Veterinary Internal Medicine, 5th edn. WB Saunders, Philadelphia, PA. 2005.
Greene’s Infectious Diseases of Dogs and Cats, 2nd edn. WB Saunders, Philadelphia, PA. 2005.
Kirk’s Current Veterinary Therapy, XIII, 2000.
31. The cat with signs of chronic vomiting
Debra L Zoran
KEY SIGNS
● Active elimination of stomach contents through the mouth.
● ± Preceded by nausea, pacing, and salivation.
● Usually digested food or liquid with acidic or neutral pH.
● ≥ 2 weeks duration.
MECHANISM?
● Vomiting occurs when the vomiting center in the medulla or when afferent impulses from the
cerebral cortex, chemoreceptor trigger zone (CRTZ), or receptors in the pharynx or abdominal
viscera is stimulated.
● Vomiting is an active process that must be distinguished from regurgitation.
● Vomitus may consist of undigested food material (if swallowed whole), partly digested or even
liquid, and may be clear, yellow (bile stained) or brown (food colored).
● The pH of vomitus is usually acidic (pH < 4), but may be neutral (pH 7) if duodenal content
is present (bile reflux).
WHERE?
● Chronic vomiting can be caused by primary gastrointestinal diseases or by extra-intestinal
diseases or disorders that may have no apparent association with the GI tract.
● Vomiting is rarely associated with primary colonic disease.
● Extra-intestinal causes of vomiting include:
● Hepatobiliary disease.
● Pancreatic disease (e.g. pancreatitis, neoplasia).
● Renal disease causing acute or chronic renal failure.
● CNS disease (e.g. vestibular disease, encephalitis, seizure disorders, neoplasia).
● Metabolic diseases (e.g. hyperthyroidism, ketoacidotic diabetes mellitus or Addison’s disease).
● Cardiomyopathy or congestive heart failure.
● Systemic illness or infection affecting the CRTZ or cortex (e.g. septicemia).
WHAT?
● Primary gastrointestinal diseases that cause chronic vomiting include:
● Parasites (e.g. Physaloptera).
● Infectious diseases (e.g. Helicobacter).
● Inflammatory diseases (e.g. IBD, gastritis or gastric ulcer disease).
● Neoplasia.
662
31 – THE CAT WITH SIGNS OF CHRONIC VOMITING 663
● Mechanical (e.g. antral pyloric hypertrophy/stenosis, obstruction, intussusception).

● Dietary disturbances (e.g. food intolerance or food allergy).
The most common causes of chronic vomiting are: inflammatory diseases (e.g. food allergy
or IBD), dietary (dietary indiscretion or food intolerance), neoplastic diseases and metabolic
or extra-intestinal disturbances (e.g. renal, hepatic or pancreatic disease).

Diseases causing signs of chronic vomiting
ANOMALY
This is a disorder of the autonomic nervous system resulting in GI signs due to motility distur-
bances in the esophagus, stomach, small and large intestine. The esophagus and colon are most
dramatically affected and thus regurgitation and constipation are more prevalent than other signs.
Chronic vomiting may occur or regurgitation may be reported as vomiting. Acute onset of
anorexia, depression, dilated pupils without blindness, prolapsed third eyelids and bradycardia are
common.
MECHANICAL
● Foreign bodies* (p 688)
Foreign bodies are often associated with an acute onset of vomiting, but string ingestion may cause
chronic intermittent vomiting when the obstruction is incomplete or motility disturbances are inter-
mittent.
● Antral pyloric hypertrophy/stenosis (p 694)
Acquired or congenital thickening of the pyloric tissue may result in vomiting due to motility dis-
turbances, obstruction of outflow or both. Vomiting usually occurs several hours after eating and
may be projectile. Rarely stenosis is functional with no evidence of thickening.
● Intussusception (p 692)
Intussusception is usually associated with acute onset of severe vomiting, but sliding, intermittent
or incomplete intussusception may have chronic, intermittent vomiting.
METABOLIC
Intermittent vomiting occurs in conjunction with weight loss, polyphagia and polyuria. Other signs
include hyperactivity, irritability, poor grooming habits and large, bulky or mucoid feces.
● Hepatic diseases (hepatic ipidosis, cholangitis, hepatic cirrhosis, portosystemic
anomalies, etc.)** (p 674)
Vomiting is often associated with hepatic diseases or failure (of any cause). Other signs of hepatic
disease include fever, weight loss, icterus, anorexia and lethargy. Cats in severe hepatic failure may
show signs of hepatoencephalopathy, including drooling, apparent blindness, stupor, pica or altered
behavior.
continued
continued
● Chronic renal failure* (p 680)

Intermittent vomiting is due to the effects of azotemia and hypergastrinemia on the gastric mucosa.
The most common signs are polyuria, polydipsia, weight loss and decreased appetite.
● Congestive heart failure* (p 689)
Intermittent vomiting often occurs in the late stages of the disease, in addition to the signs of car-
diovascular and respiratory distress or failure.
● Diabetes mellitus* (p 681)
One third of cats with diabetes have a history of vomiting. Cats with severe ketoacidosis secondary
to unregulated diabetes mellitus often present with signs of anorexia, weight loss and a sudden
onset of vomiting and depression. Polyuria and polydipsia are also present and may have been
ongoing for several months prior to the development of the severe signs of illness.
● Hypercalcemia* (p 683)
Vomiting often occurs secondary to hypercalcemia. Other clinical signs associated with hypercal-
cemia include polyuria/polydipsia, anorexia and lethargy. Severe hypercalcemia may cause muscle
weakness and dystrophic calcification of tissues (e.g. skin, kidneys, stomach, etc.).
● CNS diseases (encephalitis, seizure disorders, vestibular disease, neoplasia)* (p 690)
Vomiting is an uncommon sign of neurologic disease, but chronic intermittent vomiting may be asso-
ciated with many different diseases of the CNS, and should be considered whenever signs of neuro-
logic disease coexist with vomiting, especially vestibular signs (e.g. head tilt, nystagmus, rolling) or
signs suggesting hepatoencephalopathy (e.g. drooling, behavior changes or apparent blindness).
● Hypoadrenocorticism (Addison’s disease) (p 691)
This is an uncommon endocrine disease in cats that often presents with only vague clinical signs
of lethargy, anorexia and weight loss. Vomiting and diarrhea are less common signs in cats, as are
changes in the electrocardiogram associated with hyperkalemia.
NEOPLASTIC
● Intestinal adenocarcinoma** (p 677)
Anorexia, weight loss and lethargy are the most common signs, but vomiting often occurs when
the tumor reaches a size that causes motility disturbances or bowel obstruction. The most common
location is the distal small intestine.
● GI lymphosarcoma** (p 675)
This tumor tends to be more infiltrative and may involve large segments of small bowel, stomach
or colon. Signs range from anorexia and weight loss to vomiting or diarrhea, depending on the
location of the tumor.
● Intestinal mast cell tumor* (p 687)
These tumors are often solitary and primarily affect the distal small intestine, and may cause no
signs, other than weight loss and anorexia, until late in the disease when vomiting develops either
secondary to tumor size or presence of metastatic foci.
● Systemic neoplasia (generalized lymphoma, systemic mast cell tumor)* (p 689)
Vomiting may occur due to neoplasia involving abdominal organs resulting in direct effects, organ
dysfunction or the release of vasoactive substances (e.g. mast cell tumor) that cause gastritis. The
most common clinical signs associated with neoplasia include anorexia, weight loss or lethargy
and usually occur in older cats.
● Other intestinal neoplasia (fibrosarcoma, carcinoids, plasmacytoma, leiomyosarcoma,

etc.) (p 693)
The presence of vomiting as a clinical sign depends on the location and size of the tumor(s) and its
effects on the local (abdominal) environment.
● Gastrinoma (p 696)
Gastrinoma may cause chronic vomiting due to gastritis or gastric ulcer disease that is unrespon-
sive to routine therapy.
NUTRITIONAL
● Food intolerance* (p 669)
Food intolerance is a non-immune-mediated condition associated with intermittent diarrhea or vom-
iting, with no pattern or association with eating, and it resolves when the food source is changed to
omit the offending substance from diet. The clinical significance of food intolerance is unknown
relative to other causes of vomiting because of the difficulty in obtaining a definitive diagnosis.
IMMUNOLOGIC
●Food allergy (dietary hypersensitivity)* (p 667)
Chronic vomiting is a common clinical presentation in cats with food allergy, and cutaneous signs
may also be present.
● Idiopathic inflammatory bowel disease (IBD)* (p 671)
IBD causes chronic, intermittent or recurrent vomiting, anorexia, weight loss and diarrhea in cats.
It is a diagnosis of exclusion and requires histopathologic confirmation.
INFLAMMATORY
● Chronic pancreatitis** (p 673)
Pancreatitis in cats is often not associated with vomiting, especially chronic pancreatitis. The most
common signs are anorexia, lethargy and weight loss.
● Gastritis/gastric ulcer disease (p 679)
This is usually associated with an acute onset of vomiting, but low-grade gastritis may result in
intermittent signs that do not prompt immediate attention.
INFECTIOUS:
Viral:
● Feline viral diseases (FeLV, FIV, FIP) (p 684)
Vomiting is not a common presenting sign for any of the primary feline viral diseases, but is asso-
ciated with FeLV or FIV primarily secondary to the systemic disease that is occurring as a result
of the infection. In cats with FIP, vomiting may be associated with focal granuloma formation in
the GI tract or abdomen or may occur secondary to systemic disease (hepatic, CNS, renal). Other
common clinical signs are anorexia, lethargy, fever or dyspnea.
Bacterial:
● Helicobacter spp.* (p 682)
The true importance of Helicobacter organisms in cats as a cause of chronic gastritis and vomiting
is still not known, but there have been increasing numbers of cats with chronic gastritis and pres-
ence of these organisms that respond to appropriate therapy.
continued
continued
Protozoal:
Intermittent vomiting is a common sign in infected cats, but will occur in conjunction with other signs
of systemic disease (respiratory, CNS, ocular).
Fungal:
● Histoplasmosis* (p 685)
GI histoplasmosis is less common than respiratory or disseminated disease, but vomiting will still
often be observed, especially when there is hepatic involvement. The most common signs are res-
piratory (e.g. coughing or signs of respiratory distress) or lethargy, anorexia and weight loss asso-
ciated with disseminated disease.
Parasitic:
●Physaloptera (p 690)
Chronic intermittent vomiting may be associated with undiagnosed infection with the stomach
worm Physaloptera.
● Heartworm disease (Dirofilaria immitus) (p 691)
Dirofilariosis is a disease with primarily regional importance. Cats with heartworm disease may
not have signs of respiratory or cardiovascular disease (e.g. coughing or changes in breathing pat-
tern), but instead present with intermittent vomiting, anorexia or weight loss.
Toxin/drug:
● Pharmacologic (drug-associated vomiting)** (p 678)
Drugs are a common cause of acute vomiting in cats. However, chronic vomiting may occur in
cats that are on long-term drug therapy (e.g. chemotherapy, theophylline, etc.).
● Lead poisoning (p 692)
Lead poisoning is an uncommon cause of vomiting in cats, as they are generally more fastidious in
their eating habits. In cats ingesting lead-containing materials, both gastrointestinal (vomiting,
diarrhea, anorexia) and neurologic (seizures, ataxia, megaesophagus, tremors) signs are typical.
Vomiting is an active process that must be distin-

INTRODUCTION guished from regurgitation.
Vomiting in cats is associated with abdominal muscle
MECHANISM? contraction, considerable muscular effort and anxi-
Vomiting occurs when the vomiting center in the ety prior to the event.
medulla is stimulated, which can occur by several
Vomitus may consist of undigested food material (if swal-
mechanisms:
lowed whole), partly digested or even liquid, and may be
● Effect of blood-borne toxins or drugs.
clear, yellow (bile stained) or brown (food colored).
● Afferent impulses from the cerebral cortex,
chemoreceptor trigger zone (CRTZ), or receptors in Vomitus is not typically tubular in form, nor does it
the pharynx or abdominal viscera. contain large amounts of white frothy material.
The CRTZ is stimulated by: The pH of vomitus is usually acidic (pH < 4), but
● Blood-borne toxins or drugs. may be neutral (pH 7) if duodenal content is present
● Impulses from the vestibular apparatus. (bile reflux).
computed tomography, etc.), endoscopic examination

WHERE?
and biopsy or surgical exploratory with biopsy.
Vomiting may be associated with gastrointestinal dis-
Many diseases that cause chronic vomiting are
ease or extra-intestinal tract diseases.
diseases from which complete recovery is not possi-
Gastrointestinal disease involving the stomach and/or ble (e.g. IBD, food allergy, motility disturbances,
small intestine causes vomiting. chronic renal disease, etc.) and thus, long-term ther-
apy including dietary or pharmacologic treatment
Vomiting is rarely associated with primary colonic
will be necessary.
disease.
In some cases, the prognosis will be very guarded to
Extra-intestinal causes of vomiting include:
poor for long-term survival (e.g. neoplasia, cardiomy-
● Hepatobiliary disease.
opathy), and this should be discussed with the owner.
● Pancreatic disease (e.g. pancreatitis, neoplasia).
● Renal disease causing acute or chronic renal failure. Occasional vomiting is considered a normal phe-
● CNS disease (e.g. vestibular disease, encephalitis, nomenon in cats, both for removal of ingested hair, but
seizure disorders, neoplasia). also as a protective mechanism following consumption
● Metabolic diseases (e.g. hyperthyroidism, ketoaci- of new or unusual foods. This should be taken into con-
dotic diabetes mellitus or Addison’s disease). sideration when evaluating a cat for chronic vomiting.
● Cardiomyopathy or congestive heart failure.
● Systemic illness or infection affecting the CRTZ or
cortex (e.g. septicemia). DISEASES CAUSING SIGNS OF
CHRONIC VOMITING (>3 WEEKS
DURATION)
WHAT?
FOOD ALLERGY (DIETARY
Primary gastrointestinal diseases that cause chronic HYPERSENSITIVITY)***
vomiting include:
● Parasites (e.g. physaloptera, etc.). Classical signs
● Infectious diseases (e.g. Helicobacter).
● Chronic vomiting, usually < once per day,
● Inflammatory diseases (e.g. IBD, gastritis or gastric
immediately to > 12 h after eating.
ulcer disease).
● Diarrhea is less frequent and more often
● Neoplasia.
large bowel in character.
● Mechanical (e.g. antral pyloric hypertrophy/steno-
● Weight loss.
sis, obstruction, intussusception).
● Dermatological signs in some cats (miliary
● Dietary disturbances (e.g. food intolerance or food
dermatitis, pruritus).
allergy).
The most common causes of chronic vomiting are:
dietary (indiscretion or food intolerance), neoplastic
Pathogenesis
diseases, metabolic or extra-intestinal disturbances
(e.g. renal, hepatic or pancreatic disease) and inflam- Food allergy is an immunologic reaction usually to
matory diseases (e.g. IBD). the protein (or glycoprotein) component of food.
Diagnosis is based on the minimum data base, multiple Food allergy may also be associated with dermatologi-
fecal examinations, survey or contrast radiography, cal signs.
radionucleotide or scintigraphic studies (e.g. thyroid
Approximately 25% of cats with GI signs from food
disease, motility studies, evaluation for portosystemic
allergy also have dermatologic signs consisting of pru-
shunts, vascular diseases, etc.), ultrasound examina-
ritus, miliary dermatitis and alopecia.
tion, endocrine testing, evaluation of serum TLI, cobal-
amin/folate assays, titers for various infectious agents, The pathogenesis of food allergy is poorly understood,
neurologic examination and diagnostics (e.g. CSF, but is thought to be a combination of two main
mechanisms. Firstly, direct toxicity caused by the Dermatologic signs occurred in 25% of cats and con-
ingestion of the food causing release of histamine and sisted of miliary dermatitis, pruritis and alopecia.
other vasoactive amines. Secondly, indirect effects are
mediated via an amplification system, which responds
to the food by releasing mast cell products, the produc-
Diagnosis
tion of eicosanoids and other inflammatory mediators,
initiation of the kinin cascade, and other events that The diagnosis of food allergy is confirmed by per-
result in the clinical syndrome. forming elimination/challenge trials. However, the
diagnosis of food allergy may require a more specific
approach to the elimination/challenge trials than is
Clinical signs
possible with commercially available diets because
Signs associated with food allergy are non-seasonal, of the difficulty in removing all sources of allergy from
affect a wide range of ages, breeds and both sexes, and are commercial diets.
present in one or all three of these systems: the gastro-
The best elimination diet for making a definitive diag-
intestinal tract, the skin or the respiratory tract.
nosis in these cases is a home-prepared diet contain-
Cats with food allergy may have vomiting/diarrhea, ing novel protein and carbohydrate source, e.g.
anorexia and weight loss, but may also have derma- lamb, venison, duck, kangaroo, crocodile or ostrich
tologic signs, which may include rodent ulcers, with potato or rice (and added vitamin and mineral sup-
eosinophilic plaques, miliary dermatitis, otitis externa plementation).
or generalized pruritus, alopecia and erythema. A com-
Gastrointestinal signs usually resolve within 1–3 weeks
bination of GI and dermatologic signs should raise the
but dermatologic signs may require that these diets be
index of suspicion of a food-related problem.
fed a minimum of 6–8 weeks or 2 weeks after all
Head and neck pruritus appears to be especially com- symptoms resolve.
mon in cats with food allergy.
The cat should then be changed to a hypoallergenic
In some cats, food allergy may be associated with sys- commercial cat food (e.g. IVD Limited diets, Hill’s
temic signs such as feline asthma, rhinitis, stomatitis or d/d diet or z/d diet, Royal Canin’s Selected protein
other respiratory tract signs. However, this is poorly diets, or Eukanuba’s Response Formula feline) contain-
documented. ing food ingredients the cat has been successfully tested
with or never exposed to.
In a study of cats with documented food sensitivity
(food intolerance and food allergy), there was a history Skin tests are inadequate for diagnosis of food aller-
of vomiting (56%), diarrhea (25%), or vomiting and gies because they have a high incidence of false posi-
diarrhea (19%). tives and negatives, and are only useful in determining
which adverse reactions to foods have an IgE-mediated
Vomiting usually occurred less than once daily, a few
pathogenesis.
minutes to > 12 h after eating and most commonly con-
sisted of bile. Serum radioallergosorbent (RAST), ELISA, or tests
that are variations on the theme, are all available com-
Large bowel signs (mucus and fresh blood in feces or
mercially to test for the presence of antigen-specific
excessive straining to defecate) were slightly (57%)
IgE in the serum. However, the difficulties present with
more common than small bowel signs. Flatulence
skin testing still exist, i.e. non-IgE-mediated and
occurred in 38% of cats.
delayed hypersensitivity reactions will also be missed.
Weight loss occurred in 70% of cats. Not all food allergies cause systemic effects or cause
increased systemic levels of IgE and so will be negative
Appetite was variably affected and either normal,
using serum IgE testing. Findings of a recent study sug-
increased or decreased.
gest that type I hypersensitivities account for only 25%
Some cats were reported as irritable (38%) or lethargic of gastrointestinal food sensitivities in cats. Gastroscopic
(25%). food sensitivity testing has been tested in humans and
dogs, but not in cats, and its utility remains to be estab- possible and affected animals will have recurrent or
lished for the routine diagnosis of food hypersensitivity. persistent clinical signs.
Differential diagnosis FOOD INTOLERANCE***

The main differential diagnosis for food allergy is food
Classical signs
intolerance and they are usually clinically indistin-
guishable. ● Chronic vomiting, usually < once per day,
immediately to >12 h after eating.
Cats with food allergy causing dermatologic signs
● Diarrhea is less frequent and more often
must be differentiated from cats with atopy, flea allergy
large bowel in character.
dermatitis, psychogenic alopecia or insect bite hyper-
● Weight loss.
sensitivity.
● Dermatological signs in some cats (miliary
The gastrointestinal signs of either syndrome can dermatitis, pruritus).
mimic many other causes of chronic GI disease, includ-
ing gastritis, pancreatitis, and small bowel diseases such
Pathogenesis
as IBD or colitis. The severity and duration of each event
depends on the amount of antigen ingested, the immune Food intolerance is a non-immunologic reaction to
response and the sensitivity of the patient. The more a substance or multiple substances in food. This
severe the presentation, the more differentials that must reaction can occur to proteins or other food compo-
be included, e.g. neoplasia, extra-intestinal disease, etc. nents, but it can also be associated with food coloring,
additives, preservatives or flavorings. Naturally occur-
ring chemicals such as amines, salicylates and
Treatment
monosodium glutamate are present in food, especially
Treatment is initiated during the diagnostic phase by highly flavored rich food.
feeding the elimination diet. The key to effective ther-
These distinctions are difficult to distinguish clini-
apy is to find the offending agent(s) and remove
cally.
them from the diet.
Food sensitivity may also be associated with dermato-
Corticosteroids may provide partial relief, especially
logical signs.
where type I hypersensitivity reactions are involved,
but in general are not effective in maintaining remission Approximately 25% of cats with GI signs from food
or symptomatic relief for cats with food allergies. sensitivity also have dermatologic signs consisting of
pruritus, miliary dermatitis and alopecia.
Antihistamines have not been proved effective in
preventing the gastrointestinal symptoms associated The pathogenic mechanisms of food intolerance are
with food allergy. poorly understood, but a combination of direct toxicity
caused by the ingestion of the food causing release of
Some animals will eventually develop allergies to com-
histamine and other vasoactive amines, and indirect
ponents in the elimination diet. In these cases, feeding
effects that are mediated via an amplification system
diets containing protein hydrolysates will be most
which responds to the food by releasing mast cell prod-
effective. Unlike regular protein molecules, the molec-
ucts, production of eicosanoids and other inflammatory
ular size of these hydrolysates is too small to crosslink
mediators, initiation of the kinin cascade, and other
IgE bound to mast cells.
events that result in the clinical syndrome.

The prognosis for control of food allergy is excellent if Cats with food intolerance traditionally have been
the offending agent(s) can be identified and eliminated thought to have gastrointestinal tract signs only,
from the diet. However, in some cases, that is not because the syndrome is not an immunologic reaction.
However, humans with food intolerance may have Treatment

dermatologic signs, mouth ulcers and other systemic
signs. In cats, vomiting, diarrhea, weight loss, poor Food intolerance is highly diet-responsive once the
coat condition and lethargy are the most frequently offending agent(s) has been identified. This is usually
observed clinical signs. It is unknown whether der- done by using an elimination diet.
matologic signs also occur with food intolerance in
cats. Since the condition is not immunologically mediated,
drugs that modify or suppress the immune response are
The most common clinical signs of food intolerance are unlikely to be beneficial.
the same as food allergy, i.e. vomiting and/or diarrhea.
The vomiting is often intermittent and may not neces-
sarily follow any particular pattern in relation to eating. Prognosis
If diarrhea occurs, it is probably more likely to be large Once the inciting food(s) has been eliminated from the
bowel in character (mucus and fresh blood in feces or diet, food intolerance has an excellent prognosis.
excessive straining to defecate) than small bowel (low
frequency, loose to watery feces passed without strain-
ing or mucus). HYPERTHYROIDISM**
Weight loss may occur, along with a change in appetite. Classical signs
● Weight loss.
● Polyphagia.
Diagnosis ● Vomiting and/or diarrhea.
The diagnosis of food intolerance is confirmed by per-
● Hyperactivity.
forming elimination/challenge dietary trials.
● Poor grooming habits.
An elimination trial (either using commercial hypoal- See main reference on page 304 for details.
lergenic diets or premium diets that have reduced food
colorings, preservatives, additives, etc.) of 4–6 days
should be embarked upon first before proceeding to a Clinical signs
more specific food elimination trial requiring con- Weight loss despite a voracious appetite (polypha-
trolled food preparation (single novel protein and car- gia) is the most common owner complaint.
bohydrate source). Gastrointestinal signs usually
resolve quickly. Vomiting may cease immediately and Vomiting and polyuria/polydipsia occur in a third of
diarrhea usually within 3 days. Recrudescence of GI cats.
signs with challenge usually occurs within 4 days but Other signs that occur less commonly are restlessness
may take up to 10 days with dermatologic signs. or irritability, poor grooming habits, decreased appetite,
lethargy, panting or dyspnea and large bowel diarrhea.
The most prevalent physical exam findings are a pal-
pable thyroid nodule, thin body condition, tachycardia
Food intolerance and food allergy are clinically or heart murmur and hyperactivity or irritability.
indistinguishable as they both present with the same
There is no breed or sex predilection for hyperthy-
clinical signs and are usually highly diet responsive.
roidism, but most (90%) are old cats (> 10 years).
Other chronic causes of GI signs include gastritis, Cats < 6 years of age are rarely affected.
pancreatitis and small bowel diseases such as IBD or
colitis. As a general rule, more severe clinical presenta-
Diagnosis
tions require a more thorough clinical workup to elim-
inate a wider range of differential diagnoses, e.g. Presumptive diagnosis is often suggested by the age,
neoplasia and extra-intestinal disease. history and clinical presentation.
Hematology changes include erythrocytosis, and a only short term. Thus, it is not useful in long-term man-
stress leukogram (leukocytosis, neutrophilia, lym- agement of the disease.
phopenia).
Adjunctive therapy for hyperthyroid heart disease:
Serum biochemistry profile changes: increases in liver beta-adrenergic receptor-blocking agents (propranolol,
enzyme activities (ALT, SAP, GGT, LDH, AST) atenolol for heart rate control, and furosemide, calcium
occur in greater than 50% of cases, hyperglycemia channel antagonists and ACE-inhibitors as needed for
and pre-renal azotemia are less common. Hyper- heart failure (see page 132).
phosphatemia and hyperbilirubinemia are uncommon
Surgical thyroidectomy is a highly effective treatment,
(< 10% of cats).
especially for unilateral disease, but requires an anes-
The urine specific gravity will usually be > 1.035 thetic procedure and careful technique to preserve the
(>50%), but cats with polydipsia/polyuria or underly- parathyroid glands. If bilateral thyroidectomy is required,
ing renal disease will have unconcentrated urine (urine the patient will require oral thyroid hormone supplemen-
SG < 1.035). tation. Recurrence of hyperthyroidism in the remaining
gland or tissue is common.
Definitive diagnosis is made by finding elevated
serum thyroxine (total T4) levels in most cats (98%). Radioiodine therapy is the simplest, safest and most
effective therapy for the majority of cats, except cats
In a few cats the total T4 is in the upper half of the nor-
with chronic progressive renal disease/failure and cats
mal range and measurements of free T4, a T3 suppres-
that will not eat in confinement. The major disadvan-
sion test (useful for diagnosis of mild hyperthyroidism,
tage is the requirement for special facilities for use of
but takes 3 days), TRH stimulation test (preformed over
radioisotopes and the cat cannot be handled for
4 hours, side effects common from TRH administration)
7–21days. This makes fluid therapy difficult if the cat
or radionuclide (99Tc, pertechnate) imaging examina-
goes into renal decompensation during that time, or
tion (requires special equipment and isolation for 24
requires other medication.
hours) may be required to make the diagnosis.
Differential diagnosis IDIOPATHIC INFLAMMATORY BOWEL

DISEASE (IBD)*
Diabetes mellitus, chronic renal failure, liver disease
are common extra-intestinal causes of vomiting, weight
Classical signs
loss and polyuria/polydipsia that must be differentiated
from hyperthyroidism. ● Vomiting with or without diarrhea.
● Weight loss and anorexia or decreased
Primary GI diseases that may cause similar signs are
appetite.
food intolerance/food allergy, IBD and gastrointestinal
neoplasia.
Pathogenesis
Treatment Inflammatory bowel disease (IBD) is an idiopathic
inflammatory disease of the feline GI tract character-
Medical therapy with anti-thyroid drugs that inhibit the
ized by infiltration of the lamina propria and
synthesis of thyroid hormones, such as methimazole or
mucosa with inflammatory cells of various types
carbimazole (2.5–5 mg/kg q 8–12 h, PO) are com-
(lymphocytic, plasmacytic, granulocytic, granuloma-
monly used treatments. However, these drugs must be
tous, eosinophilic or combinations of these).
administered daily and have side effects which are
potentially problematic. Vomiting and anorexia are rela- A lymphocytic/plasmacytic infiltration is the most
tively common side effects, while hematologic abnor- common lesion in cats.
malities are rare.
The etiology is unknown but believed to involve
Calcium ipodate (15 mg/kg PO q 12 h) decreases serum genetic, immunologic, dietary, bacterial and mucosal
T3 (but not T4) concentrations acutely, but the effect is factors.
Lymphocytes and plasma cells are normal compo- It is especially important to rule out parasitic, infec-
nents of the feline GI tract, and increased numbers in tious, dietary and extra-intestinal (e.g. hepatic, renal
the GIT occur in response to many infectious agents. or pancreatic) causes of disease, as these may cause
Differentiation of feline IBD from other diseases similar lesions to IBD.
requires a complete examination to rule-out other
The only means of ruling out dietary causes of vomit-
causes for the infiltration. In IBD, there should also
ing is via an elimination trial, which must be conducted
be evidence of mucosal disease (e.g. erosion, villous
using an elimination diet prior to making a diagnosis of
blunting, loss of normal structure in other ways, loss of
IBD.
normal function).
Endoscopic examination and biopsy is the most com-
Eosinophilic IBD is rare in cats, and in some cases it
mon procedure used to obtain the diagnosis. Multiple
is found in association with hypereosinophilic syn-
(6–8), good-quality (containing submucosa and prop-
drome (infiltration of eosinophils in many body tissues
erly oriented) biopsies should be obtained from the
including liver, spleen, lymph nodes, etc.).
small intestine and stomach. Biopsies should be taken
Other forms of IBD, such as granulomatous and neu- from all regions of the stomach and lymphoid follicles
trophilic IBD are also rare in cats. should be avoided when obtaining biopsies from the
duodenum. Full-thickness biopsies obtained surgically
Most forms of IBD involve the small intestine, spar-
are also acceptable if endoscopy is unavailable, and
ing the stomach and colon, however, enterocolitis and
equal care should be taken to assure biopsy quality
gastritis may also occur.
(proper handling to minimize artifact and orientation on
Recently an association has been observed between the biopsy sponge to prevent curling and crush artifacts).
cats with idiopathic IBD and concurrent cholangitis
The major difficulty associated with endoscopic
and pancreatitis. The true relationship between these
diagnosis of IBD is differentiation of IBD from lym-
observations and clinical IBD is not known.
phoma, which will not be possible if the biopsy sam-
ples are not deep enough (contain submucosa) or if they
Clinical signs have significant mucosal artifacts that prevent adequate
assessment of mucosal abnormalities. In some cases
Vomiting and weight loss are the most common
where histologic differentiation is impossible, immuno-
signs, but diarrhea and anorexia are also frequently
cytochemistry techniques may have to be employed to
observed signs.
distinguish the cell origin (e.g. lymphoma cells tend to
Middle-aged (> 4 years) cats are most frequently be monoclonal, while lymphocytes from cats with IBD
affected, but all ages have been reported to have IBD. will be polyclonal).
There is no breed or sex predilection, but purebred Non-specific laboratory abnormalities that may be
cats may be at increased risk compared to DSH cats. found in cats with IBD include: hypoproteinemia,
hyperglycemia (stress induced), hypokalemia, ele-
If there is concurrent cholangitis or pancreatitis, cats
vated liver enzyme activities and a stress leukogram.
may also present with icterus, abdominal pain or fever.
Serum cobalamin and folate levels may be decreased
in cats with IBD due to malabsorption.
Diagnosis
Radiography and ultrasonography generally do not
The diagnosis is based upon several factors: (1) his-
assist with the diagnosis, but are important in ruling
tologic infiltration of inflammatory cells, usually lym-
out other causes of the clinical signs, e.g. neoplasia.
phocytes and plasma cells in the GI tract; (2) the
presence of inflammatory cells is associated with
mucosal abnormalities and functional disturbances;
(3) there are no other identifiable causes for the infil-
tration identified; and (4) the signs of the disease are Neoplasia (lymphoma is of special mention because
chronic (> 3 weeks in duration). it may have a similar histologic appearance to IBD).
Food intolerance or hypersensitivity (food allergy). Prognosis

Parasitic infections of the GI tract, especially giardia, Guarded. Cats will frequently respond well to dietary
which are difficult to diagnose. and pharmacologic therapy, but relapses are common
Infectious diseases such as Campylobacter, salmonel- and long-term management is required. There is no
losis, Clostridium, etc. known cure for IBD and owners should be educated
about the nature of the disease to encourage compliance
Extra-intestinal causes of vomiting such as hyperthy- and understanding.
roidism, uncontrolled diabetes, renal failure and pan-
creatitis.
CHRONIC PANCREATITIS*
Classical signs
Treatment ● Lethargy.
In most cats, a combination of dietary modification ● Anorexia.
and pharmacologic therapy (anti-inflammatory, ● Vomiting is observed in less than 30% of
immunosuppressive) is successful in controlling the cases.
clinical signs.
Dietary therapy involves three main strategies: (1)
low-residue, highly digestible diets; (2) hypoallergenic,
elimination diets aimed at controlling food allergies; or
(3) high-fiber diets for cats with IBD that primarily Clinical signs
involves the large bowel.
Lethargy and anorexia have been the most commonly
The mainstay of pharmacologic therapy in cats with observed clinical signs.
IBD is prednisone (2–4 mg/kg PO q 12–24 h). This dose
is tapered after the first 2 weeks to the lowest dose that will In general, vomiting and anterior abdominal pain
maintain remission. Some cats can be weaned off pred- occur less frequently.
nisone after 3–6 months and maintained on a controlled Signs may be protracted, with low-grade vomiting
diet (or diet with metronidazole), while others will require occurring in some cats, while others have acute signs.
life-long steroid therapy.
In refractory cases, dexamethasome (0.25 mg/kg PO q
Diagnosis
12–24 h) may be used as well, but is not suitable for
alternate day therapy because of the long half life. A certain degree of clinical suspicion is required to
make the diagnosis of pancreatitis in cats because the
Metronidazole is often added (10–15 mg/kg PO q 12 h)
signs are so vague.
to the treatment plan because of the anaerobic, antipro-
tozoal and immunomodulating effects of the drug. Cats with chronic pancreatitis may develop secondary
complications such as exocrine pancreatic insuffi-
Other antibiotics that may be useful include tetra-
ciency, diabetes mellitus, obstruction of the common
cycline (20 mg/kg PO q 8 h), doxycycline (5–10 mg/kg
bile duct or cholangitis.
PO q 12 h) or tylosin powder (10–20 mg/kg PO q 12 h).
Hematology and serum chemistry profiles are non-
In cats that do not completely respond to corticos-
diagnostic, but may show dehydration, electrolyte
teroids or that become refractory to standard treatment
imbalances, elevated liver enzymes, mild hyperbiliru-
approach, chlorambucil (1 mg PO q 3 days) or aza-
binemia or a leukocytosis.
thioprine (0.3–0.5 mg/kg PO q 2–3 days) can be added
to the regimen. Toxicity (leukopenia) is a major risk Serum lipase and amylase values are not helpful, as
with azathioprine use, and should be monitored by they may be elevated, normal or low in normal cats or
hemograms every 2–3 weeks. cats with pancreatic disease.
Imaging studies are the most useful way to obtain a Steroid therapy may be indicated in cats with concur-
presumptive diagnosis of pancreatitis. Radiographs of rent IBD or cholangitis.
the anterior abdomen may reveal evidence of local
peritonitis, gas in the duodenum or anterior jejunum, or
HEPATIC DISEASES (HEPATIC LIPIDOSIS,
a mass. Ultrasound examination remains the most
CHOLANGITIS, HEPATIC CIRRHOSIS,
reliable technique to evaluate the pancreas and
PORTOSYSTEMIC ANOMALIES)
determine the presence of swelling, abscess or fibrosis.
It is important to note that ultrasonographic changes
Classical signs
in chronic pancreatitis persist for months.
● Lethargy or depression, vomiting, anorexia
Elevations in serum trypsin-like immunoreactivity
and weight loss are common signs.
(TLI) assay have been suggested as a means of detect-
● Icterus, ascites, hepatomegaly or
ing pancreatitis, but this has not be shown to be con-
microhepatica are variable.
sistently accurate either, and is of less use in chronic
pancreatitis.
See main references on page 421 for details (The
The assay for feline pancreatic lipase (fPLI) has been Yellow Cat or Cat With Elevated Liver Enzymes).
developed and is a sensitive and highly specific test for
acute pancreatitis. However, in cats with chronic pan-
Clinical signs
creatitis, the fPLI may be normal, or mildly increased
but below levels diagnostic for pancreatitis, which can Vomiting occurs primarily because of the gastritis
make test interpretation difficult. that occurs secondary to changes in blood flow and
release of GI hormones, and because of mediator
release (stimulation of the vomiting center) secondary
to presence of toxins from decreased hepatic clearance
The list of problems causing anorexia and lethargy in or function.
cats is lengthy and includes multiple organ systems and
Liver diseases often present with the relatively non-
abnormalities.
specific signs of anorexia, weight loss, vomiting, and
lethargy or depression with or without icterus.
Treatment
Other signs include ascites, edema formation, bleed-
Nothing should be fed for 1–2 days if the cat is vomiting disorders due to deficiency of coagulation factors
ing until the vomiting can be controlled. However, a fast or DIC, and in cases with severe hepatic failure, signs
of longer than 3 days is to be avoided if at all possible in of hepatoencephalopathy (dementia, personality
most cats. changes, seizures, stupor or coma). Prolongation of clot-
ting times is quite common in cats with hepatopathy.
Intravenous fluid therapy should be administered,
using a balanced electrolyte solution (either replace-
ment or maintenance fluids) to maintain hydration, cor- Diagnosis
rect pancreatic ischemia and reduce the risk of
Icterus (hyperbilirubinemia) may be caused by pre-
complications of pancreatitis.
hepatic (hemolysis), hepatic or post-hepatic (bile duct
Anti-emetics (e.g. metoclopramide 0.1–0.2 mg/kg) obstruction) diseases which all must be considered.
may be used if the cat is vomiting.
The hemogram is important in differentiating hemol-
Cats with severe pancreatitis may be unable to eat for ysis from hepatic causes of icterus. Anemia is a
several days (3–5), thus, parenteral or partial enteral common problem and may be either regenerative (sec-
nutrition will be necessary to prevent development of ondary to blood loss or hemolysis) or non-regenerative
malnutrition, feline hepatic lipidosis and impaired (e.g. anemia of chronic disease, bone marrow suppres-
immunity. sion). Typically the anemia of chronic disease is
less severe (PCV > 20), than that seen with hemolysis gitis, and hepatic lymphoma or carcinoma) are the most
or severe blood loss. common diseases.
Target cells (leptocytes) on the blood smear are also Cats with ascites: Ascites may be caused by pre-
suggestive of liver disease. hepatic (cardiac), hepatic or post-hepatic (GI lymphatic
obstruction, protein-losing enteropathy, severe protein-
Serum biochemical profile results will be supportive of
losing nephropathy or mesenteric hypertension (tor-
the diagnosis, with the most common findings being
sion) or venous thrombosis or vasculitis), and these
elevated liver enzymes, hyperbilirubinemia,
must be separated. Ascites due to cardiac failure is
decreased BUN, decreased albumin and total protein,
very rare in the cat. Hepatic disease, vasculitis from
hypocholesterolemia, and electrolyte disturbances con-
feline infectious peritonitis or lymphatic obstruction
sistent with vomiting (hypokalemia, hypochloridemia,
associated with neoplasia are the most common causes
hypernatremia).
of ascites in cats.
A serum bile acid assay is the most reliable, easiest to
perform and most readily available liver function test.
A pre- and 2-hour post-prandial assay should be Treatment
submitted to evaluate liver function. Other function
Treatment is based upon identifying the primary
tests include blood ammonia and bromosulfophthalein
problem. The reader is referred to the main reference
(BSP) retention.
(page 421) for details.
Measurement of sulfated bile acids in urine is a newly
developed test to diagnose liver disease. In many cats
that will not eat, obtaining a serum post-prandial bile GI LYMPHOSARCOMA**
acid sample is difficult, and this test may provide addi-
tional information about the status of liver function in Classical signs
inappetent cats.
● Weight loss.
Imaging studies (radiographs, ultrasound) are used to ● Intermittent or persistent vomiting.
assess liver size, morphology and structure, and may be ● Small or large bowel diarrhea.
used to obtain aspirates or biopsies of liver via ultra- ● Lethargy or depression.
sound-guided techniques.
In all cases of suspected liver failure, evaluation of Pathogenesis
coagulation function is essential, not only for thera-
In the United States and other countries where feline
peutic purposes (e.g. determining the presence of DIC,
leukemia virus (FeLV) is prevalent, FeLV infection
coagulopathies), but also prior to obtaining tissue for
is the most common cause of all types of lymphoma
biopsy.
except the alimentary form, which is only associated
The definitive diagnosis typically requires histopatho- with viremia 25–30% of the time. In areas where FeLV
logic examination of liver tissue, however, in cases of infection is rare (e.g. east coast of Australia), most
suspected vascular anomalies, a venous portogram or cats with lymphoma are FeLV negative.
portal scintigraphy is necessary to define the abnormal
Some evidence suggests that the alimentary form of
vascular structures.
lymphoma arises from transformed multipotent lym-
phoid or monocyte precursors or from FeLV-transformed
Differential diagnosis B-lymphocytes, and thus may still be associated with
FeLV.
Icteric cats: Immune-mediated hemolytic anemia, pan-
creatic or gastric abscess or tumor obstructing common Alimentary lymphoma is the second most common GI
bile duct, hemolytic anemia secondary to red cell para- tumor (adenocarcinoma is first), and occurs in older
sites, primary liver diseases (hepatic lipidosis, cholan- cats (> 8 years).
The most common site for lymphoma is the jejunum The definitive diagnosis is made by histopathologic
or ileum, with the duodenum being a rare site of occur- evaluation of affected segments of bowel. Ultrasound-
rence. Lymphoma is the most common tumor found in guided aspirates often will provide sufficient tissue
the feline stomach (although it is still a rare disease), sample for the diagnosis (intestinal wall, mass or lymph
but is found unfrequently in the colon compared to nodes).
adenocarcinoma.
If the lesion is in a location accessible by endoscopy,
Lymphoma can occur as a solitary mass causing an biopsies can be obtained by this method. However,
obstructive lesion, or as diffuse disease affecting endoscopic biopsy samples can be easily misread as
many sections of the GI tract and occurring throughout IBD or visa versa, and the diagnosis can be missed if
all layers of the bowel wall. the lesion is present only in the submucosa.
If these diagnostic modalities are not available or pro-
Clinical signs vide inconclusive results, full-thickness biopsies
obtained by surgical exploratory are usually definitive.
The most common clinical signs associated with intes-
tinal lymphoma in cats are anorexia, lethargy and Staging the disease requires histologic evaluation of
weight loss. regional (mesenteric) lymph nodes, liver and spleen,
radiographic evaluation of lungs and examination of
Vomiting and diarrhea are variably observed, bone marrow aspirates (if indicated) for evidence of
depending on the location of the lesion, the nature of dis- metastasis.
ease (diffuse vs. a solitary mass) and duration of disease
e.g. fever, hematemesis, icterus, ascites and melena.
Cats that are FeLV positive may also have clinical signs
consistent with the disease in other locations (e.g. ane- The major differential is lymphocytic plasmacytic
mia, leukemia, etc.). IBD.
Intestinal adenocarcinoma, foreign body, FIP, fungal or
algal infections of the GIT, other intestinal tumors
Diagnosis
(e.g. mast cell tumor) and hyperthyroidism must all be
Hematology may be normal or there may be an ane- considered.
mia of chronic disease (that may be masked by dehy-
dration) in cats that are FeLV negative. FeLV-positive
Treatment
cats may have a wide variety of hematologic changes,
which should be further investigated with a bone mar- Chemotherapy is provided in stages: induction of
row examination. remission, intensification, maintenance and rescue. In
general, cats are more difficult to rescue (compared
Serum biochemistry profile values also may be
to dogs) once the cancer is out of remission, which is
within normal limits, or there may be increases in
why their survival times are shorter than dogs.
liver enyzmes, hypercalcemia or hypoproteinemia.
Pre-renal azotemia and electrolyte disturbances may A typical protocol used to induce remission is the
occur in cats with severe vomiting. COAP protocol: cyclophosphamide (200–300 mg/m2
PO q 3 weeks), vincristine (0.5 mg/m2 IV q 1 week),
The majority of cats (70–75%) are FeLV antigen
cytosine arabinoside (100 mg/m2 IV or SC for 2 days
negative.
only), and prednisolone (50 mg/m2 PO q 24 h for 7 days,
Radiographs may be normal or may reveal thickened then EOD). If remission is only partially achieved, inten-
bowel loops or a solitary mass lesion. sification with doxorubicin (25 mg/m2 IV q 3 weeks) or
mitoxantrone (4–6 mg/m2 IV q 3 weeks) can be tried.
Ultrasonography is useful for localizing solitary
masses, evaluating mesenteric lymph nodes (which are Maintenance chemotherapy protocols may include
also typically involved), and for identifying thickened continuation of the COAP protocol or use of the LMP
intestinal loops. protocol (chlorambucil, methotrexate, prednisone).
In cats with small cell (highly differentiated) lym-

INTESTINAL ADENOCARCINOMA**
phoma of the GIT, the combination of chlorambucil
(20 mg/m2 PO every other week) and prednisolone
Classical signs
(20 mg/m2 PO EOD), with or without methotrexate
(2.5 mg/m2 PO EOD) is often successfully used. ● Weight loss and lethargy or depression are
the most prevalent signs.
Other protocols that have been successfully used to
● Intermittent to persistent vomiting or
treat feline lymphoma include COP (cyclophos-
hematochezia develop as the tumor
phamide, vincristine and prednisone), VCM (vincristine,
obstructs or ulcerates the epithelial
cyclophosphamide and methotrexate), or VCM plus
surface.
L-asparaginase.
Nutritional support should be used as needed (espe-
cially in cats that are vomiting or not eating enough to
Pathogenesis
maintain normal function).
The most common non-hematopoietic tumor of the
Control of secondary infections is also sometimes
feline GI tract is the adenocarcinoma.
necessary and should be implemented as required. In
cats with alimentary lymphosarcoma, metronidazole is Most intestinal adenocarcinomas occur in the jejunum
often used as the antibiotic choice. and ileum, with the duodenum rarely affected. Colonic
adenocarcinoma is uncommon and usually occurs in
very old cats (e.g. 16 years).
Prognosis Siamese cats represented 70% of 225 reported cases of
intestinal adenocarcinoma and had a mean age of
FeLV status does not influence whether or not
10–11 years.
remission occurs, but is a significant predictor of
survival, with FeLV-negative cats having much Domestic shorthair cats had the most reported cases
longer survival times. FeLV-positive cats in stages of colonic adenocarcinoma.
III–V had no differences in survival than FeLV-
Feline leukemia virus appears to have no role in the
negative cats, but in stage I–II, survival is 18 months
pathogenesis of this disease, since all 28 cats in one
versus 4 months, respectively, for negative cats and
study that were tested were found to be FeLV negative.
cats with the virus.
Adenocarcinomas occur either as annular or intra-
The overall prognosis is guarded to poor in cats with
luminal tumors.
alimentary lymphoma. Most cats with alimentary lym-
phoma respond poorly to chemotherapy, but those that Metastasis of adenocarcinomas is typically within the
do respond may have a survival time of more than one abdominal cavity and not to the lungs.
year. Cats with a solitary mass in the GIT that can be
resected have a better prognosis.
Most cats with lymphoma treated with multiple Clinical signs
agent chemotherapy protocols are expected to live
The most commonly observed clinical signs are
3–9 months, with 20% living longer than 1 year.
anorexia, lethargy, weight loss and vomiting.
Untreated cats can only be expected to survive 4–8
weeks. Cats that are FeLV positive also have shorter Hematochezia, melena or diarrhea are primarily
survival times. observed in cats with colonic disease.
Survival does not appear to be influenced by the In cats that are not eating and are vomiting persistently,
extent of the disease, anatomic location or clinical dehydration may also occur. Fever and abdominal effu-
stage, which is an important predictor in some types of sion are also late-stage findings associated with metas-
lymphoma. tasis of the tumor.
Diagnosis Nutritional support may be necessary in cats that do

not eat enough to meet at least resting energy require-
Hematologic and serum biochemical profiles are ments (RER = 30 × BW (kg) + 70) and cats with can-
often normal. cer may require additional calories (RER × 1.5).
Abnormalities may include: hemoconcentration, non- Cats with large colonic resections may require very
regenerative anemia of chronic disease, electrolyte highly digestible diets to reduce the fecal volume and
imbalances or pre-renal azotemia, hypoproteinemia or load on the colon.
hypoalbuminemia due to GI protein loss, or elevated
liver enzyme activities (metastatic disease).
Prognosis
Radiographs of the thorax rarely reveal metastatic
lesions. The presence of metastatic disease is not necessarily
a poor prognostic sign in cats with adenocarcinoma,
Abdominal radiographs may show a mass, enlarged and should not be a disincentive for performing a sur-
lymph nodes or signs of an intestinal obstruction (e.g. gical resection and anastomosis.
dilated, air-filled bowel segment, abnormal gas pat-
terns, or differences in bowel size or location relative to The average survival for cats with the disease is 4–15
neighboring bowel). Some cats will have tumors with months (with or without metastatic disease), but some
osseous metaplasia (mineralization) or ascites that cats live several more years following aggressive surgi-
will imply neoplasia. Contrast studies may be very use- cal resection.
ful in delineating intraluminal or annular lesions.
Ultrasonography is also very helpful in identifying PHARMACOLOGIC (DRUG-ASSOCIATED
mass lesions and their extent for staging, and can be VOMITING) **
used to direct fine-needle aspirates or biopsies for
diagnosis. Classical signs
In cats with colonic disease, colonoscopic evaluation ● Vomiting observed after administration or
and biopsy may also be useful. ingestion of a drug.
Surgical exploratory is the best way to obtain the See main reference on page 642 for details.
definitive diagnosis, get accurate staging informa-
tion, and will also allow resection of the affected seg-
ment of bowel if that is indicated. Clinical signs
In some cases, vomiting is expected following drug
Differential diagnosis administration (e.g. chemotherapy, xylazine), while in
others it is not usual (e.g. tetracycline, erythromycin),
Intestinal foreign body or obstruction, other intestinal
and in others it represents toxicity or accidental expo-
neoplasia, inflammatory bowel disease, vomiting and
sure (NSAIDs, narcotics, digitalis).
weight loss due to extra-intestinal disease (chronic
renal failure, etc.), fungal or algal diseases of the intes- The signs observed will depend on the drug that is
tine, and FIP granuloma should all be included in the administered, e.g. chemotherapy drugs may cause
differential list. vomiting, anorexia, lethargy, hair loss, etc., while vom-
iting caused by chloramphenicol or erythromycin may
be the only clinical sign.
Treatment
The only reported and effective treatment for intes-
tinal adenocarcinoma in cats is surgical resection. Diagnosis
The role of adjuvant chemotherapy for feline intes- Diagnosis is largely dependent upon obtaining an
tinal adenocarcinoma has not been explored. extensive, accurate history that includes a complete
history of drugs the cat is taking or has taken, toxins it

GASTRITIS/GASTRIC ULCER DISEASE
has been exposed to and the potential for accidental or
malicious poisoning.
Classical signs
Some commonly used drugs known to cause vomit-
● Frequent vomiting is typical, but
ing in cats include many, if not most, antibiotics (e.g.
intermittent vomiting will occur in some
amoxicillin, cephalexin, enrofloxacin, tetracycline,
cats.
erythromycin, metronidazole, clindamycin), chemo-
● Hematemesis or melena occurs with
therapy drugs (dacarbazine, cisplatin, doxorubicin,
severe gastritis or bleeding ulcers.
methotrexate, cyclophosphamide), methimazole, potas-
sium bromide, glipizide, and antifungal drugs (e.g.
itraconazole, amphotericin).
In some cases, determination of blood levels of a spe-
cific drug will confirm the presence of a drug or toxin
Clinical signs
that was unknown or unexpected. Alternatively, hair
and urine samples can also be used in some cases to Vomiting, either frequently or intermittently, is the pri-
determine the presence of metabolites of various drugs mary clinical sign. Severe gastritis and ulcer disease
or chemicals. will result in anorexia, abdominal discomfort,
lethargy or weight loss.
If the suspected exposure is recent, evacuation of the
stomach and analysis of its contents will also provide a Cats with severe gastritis or ulcer disease may also have
means of determining the presence of drugs or chemicals. hematemesis or melena from mucosal bleeding.

Other acute causes of vomiting such as food intoler- Endoscopic examination of the gastric mucosa will
ance/dietary indiscretion, parasitic diseases, infectious often reveal the surface erosions or ulcers, however,
diseases, foreign bodies or gastritis due to other causes histologic examination of the tissue is required to
should be considered when the history is not helpful in make a diagnosis of gastritis. Mild or chronic gastritis
identifying exposure. lesions may not have an abnormal mucosal appearance.
Gastric or duodenal ulcers can also be identified by con-
trast radiography and by ultrasonography in some
Treatment
cases, but these techniques are not as useful as endoscopy.
Choice of treatment depends on whether the vomiting is
Most cats with gastritis will have a normal hemogram
expected (e.g. chemotherapy) and can be controlled with
and chemistry profile. Cats with bleeding ulcers may
anti-emetics (e.g. metoclopramide or chlorpromazine),
have evidence of acute (non-regenerative if peracute,
or is due to unexpected toxicity or accidental ingestion.
regenerative if recent) or chronic blood loss (may be
Supportive care for toxicity or accidental ingestion either regenerative or non-regenerative depending on
includes removal of stomach contents and gastric amount of hemorrhage).
lavage, administration of activated charcoal to reduce
absorption of contents, administration of gastric protec-
tants as indicated (NSAID ingestion will cause gastri-
tis), anti-emetics (metoclopramide or chlorpromazine), Helicobacter spp. infection, parasites (Physaloptera,
and fluid support to prevent or treat dehydration. Ollanus spp.), IBD, neoplasia, gastritis due to other
extra-intestinal diseases.
In cats with vomiting due to intolerance (e.g. tetra-
cycline), changing the drug protocol to another that will In cats with ulcers that do not respond to standard
be effective is generally all that is indicated. therapy, ulcer disease due to a gastrinoma should be
ruled out. Diagnosis of a gastrinoma is made histolo- Clinical signs

gically by finding a neuroendocrine tumor, usually in
the abdomen, and by confirming the presence of hyper- Polyuria/polydipsia, anorexia or decreased appetite,
gastrinemia (serum gastrin levels that are extremely and weight loss are the most common clinical signs of
elevated) not due to secondary causes. chronic renal failure.
An unkempt hair coat, decreased grooming and
Treatment reduced overall activity level are also often observed.
Specific treatment is aimed at identifying and correct- Intermittent vomiting or diarrhea due to hypergastrine-
ing the underlying cause. mia and uremia and uremic ulcers or stomatitis occur in
severe cases.
Non-specific treatment for gastritis or gastric ulcers
involves reduction of gastric acid secretion, protection Polyuria is profound until the late stages of the disease,
of the mucosa to allow healing and reduction of gastric when oliguria gradually develops with the progression
retention or vomiting. This is accomplished by: to end-stage kidney disease.
Histamine-2 blockers: ranitidine (0.5–1.0 mg/kg PO q

12 h), famotidine (0.5–1.0 mg/kg PO q 12–24 h). Diagnosis
Proton pump inhibition: omeprazole (0.5–1.0 mg/kg History and physical examination findings are sugges-
PO q 24 h), note: this drug is difficult to dose in cats as tive of the diagnosis in a geriatric cat.
it must be recompounded, but is the most effective acid
Hematology, serum biochemistry profile and urinaly-
suppression drug.
sis will confirm the presence of azotemia, isos-
Mucosal protection: sucralfate (250–500 mg PO q 8–12 thenuria or poorly concentrated urine (1.015–1.035),
h) note: give at least 2 hours before giving H2 blockers. mild to moderate non-regenerative anemia, dehydra-
tion may also be present, along with hypokalemia,
Anti-emetics: metoclopramide (0.1–0.2 mg/kg PO q
hyperphosphatemia, and evidence of chronic meta-
8–12 h) as needed to control vomiting, promote gastric
bolic acidosis (low total CO2).
emptying and reduce gastroesophageal reflux.
Feed only highly digestible, low-fat foods (e.g. Hill’s
i/d diet, Purina EN, Iams low-residue diet, etc.) in Differential diagnosis
small amounts. In some cats, it is best to give them
Hyperthyroidism, diabetes mellitus, hepatic disease
nothing per os until the gastritis/ulcer healing has
(hepatic lipidosis if cat is/was obese) and neoplasia
begun and the vomiting is under control (1–3 days).
(lymphoma, adenocarcinoma, etc.) are important dif-
Hydration should be maintained with IV or SQ fluids as ferentials in an old cat with polyuria/polydipsia and
needed, if the cat is unable to eat or has severe vomiting. weight loss.
CHRONIC RENAL FAILURE*

Treatment
Classical signs Supportive. Fluid therapy as needed. Sub-cutaneous
fluids may be very important adjunctive therapy in
cats that do not drink enough or are vomiting, and have
● Weight loss.
severe polyuria that results in dehydration and worsen-
● Anorexia.
ing azotemia.
● Lethargy.
● Poor/hair coat/unkempt appearance. Dietary manipulation. Feeding a diet that has a mod-
● Vomiting. erate or low quantity of high-quality protein,
reduced phosphorus, and relatively high in calories,
See main reference on page 235 for details (The Cat to maintain weight, decrease azotemia and reduce the
With Polyuria/Polydipsia). effects of renal secondary hyperparathyroidism.
Phosphorus binders (e.g. amphogel) may be needed Diagnosis

when dietary manipulation no longer is effective in
reducing serum phosphorus levels. The clinical signs and history of polyuria/polydipsia
suggest that diabetes mellitus should be considered.
Potassium supplementation (potassium gluconate) is
needed in most cats with chronic renal failure due to The hemogram is non-specific, hemoconcentration
potassium wasting and total body potassium depletion and a stress leukogram are common, however, some
that occurs. cats have an inflammatory leukogram secondary to
infection (a common sequelae of unregulated diabetes
In cats with frequent vomiting, histamine-2 blockers mellitus).
(famotidine 0.5–1.0 mg/kg PO q 24 h, ranitidine
0.5–1.0 mg/kg) may be helpful in reducing hyperacid- A serum biochemistry profile and urinalysis will be
ity and gastritis that occurs secondary to azotemia and diagnostic. The finding of hyperglycemia with gluco-
hypergastrinemia. suria with or without ketonuria, and in some cases
bactiuria/pyuria is typical. Other abnormalities likely
Cats in more advanced stages of renal disease may have to be observed include elevated liver enzymes,
a significant non-regenerative anemia (PCV < 20) hypokalemia (may be severe), hypophosphatemia (may
due to the lack of erythropoietin production from the be severe), hypomagnesemia, low total CO2 values
failing kidney, which may respond, for a limited period (supportive of acidosis), and azotemia (may be pre-
of time, to treatment with recombinant human renal or renal in origin).
erythropoietin.
Other studies, such as imaging, blood gas analysis,
etc. are used to further characterize the disease relative
DIABETES MELLITUS* to severity and cause (e.g. pancreatitis, etc.), but should
not be done at the expense of initiating appropriate
Classical signs and immediate therapy.
● Weight loss. Differential diagnosis
● Polyphagia or anorexia.
● Lethargy, weakness and/or depression. The differentials are numerous, based upon the his-
● Vomiting. tory and clinical signs (e.g. renal failure, hepatic dis-
ease, poisoning, neoplasia and inflammatory bowel
See main reference on page 236 for details (The Cat disease) but a minimum data base will serve to confirm
With Polyuria and Polydipsia). the presence of diabetes mellitus.
Treatment
Clinical signs
Ketoacidotic diabetes mellitus can be a medical
Signs of polydipsia, polyuria, polyphagia and weight
emergency, as many cats will have severe metabolic
loss may be present for months prior to diagnosis.
acidosis, dehydration and electrolyte disturbances that
Approximately one-third of cats with diabetes melli- are life threatening unless addressed.
tus have a history of vomiting. An acute onset of
Fluid therapy (0.9% NaCl or Normosol) is the essen-
vomiting may occur with ketoacidosis.
tial, but must be used judiciously in conjunction with
The classical signs of ketoacidosis include polyuria, replacement of potassium, phosphorus and magne-
polydipsia, anorexia, weight loss, dehydration, vom- sium, which are often severely depleted. Serum potas-
iting, weakness and depression. sium may rapidly decrease during initial therapy and
should be monitored very closely (q 2–4 h).
In some cats, other clinical signs may include periph-
eral nerve dysfunction (plantegrade stance), demen- Insulin replacement is instituted with a short-acting
tia or stupor/coma. insulin (e.g. regular insulin, 0.1–0.2 U/kg, IV or IM q
2–6 h or as a constant rate infusion). Frequent moni- other instruments, or via contact with oral secretions
toring (q 1–2 h) of blood glucose concentrations is directly.
necessary so that when the blood glucose level drops
Infection with Helicobacter organisms results in
below 16.8 mmol/L SI (300 mg/dl), 5% dextrose is
increased infiltration of the mucosa with polymor-
added to the fluids.
phonuclear cells and mononuclear cells, and is clas-
In cats that are not severely acidotic, and are still eating sified as chronic gastritis.
and not vomiting, insulin treatment may be instituted
Persistent infection is associated with increased
with NPH insulin (0.25–0.5 U/kg, SQ q 12 h), or where
development of gastric lymphoid follicles, especially
available PZI or glargine, with monitoring of blood glu-
in the antrum, the location of heaviest concentration of
cose levels (q 2–3 h).
organisms in most cats.
Cats that have urinary tract or other infections
At this time, there does not appear to be a breed or sex
should be treated with appropriate antibiotics.
predilection for infection or development of signs.
Vomiting is controlled with metoclopramide
The classical sign is chronic vomiting due to gastri-
(0.1–0.2 mg/kg q 12 h) as needed.
tis, but the incidence and true importance of
Cats that are able to eat without vomiting should be fed Helicobacter spp. in gastritis in cats is not known.
a highly palatable diet (see page 238). High-protein,
reduced-carbohydrate diets are advantageous in both
Clinical signs
thin and obese diabetic cats unless they have concurrent
renal disease and need to eat a lower-protein diet. Chronic vomiting, weight loss and in some cases, pica
are reported in clinically affected cats.
HELICOBACTER SPP.* However, these organisms will be present in clini-
cally healthy animals, so a direct cause-and-effect
Classical signs relationship cannot be established.
● The classical sign is vomiting.
Diagnosis
Pathogenesis The diagnosis is made by histologic examination of
gastric mucosal tissue (usually obtained via
Helicobacter organisms known to colonize the feline
endoscopy). Either a special silver stain or modified
stomach include: H. pylori, H. felis, and H. bizzoze-
Giemsa stain must be used to identify the organisms.
ronii. Other Helicobacter spp. that have been identified
in the small intestine and liver of cats include Culture and organism identification is also required
H. cinaedi and H. fennelliae. The significance of these to make a definitive diagnosis, since not all spiral
organisms and their ability to cause clinical disease is organisms are pathogens or Helicobacter spp. Helico-
unknown. bacter spp. require special media and handling for
successful culture in vitro.
H. felis is commonly found in the stomach of cats and
may not be a feline pathogen, but H. pylori, which Helicobacter spp. produce urease that can be used to
causes peptic disease in humans, is believed to also be provisionally diagnose their presence, by placing
associated with gastritis in cats, especially cats in biopsy samples in urea broth or by using the com-
colonies or catteries. H. bizzozeronii is the most commercially available test (CloTest). However, this test
mon gastric colonizer in cats, and has experimentally is neither sensitive nor specific for Helicobacter
produced chronic gastritis in kittens. infection.
Infection is primarily transmitted via the oral–oral Serologic assays used in humans are not reliable for
route. Organisms are present in vomitus, oral secre- testing in cats because of the cross-reactivity between
tions and saliva, and may be transmitted via improp- other spiral organisms (commonly present in normal
erly disinfected dental equipment, endoscopes and cats) and H. pylori (the suspected pathogen).
Differential diagnosis Most epidemiologic studies do not incriminate pet

contact with human infection, and only contact with
Chronic gastritis due to other causes such as hepatic commercially reared cats has been shown to have any
disease, pancreatitis, chronic renal failure or IBD may potential for risk, suggesting the possibility of a reverse
result in a similar clinical presentation. zoonotic infection.
Treatment HYPERCALCEMIA* (MALIGNANCY,

There have been various treatment regimens recom- CHOLECALCIFEROL TOXICITY,
mended for cats with Helicobacter infection, but none CHRONIC RENAL FAILURE,
have been well substantiated. HYPERPARATHYROIDISM, IDIOPATHIC
HYPERCALCEMIA)
The triple therapy regimen has been the mainstay of
treatment for Helicobacter infection. This is bismuth Classical signs
(0.5–2 ml/kg PO q 4–6 h), metronidazole (62.5 mg PO
q 24 h), and amoxicillin (15–20 mg/kg PO q 12 h). This ● Signs vary with the cause of
regimen with the addition of famotidine (0.5–1.0 mg/kg hypercalcemia.
PO q 24 h) has been recommended in refractory or ● Anorexia, vomiting and weight loss are
severe cases. typical.
● Polyuria and polydipsia are late signs, due
Famotidine (0.5–1 mg/kg PO q 24 h), ranitidine (1–2 to renal failure.
mg/kg PO q 12 h), or omeprazole (0.5–1.0 mg/kg PO q ● Muscle weakness or tremors may occur
24 h), in addition to antibiotic therapy have more acutely.
recently been recommended.
Other antibiotics that may be used include tetracycline See main reference on page 245 (The Cat With
(22 mg/kg PO q 8 h), clarithromycin (7.5 mg/kg PO q Polyuria and Polydipsia) for details.
12 h), or azithromycin (5 mg/kg PO q 24–48 h).
Pepto-bismol can be used (1 ml/kg PO q 24 h) to con-
trol gastritis due to Helicobacter infection, but salicy- Clinical signs
late toxicity has occasionally been observed in Vomiting may be due to the disease causing the
individual cats. increased serum calcium or to the direct effects of ele-
The duration of treatment for infected cats has also vated calcium stimulating vomiting receptors both
not been well substantiated, but 14–28 days has been peripherally or centrally.
the standard recommendation. The signs are dependent upon the cause of hyper-
calcemia, which can be due to the presence of
malignancy, ingestion of cholecalciferol-containing
Prevention rodenticides, endocrinopathies (primarily primary
Unknown, but careful attention to cleanliness of endo- hyperparathyroidism) or idiopathic.
scopes and dental equipment is advised. Signs associated with large elevations in serum calcium
include anorexia, vomiting, muscle weakness, polyuria
and polydipsia, shaking/tremors and weight loss.
Public health
Hypercalcemia has also been associated with the devel-
H. felis and H. heilmannii both are capable of coloniza-
opment of calcium-containing nephroliths or uroliths,
tion of humans and cats, but are not particularly patho-
which may cause signs of renal or bladder dysfunction.
genic. H. pylori has not been isolated reliably from pet
cats, so the zoonotic potential of Helicobacter in pet Generally, in cats, hypercalcemia is rare, but if pres-
cats as a cause of human gastritis (a significant prob- ent is most commonly caused by renal failure or is
lem) has not been shown. secondary to malignancy. In some cats, the cause cannot
be identified. Other rarer causes include vitamin D toxi- fluid diuresis with physiologic saline (60–180
cosis, primary hyperparathyroidism, hyperthyroidism, ml/kg/day) and administration of drugs that induce
hypoadrenocorticoism and granulomalous disease. calciuresis (furosemide 2–4 mg/kg PO q 12 h, or pred-
nisolone 1–2 mg/kg PO q 12 h).
In severe, life-threatening hypercalcemia, where the
Diagnosis
above measures are inadequate, sodium bicarbonate
Hypercalcemia of malignancy is most often second- (0.5–2 mEq/kg in IV fluids over 6 hours), salmon cal-
ary to lymphoma, but may be due to multiple myeloma, citonin (4 U/kg IV q 12–24 h) and dialysis (peritoneal
adenocarcinoma and squamous cell carcinoma. or hemodialysis) may be necessary.
Diagnosis of this disorder is based upon finding the pri-
Other long-term therapeutic measures include feeding
mary tumor, an elevation of PTH-rP but not of iPTH in
a low-calcium diet (Hill’s k/d, u/d).
serum, and a response to therapy.
Primary hyperparathyroidism is rare in cats, but
FELINE VIRAL DISEASES (FeLV, FIV, FIP)
will be associated with an increased iPTH assay,
a decrease in serum phosphorus and lack of other pri-
Classical signs
mary abnormalities.
● Weight loss, anorexia and lethargy are the
Cholecalciferol poisoning is associated with a
most common signs.
decrease in both the iPTH assay and PTH-rP assay,
● Vomiting is less common.
hyperphosphatemia and often evidence of mineraliza-
● ± Fever
tion of abdominal and other soft tissues.
Chronic renal failure (renal secondary hyper- See main reference on pages 540, 339, 372 for details.
parathyroidism) is associated with an elevated iPTH
and PTH-rP assay, but normal or decreased ionized cal-
Clinical signs
cium. Ionized calcium will be elevated with all other
causes of hypercalcemia. Specific signs depend upon the effect of the infection
on the individual cat, e.g. development of neoplastic
Recently, idiopathic hypercalcemia has been reported
disease, bone marrow involvement, secondary infec-
in cats and acidifying diets were implicated. This is
tions and local (granuloma formation in FIP) or sys-
associated with an increased serum total calcium or
temic disease (CNS, respiratory, hepatic, effusions).
serum ionized calcium concentration, or both. Serum
iPTH concentrations are low or in the low–normal The most common signs are weight loss, anorexia
range, while serum PTHrP is usually undetectable. and lethargy or depression.
Serum 25-hydroxycholecalciferol (vitamin D3) con-
Feline leukemia virus (FeLV) is often associated with
centrations are normal in affected cats, as are serum
neoplastic disease (lymphoma, bone marrow infiltra-
phosphorus and albumin levels.
tion) or bone marrow dyscrasias (cytopenias,
Phosphorous concentrations are normal or low–nor- myelodysplasias, etc.). Vomiting may occur associated
mal in all causes of hypercalcemia except cholecalcif- with lymphoma.
erol toxicity or renal failure, unless renal failure
Feline immunodeficiency virus (FIV) results in
develops secondary to hypercalcemia.
immunodeficiency disease that often results in second-
ary infections being the cause of significant morbidity
and mortality. The skin, respiratory system and the gas-
Treatment
trointestinal tract are most often affected.
Specific treatment of hypercalcemia is directed at cor-
The classical presentation of effusive feline infec-
recting the underlying cause if possible.
tions peritonitis (FIP) is anorexia, lethargy, fever,
Supportive therapy measures to control or reduce weight loss, abdominal enlargement and dyspnea due
hypercalcemia include correction of fluid deficits and to the pleural and peritoneal effusion of fluid.
Non-effusive FIP may present with a wide variety of

HISTOPLASMOSIS*
clinical signs depending on the system involved,
including chorioretinitis, fever, vomiting and/or diar-
Classical signs
rhea, abdominal pain (renal, liver), anorexia, lethargy
and weight loss. ● Dyspnea, wheezing or coughing are
classical signs.
Diagnosis ● Signs of gastrointestinal, CNS, or
hemolymphatic system disturbances occur
Diagnosis of FeLV is by ELISA antigen testing and
with systemic involvement.
confirmation with serum or bone marrow IFA if the
diagnosis is in doubt. PCR testing can also be per-
formed in FeLV-suspect cats for confirmation.
FIV infection is detected by an antibody test and con-
Clinical signs
firmed either via western blot analysis or PCR testing
for the presence of viral proteins. (Note: vaccinated cats The classical presenting signs are respiratory: dysp-
will test positive on the antibody test.) nea, wheezing or coughing.
Diagnosis of FIP is a very difficult process because of In cats with systemic histoplasmosis, the gastrointesti-
the lack of a definitive test that is sensitive and specific nal tract, CNS or the skeletal system may be involved.
enough to differentiate enteric corona viral infections The GI tract signs are typically associated with diar-
from FIP (a mutant of enteric corona virus). rhea, but in some cases, vomiting is observed, along
with anorexia, weight loss and lethargy.
Antibody titers are available, but detect the pres-
ence of any corona virus (feline enteric, canine In generalized histoplasmosis, more non-specific signs
enteric, FIP, etc.). Most cats from catteries, shelter situ- may occur, such as anorexia, weight loss, fever, lymph-
ations or large, multi-cat populations will be exposed to adenopathy and lethargy.
enteric corona virus because of the ubiquitous nature of
Nervous system signs are rare and typically associated
the virus in these settings (up to 85–90%). Thus, anti-
with seizures, changes in mentation or meningitis (neck
body testing of cats from these environments will be
or back pain, other neurologic signs such as ataxia, cra-
quite difficult to interpret. Specific ELISA tests for the
nial nerve signs or weakness).
7B protein in FIP have not proved to be reliable in the
field. The hemolymphatic system involvement is manifest
primarily as bone marrow infiltration with the fungus,
Serum PCR testing for FIP shows great promise for
which crowds out the red cell, white cell and/or platelet
becoming a definitive diagnostic test, but the currently
precursors, so the clinical signs are variable depending
available serum tests still are not reliable tests for dis-
on the extent of marrow destruction.
tinguishing FIP versus enteric corona virus. The PCR
test is an excellent means of ruling out FIP (negative
Diagnosis
test means the cat does not have FIP). However,
a positive serum PCR test does not prove the cat has This disease has a regional occurrence, so a support-
FIP. ive history in a cat from an endemic area is suggestive.
The definitive diagnosis of FIP still requires histo- In cats with pulmonary histoplasmosis, there may be
logic examination of tissues for the classical changes very few hematologic or serum biochemical changes
or virus isolation. This is not usually necessary in cats (e.g. leukocytosis, mild anemia, hyperproteinemia due
with effusive FIP, but non-effusive FIP has such vari- to increased gamma globulins).
able clinical signs and progression that the diagnosis is
Disseminated histoplasmosis will often be associated
quite challenging.
with increases in liver enzyme activities, abnormal
PCR on tissue samples which have classic changes is hemogram (bone marrow involvement causing anemia,
also a good diagnostic test for FIP. thrombocytopenia, etc.), or changes associated with
protein losing enteropathy (hypoproteinemia, hypo- infected, especially those with FIV or feline leukemia
albuminemia, hypocholesterolemia, altered serum elec- virus infection.
trolytes).
Infected cats most frequently have respiratory tract
Radiographs will be useful in cats with pulmonary disease (dyspnea, coughing, rhinitis), CNS disease
disease, but less helpful with evaluation of other (ataxia, behavioral changes, seizures, circling),
organs. Cats with intestinal histoplasmosis often have hepatic disease (vomiting, diarrhea, icterus, anorexia,
thickened loops of bowel that can be seen radiographi- lethargy, weight loss, abdominal effusion or discom-
cally or via ultrasound imaging. Ultrasound may be fort), cardiac disease (arrhythmias, sudden death) or
useful in assessing liver and GI tract involvement. ocular disease (chorioretinitis, anterior uveitis, optic
neuritis, blindness, anisocoria, glaucoma or retinal
Serology is available for detection of systemic fungal
detachment).
infections, including histoplasmosis, but the tests have
a high percentage of false negatives in cats. Adult cats with FIV have more multi-systemic signs,
while cats without FIV often have ocular or neurologic
The definitive diagnosis is obtained by finding
signs only.
organisms in the affected tissues.
Occasionally, toxoplasma granulomas (tissue cysts)
Endoscopic or surgical biopsy, fine-needle aspirates by
form in the GIT or pancreas, rather than encysting in
ultrasound guidance, bone marrow examination or
muscle, and result in chronic vomiting. The encysted
bronchial washing are necessary to obtain the diagnosis.
organisms cause immune complex formation that is
In cats with signs of GI disease, especially diarrhea, rec-
responsible for the granuloma formation and the
tal scrapings may also reveal the organism.
chronic, but sublethal clinical disease.
TOXOPLASMOSIS*
Diagnosis
Classical signs
Hemogram abnormalities: non-regenerative anemia,
● Toxoplasmosis is a systemic disease neutrophilic leukocytosis, lymphocytosis and
involving multiple organs systems. eosinophilia are most commonly observed.
● Respiratory tract signs (dyspnea, coughing,
Lymphopenia may be present in cats with FIV or end-
rhinitis).
stage disease.
● CNS signs (ataxia, behavioral changes,
seizures, circling). Biochemical abnormalities are common with systemic
● Hepatic disease signs (vomiting, diarrhea, disease and include: hypoproteinemia, hypoalbumine-
icterus, anorexia, lethargy, weight loss, mia, hyperglobulinemia, elevated liver enzyme activities
abdominal effusion, or discomfort). (hepatic involvement), increased creatine kinase (muscle
● Cardiac signs (arrhythmias, sudden death). involvement), hyperbilirubinemia (cats with cholangi-
● Ocular signs (chorioretinitis, anterior tis), proteinuria is also relatively common.
uveitis, optic neuritis, blindness,
In focal GIT Toxoplasma granuloma, biochemical
anisocoria, glaucoma or retinal
abnormalities may be minimal.
detachment).
● Rarely GIT granuloma causing vomiting. Diagnosis is based on finding the organism in tissues
(cytology or histopathology) or by serologic testing.
Thoracic radiographs in cats with acute disease will
reveal a diffuse interstitial pattern with a mottled lobar
distribution.
Clinical signs
Fecal examination for oocysts in cats is usually not
Toxoplasmosis is a systemic, multi-organ disease helpful since less than 1% of infected cats shed the
that often affects young kittens, but adult cats are also oocysts on any given day.
Serologic testing is currently the best method of detec- Intestinal mast cell tumors are usually solitary, and
tion, but because of the presence of antibodies in both affect the distal small intestine, but multiple masses
healthy and diseased cats, titers must be used cau- can occur. Typically, they appear as a segmented
tiously. No single serologic test can definitively con- nodular thickening in the small intestine.
firm toxoplasmosis.
Mast cell tumors of the GI tract are usually poorly dif-
Serum ELISA tests for IgM, IgG and IgA are readily ferentiated (thus cytologic examination is difficult)
available and have been used to try to distinguish acute and highly malignant, with metastasis to the mesen-
from chronic infections in cats. Finding of a high IgM teric lymph nodes, liver and spleen. They are generally
titer, along with a four-fold increase over 2–3 weeks not functional tumors and are not typically associated
(or decrease) in IgG titer (in the presence of appro- with gastrointestinal ulcer disease. However, there
priate clinical signs, and response to anti-toxoplasma may be chronic bleeding from the tumor into the GIT.
drugs, e.g. clindamycin) is suggestive of recent or
No association with FeLV, FIV or FIP has been
active toxoplasmosis.
reported.
Other tests of serum IgG supportive of toxoplasma
infection are the modified agglutination test (MAT)
and the latex agglutination test (LAT). The MAT is the
Clinical signs
most sensitive test of IgG antibody, but is not uniformly
available. The LAT cannot distinguish antibody classes, The most common clinical signs in cats with an intes-
thus is less useful. tinal mast cell tumor are weight loss, lethargy and
anorexia.
Aqueous humor and CSF titers are also useful, but
should be compared with serum titers to determine if Intermittent or persistent vomiting, diarrhea and
local immunoglobulin production is occurring. lethargy or depression become more prevalent with
advancing disease.
Vomiting and/or diarrhea may also be observed, but
INTESTINAL MAST CELL TUMOR* often not until late in the disease.
Other signs include ascites, splenic enlargement
Classical signs
(metastasis), and rarely, mast cells in circulation (bone
● Weight loss and anorexia are the most marrow involvement).
common early signs.
● Intermittent or persistent vomiting,
Diagnosis
diarrhea and lethargy or depression
become more prevalent with advancing Palpation of an intestinal mass in an older cat is sug-
disease. gestive of neoplasia, but these tumors may be very
small.
Abnormalities of the hemogram or serum chemistry
Pathogenesis profile are uncommon, but may include anemia (non-
regenerative), hypoproteinemia and elevated liver
Mast cell tumors of the intestine are the third most
enzyme activities.
common GI tract neoplasm in cats behind lymphoma
and intestinal adenocarcinoma. Survey radiographs may identify a mass, evidence of
intestinal obstruction, or mild peritoneal effusion, but
These are tumors of old (mean age = 13 years) cats,
contrast radiography will be required to identify the
with no breed or sex predilection. They occur with
location and extent of many of these tumors.
about the same frequency as mast cell tumors of the
lymphoreticular system (e.g. spleen, lymph nodes and Ultrasonography is a useful tool in identifying the
bone marrow), but cats with intestinal mast cell location, extent and presence of metastatic lesions.
tumors typically do not have circulating mast cells. Fine-needle aspiration or biopsy of these masses by
ultrasound guidance may be useful, but because of the Despite surgical removal, cats with intestinal mast
poorly differentiated nature of the tumor they may also cell tumors rarely live longer than 4 months.
be non-diagnostic.
Analysis of peritoneal effusion fluid may be helpful if FOREIGN BODIES*
mast cells are present, but as with fine-needle aspirates,
the effusion may be suggestive of neoplasia, but not Classical signs
necessarily give a definitive diagnosis.
● The classical sign is an acute onset of
Definitive diagnosis requires histopathologic exami- frequent vomiting.
nation of the tissue, which is usually best achieved by ● Intermittent vomiting will occur in some
wide surgical resection and anastomosis. cats with foreign bodies that are causing
an intermittent or incomplete obstruction
Staging of the tumor is achieved by biopsy of mesen-
(e.g. string).
teric lymph nodes, spleen, liver and bone marrow aspi-
ration (if indicated). The tumor rarely metastasizes
out of the abdomen.
Clinical signs
The classical sign is an acute onset of frequent vom-
Other intestinal neoplasia, foreign body, fungal or algal
iting, but intermittent vomiting will occur in some cats
disease, inflammatory bowel disease, and extra-
with foreign bodies that are causing an intermittent or
intestinal causes of anorexia, weight loss and vomiting
incomplete obstruction (e.g. string).
(chronic renal failure, hyperthyroidism, etc.) are all dif-
ferentials that should be considered. There may or may not be palpable abnormalities in the
intestinal tract, and most cats will be clinically normal
otherwise.
Treatment
Surgical resection is the only known treatment.
Surgical margins must be > 5 cm beyond the visible Diagnosis
edge of the lesion because of the cellular invasion that The definitive diagnosis is usually made by contrast
occurs along the tumor mass. radiography, however, survey radiographs or ultra-
Metastasis occurs early in the course of the disease sound examination may also reveal abnormalities that
to the spleen, liver and regional lymph nodes. are consistent with a GI foreign body.
Other forms of therapy (chemotherapy, radiation, etc.) String foreign bodies often are found attached to the
have either been ineffective or not evaluated. base of the tongue, thus a thorough oral exam is
Adjunct therapy with cimetidine, anti-histamines always essential in cats with a suspected GI foreign
and prednisone may be tried to control signs associated body.
with mast cell degranulation, but are often not helpful Some foreign bodies can be found and retrieved by gas-
because these tumors are typically poorly differentiated trointestinal or colonic endoscopy. In many cases,
and do not produce granules or GI ulcer disease. these foreign objects are metallic and will be visible on
Nutritional support (enteral or parenteral nutrition) survey radiographs.
may be required for cats that do not want to eat or are
vomiting.
Gastric parasites, heartworm disease, Helicobacter spp.
Prognosis
gastritis, food intolerance, food allergy, and antral
The prognosis is poor for cats with this disease. pyloric hypertrophy or stenosis are primary differentials
because they all may cause vomiting in the absence of Diagnosis

other signs of disease.
History and physical examination findings will be
suggestive of congestive heart failure, especially if the
Treatment cat has a murmur, gallop rhythm or other signs refer-
Surgical removal of the foreign body is required if it able to primary heart disease.
is not able to be retrieved and removed via an endo- Hematology and serum biochemical profile data
scopic procedure. may reveal mild, non-specific changes, such as ane-
mia of chronic disease, prerenal azotemia, elevations in
liver enzyme activities secondary to congestion, and
CONGESTIVE HEART FAILURE* changes in electrolytes and proteins consistent with
dehydration. If myositis is a differential for the cause of
Classical signs heart failure, elevated creatine kinase values may be
● Coughing or dyspnea. useful additional information.
● Lethargy. Imaging studies are necessary to make a definitive
● Anorexia. diagnosis. In particular, thoracic radiographs will be
● Exercise intolerance. helpful in assessing cardiac size and pulmonary
● Weight loss. involvement (edema vs. pleural effusion, etc.).
Cardiac ultrasound examination is the best diagnos-
See main reference on page 124 for details (The Cat tic test for evaluating cardiac muscle function, size and
With Abnormal Heart Sounds and/or an Enlarged Heart). presence of valvular or other defects.
Electrocardiography may also be useful to detect or
Clinical signs document any arrhythmias.
Classical signs of congestive heart failure include dys-
pnea, coughing, cyanosis, pale mucous membranes,
poor pulse quality, inappetence, exercise intolerance/ SYSTEMIC NEOPLASIA*(GENERALIZED
weakness and lethargy. Cats are usually presented with LYMPHOMA, SYSTEMIC MASTOCYTOSIS)
acute dyspnea and cyanosis.
The signs may be quite variable depending on the Classical signs
cause of heart failure. Valvular disease is often associ- ● Weight loss.
ated with an audible murmur, while heart muscle ● Lethargy or depression.
diseases often are associated with tachycardia, gallop ● Anorexia.
rhythm and weak pulses. ● Enlarged spleen or liver, lymph nodes or
Other signs that may be observed in cats with heart bone marrow involvement.
failure include collapse, vomiting, weight loss, limb
paresis/paralysis due to thromboembolic disease, and
Clinical signs
rarely, abdominal distention.
The most common clinical finding is marked
Other cats may develop pleural effusion that increases
hepatomegaly or splenomegaly along with enlarged
respiratory effort but is not associated with coughing or
lymph nodes (mesenteric).
increased lung sounds (decreased or absent lung sounds
are present). Other common signs are vomiting and anorexia.
Vomiting episodes are typically chronic, but infre- In some cases, peritoneal effusion will be present,
quent and more commonly associated with heart mus- which along with the hepatomegaly or splenomegaly
cle disease (myopathy) rather than valvular disease. will be observed as profound abdominal enlargement.
Diagnosis Diagnosis
Definitive diagnosis is obtained by fine-needle A thorough neurologic examination is the first step in
aspiration of the enlarged liver, spleen or lymph determining if neurologic disease is present and in
nodes. attempting to determine if the disease is affecting the
central, spinal or peripheral nervous system.
Mast cells or lymphoblasts/cytes may also be found in
the systemic circulation on routine hematology, and Other important diagnostic tests for diseases in the
will also be found on examination of bone marrow CNS include CSF analysis, including culture and serol-
aspirates. In addition, anemia and cytopenias are ogy (FIP, toxoplasmosis, fungal disease), computed
also common findings on hematologic exams. tomography or MRI imaging, electroencephalogram, and
brainstem auditory-evoked response (middle/inner ear).
Ultrasound or radiographic evaluation will reveal
the extreme size of the liver and spleen and ultrasound Radiographs of the middle/inner ear areas are non-
guidance can be used in obtaining fine-needle aspirates specific and very difficult to evaluate, and have largely
(especially of lymph nodes or sections of the liver that been replaced by CT as a means of assessing this
have obvious structural abnormalities). region. However, middle and inner ear infections can
also be diagnosed via myringotomy and culture of
fluid from the middle ear.
CNS DISEASES* (ENCEPHALITIS,
Unless a systemic disease process is the cause of the
VESTIBULAR DISEASE, SEIZURE
CNS signs, the minimum data base is likely to be
DISORDERS, NEOPLASIA)
normal.
Classical signs
PHYSALOPTERA
● Neurologic signs localized to the region of
the CNS that is affected (e.g. vestibular Classical signs
disease is associated with loss of balance,
ataxia, falling to one side, head tilt, ● The classical sign is frequent vomiting, but
nystagmus, etc.). intermittent vomiting will occur in some
● Vomiting is infrequent. cats.

Clinical signs With Signs of Acute Vomiting).
The predominant clinical signs will be neurologic

signs that are localized to the region of the CNS that Clinical signs
is affected. Vestibular disease can be associated with The predominant clinical sign is vomiting. Most cats
vomiting, but typical signs include loss of balance, will present with an acute onset of vomiting, but others
ataxia, falling to one side, head tilt and nystagmus. may have intermittent, chronic vomiting.
Most neurologic diseases that cause vomiting affect
the CNS, not the spinal cord or peripheral nervous sys-
Diagnosis
tem, except for the peripheral parts of cranial nerve
VIII located in the inner ear. Fecal floatation and finding of the larvated eggs in the
feces (shedding is intermittent, so multiple feces are
Vomiting is an infrequent but still important sign of
required) is diagnostic, but unrewarding.
CNS disturbance most often associated with involve-
ment of the peripheral vestibular system. Finding of small worms in vomitus or on endoscopic
examination.
Cats with signs of hepatoencephalopathy (changes in
behavior, stupor, drooling or ataxia) may vomit from Response to a therapeutic trial with fenbendazole
the effects on the CNS or the GIT. (25 mg/kg PO q 24 h for 3–5 days).
Ultrasound can also be used to identify worms in the

HEARTWORM DISEASE (DIROFILARIA
main pulmonary artery or right ventricle, but the sensitiv-
IMMITIS)
ity of this test is highly dependent on operator experience.
Classical signs A heartworm antibody test is the recommended
screening test for cats, and while it does not confirm
● Signs are variable.
infection, it is an accurate means of confirming expo-
● No signs may be present.
sure. However, it may remain positive for 18 months
● Signs of respiratory disease (tachypnea,
or more after resolution of infection, and also may
dyspnea).
be positive if arrested larval infection has occurred.
● Intermittent vomiting.
● Signs of cardiovascular disease (lethargy, Because cats generally have only 1–2 worms present, the
anorexia, coughing, weakness). standard heartworm antigen tests used in dogs are
● Sudden death. often not sensitive enough to detect the disease in cats.
A feline antigen test has been developed, and detects
the presence of a single male worm, but false-negative
tests still occur. Antigen tests should not be the sole
means of evaluating cats for heartworm infection.
Clinical signs
Anorexia and weight loss are the most common signs
observed in cats with dirofilariasis. HYPOADRENOCORTICISM (ADDISON’S
DISEASE)
Respiratory signs such as wheezing, dyspnea, and
occasionally coughing are less common than in dogs,
Classical signs
and often mimic feline asthma.
● Lethargy, anorexia and weight loss are
Intermittent vomiting is a relatively frequent sign
most common.
associated with feline heartworm disease that may
● Vomiting.
occur in the absence of other clinical signs.
● Polyuria, polydipsia.
Sudden death is a complication of heartworm disease in ● Clinical signs may wax and wane.
cats, and may occur in 20–30% of infected cats.
Diagnosis
Clinical signs
A history of living in a heartworm endemic area
This is a very rare disease in cats.
along with the appropriate clinical signs in the
absence of heartworm preventative use should arouse The classical signs are lethargy, anorexia and weight
clinical suspicion. loss. Other signs that may be seen are vomiting,
polyuria/polydipsia, weakness and waxing/waning signs.
Hematology may reveal an eosinophilia or basophilia.
Most cats (> 50%) will be hypothermic, dehydrated
Unless cats have developed heart failure, the chemistry
or depressed on physical examination, but other signs
profile and urinalysis are usually normal. Cats that are
such as weak pulses, bradycardia and collapse are less
in right congestive heart failure may have elevated liver
common.
enyzme activities or azotemia.
Radiographs of the thorax will reveal the classic
Diagnosis
changes associated with heartworm disease, which
are enlarged pulmonary arteries, arterial tortuosity or The history and clinical signs will be vague in early
blunting, pulmonary interstitial pattern and right-sided cases, so that a degree of clinical suspicion is required
cardiac enlargement. to make the diagnosis.
Anemia, lymphocytosis and eosinophilia are rela- To differentiate pituitary or hypothalamic disease
tively uncommon (< 20%) findings in cats. from exogenous drug administration as the cause of
secondary hypoadrenocorticism, plasma ACTH con-
Serum biochemistries and urinalysis show hypona-
centration is measured.
tremia, azotemia (pre-renal or renal), and hyper-
phosphatemia in the majority of cats. Hyperkalemia
and hypochloridemia are also common, but not seen in INTUSSUSCEPTION
every case.
Classical signs
Other less common (< 30% cases reported) abnormali-
ties include metabolic acidosis, increased liver enzyme ● The classical sign is an acute onset of
activities, hypercalcemia and hyperbilirubinemia. frequent vomiting.
● Intermittent vomiting will occur in some
Slightly more than 50% of affected cats will have an
cats.
unconcentrated urine sample (SG < 1.030), support-
ing renal azotemia.
The definitive diagnostic test for hypoadrenocorticism
is an ACTH stimulation test, which will reveal a low
Clinical signs
resting cortisol concentration, and no response (no
increase in cortisol levels) following administration of An acute onset of vomiting, abdominal pain or
ACTH (Cosyntropin 0.125 mg/cat, IM), at either the 30 anorexia is the most common sign. However, in some
or 60 min post-administration sampling times. cats with sliding, intermittent or incomplete intus-
Administration of steroids by any route (oral, parenteral susception, the signs may be intermittent. Weight loss
or topically) or progestins (e.g. megestrol acetate) will and vomiting will be more prevalent in these cats.
suppress cortisol response to ACTH. This suppression
may persist for weeks after the last time of administra-
Diagnosis
tion, especially if administration was chronic.
A palpable abdominal mass may help direct the diag-
Radiographic changes include microcardia and
nostic approach if it is present.
hypoperfusion of the lungs due to hypovolemia. ECG
changes classically observed in dogs, such as peaked Contrast radiographs or ultrasound examination of
T waves, reduced or absent P waves, or atrial standstill the GI tract are the most definitive means of making the
are not seen in cats. diagnosis.
If serum electrolyte concentrations are normal, but a Intussusception rarely presents as a chronic prob-
subnormal response to ACTH administration is lem, so in these cases, abnormalities associated with
observed, the cat may have: (1) residual mineralocorti- chronic GI dysfunction (e.g. hypoproteinemia, hypoal-
coid secretion; (2) secondary hypoadrenocorticism buminemia) may be present.
from pituitary or hypothalamic disease causing only
glucocorticoid deficiency but this has not yet been
LEAD POISONING
reported in cats; or (3) secondary hypoadrenocorti-
cism due to exogenous administration of glucocorti-
Classical signs
coids or progestogens. Although this is the most
common cause of secondary hypoadrenocorticism and ● Gastrointestinal signs include anorexia,
suppressed adrenal response to ACTH, it rarely causes vomiting, diarrhea and abdominal pain.
sufficient lethargy for veterinary attention to be sought. ● Neurologic signs include aggression,
If clinical signs consistent with hypoadrenocorticism nervousness, tremors, seizures, blindness
are present in a cat with a suppressed ACTH stimula- and dementia.
tion test secondary to steroid administration, the signs
are most likely caused by another disease. See main reference on page 596 for details.
Clinical signs If the cat is debilitated and anorectic, nutritional sup-

port may also have to be instituted.
Gastrointestinal signs include anorexia, vomiting,
diarrhea and abdominal pain. Weight loss is common.
Neurologic signs include aggression, nervousness, OTHER INTESTINAL NEOPLASIA
tremors, seizures, blindness and dementia. (FIBROSARCOMA, CARCINOIDS,
GI signs tend to occur acutely and before neurologic PLASMACYTOMA, LEIOMYOSARCOMA,
signs. CNS signs are associated with severe toxicity or ETC.)
chronicity.
Classical signs
Diagnosis ● Weight loss.
There may be a history of exposure to lead-containing ● Anorexia.
materials in the environment (paints, roofing materials, ● Vomiting and/or diarrhea.
batteries, used motor oil, lead shot, etc.).
Characteristic clinical signs (the combination of gas-
trointestinal and neurologic signs) are suggestive. Clinical signs
There are typical hemogram changes including The clinical signs observed will depend upon the
basophilic stippling of RBCs, and increased numbers of tumor location in the GI tract.
nucleated RBCs, although these are not as common in
the cat as in the dog. In cats, anorexia, weight loss and lethargy are the
most common clinical signs of any gastrointestinal
Radiographs may reveal radiopaque material in the GIT. neoplastic disease.
The definitive diagnosis is made by measurement of a Vomiting and/or diarrhea may be observed, but will
blood lead level (> 0.5 ppm is diagnostic). be variable depending on whether the tumor is in the
small intestine or colon, and whether it is diffuse or
Treatment solitary in extent.
Gastric lavage or induction of emesis should be per-

formed to remove the offending materials from the
stomach, if ingestion was recent. If the material can be Diagnosis
retrieved by endoscopy or surgical removal (e.g. it is a
Palpation of an intestinal mass is an important diag-
large object) it should be done.
nostic tool, since many of these tumors are solitary and
Oral activated charcoal should be administered to produce strictures or obstructions.
reduce the absorption of the material from the GIT.
Hematology and serum biochemistry profiles may
An IV catheter should be placed and supportive fluid be within normal limits in cats with intestinal neopla-
therapy (Normosol or LRS, 40–60 ml/kg IV) should sia.
be commenced.
Abnormalities associated with secondary effects of the
Calcium EDTA to chelate lead and hasten excretion tumor include dehydration, electrolyte imbalances,
can also be used (25 mg/kg q 6 h IV as 10 mg Ca anemia of chronic disease, etc.
EDTA/ml in dextrose, maximum 2–5 days).
Radiographs of both the thorax and abdomen are an
If seizures or other severe neurologic signs are present, important, but sometimes non-diagnostic, tool.
appropriate seizure control (e.g. IV valium 2.5–5 mg Radiographs are best for assessment of pulmonary
or phenobarbital 1–4 mg/kg IM) should be used. metastasis.
Ultrasound is an invaluable tool for lesion local- Acquired pyloric hypertrophy has a more variable
ization, determination of lesion extent and in some presentation, but is usually associated with intermit-
cases, obtaining a fine-needle aspirate or biopsy of tent vomiting of digested food several hours after
the lesion. consumption. If the pylorus is completely obstructed
the vomiting may be projectile.
Definitive diagnosis is by histopathologic evaluation
of a biopsy or tissue obtained after surgical resection. Chronic intermittent vomiting and gastric distention
may lead to gastroesophageal reflux or esophagitis
which may be associated with regurgitation or inap-
ANTRAL PYLORIC
petence and weight loss.
HYPERTROPHY/STENOSIS
Classical signs
Diagnosis
● Vomiting several hours after eating.
History and signalment will be suggestive of a gastric
● Projectile vomiting will be observed if the
emptying disturbance.
pylorus is obstructed.
● Abdominal distention or pain may be Hemogram, serum chemistries and urinalysis are
observed due to gastric distention. typically unremarkable.
Survey radiographs of the abdomen may be normal,
Pathogenesis show gastric distention, or pyloric abnormalities.
Contrast radiographs may identify hypertrophic gas-
Antral pyloric hypertrophy is a condition that involves
tric mucosa or a narrow gastric outflow pathway (“beak
hyperplasia of the pyloric musculature, pyloric
sign”).
mucosa or both, which results in narrowing or com-
plete obstruction of the gastric outflow tract. Ultrasonography may detect a thickened pyloric
antrum if it is present.
The condition can be congenital or acquired, but in
either case, the exact cause is unknown. Fluoroscopy or scintigraphy can be used to evaluate
gastric peristalsis and emptying, but are not univer-
Both neural dysfunction and endocrinopathies
sally available.
(hypergastrinemia) have been proposed to be involved
in the disease. Gastric endoscopy may be normal or may reveal
thickened folds of mucosa, the pyloric antrum may not
The obstruction of gastric outflow results in gastric
insufflate normally, or the pylorus may be too stenotic
retention and subsequent gastric distention. Gastric
to allow passage of the endoscope through the orifice.
distention stimulates gastrin secretion which is
trophic to antral tissues and may further contribute to Definitive diagnosis requires an exploratory laparo-
mucosal hypertrophy. tomy and histopathologic examination of tissue for
antral pyloric hypertrophy, but motility disturbances
In some cases of congenital pyloric stenosis there is
can only be diagnosed via fluoroscopy/scintigraphy,
no antral hypertrophy. The gastric retention is believed
and hypergastrinemia can be detected by measurement
to be due to a motility disturbance that results in a
of serum gastrin levels.
functional obstruction.
For reasons that are yet unknown, the disorder has been
observed primarily in Siamese cats. Differential diagnosis
Neoplasia (gastric adenocarcinoma, leiomyosarcoma,
lymphosarcoma) of the gastric, pancreatic or duodenal
Clinical signs
tissues resulting in pyloric thickening and obstruction
Vomiting is the most common sign. should be considered, especially in older cats.
In congenital pyloric stenosis, kittens begin to vomit Neoplasia of surrounding tissues resulting in gastric out-
shortly after they commence solid food. flow obstruction from an external source, or a gastric
foreign body resulting in obstruction or decreased out- Clinical signs

flow may also result in similar clinical signs.
Lethargy and anorexia are present in almost all cats
Gastric ulcer disease may result in chronic vomiting and usually develop over a 48-hour period.
and abnormal motility.
The classical signs are associated with the dysfunction
Extra-gastrointestinal causes of vomiting include of both sympathetic and parasympathetic nervous
hepatic, renal, metabolic, inflammatory (pancreatitis) system. Ocular signs include dilated pupils, decreased
or endocrine causes. or absent pupillary light reflex and protruding nictitans,
but have normal vision.
Treatment
Gastrointestinal signs are present in about 95% of
Definitive treatment for pyloric antral hypertrophy/steno- cats and include constipation, regurgitation (secondary
sis is surgical correction of the outflow obstruction. to megaesophagus) and dry mouth. Vomiting may
In cats with motility disturbances, gastric prokinetic occur or regurgitation may be reported as vomiting.
therapy (metoclopramide 0.1–0.2 mg/kg PO q 12 h, or Less commonly observed signs are bradycardia, hypoten-
cisapride 5 mg/cat PO q 8–12 h) may improve move- sion, urinary incontinence or a distended, easily com-
ment of ingesta and reduce clinical signs. pressed bladder, proprioceptive deficits and transient
However, in early cases, medical management with feed- syncopal episodes.
ing of small meals consisting of highly digestible foods
(low residue, low fat, low fiber) may also be helpful. Diagnosis
Following surgical correction of the outflow obstruc- There is no definitive, antemortem diagnostic test for
tion, some animals will still require medical therapy dysautonomia.
with gastric prokinetics because of residual motility
disturbances. Diagnosis is made by using the clinical presentation
along with radiographic evidence of megaesophagus
Prognosis and its associated complications, and use of pharma-
cologic testing to evaluate the function of the sympa-
The prognosis is guarded to good with surgical man- thetic and parasympathetic nervous system.
agement, as some animals may still require life-long
medical management following surgery to control the Direct-acting parasympathomimetic and sympath-
clinical signs. omimetics produce an effect in diseased cats but not
in normal cats because of post-ganglionic denervation
Cats that develop esophagitis due to reflux disease may hypersensitivity in affected cats. Indirect (pregan-
have a more guarded prognosis because of the problems glionic) acting agents produce an ocular effect in nor-
associated with esophagitis (stricture development). mal cats but not diseased cats.
Ocular testing with sympathomimetic agents, e.g. 1%
DYSAUTONOMIA hydroxyamphetamine (indirect acting) produces no
mydriasis, and 1% phenylephrine (direct acting) pro-
Classical signs duces rapid mydriasis in affected cats.
● Depression and anorexia. Ocular testing with parasympathomimetic agents, e.g.
● Mydriasis, reduced pupillary light reflex, 0.5% physostigmine (indirect acting) produces no mio-
protruding nictitans, normal vision. sis, and 0.1% pilocarpine (direct acting) produces rapid
● Xerostomia (dry mouth and mucous miosis in affected cats.
membranes) and keratoconjunctivitis sicca.
● Retching, regurgitation or vomiting. Systemic testing using 0.04 mg/kg atropine, subcuta-
● Fecal incontinence or constipation. neously, will increase the heart rate if the sympathetic
nervous system is normal. Note: Do not use ephedrine,
See main reference on page 792 for details (The Con- epinephrine or other sympathomimetics, because fatal
stipated or Straining Cat). arrhythmias can be induced.
Failure to demonstrate a wheal and flare response fol- Diagnosis

lowing intradermal injection of histamine (1:1000)
indicates a defect in the sympathetic innervation of The gastritis and gastric ulcer disease are diagnosed by
cutaneous blood vessels. endoscopy and histologic examination of the stom-
ach and duodenum.
GASTRINOMA However, to make a definitive diagnosis of

Zollinger–Ellison syndrome, a serum gastrin level
Classical signs must be obtained along with the finding of a discrete
tumor on the pancreatic islets. Very high levels of
● Chronic vomiting unresponsive to routine serum gastrin are obtained in cats with gastrinoma.
therapy for gastritis and gastric ulcer
disease.
These are rare tumors of the GI tract, so even finding
Pathogenesis elevated serum gastrin levels is not sufficient, since
Chronic gastritis and gastric ulcer disease are pro- there are other causes for elevations in serum gastrin
duced secondary to a gastrin-secreting tumor that levels (e.g. chronic renal failure, etc.).
arises from the pancreatic islet cells (called Other causes of chronic gastritis, including Helicobacter
Zollinger–Ellison syndrome). spp., liver disease and pancreatitis should be explored.
This is a rare disease that has only been described in
three older cats. Treatment
The pancreatic tumor may occur as a solitary lesion, or Surgical removal of the tumor, if possible, is the treat-
there may be multiple lesions on the liver due to metas- ment of choice. Management of the gastritis and gastric
tasis. ulcer disease is as for other primary causes of this prob-
lem (see section on gastritis for details, page 680).
Clinical signs
Typical signs include chronic vomiting, weight loss
and anorexia in a cat previously diagnosed with gas-
tritis or gastric ulcers on histopathologic examination
of the stomach, but unresponsive to routine therapy.
RECOMMENDED READING
August JR. Consultations in Feline Internal Medicine, 2001.
Rosser J. In: August J (ed) Food Hypersensitivity: New Recommendations for Diagnosis and Management. WB
Saunders Company, Consultations in Feline Internal Medicine, 1997, pp. 209–214.
Guilford WG, Jones BR, Markwell PR, et al. Food sensitivity in cats with chronic idiopathic gastrointestinal
problems. J Vet Intern Med 2001; 15: 7–13.
Kirk’s Current Veterinary Therapy XIII, 2000.
Krecic MR. Comp. Cont. Ed., 2003; 23 (11): pp. 951–973.
32. The cat with signs of acute small
bowel diarrhea
Debra L Zoran
KEY SIGNS
● Loose to watery feces.
● ± Melena.
● No mucus or fresh blood.
● < 3 weeks duration.
MECHANISM?
● There are four recognized pathophysiologic mechanisms of diarrhea include osmotic, secre-
tory, increased permeability and altered motility.
Small bowel diarrhea is characterized by:
● Increased volume of feces.
● Normal to increased frequency of defecation.
● No straining or tenesmus associated with defecation.
● If blood is present in feces it occurs as melena.
● Increased mucus is not present in the feces.
● Weight loss and vomiting are commonly observed concurrently.
WHERE?
● Small intestinal tract (duodenum, jejunum and ileum).
WHAT?
● Mild, acute small bowel diarrhea is a common problem that may be caused by a variety of self-
limiting factors, including dietary, infectious, parasitic or toxic agents. However, severe small
bowel diarrhea may be life-threatening and associated with severe systemic or GI disease.
Some diseases typically produce chronic diarrhea, but in the early stages are perceived as pro-
ducing acute diarrhea.
697

Diseases causing signs of acute small bowel diarrhea
MECHANICAL
● Foreign bodies* (p 713)
Diarrhea commonly occurs either due to motility disturbances or irritating effects of the foreign
object that may cause increased secretion.
● Intussusception* (p 712)
Acute onset of diarrhea may occur due to alterations in gut motility, however, vomiting is a more
prominent clinical sign.
● Motility disturbances
Primary motility disturbances are rare, but secondary causes of abnormal GI motility such as post-
operative ileus, post-obstructive disease or metabolic or endocrine causes of ileus are more impor-
tant causes of diarrhea.
● Short bowel syndrome (p 730)
Spontaneous short bowel syndrome occurs acutely with intussusception, bowel strangulation and
intestinal volvulus. Iatrogenic syndrome associated with resection of 75–90% of the small intestine
results in severe diarrhea and weight loss. Congenital forms of short bowel syndrome are reported,
but are rare.
METABOLIC
● Hyperthyroidism* (p 711)
Intermittent diarrhea, vomiting or voluminous stools in an older cat with a good to ravenous
appetite, obvious weight loss and poorly groomed coat are characteristic of this disease.
● Inflammatory hepatobiliary disease (cholangitis)* (p 710)
The clinical presentation of cholangitis is non-specific: anorexia, lethargy, weight loss, vomiting,
diarrhea, dehydration, hepatomegaly and icterus. The disease primarily affects male cats greater
than 4 years of age.
● Shock (hypovolemic, septic, endotoxic)* (p 722)
Acute diarrhea occurs secondary to gastrointestinal ischemia from severe hypovolemia or sepsis
and may contribute to patient morbidity.
● Exocrine pancreatic insufficiency (p 730)
A rare disease in cats, but is typically associated with small bowel diarrhea, weight loss and a rav-
enous appetite. Diarrhea is typically chronic but may be perceived as acute onset.
NUTRITIONAL
● Food intolerance*** (p 704)
Indiscretion is associated with an acute onset of diarrhea due to overeating, eating too quickly or
ingesting a foreign substance (food or non-food). Intolerance presents with intermittent diarrhea or
vomiting, with no pattern or association with eating, and resolves when the food source is changed
to omit offending substance from diet.
● Food allergy (dietary hypersensitivity)* (p 709)
Vomiting appears to be more common than diarrhea in cats with food allergy, but it is more likely
to occur when the disturbance affects more distal aspects of the GI tract.
32 – THE CAT WITH SIGNS OF ACUTE SMALL BOWEL DIARRHEA 699
NEOPLASTIC
● Tumors of the small intestine* (p 715)
The most common tumor of the feline digestive system is alimentary lymphoma. Other tumors that
occur in the small intestine are adenocarcinomas (second), and mast cell tumors (third), with
fibrosarcomas, leiomyosarcomas and carcinoids occurring rarely. With the exception of lymphoma,
which can occur at any age, most tumors occur in old cats. The clinical signs most often observed
are anorexia and weight loss, with vomiting or diarrhea less common. The diarrhea is often chronic,
but the onset may be acute.
IMMUNOLOGIC
● Idiopathic inflammatory bowel disease (IBD) (p 714)
Generally considered to be a disorder associated with chronic, intermittent vomiting, diarrhea or
weight loss, but acute exacerbations of diarrhea may occur. IBD is described primarily by the pre-
dominant inflammatory cell type infiltrating the mucosa. Lymphocytic plasmacytic enteritis is the
most common form of IBD, but eosinophilic and suppurative forms of the disease occur as well.
INFECTIOUS
● Coccidiosis (isosporosis, cryptosporidiosis, toxoplasmosis)** (p 705)
Infections that result in mild to moderate diarrhea are most common in neonates and immunosup-
pressed adults. Most adults have asymptomatic infestations. The species of coccidia most com-
monly associated with disease in cats are Isospora spp., Cryptospordium parvum and occasionally
Toxoplasma gondii.
● Giardiasis** (p 707)
Acute or chronic small bowel diarrhea is the most common clinical presentation, however in some
cats large bowel diarrhea also may occur.
● Nematode parasites (roundworms, hookworms)* (p 717)
Common signs occurring in kittens with roundworms (Toxocara cati, Toxascaris leonina) include
unthriftiness, diarrhea and pot-bellied appearance, however, vomiting may also occur.
● Salmonellosis* (p 719)
Diarrhea, weight loss and systemic illness are primarily problems in young or debilitated cats, as
most cats are asymptomatic carriers. The disease is most important clinically in young kittens or
geriatric cats that develop septicemia due to Salmonella spp., and may die acutely. Salmonellosis is
a zoonotic disease.
● Clostridium perfringens enterocolitis* (p 721)
Diarrhea occurs due to sporulation of clostridial organisms and release of enterotoxin resulting in a
secretory diarrhea that is usually small bowel in character, but can also have a large bowel component.
● Feline coronavirus infections (feline enteric coronavirus/feline infectious
peritonitis* (p 718)
Feline enteric coronavirus causes mild, transient diarrhea in young kittens, and is the source of
feline infectious peritonitis virus (FIPV). Systemic infectious disease by FIPV is characterized by
vasculitis and granulomatous lesions in affected organs. Since FIPV rarely affects the GI tract sin-
gularly, vomiting is often associated with the disease effects on the liver, kidneys or other organs.
Rarely FIPV causes intestinal granulomas that obstruct the GI tract and cause vomiting or diarrhea
that is usually chronic, but may have an acute onset.
continued
continued
● Feline panleukopenia virus (p 722)

Infectious viral enteritis of young cats that is often fatal in unvaccinated populations. Typically,
there is a sudden onset of depression and anorexia. Vomiting is followed by diarrhea, varying from
mild to severe. Panleukopenia may result in systemic septicemia and rapid death. A relatively rare
problem in vaccinated cats due to the vaccine efficacy.
● Peritonitis (p 729)
Abdominal pain, distention, fever, decreased appetite and lethargy are the most common present-
ing signs. Vomiting or diarrhea may occur, but is not a consistent problem.
● Feline leukemia virus (p 725)
Systemic retroviral disease associated with neoplasia and bone marrow disease in cats. Diarrhea
occurs most commonly secondary to development of GI lymphoma.
● Feline immunodeficiency virus (p 726)
Diarrhea is not a common presenting sign of cats with FIV, but diarrhea can occur secondary to
the immunodeficiency disease or result from a purulent form of colitis that can occur in a small
number of cats that are infected with FIV.
● Campylobacteriosis (p 726)
An uncommon cause of diarrhea in cats, but will cause mucoid, bloody diarrhea, weight loss,
anorexia and fever in affected kittens or young cats. Most affected cats are from shelters or catter-
ies that have crowded conditions and poor hygiene. In adult cats, the disease is usually self-limit-
ing, but it is an important zoonosis.
● Bacillus piliformis (Tyzzer’s disease) (p 732)
Produces clinical signs that are identical to panleukopenia.
IDIOPATHIC
● Acute gastroenteritis*** (p 702)

This acute, mild small bowel diarrhea may be caused by a number of dietary, bacterial, parasitic or
toxic agents that are usually self-limiting.
Rare disorder that is associated with eosinophilic IBD and systemic eosinophilia (increased circu-
lating eosinophils and increased eosinophils in lymph nodes, etc.). It is usually associated with
chronic vomiting, diarrhea and weight loss, and is poorly responsive to treatment.
● Idiopathic juvenile diarrhea (p 727)
This is a condition of kittens and young cats less than one year of age. It causes chronic small
bowel diarrhea, which is self-limiting once the kitten reaches adulthood.
Toxic:
● Pharmacologic (antibiotic-induced diarrhea)** (p 705)
Acute onset of diarrhea or vomiting after initiating antibiotic therapy. Antibiotics often associated
with inducing diarrhea: ampicillin, cephalosporins, clindamycin, metronidazole, tetracycline, etc.
● Pyrethrins/pyrethroids/permethrins/organophosphates* (p 718)
Vomiting, diarrhea, hypersalivation, contact dermatitis, ataxia, excitation, seizures and dyspnea are
all reported signs of toxicity to these insecticides.
● Heavy metals (lead, arsenic) (p 724)

The two most common heavy metal intoxications are ingestion of lead and arsenic. Both cause
severe GI signs: vomiting, diarrhea, anorexia, and depression, but lead poisoning will progress to
neurologic signs (e.g. ataxia, tremors and seizures), while arsenic is nephrotoxic and hepatotoxic.
● Plant ingestion/toxicity (p 728)
Plants may irritate mucous membranes and cause acute drooling, vomiting or diarrhea. Plant tox-
ins that result in renal or hepatic failure may cause more severe and prolonged vomiting, diarrhea,
depression and anorexia.
Increased secretion of water and electrolytes is

INTRODUCTION another cause of diarrhea which occurs primarily as
a result of activation of cellular second messenger path-
ways (cAMP, cGMP, etc). The causes of secretory
MECHANISM? diarrhea in cats include Salmonella, Clostridium,
Acute small intestinal diarrhea is a common clinical Campylobacter, E. coli, and Staphylococcus. Diarrhea
problem that is often mild or self-limiting. due to hyperthryoidism may also be due to a secretory
mechanism, but this is unproven.
In general, small bowel diarrhea tends to be milder in
cats than in dogs because of the capacity of the feline The presence of increased intestinal permeability
GI tract to absorb water. due to inflammation, erosion/ulceration or necrosis
is also an important cause of diarrhea. A major cause of
Some diseases which typically produce chronic diar-
increased permeability diarrhea in cats is IBD, but
rhea may present as acute diarrhea.
lymphoma or other causes of intestinal inflammation,
In some cats, life-threatening illness develops due to such as the enteroinvasive bacteria (e.g. E. coli) can
the severity of fluid loss or as a result of the primary also cause diarrhea by this mechanism.
problem causing the small bowel diarrhea (endotoxe-
Altered intestinal motility, either increased or
mia, neoplasia, etc.).
decreased segmentation or propulsion movements will
There are many different causes of diarrhea, which lit- cause diarrhea. While it is difficult to prove that altered
erally is the presence of increased water in the feces. motility is the primary cause of diarrhea in many cases,
it may occur in hyperthyroidism, dysautonomia, some
The increase in fecal water may be due to a physical,
infectious enteropathies and in GI neoplasia.
functional or physiologic disturbance in the small intes-
tine, the colon, or both. The main consequences of acute small bowel diar-
rhea are dehydration and development of metabolic
Characteristics of small bowel diarrhea include:
acidosis as a result of fluid and electrolyte losses.
● A large volume of watery or very soft feces.
● No mucus or hematochezia, if blood is present it Infectious and parasitic causes of small intestinal
occurs as melena. diarrhea may be either self-limiting or severe, depend-
● There is little or no straining or tenesmus. ing on the pathogenicity of the organism.
● Weight loss and vomiting are commonly observed.
Inflammatory bowel disease, neoplasia and other more
● The frequency of defecation is normal to increased.
severe diseases that cause small bowel diarrhea are often
Diarrhea may be due to increased osmotically active associated with other signs of systemic or GI disease,
substances present in the lumen. The most common such as weight loss, anorexia, vomiting or depression.
causes of this type of diarrhea are dietary
overload/indiscretion and malabsorption, which can
WHERE?
be due to deficiency of pancreatic (e.g. EPI) or intestinal
brush border enzymes, or upper small bowel diseases Small bowel diarrhea can be the result of disease in the
(e.g. mucosal or intramural), such as IBD or lymphoma. small intestine (duodenum, jejunum, ileum) or occur
secondary to systemic illness (peritonitis, septicemia), Pathogenesis

organ failure (hepatic, renal or pancreatic disease) or
other miscellaneous causes such as hyperthyroidism. Mild, acute small bowel diarrhea is a common pre-
senting complaint, and may be caused by a variety of
A careful history and physical examination will deter- self-limiting disturbances, including dietary, parasitic,
mine whether the problem is likely related to the GI infectious or toxic agents.
tract or a systemic problem.
Small bowel diarrhea can be caused by osmotic
In otherwise healthy cats with acute diarrhea that is (increased unabsorbed substances present in the lumen,
likely due to dietary indiscretion, mild infectious enteri- such as occurs in overeating or malabsorption), secre-
tis or exposure to a self-limiting toxin, a minimal diag- tory (increased secretion of ions and water into the
nostic approach is needed. lumen, which is mediated by second messengers such as
In cats that are dehydrated, clinically depressed, cAMP or cGMP and often stimulated by bacterial or
anorectic or vomiting, a more aggressive approach that viral agents), increased permeability (increased intes-
includes a hemogram, chemistry profile, fecal analy- tinal permeability occurs from diseases that cause
sis, and radiographs or ultrasound is indicated. increased inflammation, erosion, ulceration or necrosis),
and altered intestinal motility (increased or decreased
WHAT? intestinal motility can result in diarrhea, especially
when it affects segmentation contractions in the colon).
The most common causes of mild, self-limiting small
bowel diarrhea include food intolerance or dietary Cats with self-limiting gastroenteritis require minimal
indiscretion, and some infectious or parasitic agents. diagnostic testing and will respond to symptomatic
treatment.
Cats with small bowel diarrhea of a more serious nature
often have systemic illness/organ failure (e.g. hepatitis, Certain strains of E. coli may behave as gastrointestinal
renal failure, or pancreatic disease such as pancreatitis), or pathogens. Very little is known about diarrheagenic
severe intestinal disease such as neoplasia or inflamma- E. coli in cats and further epidemiological investigations
tory bowel disease, which must be carefully evaluated. on this subject are needed. One recent study showed no
difference in the strains of E. coli isolated from a group
Diagnosis is based upon history and physical examination of cats with diarrhea and a control group of cats that did
findings, radiography, hematology and serum chemistry not have diarrhea.
profiles, serology if indicated for FeLV/FIV, serum TLI,
fecal analysis, fecal cytology or alpha-1 protease inhibitor
testing, serum cobalamin/folate assays and histopathology. Clinical signs
Acute onset of vomiting, diarrhea, anorexia or
DISEASES CAUSING SIGNS OF lethargy in an otherwise healthy cat.
ACUTE SMALL BOWEL DIARRHEA Dehydration may occur if the signs are severe.
(<3 WEEKS DURATION)
Rarely associated with hematemesis, hematochezia or
melena.
ACUTE GASTROENTERITIS***

● Vomiting, anorexia or reduced appetite are Acute idiopathic gastroenteritis is a pathological
common. description and not a diagnosis. One of the many eti-
● Acute gastroenteritis is more common in ologies listed in this chapter is the likely cause.
young cats or kittens, but can occur in any However in cats that are otherwise healthy, but have
age, breed or sex. mild signs of gastroenteritis and no clinical evidence of
● Mild to severe small bowel diarrhea may dehydration, an extensive diagnostic work-up is rarely
also be observed. indicated or performed so the cause of the signs
remains unknown.
A PCV, TP and fecal examination are simple, inex- Deficits should be replaced over 4–6 hours or more,
pensive tests that should be used in cats that seem and ongoing losses estimated and additional fluid
lethargic or dehydrated. amounts added to the maintenance fluid rate calculated.
In cats with more persistent or severe clinical signs, Potassium supplementation of intravenous fluids
a dietary change, more extensive fecal analysis (zinc should be initiated once the cat is rehydrated and
sulfate flotations, culture or cytology) and additional should be monitored and adjusted based upon serum
evaluation of the hemogram or chemistry profile is potassium levels.
indicated.
Antimicrobial therapy is not routinely indicated for
treatment of acute, mild forms of gastroenteritis.
The choice of antibiotic should be based on the sus-
Food intolerance (ingestion of substances that cause pected or known causative organism (Campylobacter,
an adverse response that is not immunologically medi- Clostridium spp., etc.).
ated, e.g. not food allergy) or dietary indiscretion
Cats with severe mucosal injury as evidenced by blood
(ingestion of foreign or usual foods or non-food sub-
loss or hypoproteinemia have the potential to develop
stances that cause GI disturbance) is a common cause
septicemia, or signs of systemic sepsis (fever, depres-
of acute gastroenteritis.
sion, leukocytosis, hypoglycemia, etc.). These cats
Bacterial or viral infections of the GI tract may be should receive broad-spectrum, parenteral antibiotics
mild and self-limiting, or severe and life-threatening, so effective against enteral pathogens (e.g. either alone or in
the clinical presentation must be carefully evaluated. combination: ampicillin, enrofloxacin, trimethoprim-
sulfadimethoxine, metronidazole or cephalexin).
Other causes of acute, mild gastroenteritis are inges-
tion of toxic substances (plant material, oil or other The most effective motility-modifying drugs for treat-
materials attached to hair coat, etc.). ment of diarrhea are the opioids (loperamide 0.08–0.16
mg/kg q 12 h or diphenoxylate 0.05–0.1 mg/kg q 12 h).
Opioids should be used with care in cats because safe,
Treatment effective dosages have not been established.
Fluid therapy is indicated if there are clinical signs of Anticholinergic drugs have no useful role in the
dehydration, or if the cat is unable to drink. symptomatic treatment of diarrhea in cats with gas-
troenteritis, because they reduce both peristaltic and
Balanced isotonic replacement electrolyte solutions
segmental intestinal motility contractions.
are the best fluid choices for cats with mild to moder-
ate metabolic acidosis and dehydration secondary to Intestinal protectants and absorbent agents (kaolin,
acute diarrhea. pectin, activated charcoal, barium, bismuth subsalicy-
late) may or may not be clinically effective, but are not
Fluids may be given subcutaneously in cats that are
harmful and are likely most beneficial when used in
only mildly dehydrated.
acute, non-specific enteritis.
In cats with severe dehydration or who are intolerant of
Bismuth subsalicylate, 0.25 ml/kg q 4–6 h, has been
subcutaneous fluid administration, intravenous replace-
shown to be most effective in acute small-intestinal
ment of fluid deficits is necessary.
diarrhea, but should be used cautiously in cats to
Oral rehydration therapy is effective in patients that decrease the possibility of salicylate toxicity.
are mildly dehydrated and can ingest oral fluids.
If vomiting is a concurrent problem, anti-emetic ther-
The maintenance rate for fluid therapy is 40–60 apy should also be initiated. Metoclopramide, 0.2–0.5
ml/kg/day, and replacement of fluid deficits is calcu- mg/kg q 6–8 h, or prochlorperazine, 0.1–0.5 mg/kg q 8 h,
lated by: are two commonly used anti-emetics. Anti-emetic
therapy should not be used if a gastric outflow
BW (kg) ¥ % dehydration = fluid deficit (liters) obstruction is suspected.
Withhold food for 24–48 hours in cats with acute opment of food intolerance, as it is this tissue that
small bowel diarrhea, and only offer water or oral iso- is responsible for promoting tolerance and hyporespon-
tonic glucose, amino acid and electrolyte solutions. siveness to harmless dietary antigens.
Because most diarrheas in cats are osmotic rather Intolerance may develop as a result of abnormal
than secretory, feeding through an acute diarrhea will mucosal barrier function, disturbances in immuno-
worsen the signs and may exacerbate the condition. regulation (decreased tolerance) or simply an abnor-
This is in contrast to humans with secretory diarrhea, mal recognition or response to certain dietary
where feeding is advantageous. antigens.

In general, for the majority of cats with acute, non- Intermittent but persistent vomiting or diarrhea are
specific gastroenteritis, the prognosis is excellent. the most common signs.
The prognosis is guarded for cats with severe diarrhea Poor hair coat, pruritus, inappetence or failure to
or diarrhea occurring secondary to problems in other thrive may also be noted but these are less common.
body systems.
Presence of concurrent dermatologic and gastrointesti-
nal signs should prompt consideration of a food allergy.
Prevention
Reduce opportunities for ingestion of toxic or irritating
Diagnosis
substances.
There is no diagnostic test for this problem other than
to observe a beneficial response to an appropriate
FOOD INTOLERANCE***
dietary trial. This should be carried out for a minimum
of 3 weeks.
Classical signs
Use a highly digestible diet or an elimination diet,
● Intermittent vomiting or diarrhea.
either a commercial diet containing a single novel pro-
● Inappetence.
tein source, or a homemade diet of boiled white rice
and a novel meat source such as duck, venison, rabbit,
Pathogenesis kangaroo, tofu, horsemeat, etc.
Food intolerance is a non-immunologic, adverse reac-
tion to a substance(s) present in food. This reaction Differential diagnosis
may be to a food component such as the type of protein
or carbohydrate, a particular component (e.g. wheat Acute, intermittent diarrhea in an otherwise healthy
gluten) or it may be to food colorings, preservatives, cat suggests early inflammatory bowel disease, GI par-
flavorings, etc. asites, dietary indiscretion, or acute gastroenteritis due
to infectious causes.
Food intolerances may result from an inability to ade-
quately digest a dietary constituent (e.g. lactose) or In some cats, this may be a sign of early renal or liver
from metabolic, toxic or pharmacological responses disease, hyperthyroidism and other primary GI abnor-
to food components such as histamine in foods, lectins malities such as neoplasia.
or from the metabolism of dietary residues by the large
intestinal microflora.
Treatment
The precise mechanism associated with vomiting or
The diet should be changed so that it does not con-
diarrhea due to food intolerance is unknown.
tain the offending substance. This may be as simple
The mucosa (formerly gut) associated lymphoid tis- as changing from a grocery store brand to a premium
sue is believed to be a major component in the devel- brand food (or vice versa), but also may require changing
to a hypoallergenic food product (e.g. IVD’s Limited Clinical signs

diets, Hill’s d/d, Eukanuba Response formula, Royal
Canin, etc.) or in unresponsive cases, formulating Anorexia or a decrease in appetite and vomiting are
a novel homemade diet that is complete and nutrition- common occurrences following antibiotic use.
ally balanced. Diarrhea may be liquid and explosive (consistent with
In food intolerance, the abnormal gastrointestinal small bowel diarrhea) or unformed, soft feces with
response is non-immunologic, thus the use of oral increased mucus (large bowel character).
prednisolone is not indicated and is unlikely to be There are no age, breed or sex predispositions to
beneficial. adverse effects, but in many cats, once an adverse effect
occurs due to one antibiotic, other closely related antibi-
otics may cause similar problems.
Prognosis
Good if the appropriate diet can be found, which is usu- Diagnosis
ally not a difficult problem. However, the cat may have
to remain on the diet indefinitely. The diagnosis is not difficult because it is based upon
an appropriate history and physical examination
findings (e.g. no other abnormalities are found).
Prevention A fecal exam and appropriate dietary history will rule
out the other potential causes of acute diarrhea.
There is no known method to predict which cats are
susceptible to food intolerance, and further, no way to
prevent the development of food intolerance. Treatment
The best approach is to stop the use of the antibiotic
in question, and if antibiotic therapy is still required,
PHARMACOLOGIC** (ANTIBIOTIC- switch to an appropriate antibiotic of another class.
INDUCED DIARRHEA)
Prevention
Classical signs
There is no known way to predict a cat’s response to
● Anorexia, vomiting or diarrhea may all antibiotic therapy, but certain antibiotics (e.g. clin-
occur following administration of damycin, cephalosporins, and amoxicillin) are the
antibiotics. most common culprits.
COCCIDIOSIS** (ISOSPOROSIS,
Pathogenesis CRYPTOSPORIDIOSIS, TOXOPLASMOSIS)
Vomiting or diarrhea associated with antibiotics is
a common occurrence and can occur with almost all Classical signs
of the popular antibiotics, including: amoxicillin, ● Acute small bowel diarrhea is most
cephalexin, erythromycin, lincomycin, sulfasoxazole, common in young cats or kittens.
tetracycline, trimethoprim-sulfadiazine, metronidazole ● In severely infected kittens, weight loss,
and clindamycin. anorexia and dehydration may also occur.
The mechanism for induction of nausea, vomiting or
● Most adult cats will be asymptomatic or
diarrhea varies for each drug. have subclinical infections.
Diarrhea often occurs due to a disruption of the

Pathogenesis
enteric microflora that results in overgrowth of patho-
genic species or sporulation of normal flora resulting in Coccidian parasites (Isospora, Cryptosporidia, etc.) are
release of toxins that cause diarrhea. common intestinal inhabitants that may occur as
commensals or pathogens, depending on the circum- mesenteric lymphadenopathy due to intestinal hyper-
stances. secretion and malabsorption.
Isospora felis and I. rivolta are the two Isospora
species (also called Cystoisospora) that infect cats. Diagnosis
Cryptosporidium parvum is generally accepted to be Diagnosis is made by identification of isosporoid
the cause of feline cryptosporidiosis. oocysts in fresh feces.
Immunocompetent cats will only develop Crypto- The oocysts of cryptosporidia are smaller than
sporidia infections in the GI tract, but immunocom- RBCs, 1/10th the size of isospora, and 1/16th the size
promised cats can have infections of the liver, pancreas, of a Toxocara oocyst.
gall bladder and respiratory tract in addition to the GI ● Special flotation media (Sheather’s sugar or zinc
disease. sulfate flotation) is required along with special
staining (Kinyoun’s carbolfuchsin negative) or
Cryptosporidiosis has been primarily reported in cats
phase contrast microscopy, to identify Crypto-
with immunosuppressive or immune-mediated dis-
sporidia.
eases such as FeLV, IBD and intestinal lymphosarcoma.
● Because of their small size, the operator needs to
Unlike most coccidian parasites, the life cycle of focus up and down on the sample to be able to iden-
Cryptosporidium occurs entirely within one host. tify the oocysts.
In other coccidian parasites infection occurs by inges- Other methods of identification of fecal Cryptosporidia
tion of infective (sporulated) oocysts or tissues from include an ELISA test, however, its effectiveness in
an infected paratenic host (wildlife, large animals, identifying feline species of Cryptosporidia is unknown,
etc.). a PCR test for Cryptosporidium DNA in the feces, or
electron microscopy of intestinal biopsy samples.
Concurrent disease, malnutrition, stress and
immunosuppression appear to be important contribut- Fecal samples submitted to the laboratory should be
ing factors in the development of clinical disease. preserved in formalin to minimize the risk of human
infection.
Clinical disease is most common in young kittens
from crowded, unsanitary, high-stress conditions.
Natural infections of healthy kittens and cats result in
asymptomatic infections in almost all cases. The primary differentials are other intestinal parasites
or protozoa (giardiasis), infectious diarrhea, toxin-
Diarrhea is present in about 10% of cats with the induced diarrhea or dietary disturbances, which are
enteroepithelial form of toxoplasmosis but is more common in young cats adjusting to new foods.
common in kittens infected before weaning. Acute
diarrhea is most common in neonatal kittens.
Treatment
Sulfonamides are the drugs of choice for Isospora,
Clinical signs however they are coccidiostatic, not curative.
Sulfadimethoxine (15 mg/kg q 12 h × 14 days) alone,
The principal clinical sign of coccidiosis is diarrhea,
or in combination with trimethoprim, is the drug of first
which may be bloody, mucoid or watery.
choice.
Other signs that may be observed include vomiting,
Other drugs that may be considered if treatment fail-
weight loss, lethargy and dehydration.
ure occurs are nitrofurazone, tetracycline, quinacrine,
Adult cats that are infected with coccidian parasites spiramycin or roxithroromycin.
(including cryptosporidia) are typically asymptomatic.
Treatment of subclinical infections of isospora or
Young or immunocompromised cats with crypto- cryptosporidiosis is not indicated or necessary, as full
sporidiosis will have profuse, watery diarrhea and recovery will occur.
Cats or kittens with clinically significant crypto- Pathogenesis

sporidiosis may be treated with tylosin, clindamycin
or azithromycin, however, the clinical effectiveness of Giardia intestinalis is a commonly encountered flagel-
these drugs is not well tested. late protozoan parasite, with a direct life cycle.
Cats or kittens that are dehydrated and anorectic will Giardia cysts are ingested from contaminated water,
require supportive care in the form of fluid replace- or directly from animal to animal (e.g. in kennels or
ment therapy or nutritional support or both. catteries).
Excystation of the ingested cysts releases two motile
Prognosis trophozoites in the small intestine.
The prognosis for complete recovery in immunocom- Cysts are approximately 9–13 microns in size but are
petent cats and kittens is excellent. not routinely identified in flotation solutions because
Any adult cat with coccidiosis or cryptosporidiosis they are not shed consistently and are small.
should be carefully evaluated for the presence of other Sugar flotation solutions will cause the cysts to shrivel.
immunodeficiency (e.g. FIV) or immune-compromising
diseases (e.g. neoplasia, IBD, etc.). Trophozoites are slightly larger, tear-drop-shaped,
have four pairs of flagella and are binucleated. The
Prevention trophozoites attach to the mucosal brush border to
absorb nutrients. Little is known about encystation and
Coccidiosis is primarily a problem of poor sanitation, what triggers it.
and over-crowded, high-stress conditions that occur in
catteries, shelters and other population-dense situations. Cysts are susceptible to desiccation, but can exist for
months in a cool, moist environment.
Because the oocysts (both Isospora and Cryptosporidia)
are environmentally resistant, only aggressive sanita- The pathogenesis of Giardia infection is not well
tion measures (daily fecal removal, disinfection of understood but is believed to involve malabsorption,
cages, runs and food utensils with steam cleaning or 10% disturbances in brush border enzyme function and
ammonia solutions) will prevent contamination. possible enterotoxin production.
Severe clinical disease is more common in young
Public health cats, but adults can become infected and symptomatic.
Cryptosporidiosis is a significant zoonosis, and thus, Protective immunity appears to protect cats from the
careful precautions must be taken in handling infected development of clinical signs, but may not protect from
animals, their feces and their environments. shedding, since some animals will continue to shed
organisms despite treatment.
Even though the association between human infection
and feline cryptosporidiosis is weak, this problem
should not be taken lightly, especially in cases of cats Clinical signs
owned by immunocompromised humans. Most adult cats infected with Giardia spp. remain
asymptomatic.
GIARDIASIS** The most common sign observed is the presence of
liquid to semiformed diarrhea, associated with
Classical signs increased frequency and quantity of defecation, in an
● The most common sign is liquid, to otherwise healthy cat.
semiformed, diarrhea with increased Vomiting, dehydration, lethargy and anorexia may be
frequency and urgency. observed in severe cases, but are uncommon.
● Some animals are asymptomatic, and most
remain bright, alert and afebrile. Occasionally, chronic small bowel diarrhea with weight
loss and poor body condition are observed.
Cats are more likely to also have evidence of acute such as seizures, coma and behavioral changes. All of
or chronic large bowel diarrhea (with hematochezia, these are less common in cats than in dogs and are
increased mucus and tenesmus) than are other species reversible with discontinuation of treatment.
affected.
Other drugs that have been recommended for treatment
of giardiasis are quinacrine and furazolidine, but
Diagnosis these drugs may not eliminate the infection, only
improve the clinical signs.
The diagnosis is made by appropriate fecal examination
techniques. Zinc sulfate flotation is considered to be Albendazole and fenbendazole have been recently
the most accurate and practical test. Three consecu- shown to be effective in treatment of dogs and cats with
tive zinc sulfate flotations will identify 95% of giardiasis. Albendazole (25 mg/kg q 12 h × 2 days) is
infected animals. not approved for use in cats in the United States and is
teratogenic, hepatotoxic and causes bone marrow sup-
Other methods include examination of fresh fecal
pression, and thus is not recommended. Fenbendazole
saline smears (1 drop saline with a small amount of
(50 mg/kg/day × 3 days) has been recommended for
feces that is spread thin enough to read a newspaper
treatment of giardiasis in cats.
through) for trophozoites (only 40% of infected ani-
mals will be identified), duodenal aspiration (e.g. Proper disposal of feces and good sanitation is
instill 10 ml of saline into the duodenum, either through essential to remove any environmental contamination.
the accessory channel of the endoscope or injected
directly during laparotomy, and then aspirate the fluid
Prognosis
for examination) of fluid looking for trophozoites
(requires endoscopy or laparotomy, but is 88% effec- With proper diagnosis, treatment and sanitation proce-
tive), or fecal ELISA testing for Giardia specific anti- dures, Giardia infections can be completely controlled.
gens (95% sensitivity, but low specificity).
At this time, the zinc sulfate flotation test appears to be Prevention
the easiest, most reliable and most accurate method of
Since the cysts are susceptible to drying and many
identifying Giardia infections.
common disinfectants, good sanitation can prevent
Because of the small size of the cysts (1/8 the size of a once contaminated area from being a source of addi-
a Toxocara oocyst), the operator needs to scan the slide tional infections.
carefully and focus up and down through the different
Avoid allowing cats access to drinking water that may
planes to identify the cysts in the preparation.
have fecal contamination.
A vaccine is now available that purports to reduce
shedding of Giardia cysts, however, immune system
Other infectious, parasitic, dietary, toxic and idiopathic activation has been shown to decrease shedding without
causes of small bowel diarrhea must be considered having an effect on the infection itself. The vaccine
since many cats have only mild signs. does not prevent infection or reduce severity, and in
a study in cats made no significant difference overall.
Treament
Metronidazole (50 mg/kg/day PO for 5 days) contin- Public health
ues to be recommended for treatment of giardiasis in
cats. However, resistant strains of the protozoan are Giardia cysts should be considered potentially zoonotic.
increasingly being reported, and thus this therapy
The infectivity of different strains of Giardia for differ-
may not be effective in all cases.
ent species is quite variable, but this fact should not
Side effects associated with metronidazole therapy preclude the need to take adequate precautions when
include gastrointestinal upset and neurologic signs, handling feces.
most cats, choosing a commercial diet that contains

FOOD ALLERGY (DIETARY
a single, novel protein source will work best for
HYPERSENSITIVITY)*
long-term management of these cats.
● Diets that contain protein hydrolysates are less
Classical signs
antigenic than intact proteins because their molecu-
● Gastrointestinal signs are variable, but can lar structure is too short to bridge IgE receptors on
include vomiting, diarrhea, weight loss or the cell membrane. The usefulness of these diets in
anorexia. cats with food allergy is unknown. Type I (IgE-
● Food allergy may also produce mediated) hypersensitivity is thought to be involved
dermatologic signs usually in the absence in only about 25% of food allergy cases. However,
of GI signs. these diets give another option for both diagnosis
and treatment of cats with food allergy.
Other diagnostic tests, including intradermal skin test-
ing, ELISA testing, RAST testing, and gastroscopic
Clinical signs food testing have all been tried in an attempt to find eas-
ier methods of making the diagnosis. However, the only
Gastrointestinal signs are more variable, but can
reliable test currently available is the food elimina-
include vomiting, diarrhea, weight loss or anorexia.
tion trial (which is also what is used in humans).
● In cats, vomiting is more common than diarrhea.
● Generally, signs of hypersensitivity involve either In most cats, the hemogram and chemistry profile
the GI tract or skin. will be completely normal or have mild non-specific
● Clinical signs can occur at any age. changes associated with inflammation.
Most common signs are dermatologic in origin (pruri-
tus, alopecia, miliary dermatitis, seborrhea), affect the
head, face, ears and inner thigh especially, and are
non-seasonal in occurrence. Other differentials such as food intolerance, parasites,
and metabolic or neoplastic diseases should be consid-
There are no known breed or sex predispositions for
ered. Inflammatory bowel disease is also a disease
food allergy.
that mimics food allergy and is very difficult to differ-
entiate from it.
Diagnosis
Flea allergy is the most common cause of dermatologic
The definitive diagnosis of food allergy is only signs of allergy, but atopy and food allergy must be
obtained by feeding an elimination diet. The signs considered.
usually start to resolve after 4–7 days but may require
6–8 weeks for complete resolution, then reintroduction
Treatment
of the offending diet results in the reappearance of
signs. Once an elimination diet has been identified that suc-
● The elimination diet chosen depends on the cat’s cessfully relieves the clinical signs, the cat should remain
preferences for food, the owner’s willingness to on that diet indefinitely. However, it is best in most cases
make homemade foods, and the clinical situation; to try to identify a commercial diet that most closely
however, the best elimination diet is a diet con- resembles the elimination diet so that the cat receives
taining a single, novel protein source (turkey, a nutritionally complete and balanced diet.
venison, duck, kangoroo, etc.) and a single, novel
After a period on one diet, cats may develop hyper-
carbohydrate source (rice, potato, etc.), with no
sensitivity to that new diet, so new (even more novel)
other additives except a pet vitamin.
diets will be necessary.
● A homemade diet (1/3 cup protein, 2/3 cup carbo-
hydrate) can be used as a diagnostic trial, but is not Most cats with food allergy respond only partially or
a balanced diet for long-term maintenance. In not at all to prednisolone.
Ultrasonography is the most useful imaging modal-

INFLAMMATORY HEPATOBILIARY
ity, and it can also be used to obtain fine needle aspi-
DISEASE (CHOLANGITIS)*
rates or biopsies. In cats with cholangitis the liver may
be normal, decreased or increased in size, but typically
Classical signs
will have a hyperechoic pattern due to the presence
● Weight loss, anorexia and depression. of inflammatory infiltrates.
● Vomiting.
The results of tru-cut biopsies do not always reflect
● Icterus.
the histopathologic diagnosis of surgically obtained
wedge biopsies. This was illustrated in a recent study
of 189 biopsies, where > 60% of the cats had tru-cut
biopsies that failed to confirm the presence of cholan-
Clinical signs gitis, which was confirmed by wedge biopsies.
Weight loss (often dramatic), anorexia, vomiting, Liver biopsies taken via surgical exploratory are
icterus and depression are the most common signs. more diagnostic, and will also allow placement of
a feeding tube (gastrostomy or jejunostomy tube) dur-
Other signs may include ascites, diarrhea or fever.
ing the procedure, which is essential for any cat that
Most affected cats are middle-aged or older. has not eaten for 3–5 days.
In addition to liver histopathology, samples of hepatic
Diagnosis tissue should also be submitted for aerobic and anaer-
obic culture.
The presence of icterus helps to narrow the differentials
list to hepatic, pre-hepatic and post-hepatic diseases.
The hemogram in cats with hepatic disease is often Differential diagnosis
abnormal (e.g. mild, non-regenerative anemia, with
abnormal RBC morphology including schistocytes, Cats that have vomiting, diarrhea, and weight loss
leptocytes or target cells), but the changes are not spe- in addition to icterus, the list of differentials is nar-
cific for liver disease. However, it does help rule out rowed to pre-hepatic causes (hemolysis), hepatic
pre-hepatic causes of icterus which are rare in cats. causes (hepatic lipidosis, hepatic necrosis, hepatic fail-
ure, etc.), and post-hepatic causes (pancreatitis, neo-
Serum chemistry abnormalities may include elevated plasia of stomach, pancreas, duodenum or bile duct,
liver enzyme activities (sometimes dramatically), and common bile duct obstruction).
hyperbilirubinemia, hypocholesterolemia, hypo-
albuminemia, decreased BUN and electrolyte alter- In cats that are not icteric, the list of potential causes
ations (consistent with vomiting or dehydration, e.g. broadens extensively to include the spectrum of meta-
hypokalemia, hypernatremia). bolic, neoplastic, toxic and infectious causes of both
systemic and primary gastrointestinal origin.
Bilirubinuria is common, but some cats may have
urate crystalluria if the liver failure is severe.
Bile acid assay (pre- and 2 hours post-prandial) will Treatment
show mild to moderate elevations.
Therapy for cats with cholangitis is largely supportive,
Urine sulfated bile acids are a new test of liver func- but the histopathologic findings are crucial in deter-
tion that may be useful in situations where obtaining mining severity, the type of inflammatory infiltrate
post-prandial bile acids is impossible, for example in (which is essential to choosing appropriate therapy),
inappetent cats. and the overall prognosis for the disease.
Coagulation function (platelet numbers and function, Most cats with severe liver disease will require fluid
and coagulation factors) should be evaluated since liver therapy to replace deficits, provide maintenance fluid
disease often adversely affects these functions. support during the recovery period, and induce diuresis
to assist removal of hepatotoxins and prevent tubular stant rate infusion of food over 24 hours is less labor
sludging from bilirubinuria and casts. intensive than using initial 1–2 hour feedings of small
volumes of food. After the initial introductory period,
The fluids should be isotonic, balanced electrolyte
the goal is to achieve a daily caloric intake near the
solutions, but preferably not containing lactate,
resting energy requirement (RER), calculated as
which is not converted to bicarbonate in cats with liver
BER = [70 + body wt (kg) × 30].
failure and thus serves as an additional source of acid.
Ringers solution and Normosol-R are replacement Most anorectic or ill cats will benefit from addition of
electrolyte solutions without lactate. B vitamins to the fluids, however, fat-soluble vitamin
deficiency may also develop in cats that are anorectic or
Vomiting should be controlled with a combination
have malabsorption. Supplementation with vitamin K
of anti-emetic therapy (e.g. metoclopramide or
and in some cases, vitamin E should be considered in
dolasetron) and acid-blocking therapy (H2 antagonists
those cats. Supplementation with L-carnitine may also
such as famotidine), since cats with liver disease are
be beneficial.
prone to development of hypergastrinemic gastritis.
Potassium and phosphorus should be supplemented
Diarrhea is rarely severe enough to require therapy
in cats with low serum levels using potassium chloride
and often resolves as the anorexia worsens.
and potassium phosphate.
Cholerectic agents (Actigall) should be used to reduce
Antioxidant therapy with S-adenosylmethionine (SAMe)
bile sludging and improve bile salt flow.
(20 mg/kg/day PO) is indicated in all cats with cholangitis.
Cats with neutrophilic cholangitis should be given
broad-spectrum parenteral antibiotics. A penicillin
HYPERTHYROIDISM*
combined with a fluorinated quinolone provides a good
spectrum of activity for enteric pathogens. Ideally, the
Classical signs
antibiotic choice should be based upon culture
results, but if the culture is negative or the cat is sys- ● Weight loss despite a good to ravenous
temically ill, broad-spectrum antimicrobial chemother- appetite.
apy should be initiated. ● Polyuria/polydipsia.
● Vomiting, diarrhea or voluminous feces.
Lymphoplasmacytic cholangitis is believed to be an
● Hyperactivity or irritability.
immune-mediated disease and has recently been
● Poor coat condition.
shown to occur in association with inflammatory bowel
disease and pancreatitis. Prednisolone therapy (2–4
mg/kg/day) is indicated in cats with lymphocytic plas-
macytic hepatic infiltrates.
Clinical signs
Nutritional support is often overlooked in cats that do
not have hepatic lipidosis, but is crucial for all sick cats Typical signs include weight loss despite a good to
due to their requirement for essential amino acids and ravenous appetite, hyperactivity, polyuria/polydip-
fatty acids to be provided in the daily diet. Nutrition can sia, and a poor coat condition.
be provided in the short term (1–3 days) via naso-
Vomiting, diarrhea or voluminous feces are common,
esophageal feeding tubes, but for longer periods,
and may be observed as an acute problem.
esophageal feeding tubes or a percutaneous endo-
scopic gastrostomy (PEG) tube should be placed to Most cats will have tachycardia, a gallop rhythm or
allow larger amounts of food per feeding as well as other signs associated with congestive heart failure
feeding a blenderized cat food rather than liquid enteral (coughing, increased respiratory rate, weakness) sec-
diets. ondary to thyrotoxic heart disease.
When initiating enteral feeding in sick cats, the volume Gastrointestinal signs associated with hyperthyroidism
of food must be gradually increased over 3–5 days, are often intermittent or relatively mild, with the excep-
to reduce vomiting and gastric retention of food. A con- tion of weight loss and appetite changes.
Diagnosis There are three commonly used therapeutic

approaches to treatment of the hyperthyroid condition
The definitive diagnosis is an elevated serum total in cats: (1) medical management with methimazole;
thyroxine concentration (T4). (2) surgical removal of the adenomatous thyroid; and
Other non-specific abnormalities of the hemogram (3) radioactive iodine treatment of the cat to obliter-
or chemistry profile may include hemoconcentration, ate the hyperactive gland(s).
mild anemia, increased liver enzyme concentrations, The treatment method chosen depends on several
including elevated serum alanine aminotransferase factors: (1) the condition of the cat (requires assess-
activity, or hyperglycemia. ment of anesthetic and surgical risks, renal function,
A thorough assessment of renal function should be cardiovascular function; (2) the availability of radioac-
undertaken (BUN, creatinine, UA) before initiating tive therapy; (3) the owner’s wishes (financial and
treatment of hyperthyroidism in cats since the increased other considerations), and the clinical judgment of the
renal blood flow associated with hyperthyroidism attending veterinarian.
may result in acute renal decompensation when the Prior to surgical or radioiodine therapy, evaluation of
thyroid disease is treated (especially with surgical or renal function and cardiovascular status is extremely
radioactive iodine therapy). important. Cats with marginal renal function may not
Most cats will have a palpable thyroid nodule. be good candidates for thyroidectomy or radioiodine
therapy which will reduce renal blood flow and metab-
Cats with signs of hyperthyroidism but serum total T4 olism dramatically and may induce an acute exacerba-
in the upper half of the normal range should be tested tion of renal failure.
using free T4 levels, as false lowering of the T4 level
may occur due to non-thyroidal illness. Some cats with thyrotoxic heart disease may require
calcium channel or beta-blocker therapy, furosemide if
In cats with suspected hyperthyroidism, but normal they are in heart failure, or aspirin (efficacy unproven)
serum total or free T4 levels, a T3 suppression test or to reduce the risk of thromboembolism. Many cats
radioactive thyroid scan can be performed to confirm with thyrotoxic heart disease respond to treatment
the diagnosis. of hyperthyroidism alone.
Cats with signs of cardiovascular disease should also
have thoracic radiographs and an echocardiogram INTUSSUSCEPTION*
performed to determine the extent of thyrotoxic heart
disease and need for therapy. Classical signs
● Anorexia, inappetence or normal appetite
Differential diagnosis are all possible, depending on the location
The major differentials for an older cat with weight and severity of the obstruction.
loss, vomiting or diarrhea include neoplasia, exocrine ● Weight loss.
pancreatic insufficiency, hepatic or renal disease and
inflammatory bowel disease. However, the presence of
Clinical signs
cardiovascular signs, a ravenous appetite or hyperactive
behavior with the GI signs should point to hyperthy- Intussusceptions are rare in cats compared to dogs.
roidism first. When they occur, they tend to be in the jejunum.
With high intussusceptions, vomiting, abdominal dis-
Treatment comfort, anorexia, lethargy, dehydration and hypovo-
lemia leading to shock are the most common clinical
Treatment for hyperthyroidism includes both control
signs.
of the over-secretion of thyroid hormone as well as
its effects on the remainder of the body (e.g. thyro- Low intussusceptions (at the ileocolic junction) typi-
toxic heart disease). cally present with bloody, mucoid diarrhea, tenesmus,
intermittent vomiting and weight loss. In many of these After surgical correction, if gastric ulceration is not
cases, the intussusception can be palpated. a complicating factor, oral alimentation should be
instituted in the first 24 hours, to enhance the return
Depending on the location and severity of the obstruction,
of normal motility and reduce the possibility of post-
there may be anorexia or inappetence and vomiting.
operative ileus.
Diagnosis
Hemogram and serum biochemistry profiles are
FOREIGN BODIES*
variable depending on the severity and location of the
intussusception, however, dehydration, electrolyte
Classical signs
abnormalities, anemia and leukocyte changes have
all been observed depending on the cause of the intus- ● Weight loss, anorexia or inappetence
susception. ● Acute onset of vomiting or gagging,
occasionally diarrhea is observed.
Radiographs and/or ultrasound examination of the
gastrointestinal tract are the best means of confirming
the diagnosis. Contrast studies may be used but should
not be done at the expense of delaying treatment in
severely ill cases.
Clinical signs
The signs depend upon the location of the foreign
used to obtain a diagnosis, especially with low intus-
object.
susceptions.
With gastric or upper small intestinal obstructions,
acute onset of frequent vomiting or gagging is com-
mon.
Many diseases that can precipitate an intussusception
Dehydration, lethargy and anorexia are common in
(viral enteritis, foreign bodies, gastroenteritis, intestinal
these cats, and they may show evidence of abdominal
parasitism, etc.) also have clinical signs that mimic it.
discomfort (either on palpation or by posture).
Therefore, a thorough physical examination, diagnostic
evaluation, and close patient monitoring are essential. In cats with a lower intestinal obstruction, diarrhea
Mesenteric volvulus is a very difficult condition to dif- will be more prevalent and vomiting less frequent.
ferentiate from intussusception both clinically and radio-
If the foreign body is of significant size or if intestinal
graphically, but fortunately is very rare in the cat.
plication from a linear foreign body is present, these
abnormalities may be palpable.
Treatment
Cats that develop an intestinal perforation as a result
Intussusception must be considered a surgical emer- of the foreign body may be quite ill (depression, fever,
gency. Cats with signs of shock or endotoxemia hypovolemia/shock).
should be prepared for surgery by correcting fluid and
Depending on the location and severity of the obstruc-
electrolyte imbalances, administration of broad-
tion, there may be an acute onset of anorexia or inap-
spectrum, parenteral antibiotics (combinations such
petence.
as ampicillin/amoxicillin or cefazolin and enrofloxain,
amikacin, cefoxitin or imipenam), and use of hista-
mine-2 blockers (ranitidine or famotidine) or protec- Diagnosis
tants if gastric erosions or ulceration is suspected.
History and physical examination findings are very
Motility-enhancing drugs, such as metoclopramide, important. Always examine under the tongue of vom-
are contraindicated in patients with GI obstruction iting cats for evidence of a string or thread foreign
and should not be used. body.
Hemogram and serum biochemistry profile findings Motility-modifying agents, such as metoclopramide,
will likely be normal if the condition is acute. should not be used until the obstruction is relieved.
Long-standing or severe linear foreign bodies or GI
perforation will show an inflammatory response, IDIOPATHIC INFLAMMATORY BOWEL
evidence of dehydration (hemoconcentration or ele- DISEASE (IBD) (LYMPHOPLASMACYTIC
vated proteins) and electrolyte abnormalities consis- ENTERITIS, EOSINOPHILIC
tent with vomiting (hypokalemia is most common). ENTEROCOLITIS)
The diagnosis is obtained by imaging studies, includ-
Classical signs
ing radiography (plain or contrast studies looking for
evidence of an obstructive gas pattern), ultrasonogra- ● Vomiting, anorexia and weight loss are the
phy or upper GI endoscopy. In some cases, endoscopy most common signs of upper GI IBD.
will allow retrieval of the foreign object, and is a useful ● Diarrhea can occur.
means of assessing other damage (e.g. erosions, ulcers, ● Affected cats are usually middle aged or
or tears in the mucosa). older, with no particular sex or breed
predisposition.
Acute diarrhea is not the classic clinical sign of
a foreign body, but may occur in combination with
Clinical signs
vomiting or anorexia, and can occur without these
signs if the obstruction is more distal. Typically, IBD is associated with upper GI signs
of chronic intermittent vomiting, weight loss and
Some cats with linear foreign bodies have a wax-
anorexia.
ing\waning course of vomiting, diarrhea or anorexia
that may not suggest the diagnosis immediately. Diarrhea is also observed in some cats, when the dis-
ease affects the colon or distal small intestine. This
Other differentials in those cases would include infec-
occurs less often in cats than in dogs. Acute exacerba-
tious, dietary or inflammatory gastrointestinal diseases.
tion of diarrhea may occur.
Most cats with IBD have chronic signs of GI disease.
Treatment
The disease is most prevalent in middle-aged to older
In cases where the object is still in the stomach, it is cats, but the range is from 6 months to 17 years.
sometimes possible to safely retrieve the object (nee-
There appears to be no breed or sex predisposition to
dle, small toy, etc.) via an endoscopic procedure.
IBD in most studies, but purebred cats and males
Most GI foreign bodies however, will require surgical appear to be over-represented in some studies.
removal, and some may be a surgical emergency
when GI perforation has occurred.
Diagnosis
Cats that are severely dehydrated from persistent
IBD is a diagnosis of exclusion, that requires two
vomiting, or have suspected intestinal perforation
steps: (1) the histopathologic confirmation of an
and leakage should be stabilized as much as possible
excessive inflammatory response, and (2) the elimina-
with aggressive fluid therapy and broad-spectrum
tion of the multitude of potential causes for GI
antibiotics prior to surgery (e.g. combination of ampi-
inflammation.
cillin/amoxicillin or cefazolin and enrofloxacin,
amikacin or cefoxitin). Some cats with a protracted his- The majority of cats with IBD will have a normal
tory of vomiting will benefit from histamine-2 block- hemogram and serum chemistry profile, however,
ers or GI protectants if gastritis or gastric erosions are a few abnormalities are not uncommon, but they are
suspected. not specific for IBD. These include leukocytosis, mild
non-regenerative anemia, increases in liver enzyme Treatment

concentrations, mild hypoalbuminemia and mild hyper-
glycemia. The key to successful treatment of IBD is to have a cor-
rect diagnosis (and that is a real challenge).
Fecal examination (flotation, direct exam, cytology) is
essential to rule out parasitism. Even if food allergy/intolerance has been ruled out,
a highly digestible, hypoallergenic or elimination
Ultrasound examination is very important, not only diet is important in the treatment of IBD. Cats with
in evaluation of the abdomen for structural abnormali- IBD have an abnormal gut immune system, thus the
ties, but especially for assessing bowel wall thickness presence of additional dietary antigens will only
and lymph node enlargement, which have been serve to exacerbate the inflammatory response.
shown to correlate well with the severity of IBD.
Ultrasound is also important, as it may allow fine- The mainstay of treatment of IBD in cats is immunosup-
needle aspiration of abnormalities which facilitate pressive doses of prednisolone (2–4 mg/kg/day PO).
diagnosis, but also will help determine the best Metronidazole (10–15 mg/kg q 12 h PO) is also very
approach to take when obtaining the biopsies (full thick- effective, and in some cats, may be as effective as
ness vs. endoscopic). steroid therapy. Many clinicians start with metronida-
Radiography, including contrast studies, has not been zole and dietary therapy, and then add prednisolone if
shown to be helpful in differentiating cats with IBD the response to treatment is incomplete.
and those with other diseases. In cats with severe IBD that is not responsive to
Ultimately, endoscopic examination or a surgical metronidazole, prednisolone and dietary therapy, cyto-
exploratory will be necessary to obtain biopsies of the toxic drugs may be considered. However, most cats
GI tract. Endoscopy is less invasive and allows visuali- with IBD do not require additional cytotoxic drug
zation of the mucosal surface, which may assist in the therapy, to manage their disease. Drugs have may be
evaluation of the cat. Multiple (6–8) biopsies should considered include chlorambucil (2 mg/m2), azathio-
be taken from multiple sites (stomach, duodenum, prine (0.3 mg/kg EOD) and cyclosporine (5 mg/cat/day).
ileum and colon), even if there is no visible evidence of CBCs should be monitored every 2–3 weeks to detect
disease. myelosuppression early.
Since there are no simple, easy tests for food intoler- Cats with a poor response to treatment or recurrent
ance or food allergy, dietary elimination trials should disease should be carefully re-evaluated (including
be conducted in all cats with signs of IBD or that have multiple GI biopsies) to be sure that the diagnosis is
inflammatory infiltrates of the GI tract. correct. Lymphoplasmacytic enteritis can be mistaken
for intestinal lymphoma in the early stages or a new
problem may have developed.
TUMORS OF THE SMALL INTESTINE*
The list of diseases that may mimic, cause or compli-
cate IBD (e.g. cause GI inflammation and similar
Classical signs
clinical signs) is extensive: systemic diseases (hyper-
thyroidism, pancreatic disease, liver disease, feline ● Chronic, progressive vomiting that may
viral diseases, toxoplasmosis), parasitic diseases include hematemesis.
(nematodes, Giardia, Cryptosporidia, other parasites ● Weight loss and anorexia may be the
such as coccidia, entamoeba), bacterial infection earliest, and most consistent signs.
(Helicobacter, Campylobacter, Salmonella, Clostridia, ● Lethargy or depression are also common,
etc.), metabolic diseases (exocrine pancreatic insuffi- especially later in the course.
ciency, serum cobalamin or folate deficiency), nutri- ● Diarrhea is more common with infiltrative
tional disorders (food intolerance), immunological neoplasms.
conditions (food allergy) and neoplasia (lymphoma,
adenocarcinoma, mast cell tumor). See main reference on page 675 for details.
Clinical signs may also facilitate diagnosis via fine-needle aspiration

or biopsy.
Weight loss and anorexia are the earliest and most
common clinical signs. Ultimately, histopathologic examination of the tissue
is necessary for a definitive diagnosis.
Lethargy or depression are also common.
In cats with obstructive or mass lesions, lesions
Diarrhea is most common with infiltrative neo- unreachable by the endoscope, or when ultrasound-
plasms, such as alimentary lymphoma, which is the guided fine-needle aspirates are non-diagnostic, surgi-
most common neoplasm in the feline small intestine. cally obtained biopsies and resection are the best
Vomiting is a common presenting complaint and approach.
may be associated with hematemesis.
In the USA there is no breed predilection for lym-
phoma, but Siamese cats appear to be predisposed to Differential diagnosis
adenocarcinoma. Alimentary lymphoma is easily (and often) mis-
Signs typically occur in older cats, however, alimen- taken, especially in the early stages of disease, for
tary lymphoma occurs in cats of all ages. lymphoplasmacytic enteritis (inflammatory bowel
disease).
Intestinal forms of lymphoma are usually found in
FeLV-negative cats, however, the multicentric form of Many other severe GI or systemic diseases may
lymphoma can involve the GI tract and is often asso- resemble intestinal neoplasia, including hyperthy-
ciated with FeLV-positive antigenemia where FeLV is roidism, chronic renal failure or liver disease, pancre-
frequent in the feline population. atitis, severe food intolerance or sensitivity, and severe
forms of infectious enteritis. Differentiation of these
Both adenocarcinoma and mast cell tumors of the GI diseases is based on blood testing, exploratory
tract are often associated more with vomiting and weight laparotomy and intestinal biopsy.
loss due to their mass-like, obstructive behavior.
In cats with mass-like or obstructive lesions, other
diseases to consider are intussusception or foreign
Diagnosis bodies, FIP or fungal granulomas, and focal abscesses.
Differentiation often requires exploratory laparotomy
Palpation of the abdomen may reveal a mass or or biopsy.
thickened intestinal loops.
Hematology and serum chemistry profiles are usu-
ally non-specific, but help to rule out other causes of Treatment
vomiting. The most frequent hematologic abnormal-
ity is anemia of chronic disease (normocytic, nor- For adenocarcinoma, mast cell tumors and other
mochromic), but blood loss anemia is also observed. tumors that tend to occur as solitary mass lesions,
The abnormalities found in the chemistry profile surgical removal via intestinal resection is the pri-
depend on the extent of the disease and severity of mary approach. Biopsies should be obtained of
vomiting, and are non-specific as well. liver, regional lymph nodes and mesenteric tissues
to determine if metastasis has occurred and its
The most helpful diagnostic procedures are imaging extent.
techniques: radiography, ultrasonography or possibly
endoscopy. There are no specific radiographic features of Chemotherapy has not been proven effective for
neoplasia, since it may be infiltrative or obstructive in adenocarcinoma or intestinal mast cell tumors.
nature. Ultrasound may be more helpful in identification Lymphoma of the alimentary tract is generally an
of thickened loops of bowel or mass lesions. infiltrative neoplasm and chemotherapy using com-
Depending on the location and size of the mass, ultra- bination protocols (COAP, etc.) are the treatments of
sonography will allow visualization of the lesion, and choice. See main reference on page 676 for details.
Ancylostoma tubaeforme (60 × 40 μm) is the most

NEMATODE PARASITES* (ROUNDWORMS,
common hookworm of cats, and is most prevalent in
HOOKWORMS)
tropical regions. The eggs are elliptical and slightly
smaller than roundworm eggs, but still readily identi-
Classical signs
fied on saline fecal flotation.
● Abdominal distention, colicky abdominal
Infection may be associated with peripheral eosino-
pain.
philia, hypoproteinemia, and mild to severe regenera-
● Poor body condition, not nursing or eating.
tive anemia (blood loss).
● Diarrhea or abnormal feces.
Kittens with severe intestinal parasitism may
develop a bowel obstruction or intussusception result-
Pathogenesis ing from the motility disturbance, in these kittens,
radiography, contrast studies or ultrasound exami-
Toxocara cati and Toxascaris leonina are the primary
nation will be necessary to identify the problem.
roundworms of cats. T. cati can be transmitted via
milk, and by ingestion of the ova or hosts (e.g. rodents)
containing the ova. Adult roundworms live in the small Differential diagnosis
intestine.
The age and clinical signs are usually supportive of the
Ancylostoma tubaeforme is the most common hook- diagnosis, but other protozoal, infectious or dietary
worm of cats, but is less pathogenic than the primary causes of gastroenteritis should be considered.
hookworm of dogs (A. caninum). Infections occur by
ingestion of larvae, migration of larvae through the
Treatment
skin, via paratenic hosts, or prenatally. However, hook-
worms are much less of a problem in cats than in Anthelmintics such as pyrantel (5–10 mg/kg PO once)
dogs. or fenbendazole (25–50 mg/kg PO q 24 h for 3 days)
are effective and can be used for treatment of both kit-
tens and adult cats.
Clinical signs Selemectin (oral monthly heartworm preventative, flea
Kittens are most likely to have clinical signs associ- adulticide and nematocide) may be used to treat or
ated with infestation with helminths. prevent intestinal parasites.
The clinical signs may include abdominal distention, Repeat treatment in 2–3 weeks (hookworms) and 4–6
colicky abdominal pain, poor body condition/hair weeks (roundworms) to effectively kill prepatent
coat, poor or reduced appetite, diarrhea or abnor- stages.
mal feces, and vomiting worms or vomiting due to Re-infection is prevented by good sanitation. Feces
masses of worms obstructing passage of ingesta. must be removed from the litter box or collected if out-
Ascarids of cats do not pass through the placenta, so side, and incinerated.
kittens will not develop prenatal infections like puppies
do. Prognosis
Excellent, except in cats with intestinal obstruction,
etc., which have a more guarded prognosis until the
Diagnosis
problem is surgically corrected.
Fecal flotation will reveal spherical egg (Toxocara
cati) with pitted outer shell membrane containing
Public health
a single zygote, and approximately 75 × 45 μm in size.
Toxascaris is also an ovoid egg of similar size but has Both roundworms (visceral larval migrans) and
a smooth shell. hookworms (cutaneous larval migrans) have
zoonotic potential, but are not as prone to cause larval Cats that have muscle tremors, seizures or other neu-
migrans as canine parasites. rologic dysfunction may need specific therapy such as
phenobarbital or valium for seizure control. Metho-
carbamol (a muscle relaxant) may be helpful in
PYRETRINS/PYRETHROIDS/
decreasing excessive muscle activity.
PERMETHRINS/ORGANOPHOSPHATES*
Organophosphate toxicity is treated with 2-PAM
Classical signs and/or atropine (0.2–0.4 mg/kg) to control the exces-
sive salivation and defecation.
● Acute onset of vomiting, diarrhea,
hypersalivation and agitation. The signs will be self-limiting once the chemical is
● Contact dermatitis. removed from the body, so supportive care is all that
● Ataxia and possibly seizures. is required. However, some cats may require 1–3 days
to recover.
Since cats will not drink or eat, fluid therapy may be
needed. In some cats, muscle tremors may be so severe
CLINICAL SIGNS to increase body temperature, so monitoring (and con-
Signs associated with contact exposure or ingestion of trolling) body temperature is important.
pyrethrin/pyrethroid-containing pesticides is generally
mild.
Vomiting, diarrhea, hypersalivation and agitation are FELINE CORONAVIRUS INFECTIONS*
the most common signs of organophosphate toxicity. (FELINE ENTERIC CORONAVIRUS/FELINE
INFECTIONS PERITONITIS)
Permethrins are very toxic to cats, resulting in cen-
tral nervous system signs, which include muscle Classical signs
tremors, ataxia, excitation or seizures. Cats may also
become hyperthermic secondary to prolonged mus- ● Mild to moderately severe diarrhea for 2–5
cle activity or seizures. days, usually in kittens (enteric form).
● Signs of FIP are vague and variable and
Contact dermatitis is not common, but may be include weight loss, fever and anorexia.
observed in cats with the topical preparations. ● Occasionally vomiting and chronic diarrhea
are observed in cats with FIP.
Diagnosis
History of exposure to or ingestion of products con-
Clinical signs
taining permethrin (most common) or pyrethroids.
Enteric coronavirus infection causes a mild to mod-
There is generally no need for further diagnostic testing
erate, self-limiting diarrhea, usually seen in kittens.
since signs will abate with removal of the product
from the skin or GI tract and supportive care. Diarrhea is uncommon in adults, but occasionally
can be a peracute, severe hemorrhagic diarrhea.
● Feline enteric coronavirus is important because
this virus is the source of feline infectious peritoni-
The history of recent application of a product contain- tis (FIP). This occurs by mutation of the enteric
ing these chemicals is usually definitive. virus to the pathogenic, virulent FIP coronavirus
that infects and replicates in macrophages.
Treatment
The clinical signs associated with feline infectious peri-
The first and most important step, if the cat is not tonitis (FIP) virus infection are quite variable and
seizuring, is to bath the cat to remove any remaining depend a great deal upon the stage when the cat pres-
chemical. ents to the veterinarian for evaluation.
Cats with fulminant FIP will likely be severely Pathogenesis

depressed, anorectic and have significant weight
loss. Respiratory distress from pleural effusion is also Salmonella are motile, Gram-negative bacilli that
common, as is the presence of ascites. Some of these are ubiquitous pathogens able to infect many mam-
cats will have gastrointestinal tract signs, such as mals, birds and reptiles.
vomiting or diarrhea, if there is significant intestinal, Virulence of different strains varies and this is deter-
liver or renal dysfunction. mined by the ability to invade tissues.
Cats with the so-called non-effusive or “dry” FIP, Salmonella localize in the lymph nodes and intes-
will have much more vague clinical signs, including tinal tract, and shedding of organisms occurs for 3–6
reduced appetite, fever, mild weight loss and general weeks. Reactivation of shedding or clinical illness
malaise. Some cats will have mild abdominal discom- may occur after stress, immunosuppression, other
fort, respiratory signs, neurological signs and granulo- viral infections or crowded environmental conditions.
matous retinal lesions.
Salmonella produce enterotoxins which increase
In some cats, FIP granulomas will cause more focal secretions and fluid loss in addition to the entero-
signs associated with the body system that is invasive effects.
affected. Vomiting and/or chronic diarrhea from granu-
lomas in the GI tract have been reported, as have central Endotoxemia or bacteremia may occur concurrently
nervous system signs ranging from ataxia to seizures. with intestinal infection or in the absence of GI signs.
Endotoxemia due to Salmonella is believed to only
Diagnosis occur in cats with severe immunocompromise.
The definitive diagnosis of FIP in cats antemortem

is quite difficult, especially in cases of focal or non- Clinical signs
fulminant FIP. There are several clinical syndromes that occur: gastro-
Interpretation of serologic tests can be difficult, enteritis, bacteremia/septicemia, organ localization
because most test for antibodies to FECV, rather than for and the persistent asymptomatic carrier state.
the FIPV form of the virus. While the negative predictive Acute episodes occur 3–5 days after exposure, with
index is relatively good, false-negative tests can occur in the most severe signs in kittens or old cats.
cats with FIP. Polymerase chain reaction (PCR) testing
is the best current test, but at present is only definitive for Cats will present with fever, malaise, vomiting,
confirmation that a cat does not have FIP. The PCR test abdominal pain and diarrhea.
still has false positives that prevent it from being a good The diarrhea varies from watery to mucoid and may
screening/diagnostic test. The 7B ELISA test detects anti- have hematochezia.
body to 7B protein, but both false-positive and false-
negative results are common with this test. Weight loss, dehydration, shock and death will ensue
if the cat is not treated aggressively.
Currently, the definitive test for FIP remains
histopathologic examination or immunohistochem- Other organ systems may be affected with the sys-
istry and virus isolation. temic illness, including the CNS (seizures) and respi-
ratory tract (pneumonia).
SALMONELLOSIS* Cats that are presented with endotoxemia or bac-

teremia often have a subclinical gastrointestinal
Classical signs infection.
● Abdominal distention, colicky abdominal pain. Very young kittens, less than 7 weeks old, will not
● Poor body condition, not nursing or eating. have fever despite bacteremia. Hypothermia, weak-
● Diarrhea or abnormal feces. ness and collapse may occur without the onset of GI
signs.
Organ localization occurs after clinical or subclinical bac- should be considered, in addition to Giardia, Crypto-
teremia and is less common in cats than it is in humans. sporidia, dietary indiscretion and toxicity.
The most common sites of organ localization include
pyothorax, meningitis, osteomyelitis and focal abscesses Treatment
of organs or skin.
Acute gastroenteritis, without systemic septicemia,
Songbird fever is a clinical syndrome of acute febrile is best treated with parenteral isotonic replacement
illness in cats associated with seasonal migrations of fluids. Maintenance fluid therapy is 40–60 ml/kg/day
birds in the northeastern United States. The disease is and replacement includes maintenance plus correction
characterized by fever, depression, diarrhea and of dehydration, i.e. BW × % dehydration plus addi-
anorexia in young, roaming (outdoor) cats that lasts for tional fluids to replace any ongoing losses. The
2–7 days and may be self-limiting or very severe. replacement fluids are to be given over 12–24 hours,
then the fluid rates can be adjusted to meet the patient’s
The vast majority of cats with salmonellosis (>90%)
needs for maintenance and ongoing losses.
have transient or no clinical illness. Occasionally
chronic diarrhea will occur for up to 8 weeks. Cats with severe hypoproteinemia due to GI protein
Recovered cats will shed for up to 6 weeks. loss or septicemia and endotoxemia may benefit from
plasma transfusions or colloid (Hetastarch) therapy.
Diagnosis Antibiotic therapy is not indicated in treating cats
with uncomplicated gastroenteritis, but is recom-
History (acute onset) and physical examination
mended in cats with sepsis or endotoxemia. Anti-
(fever, depression, diarrhea) will be important sug-
biotics that may be effective against salmonellosis
gestive factors but there are numerous causes of acute
include the fluorinated quinolones, aminoglycosides
diarrhea in young cats.
and trimethoprim-sulfonamide combinations.
Routine hematology and serum biochemistry profiles
Antibiotic therapy may prolong the period of shed-
are typically unremarkable in the early phases, but will
ding, and is associated with development of resistant
show evidence of dehydration, electrolyte imbalance
populations of Salmonella spp.
and leukocyte abnormalities in the later stages. Cats
with bacteremia/septicemia will have a left shift or degen- The presence of neutrophils on a rectal cytology swab
erative neutropenia, hypoglycemia, and may have hepatic justifies antibiotic therapy.
or renal compromise as a result of the endotoxemia.
Definitive diagnosis depends on the culture of Prognosis
Salmonella spp. from fecal samples, or from urine,
Excellent for cats with mild or subclinical infections,
CSF, synovial fluid or blood in cats with bacteremia.
which comprise the majority of the cases.
Serology can be used, but many subclinically
In cats with septicemia or endotoxemia, the mortal-
infected cats will have titers, thus this method is not
ity rate is high due to cardiovascular collapse, renal
an accurate means of diagnosis. It is also not use-
failure and DIC.
ful in acutely ill cats to aid treatment decisions
because of the time delay in seroconversion.
Prevention
Fecal cytologic exam will reveal large number of fecal
Enforcement of strict hygiene (litter box) and proper
leukocytes, thus suggesting an infectious organism
cleaning of cages (phenolic compounds or bleach) will
that disrupts the mucosal barrier.
reduce the risk of subclinical carriers creating disease
problems in large population groups or hospitals.
Public health
Other acute, GI infectious diseases, such as feline pan-
leukopenia virus, Campylobacter and Clostridium Salmonellosis should be considered a zoonotic disease.
The presence of the organism can be confirmed by culture

CLOSTRIDIUM PERFRINGENS
of fresh fecal specimens, however, because this is part of
ENTEROCOLITIS*
the normal flora, this approach is not definitive.
Classical signs Similar to the dog, there appears to be a poor correla-
tion between the presence of fecal endospores and
● Acute small bowel diarrhea with or without
the presence of enterotoxin.
anorexia or lethargy.
Reverse passive latex agglutination (RPLA) tests for
clostridial enterotoxin are available and have been
used in dogs and humans, but have not been evaluated
Pathogenesis
in cats. In dogs, the test does not differentiate dogs
Clostridium perfringens is an anaerobic, Gram- with clostridial diarrhea from normal dogs, as > 25%
positive, spore-forming rod that is a normal inhabi- of normal dogs are positive. An enzyme immuno-
tant of the colon in animals and people. assay (Techlab, Inc., Blacksburg, VA) appears to be
more specific in dogs. A positive enterotoxin assay
Enterotoxin formation by Clostridium spp. causes
determined by ELISA (regardless of endospore num-
increased membrane permeability and results in
bers) in the context of clinical signs consistent with
fluid and ion loss. Eventually, the epithelial cells will
clostridial infection is strongly supportive of
die and slough.
clostridial-associated diarrhea.
Most clostridia exist in the GI tract in their vegeta-
PCR tests are also utilized for testing feces for entero-
tive state, but under certain conditions (alkaline envi-
toxin, but are not universally available.
ronment, other concurrent infections, antibiotic therapy
or stress) the bacterium will undergo sporulation and
release of enterotoxin. Differential diagnosis
Following an infection, the organism can be shed for Other enteric bacterial infections, parasitic and pro-
weeks to months, and because of its stability in the tozoal infections, dietary disturbances and toxin
environment, has the potential to infect many other sus- exposure should all be ruled out first.
ceptible animals. Because this disease can occur in any age of cat, other
considerations are metabolic disease (hyperthy-
roidism), liver disease and neoplasia.
Clinical signs
The most common clinical sign is severe, watery to Treatment
mucohemorrhagic diarrhea.
In severely ill cats, parenteral fluid therapy and intro-
In most cats, the diarrhea only lasts a few days, but duction of a bland, highly digestible diet is necessary.
in some, it may persist and become chronic. Animals
The primary treatment is the use of antimicrobial
that have severe diarrhea will become dehydrated,
drugs that have a good spectrum against anaerobic
lethargic and may be anorexic.
bacteria: metronidazole, tylosin, ampicillin/amoxicillin
There is no breed, sex or age predisposition, but cats and clindamycin have all been successfully used.
from catteries or in stressed environments are at
Addition of dietary fiber (1 tbsp psyllium/cat), or
increased risk.
changing to a diet with increased dietary fiber may
greatly reduce the proliferation of clostridial organ-
Diagnosis isms in the large bowel.
The history (acute onset, predisposing conditions)
Prognosis
and physical examination findings (character of the
diarrhea) help to focus the diagnostic approach toward Good with appropriate antibiotic therapy in most
infectious, parasitic and dietary causes of diarrhea. cats.
Some cats will have recurrent bouts of diarrhea that infection (e.g. radiographs of chest, abdominal ultra-
require repeated treatment with antibiotics or may sound).
benefit from lactulose, which reduces the luminal pH
and thus will decrease sporulation.
FELINE PANLEUKOPENIA VIRUS
Classical signs
SHOCK (HYPOVOLEMIC, SEPTIC, ● Acute onset of anorexia, vomiting, pyrexia,
ENDOTOXIC)* depression, weakness and dehydration.
● The disease is most severe in kittens, and
Classical signs has a high mortality rate.
● Diarrhea occurs late in the course of the
● Acute onset of generalized depression,
disease.
fever or hypothermia.
● Tachycardia/tachypnea and signs of shock.
● Vomiting is not consistently present but
does occur, and bloody diarrhea is also Pathogenesis
occasionally observed.
Feline panleukopenia is a parvovirus that requires
rapidly dividing cells for successful infection (lym-
phoid tissue, bone marrow and intestinal mucosal
crypts).
Infections of kittens in utero, or in the immediate post-
Clinical signs
natal period, results in infection of the cerebellum,
Cats with endotoxemia or sepsis are depressed, usu- cerebrum, retina and optic nerves which may result
ally febrile (but may be hypothermic), and show in seizures, behavioral changes, cerebellar dysfunction
signs of shock. and retinal degeneration.
Vomiting or bloody diarrhea may occur in the later Damage to the intestinal crypt cells results in shorten-
stages of illness. ing and eventually loss of the villous (absorptive) cells.
Diarrhea is caused by malabsorption and increased per-
Other signs include respiratory distress, weakness,
meability.
obtundation and seizures.
Kittens infected with panleukopenia are highly suscep-
tible to secondary bacterial infections with enteric
microflora.
Diagnosis
Gram-negative endotoxemia is a common compli-
Hemogram, serum chemistry and urinalysis show
cation and cause of death in kittens.
neutrophilia if there has been time for neutrophilia to
develop, or neutropenia, thrombocytopenia, hyper- Infection of the queen early in the pregnancy can
glycemia early, progressing to hypoglycemia later. result in a wide variety of reproductive disorders,
Hyperkalemia, and elevated liver enzymes and BUN including early fetal death, infertility, abortions or fetal
are common, as is bacteriuria. mummification. Late-stage gestation infections result
in the birth of live kittens with varying degrees of
Blood culture is indicated in patients with suspected
neurologic dysfunction.
bacteremia to confirm the infection exists. Urine cul-
ture is also helpful in cases with renal seeding of the As with canine parvovirus, the feline virus is highly
infection. contagious, and is very persistent in the environment.
Imaging studies are important in further evaluating Panleukopenia is transmitted by direct contact of sus-
the extent of illness and may help identify a focus of ceptible animals with infected cats or their secretions
(feces contains the largest amount of virus). However, Secondary upper respiratory tract infections may
fomites are an important aspect of transmission occur, especially calici- or herpesvirus infections.
because of the prolonged survival of the virus in the
environment. Diagnosis
Feline panleukopenia can be inactivated by bleach The history (acute onset of depression and vomit-
and formaldehyde, but is resistant to other common ing), signalment (cat less than 1 year of age) and
disinfectants. physical examination findings (fluid- and gas-filled
intestines) are all suggestive of the disease.
The milder forms of the disease that occur in adult cats
Clinical signs can be difficult to differentiate from many other gas-
trointestinal diseases.
The majority of cases of clinical panleukopenia are
observed in kittens or young cats under 1 year age. The most consistent hematologic abnormality is pan-
leukopenia, with leukocyte counts typically ranging
Clinical signs vary from mild to very severe.
between 500 and 3000 cell/μl. Because the disease is so
Anorexia, depression and extreme lethargy are very acute, serum biochemistry values are usually within
common clinical signs in the early stages. normal limits. Hypoglycemia and elevated liver enzyme
concentrations may be detected in cats with endotoxemia.
Vomiting usually occurs but varies in severity and is
associated with dehydration. There is no licensed ELISA test kit for the feline par-
vovirus, however, the canine test kit will detect the
Diarrhea occurs 24–48 hours after the onset of
feline parvovirus in feces as well. False-positive and
depression, and may be mild or marked with severe
false-negative test results can occur.
blood-streaked or hemorrhagic diarrhea.
● False-positive test results can occur following
In the peracute form, death may occur before diarrhea recent vaccination with a modified live panleukope-
develops. nia vaccine, and false-negative results occur if the
● The cat often sits sternally with its head down kitten is tested before shedding starts, if there is
(flexed). low virus burden or late in the course when
● Abdominal palpation may reveal evidence of pain, shedding becomes more intermittent.
enlarged abdominal (mesenteric) lymph nodes and
Serologic testing is still an important diagnostic test
increased gas or fluid in the intestines.
for feline panleukopenia, but it requires paired sam-
The cat may or may not be febrile, but may become ples (acute and convalescent) that show a rise in titer
febrile if there is sepsis. In the late stages of fatal dis- to be definitive. Serology is usually only indicated in
ease, the cat will almost always become hypothermic. a multi-cat facility so appropriate preventative vacci-
Hypothermia indicates a grave prognosis. nation programs can be implemented.
Kittens affected in late gestation, or in the first 9 Other tests that can be performed include virus isola-
days after birth, are often ataxic, hypermetric, dys- tion on feces or tissues and electron microscopy for
metric, incoordinated and have a base-wide stance detection of virus particles in the feces.
when they begin to walk at 2–3 weeks of age.
Other neurologic abnormalities include seizures, Differential diagnosis
behavioral changes and retinal degeneration.
In its severe form, which is typically present in kittens,
Prenatally infected kittens may be stillborn or die as few diseases mimic feline panleukopenia.
fading kittens in the first few days of life.
Milder clinical forms of the disease in adult cats must
Many susceptible cats will be infected, but have sub- be differentiated from all other infectious causes of
clinical or mild GI signs associated with depression gastrointestinal disease (e.g. campylobacterosis, giar-
and anorexia for 1–3 days. diasis, etc.).
Feline leukemia virus can present in some cats with include are amino acids and glucose, which can be
a panleukopenia-like syndrome, but is easily distin- given via a peripheral vein or intraosseously.
guished from feline panleukopenia by the presence of
As with other parvovirus infections, aggressive sup-
FeLV antigenemia, persistent leukopenia and anemia in
portive care (fluids, antibiotics, warmth, control of
a well, vaccinated cat.
emesis, and nutrition, including gamma globulins if
Salmonella infections in cats are usually subclinical, available) is the key to success.
but can present with a fulminant gastroenteritis simi-
Treatment of adult cats is supportive, but depends on
lar to panleukopenia. In acute salmonellosis, leukope-
the severity of the clinical signs.
nia may be present.
There is no treatment for the neurological signs.
Treatment
Prognosis
Treatment is supportive, but must be aggressively
administered if it is to be successful. The prognosis for kittens or very young cats with
severe signs of feline panleukopenia is guarded to
The key is maintenance of fluid (40–60 ml/kg/day
grave, as many die. Kittens infected before 10 days of
plus correction of dehydration and treatment of ongo-
age that survive have life-long neurologic dysfunc-
ing losses) and electrolyte balance (add potassium
tion, which is not progressive, and may be acceptable
chloride to fluids) and prevention of secondary bacte-
to the owners.
rial infection until the body is able to neutralize the
virus with antibody. Adult cats are likely to survive without significant dis-
ability, and will have life-long immunity.
Antibiotics effective against enteric pathogens
(Gram-negative and anaerobic bacteria) must be given
to control secondary bacterial infections. Combination Prevention
therapy with ampicillin (10–20 mg/kg q 8 h) or
The currently available vaccines for feline pan-
cephalexin (20–30 mg/kg q 8 h) and amikacin (8 mg/kg
leukopenia are excellent. Kittens should be vaccinated
q 24 h) or enrofloxacin (5 mg/kg q 24 h) is necessary
at 8–9 weeks and then boostered at 12–14 weeks.
for broad-spectrum coverage.
Adults have traditionally been revaccinated annually,
Control of vomiting can usually be achieved with
but this is not necessary. In a recent study, protective
metoclopramide (0.2–0.5 mg/kg q 6–8 h) or prochlor-
immunity from a killed feline panleukopenia vac-
perazine (0.1–0.5 mg/kg q 6–8 h) therapy.
cine was found to persist for at least 7 years, and
Plasma or blood transfusion therapy (up to 20 ml/kg modified live vaccines are believed to impart life-long
for plasma therapy, or calculate transfusion to increase immunity.
the PCV to approximately 20%) are indicated in kittens
In young kittens, it is also important to reduce their
with severe anemia, hypoproteinemia or hypotension.
risk of exposure by isolation from unvaccinated or
Young kittens also need nutritional support to pre- ill cats.
vent the development of hypoglycemia and assist the
immune response. B vitamin supplementation is also
especially important. HEAVY METALS (LEAD, ARSENIC)
● Nutritional support may include tube feeding
(orogastric, nasogastric) with liquid enteral supple- Classical signs
ments, force feeding of canned or blenderized ● Vomiting, diarrhea, anorexia and
foods, or intraosseous/intravenous feeding (total depression occur early.
or partial parenteral nutrition). If the kitten is not ● Chronic signs of lead toxicity involve the
vomiting, the enteral route is preferred, but in central nervous system, e.g. seizures,
vomiting patients, parenteral routes of feeding tremors and ataxia are most common.
will be necessary. The most important nutrients to
(continued)
Classical signs—Cont’d nine aminotransferase and alkaline phosphatase

enzymes. Other abnormalities may include elevations
● Arsenic toxicity eventually results in in bilirubin, bile acid values and decreases in albumin
hepatic and renal failure presenting as (in end stage hepatic failure).
depression, anorexia, vomiting and
diarrhea, along with oliguria or anuria, or Nephrotoxicity associated with arsenic poisoning is
icterus and ascites. also associated with isosthenuria, azotemia and even-
tually oliguria/anuria.
See main reference on pages 596, 659 for details.
FELINE LEUKEMIA VIRUS
Clinical signs
Classical signs
There are two major categories of clinical signs with
lead poisoning: (1) gastrointestinal signs, which ● Clinical signs are incredibly variable and
occur early in the course of the disease, and (2) cen- depend on which organ(s) are affected.
tral nervous system signs, which are manifest late in ● Weight loss, inappetence.
the disease. ● Occasionally vomiting or chronic diarrhea.
● Diarrhea is rarely observed as an acute
GI tract signs occur early with lead toxicity and may
onset.
include vomiting, diarrhea, salivation, inappetence
● Anemia may be observed.
and lethargy.
Chronic signs of lead toxicity involve the central nerv- See main reference on page 540 for details.
ous system, and include seizures, tremors and ataxia.
Arsenic causes GI signs early, but is hepatotoxic and Clinical signs
nephrotoxic, resulting in depression, anorexia, vomit-
Inappetence, weight loss, and lethargy are typical
ing and diarrhea along with oliguria or anuria, or
non-specific signs.
icterus and ascites.
The clinical signs observed in cats infected with feline
Lead is commonly found in older paints, while
leukemia virus will be quite variable and depend
arsenic is primarily obtained from snail baits.
upon which body system(s) is affected.
Neoplasia, immunosuppression and bone marrow
Diagnosis
disease (especially of the red cell series causing ane-
Historical information of exposure to heavy metals is mia) are the most common clinical manifestations of
a very important means of getting the diagnosis, how- the disease.
ever, such information is not always known.
Generalized lymphosarcoma is a manifestation of
The hemogram and serum chemistry profile will be FeLV in cats, and involvement of liver and mesen-
unremarkable when the cat presents with signs of gas- teric lymph nodes results in gastrointestinal tract
trointestinal disturbance. signs, such as vomiting, anorexia, chronic diarrhea and
weight loss. While the diarrhea is generally chronic in
The most common hematologic abnormality asssoci-
nature, the owner may perceive that it is acute in onset.
ated with lead poisoning is basophilic stippling of
Occasionally, the diarrhea occurs in cats with a good to
red cells, which occurs in 30% of cats with lead expos-
increased appetite.
ure, and the presence of nucleated red blood cells
(also 30%). However, these tests are not pathogno-
monic for lead poisoning. Diagnosis
Heavy metals also cause hepatocellular necrosis, Any ill cat should be tested for infection with feline
which will be evidenced by elevations in serum ala- leukemia virus, due to its many clinical manifestations
and the poor prognosis that exists for cats that are Acute signs include fever, lymphadenopathy and
infected with the virus. inappetence. Other signs include weight loss and non-
specific lethargy.
The hemogram and serum chemistry profile will
likely be abnormal, especially in cats with systemic Chronic small bowel diarrhea is one clinical syn-
illness. The changes may be mild or subtle (mild ane- drome associated with FIV infection. Other syndromes
mia of chronic disease, mild changes in white blood include non-regenerative anemia, neutropenia, anterior
count, liver enzymes, etc.) in the early stages of the uveitis, glomerulonephritis and central nervous system
disease, and dramatic (severe non-regenerative ane- signs ranging from behavioral changes to seizures.
mia, leukopenia, elevation of liver enzymes, etc.)
when the disease finally progresses to end-stage.
Diagnosis
Radiographs and ultrasound examination are useful
History (middle-aged, male, outdoor cat) and physical
in detecting lymphosarcoma involving the GI tract.
examination (non-specific signs of weight loss, with pos-
Biopsy of the GI lesions via fine-needle, tru-cut or sible multi-system involvement) findings are suggestive.
wedge resection of tissue will be necessary to confirm
Antibodies to FIV are detected in serum by an ELISA
the diagnosis of lymphosarcoma.
test commercially available.
The definitive diagnostic test for detection of feline
Cats vaccinated for FIV will be positive to the antibody
leukemia virus infection in cats is a serum ELISA test
test and cannot be distinguished from infected cats.
which detects viral antigen. A positive test should be
confirmed using a follow-up ELISA test 8–12 weeks Confirmation of the test is not usually necessary in ill
later, or by using an immunofluorescent antibody (IFA) cats, but in healthy cats, confirmation of the positive
test on whole blood or bone marrow, as the sensitivity antibody test by western blot or PCR analysis is
and specificity of serological tests such as these are suggested.
affected by the incidence of disease in the local popu-
Kittens may obtain antibody from milk and not be
lation and the individual cat’s risk factors for infection.
infected, so a positive antibody test in kittens under
16 weeks of age should be re-evaluated in 1–2
FELINE IMMUNODEFICIENCY VIRUS months to determine whether the antibody was mater-
nal or infectious.
Classical signs
● Chronic disease of middle-aged to older
CAMPYLOBACTERIOSIS
cats.
● Most common clinical signs are weight
Classical signs
loss, chronic infections and development of
neoplastic disease. ● Abdominal distention, colicky abdominal
● Acute or chronic diarrhea is an uncommon pain, and diarrhea are the most common
problem but occasionally occurs as the signs.
only sign. ● Kittens are generally in poor body
condition, or have other concurrent
See main reference on page 339 for details. infections.
Clinical signs
Pathogenesis
Clinical signs may be due to direct effects of the virus
Campylobacter spp. are Gram-negative, motile rods
or occur secondary to the development of immun-
associated with diarrheal disease in many species.
odeficiency, but in either case, occur in middle-aged
to older, male cats that are outdoor or occasionally The disease is spread by fecal–oral mechanisms, with
fight. food and water being primary sources of infection.
The disease is most prevalent, and clinically signifi- Differential diagnosis

cant, in kittens from catteries, shelters or laboratories.
Infectious (Salmonella, Clostridium), parasitic (Giardia,
Most adult cats have asymptomatic infections, and Cryptosporidia, etc.), and dietary (intolerance or dis-
those with diarrhea often have other concurrent cretion) agents should all be considered.
enteric pathogens present that exacerbate the severity
of the disease.
Treatment
Exposure to Campylobacter results in the develop-
ment of protective immunity which may explain why Since most cats with Campylobacter infections are
kittens are more prone than adults to the development asymptomatic or associated with other infections, the
of clinical disease. effectiveness of antibiotics for treatment of this dis-
ease is unknown.
Several antibiotics appear to be effective in eliminat-
Clinical signs ing the organism, including erythromycin (10 mg/kg q
8 h PO), metronidazole (5–10 mg/kg q 12 h, PO),
In cats, clinical signs of campylobacteriosis are uncom- cephalosporins (20 mg/kg q 12 h PO), and fluorinated
mon in the absence of other pathogens. Most infec- quinolones (5 mg/kg q 24 h PO).
tions are asymptomatic.
Affected cats are usually less than 6 months of age. Prognosis
The primary clinical sign of infection is diarrhea, Excellent, especially in adult cats.
which may be watery, bloody, mucoid or a combination.
Some kittens will become systemically ill with lethargy, Public health
dehydration and anorexia observed.
Enteric campylobacters are known to be human
pathogens, and kittens can be a source of human infec-
tion.
Diagnosis
Usually kittens with diarrhea are incriminated as causes
History and physical examination findings are of human infection, however, because humans can be
important, but may be unremarkable. infected with extremely small amounts of the bacteria,
Routine hematology, chemistry profiles and imaging asymptomatic cats and kittens that are shedding can
studies are typically unremarkable. also be a source of infection.
Diagnosis can be confirmed by culturing freshly The best way to prevent human zoonosis is to stress the
obtained fecal samples. Samples can be transported importance of exercising appropriate personal hygiene
at room temperature without special handling, but when handling pet feces or litter boxes.
must be cultured in a microaerophilic atmosphere.
Campylobacter are often cultured from the feces of IDIOPATHIC JUVENILE DIARRHEA
normal cats (up to 40%), so it is important to correlate
the presence of the organism with the history and clini- Classical signs
cal signs.
● The only presenting sign is chronic
Dark-field or phase contrast microscopy can also be diarrhea.
used to identify the motile, curved bacteria on fresh
fecal samples. Gram-stained samples can also be used
Pathogenesis
to identify the gull wing-shaped rods in the feces.
However, these approaches are less sensitive and require The pathogenesis of idiopathic juvenile diarrhea is
more technical skill. unknown.

The disorder occurs in kittens and young cats under Vomiting is the most common sign following inges-
a year of age. tion of plant material, whether or not it is poison-
ous/toxic to the gastrointestinal tract or not.
The only clinical sign is presence of chronic small
bowel diarrhea. Other signs may include anorexia, drooling, dyspha-
gia or diarrhea.
Kittens are otherwise healthy, active and gain weight
Diagnosis
Diagnosis
History of exposure or ingestion is essential in many
The diagnosis is one of exclusion. Thus, infectious,
cases, because there is so much variability in presen-
parasitic, dietary and mechanical disorders must all be
tation.
ruled out.
Plants that cause vomiting due to irritation or direct
Cats with this syndrome are often purebred cats, and
GI upset include Philodendron, Diffenbachia (dumb
the diarrhea is self-limiting once they reach adult-
cane), Euphorbia (poinsettia), Caladium, Ricinus (cas-
hood.
tor bean), Robinia and Solanum (tomato, eggplant or
nightshade) spp. to name a few of the more common
Differential diagnosis plants.
Because this is a disease of kittens, bacterial, viral, par- Plants that cause vomiting secondary to nephrotoxi-
asitic, protozoal, dietary and toxic causes of diarrhea city include Lilium (lily), Rheum (rhubarb) and Oxalis
must all be carefully considered. spp.
Treatment
There is no known effective treatment for this condi-
Consider dietary indiscretion, foreign body or ingestion
tion. But, since it is self-limiting, owners should be
of other toxins if there is an acute onset of vomiting or
instructed not to give up prematurely.
diarrhea in an otherwise healthy cat.
Cats ingesting plants that are nephrotoxic will have
Prognosis
signs that are indistinguishable from other causes of
The prognosis is good once the kitten reaches adult- vomiting due to systemic metabolic, infectious or
hood. inflammatory diseases.
PLANT INGESTION/TOXICITY Treatment

In most cases, the vomiting is self-limiting after the
Classical signs
offending plant is removed from the GI tract.
● Acute onset of drooling, vomiting or
Gastric protectants (e.g. sucralfate 0.5–1 g/cat PO) or
diarrhea due to the irritant effects on
histamine-2 antagonists (e.g. famotidine, 0.5 mg/kg
mucous membranes.
PO or SQ q 24 h) may be indicated if severe gastritis
● More severe and prolonged vomiting,
develops.
diarrhea, depression or anorexia may
occur if hepatic or renal failure occurs as Gastric lavage may be helpful if large amounts of
a result of the toxicity. irritant plants are consumed and is important follow-
ing ingestion of toxic plants to reduce further absorp-
See main references on page 646 for details. tion of toxic substrates.
Other treatments that may be necessary include fluid Hydroxyurea (7.5 mg/kg q 12 h PO) may also be used
therapy, anti-emetics such as metoclopramide (0.2–0.5 to reduce eosinophil production. It is administered for
mg/kg PO or SQ q 8 h), and offering food that is 3–14-day courses, as required to maintain the cat in
bland or highly digestible. remission.
Once signs of nephrotoxicity are observed following Nutritional or fluid support is often required until the
lily plant ingestion, progression to anuric renal fail- disease is brought under control.
ure and death is unavoidable. Supportive care with
fluid therapy may slow the onset of signs, but there is
Prognosis
no effective treatment.
The prognosis is guarded to poor.
HYPEREOSINOPHILIC SYNDROME
PERITONITIS
Classical signs
● Severe, small bowel diarrhea that may be Classical signs
unresponsive to treatment.
● Abdominal pain, lethargy, ascites, anorexia
● The hemogram is characterized by
and fever are common signs.
peripheral eosinophilia and there is
● Vomiting or diarrhea are less frequent, but
infiltration of eosinophils in the bone
often observed in more severe cases.
marrow, spleen, liver, lymph nodes and
other organs.
Clinical signs
Clinical signs Intestinal perforation secondary to string or other for-
eign bodies, is the most common cause of peritonitis.
The clinical signs are similar to those of cats with IBD
Other causes include penetrating wounds and chemi-
except the intestinal wall thickening is more pro-
cal peritonitis (due to bile duct rupture).
nounced, hepatosplenomegaly is common, and
bloody diarrhea is common. The diarrhea is usually Abdominal discomfort/pain, lethargy and anorexia
chronic rather than acute. are common signs.
Some cats will cough, have skin lesions (miliary der- Vomiting or diarrhea are not common signs, but
matitis) and have peripheral lymphadenopathy, but when they occur are often associated with severe dis-
these clinical signs are less common. ease.
Fever and abdominal distention/effusion may also be
Diagnosis present.
Histopathologic examination of liver, spleen, lymph
node or intestinal biopsies provides the definitive Diagnosis
diagnosis. There is infiltration of these organs by large
Abdominal radiographs (plain, contrast) and ultra-
numbers of normal eosinophils.
sonography will suggest peritonitis and may pinpoint
location or cause (ruptured gallbladder, pancreatitis,
Treatment bowel rupture).
The cornerstone of treatment is high-dose pred- Definitive diagnosis confirming the presence of peri-
nisolone therapy (3–6 mg/kg/day PO), but relapses tonitis is with abdominocentesis or diagnostic peri-
are common, even if the high doses of steroids are toneal lavage and cytologic/bacteriologic examination
maintained. of fluid.
Hematology is non-specific: inflammatory leukogram, Diagnosis

stress leukogram or sequestration of neutrophils.
The diagnosis is presumptive if surgical resection is
the cause.
SHORT BOWEL SYNDROME
Cats are often hypoproteinemic, may be hypocholes-
Classical signs terolemic, and have other non-specific hemogram or
chemistry abnormalities.
● Severe, and in some cases intractable,
small bowel diarrhea. Imaging studies can be used to confirm the diagnosis.
● Peracute onset of vomiting, depression and
anorexia if associated with ischemic Differential diagnosis
intestinal disease. Other diseases that may cause similar signs include
severe infectious enteropathies, inflammatory bowel
disease or alimentary neoplasia.
Pathogenesis
Short bowel syndrome is classically due to surgical Treatment
resection of a large segment (75–90%) of the small If the disease is spontaneous in the adult cat, stabi-
intestine that results in fluid overload to the colon and lization and prompt surgery is required.
resultant diarrhea.
Tincture of thyme will allow the bowel to adapt when
Other causes include ischemic intestinal diseases the syndrome is iatrogenic in origin.
such as intussusception, bowel strangulation and
intestinal volvulus, which are very rare in the cat. Broad-spectrum antibiotics may be needed.
Intestinal adaptation occurs in the large bowel, Low-fat, highly digestible diets are necessary to max-
which ultimately results in a return to a soft or semi- imize absorption of nutrients.
formed fecal specimen. Fat-soluble vitamins should be administered as
If greater than 85% of the small intestine has been needed. Cobalamin 125–250 μg SQ once per week
removed the chance for adaptation is poor. until serum concentrations are normalized, then every
1–2 months to maintain levels. Folate 0.5 mg PO daily
Congenital forms of short bowel syndrome are also until serum levels normalized then as required.
rare, and will be seen in kittens with intractable diar- Vitamin E supplementation may also be needed.
rhea.
Parenteral nutrition may be required in some cats in
the early stages to support them until bowel function
Clinical signs returns.
Diarrhea, dehydration and weight loss all occur as Prognosis

a result of short bowel syndrome.
Guarded; in cats where diarrhea persists for longer
Other signs are related to intestinal malabsorption: than 2 months after the resection, the prognosis for
deficiency of proteins, vitamins or clotting factors. a return to function is poor.
Small intestinal bacterial overgrowth may also occur
resulting in vomiting or anorexia as well.
EXOCRINE PANCREATIC INSUFFICIENCY
If associated with ischemic intestinal diseases, evi-
dence of endotoxemia and shock may be present. Classical signs
Depression, anorexia and vomiting are the most ● Weight loss despite a vigorous appetite,
common signs. The acuteness and severity of the which may include pica and coprophagy.
signs depend on the extent of the bowel compromise.
Classical signs—Cont’d Vomiting and anorexia are also occasionally

reported.
● Fecal characteristics may be normal, soft
and voluminous or watery diarrhea. The feces are typically pale, loose, voluminous, and
● Poor haircoat and greasy, flaky seborrhea they may be quite malodorous.
are also common. Cats often have a greasy, flaky haircoat due to the fat
malabsorption.
Pathogenesis Deficiencies of fat-soluble vitamins can result in a

bleeding disorder (vitamin K-responsive coagulopa-
Exocrine pancreatic insufficiency (EPI) is very rare in thy), which may present as excessive bleeding from
the cat compared to the dog. venepuncture sites or spontaneous hemorrhage
The most common cause of EPI in the cat is chronic (nose bleeds, hematuria, melena, etc.).
pancreatitis.
A less common cause of EPI is infestation with the Diagnosis
feline pancreatic fluke, Eurytrema procyonis.
Results from routine hematology and chemistry pro-
Other, possible causes of EPI in cats include pancre- files will be normal in most cats. Occasionally, ele-
atic adenocarcinoma and congenital pancreatic acinar vations in hepatic enzymes or neutrophilia will be
hypoplasia or aplasia. observed.
Idiopathic pancreatic acinar atrophy, the most com- Routine abdominal radiography and ultrasonogra-
mon cause of EPI in dogs, has not been reported in cats. phy is usually normal, and is not diagnostic.
In humans with EPI caused by chronic pancreatitis, dia- Fecal proteolytic activity testing will reveal unde-
betes mellitus occurs concurrently. It is unknown tectable levels of enzymes, which is diagnostic for
whether cats with chronic pancreatitis and EPI will EPI, but the test is very labile, so false-positive tests
also progress to develop diabetes mellitus as well. occur to improper sample handling.
EPI is believed to develop when > 90% of the enzymes A recently validated radioimmunoassay for feline
of the exocrine pancreas are destroyed. These trypin-like immunoreactivity (fTLI) is available,
enzymes play an integral role in assimilating the major much like the TLI test available for use in dogs.
food components: proteins, lipids and carbohydrates.
Severely decreased fTLI concentrations are diag-
Pancreatic enzymes increase the efficiency of breakdown nostic for EPI in cats.
of macromolecules in the digestive tract and enhance the
transport mechanisms for sugars, amino acids and fatty All cats with EPI should have a serum cobalamin
acids. Thus, food substances are inefficiently broken and folate assay, since many cats with EPI are cobal-
down and cannot be readily transported across the amin deficient or have concurrent small bowel disease,
intestinal lumen without pancreatic enzymes. causing folate levels to be low.
Diarrhea occurs due to the presence of large quantities

of fats, protein and carbohydrates, which are osmotic. Differential diagnosis
Maldigestion of these important nutrients leads to The clinical signs are so non-specific that many other
weight loss and may also cause deficiencies of vita- diseases that cause polyphagia, weight loss and diar-
mins, fatty acids or other essential nutrients. rhea must be considered: hyperthyroidism, diabetes
mellitus, corticosteroid treatment or hyperadrenocorti-
cism, chronic renal failure, heart failure, liver disease,
Clinical signs dental disease, neoplasia, and chronic intestinal dis-
The most common clinical signs are polyphagia, eases such as inflammatory bowel disease and ali-
diarrhea and weight loss. mentary lymphoma.
Treatment recognized and appropriately managed, it may be pos-

sible to prevent the consequences of chronic pancreati-
Most cats with EPI can be successfully treated by tis-EPI.
dietary supplementation with pancreatic enzymes.
The powder products (1 tsp per meal) appear to be
more clinically effective than tablets. TYZZER’S DISEASE (BACILLUS
PILIFORMIS)
If the cat refuses to eat the food with pancreatic extract,
raw pancreas can be offered, but it is essential to use Classical signs
bovine pancreas to prevent transmission of
Aujeszky’s disease in porcine pancreas in areas ● The disease occurs primarily in kittens at
where the disease occurs. weaning age, but is rare.
● Rapid onset of depression, abdominal
A diet that contains low amounts of insoluble fiber discomfort.
should be fed, since insoluble fibers may interfere with ● Death within 24–48 hours is common, but
pancreatic enzyme activity. some may have signs several days before
Some cats will not respond to enzyme supplementation death.
alone, and this may be due to concurrent cobalamin
deficiency or small intestinal disease. Cobalamin Pathogenesis
supplementation should be given parenterally
(100–250 μg SC once weekly for 6–8 weeks, then Disease is caused by Bacillus piliformis, a spore-
monthly or bimonthly as needed). forming, Gram-negative, intracellular bacillus.
In cats with suspected vitamin K deficiency, supple- This is primarily a disease of laboratory rodents,
mentation should also be initiated (vitamin K1 and is very rare in cats and dogs, but may be seen in
1 mg/kg/day PO). kittens and especially weanlings.
Other supplements that should be given include: toco- The source of the infection is believed to be rodent
pherol (30 IU orally, once daily with food for the first feces.
month until levels are normalized), and folate (0.5 mg The organism proliferates in the intestinal epithe-
orally, once daily). lium producing enterocolitis and then spreads to the
It is unknown whether or not cats develop small liver and systemic circulation.
intestinal bacterial overgrowth as a complication of
EPI as is common in dogs. However, in cats that do Clinical signs
not respond as anticipated to pancreatic enzyme sup-
plementation, addition of metronidazole or tetracy- The most common signs are an acute onset of depression
cline to the treatment regime is indicated. and abdominal discomfort.
Death usually occurs within 24–48 hours, although
Prognosis weight loss and recurrent or chronic diarrhea can
occur in older cats.
Because EPI is associated with the irreversible loss of
pancreatic acinar tissue, complete recovery is not The diarrhea is typically infrequent, scant and
possible. pasty.
However, with appropriate management, cats with EPI will

gain weight, pass normal feces and can live a normal life. Diagnosis
There is no ante-mortem test for Tyzzer’s disease,
Prevention and most frequently, the diagnosis is made by necropsy.
There is no known way to prevent the development of The lesions are most severe in the ileum, colon and
EPI, however, if cats with chronic pancreatitis can be liver, with the ileum and colon being severely thickened.
Special stains (Giemsa) will reveal the filamentous Treatment

organisms in the histopathologic specimens.
There is no known effective therapy.
The organism is difficult to culture because of its
intracellular, microaerophilic nature. Supportive care with antibiotics, fluids and mainte-
nance of body functions (temperature, nutrition) are
essential.
The disease is so peracute that panleukopenia must be Prognosis
considered, as well as other infectious agents that cause
severe enteritis and systemic disease. Poor.
RECOMMENDED READING
August JR (ed). Consultations in Feline Internal Medicine II. Philadelphia, PA, WB Saunders, 2001.
Ettinger S. Textbook of Veterinary Internal Medicine, Vol. 5. 2000.
Greene CG (ed). Infectious Diseases of Small Animals, 3rd edn. Philadelphia, PA, WB Saunders; 2005.
Guilford WG, Center SA, Strombeck DR, et al (eds). Strombeck’s Small Animal Gastroenterology, 3rd edn.
Philadelphia, PA, WB Saunders, 1996.
Marks SL, Kather EJ. Bacterial-associated diarrhea in the dog: a critical appraisal. Vet Clin North Am Small Anim
Pract 2003; 33: 1029–1060.
Suchodolski JS, Steiner JS. Laboratory assessment of gastrointestinal function. Clin. Tech. Small. Anim. Pract.,
2003; 18: 203–210.
33. The cat with signs of chronic small
bowel diarrhea
Debra L Zoran
KEY SIGNS
● ± Melena.
● No mucus or fresh blood.
● > 3 weeks duration.
MECHANISM?
● Diarrhea may be defined as a change in the frequency, consistency or volume of bowel
movements.
● The four recognized pathophysiologic mechanisms that cause diarrhea include osmotic,
secretory, increased permeability and altered motility.
● Osmotic diarrhea and conditions causing increased permeability are believed to be the most
common causes of diarrhea.
● Classification of diarrhea by characteristics that tend to be more prevalent in small vs. large
intestinal disease is a helpful way to develop an appropriate diagnostic and treatment regimen.
Small bowel diarrhea is characterized by:
● Increased volume of feces.
● Normal to increased frequency of defecation.
● No or little straining or tenesmus associated with defecation.
● If blood is present in feces it occurs as melena.
● No increase in mucus on the feces.
● Weight loss and vomiting are commonly observed concurrently.
WHERE?
● The small intestinal tract (duodenum, jejunum and ileum) is the site of origin of the diarrhea.
However, diseases in other body systems may cause diarrhea in an otherwise normal
intestinal tract (e.g. liver disease, hyperthyroidism, etc.).
WHAT?
● Chronic small bowel diarrhea is a clinical sign that should be aggressively evaluated to
determine its cause.
● Cats with chronic diarrhea of small intestinal origin may have any of a number of GI or
systemic diseases or disorders, but metabolic (hyperthyroidism, renal or liver disease, etc.),
idiopathic (inflammatory bowel disease), neoplastic (lymphoma), and nutritional (food
allergy or intolerance) are common causes.
734
33 – THE CAT WITH SIGNS OF CHRONIC SMALL BOWEL DIARRHEA 735

Diseases causing signs of chronic small bowel diarrhea
ANOMALY
● Intestinal diverticulosis (p 759)
These are rare disorders that are most commonly found in the jejunum, and may be subclinical or
associated with vomiting, diarrhea or abdominal pain.
MECHANICAL
● Intussusception (p 756)
Acute onset of diarrhea may occur due to alterations in gut motility, however, vomiting is a more
prominent clinical sign.
● Short bowel syndrome (p 760)
This iatrogenic syndrome is associated with resection of 75–90% of the small intestine and results
in severe diarrhea and weight loss. Congenital forms of short bowel syndrome are reported, but are
rare.
METABOLIC
Intermittent diarrhea, vomiting or voluminous stools in an older cat with a good to ravenous
appetite, obvious weight loss and a poorly groomed coat are characteristic of this disease.
● Exocrine pancreatic insufficiency (EPI) (p 751)
This is a rare disease in cats, but is typically associated with small bowel diarrhea, weight loss and
a ravenous appetite.
● Hypoadrenocorticism (p 754)
The classic signs include depression, weakness, vomiting and diarrhea. However, GI signs do not
occur in all cases, and the cause of the vomiting or diarrhea is unknown. Some cats will not
develop concurrent mineralocorticoid deficiency with the glucocorticoid deficiency, and thus elec-
trolyte disturbances will not be apparent.
NEOPLASTIC
● Alimentary lymphosarcoma* (p 742)
This is the most common neoplasm of the feline intestine, and because of the lymphocytic infil-
trate and clinical presentation, is easily confused with IBD. Most cats with alimentary lymphoma
are FeLV antigen negative. Aggressive chemotherapy is the only effective treatment, and may
result in a 3–12-month survival time.
● Intestinal adenocarcinoma (p 750)
The intestinal tract is a much less common location for adenocarcinoma than the colon in cats.
This tumor is the second most common intestinal tumor and tends to cause obstructive lesions of
the ileum that frequently cause vomiting, but may also be associated with diarrhea. Siamese cats
may be predisposed.
● Intestinal mast cell tumor (p 753)
Intestinal mast cell tumors are the third most common neoplasm affecting the feline small bowel,
but are rare occurrences. This tumor is aggressive, poorly responsive to therapy and usually has
metastasized by the time of diagnosis.
continued
continued
● Other small intestinal neoplasia (fibrosarcoma, carcinoids, plasmacytoma) (p 757)

Other malignant and benign neoplasms that may be associated with vomiting, diarrhea, weight loss
or anorexia in cats include fibrosarcoma, plasmacytoma, hemangiosarcoma, leiomyosarcoma, etc.
Clinical signs and prognosis are dependent on the location of the tumor, the type of tumor and its
response to therapy. Tumors of the duodenum are rare and usually associated with extension of a
local neoplasm.
● APUDomas (p 758)
Neoplasms of APUD cells are rare tumors in the cat. They include insulinomas, gastrinomas,
pheochromocytomas and carcinoid tumors of the GI tract. Clinical signs will depend on the tumor
type, but carcinoid tumors are most likely to cause diarrhea.
NUTRITIONAL
● Food intolerance*** (p 740)
Food intolerance is a non-immune-mediated condition associated with intermittent diarrhea or vom-
iting, with no pattern or association with eating, and it resolves when the food source is changed to
omit the offending substance from diet. The clinical significance of food intolerance is unknown
relative to other causes of diarrhea because of the difficulty in obtaining a definitive diagnosis.
IMMUNOLOGIC
● Food allergy (dietary hypersensitivity)*** (p 739)
Chronic vomiting appears to be more common than diarrhea in cats with food allergy, and cutaneous
signs may also be present.
IBD is a chronic inflammatory disease of the GI tract of unknown etiology. It affects cats of all
ages, sexes and breeds, but is most commonly found in middle-aged, purebred adult cats.
Lymphocytic plasmacytic enteritis is the most common histologic form of IBD, but eosinophilic
and suppurative infiltrates occur as well.
● Inflammatory hepatobiliary disease (cholangitis) (p 746)
The clinical presentation of cholangitis is non-specific and presenting signs include anorexia,
lethargy, weight loss, vomiting, diarrhea, dehydration, hepatomegaly and icterus.
INFECTIOUS:
Viral:
● Feline coronavirus infections (feline enteric coronavirus/feline infectious peritonitis) (p 749)
Feline enteric coronavirus results in mild, self-limiting diarrhea or subclinical infection. In FIP, the GI
tract is rarely affected singularly, and so, vomiting or diarrhea is often associated with the effects of the
disease on other organs. Rarely, FIP causes intestinal granulomas that obstruct the GI tract and cause
vomiting or diarrhea. Systemic signs of FIP may include lethargy, anorexia, pyrexia and CNS signs.
● Feline immunodeficiency virus (p 749)
Diarrhea is not a common presenting sign of cats with FIV, but diarrhea can occur secondary to the
immunodeficiency disease or result from a purulent form of colitis that can occur in a small num-
ber of cats that are infected with FIV.
Bacterial:
● Clostridium perfringens enterocolitis/clostridial enterocolitis (p 748)
Diarrhea occurs due to sporulation of clostridial organisms and release of enterotoxin resulting in a
secretory diarrhea that is usually small bowel in character, but may also have a large bowel compo-
nent.
● Campylobacteriosis (p 750)
Campylobacter infection may cause mucoid, bloody diarrhea, weight loss, anorexia and fever in
affected kittens or young cats. Most affected cats are from shelters or catteries that have crowded
conditions and poor hygiene.
Protozoal:
● Giardiasis* (p 744)
Acute or chronic small bowel diarrhea is the most common clinical presentation. However, in
some cats large bowel diarrhea also may occur.
Fungal:
● Histoplasmosis (p 755)
Diarrhea associated with intestinal histoplasmosis is uncommon in cats compared to dogs. The
most common clinical signs in cats are associated with respiratory infection, or anorexia, fever and
weight loss associated with systemic illness.
Parasitic:
● Coccidiosis (isosporosis, cryptosporidiosis, toxoplasmosis)** (p 741)
Infections that result in mild to moderate diarrhea are most common in neonates and immunosup-
pressed adults. Most adults have asymptomatic infestations. The species of coccidia most com-
monly associated with disease in cats are Cystoisospora spp., Cryptosporidium parvum, and
occasionally Toxoplasma gondii. Toxoplasmosis has recently been observed in association with IBD.
Idiopathic:
● Idiopathic juvenile diarrhea (p 753)
This condition is associated with small bowel diarrhea and occurs in kittens or young cats less than
a year of age. There is no known cause for the diarrhea and when the cat reaches adulthood, the
diarrhea resolves.
● Protein-losing enteropathy (p 760)
This condition is much less common in cats than in dogs, but may result in chronic diarrhea, mal-
absorption, weight loss and hypoproteinemia. Primary lymphangiectasia is rare, but secondary
causes of lymphatic obstruction, such as inflammation or neoplasia, are relatively more common
and must be considered.
This rare disorder is associated with eosinophilic IBD and systemic eosinophilia (increased circu-
lating eosinophils and eosinophilic infiltrate in the lymph nodes, etc). It is usually associated with
chronic vomiting, diarrhea, and weight loss, and is poorly responsive to treatment.
also an important cause of both acute and chronic

INTRODUCTION diarrhea. Inflammatory bowel disease, lymphatic
obstruction (due to lymphangiectasia or mucosal
MECHANISM? inflammation), systemic diseases that alter GI blood
flow or mucosal integrity, neoplasia, enteric pathogens
Chronic small intestinal diarrhea is distinct from
and parasites, and toxins may all produce diarrhea by
acute diarrhea, in that the disease or disturbance caus-
this mechanism.
ing the problem is not self-limiting.
Altered intestinal motility, either increased or
Diarrhea is the most consistent manifestation of
decreased segmentation or propulsion movements will
intestinal disease.
cause diarrhea. Unfortunately, evaluation of intestinal
In cats with small bowel diarrhea for > 3 weeks dura- motility is a difficult process, and differentiating cause
tion, an aggressive search for the cause should be from effect in motility problems even more challeng-
undertaken. ing. Diarrhea due to intestinal motility disturbances
may be caused by stagnant loop syndrome, dysautono-
Characteristics of small bowel diarrhea include:
mia, ileus, loss of segmentation or peristalsis due to
● Large volume of watery or very soft feces.
drugs, toxins, etc.
● No mucus or hematochezia, and if blood is pres-
ent it occurs as melena. Chronic small bowel diarrhea is often a sign of
● There is little or no straining or tenesmus. a serious small intestinal disease (e.g. inflammatory
● Weight loss and vomiting are commonly observed. bowel disease, neoplasia, lymphangiectasia, severe
● The frequency of defecation is normal to food intolerance, or a chronic infectious disease) which
increased. should be thoroughly investigated.
Diarrhea occurs when there is an increase in fecal However, systemic disorders such as EPI, renal fail-
water, which can occur due to a variety of small or ure, liver disease and some endocrinopathies (e.g.
large intestinal disorders, but has been generally hyperthyroidism, APUD tumors and hypoadrenocorti-
grouped into four categories: osmotic, permeability, cism) will also cause chronic diarrhea and should not
secretory and motility disturbances. be overlooked.
Chronic diarrhea due to increased osmotically active

substances present in the lumen is usually associated
WHERE?
with GI malabsorption syndromes (EPI, liver failure,
severe small intestinal disease, lymphangiectasia, etc.) Small bowel diarrhea can be the result of disease in the
or dietary overload. small intestine (duodenum, jejunum, ileum) or occur
secondary to organ failure (hepatic, renal or pancreatic
Increased secretion of water and electrolytes is usu-
disease) or endocrinopathies (hyperthyroidism, hypoa-
ally a cause of acute small bowel diarrhea, which occurs
drenocorticism, or rarely APUD tumors).
primarily as a result of activation of cellular second
messenger pathways (cAMP, cGMP, etc.) by enteric A careful history and physical examination will
pathogens. Conditions that cause diarrhea by increas- determine whether the problem is likely related to the
ing secretory mechanisms include bacterial infections GI tract or a systemic problem.
with enterotoxigenic or endotoxin-producing species,
Diagnostic tests that will aid localization of the prob-
the presence of unconjugated bile acids in the small
lem include a hemogram, chemistry profile, fecal
bowel or increased secretion due to endocrine tumors.
analysis, intestinal function studies (fTLI, cob/folate)
The presence of increased intestinal permeability due and abdominal imaging studies (radiographs or ultra-
to inflammation, erosion/ulceration or necrosis is sound).
There may also be dermatologic signs, such as pruritus,

WHAT?
alopecia, miliary dermatitis, seborrhea, pustules, etc.,
Cats with small bowel diarrhea of a chronic nature which affect the head, face, ears and inner thigh espe-
often have severe intestinal disease (neoplasia, inflam- cially, and are non-seasonal in occurrence.
matory bowel disease), or systemic illness/organ fail-
Dermatologic signs need not be present to attribute
ure (hepatitis, pancreatic disease such as EPI or
GI signs to food allergy.
hyperthyroidism).
Respiratory tract hypersensitivity is reported
Diagnosis is based upon history and physical exami-
in humans but is poorly documented in cats. However,
nation findings, radiography, hematology and serum
the propensity for cats to develop airway hyper-
chemistry profiles, serology if indicated for
sensitivity may warrant further consideration of this
FeLV/FIV, etc., serum TLI, fecal analysis, including
possibility.
cytology or alpha-1 protease inhibitor testing, and
histopathology. Most cats are young adults when signs first develop,
but the signs can occur in any age, breed or sex of
DISEASES CAUSING SIGNS OF cat.
CHRONIC SMALL BOWEL DIARRHEA
(> 3 WEEKS DURATION) Diagnosis
The definitive diagnosis of food allergy is only
FOOD ALLERGY (DIETARY obtained by feeding an elimination diet. The signs
HYPERSENSITIVITY)*** will resolve after 6–9 weeks (there is usually a clinical
response within 1–3 weeks), with reintroduction of the
Classical signs offending diet resulting in the reappearance of signs
within 4–10 days.
● Vomiting or diarrhea.
● Anorexia and weight loss. Other diagnostic tests, including intradermal skin test-
● Pruritus or miliary dermatitis. ing, ELISA testing, RAST testing, and gastroscopic
● Alopecia. food testing have all been tried in an attempt to find
● Seborrhea. easier methods of making the diagnosis. However, all
of these tests are fraught with false-negative and
See main reference on page 667, Food sensitivity, in -positive results that limit their usefulness. The only
“The Cat With Signs of Chronic Vomiting” for details. reliable test currently available is the food elimina-
tion trial, which is also used in humans.
Clinical signs In most cats, the hemogram and chemistry profile
will be completely normal or have mild non-specific
Food allergy is an adverse reaction to food that has
changes associated with inflammation (e.g. eosinophilia,
a proven immunologic component.
proteinuria).
Gastrointestinal signs are variable, but can include
The elimination diet chosen to make the diagnosis
vomiting, diarrhea, flatulence, weight loss or anorexia.
will depend on the cat’s preferences for food, the
Diarrhea can be profuse and watery suggesting small
owner’s willingness to make homemade foods, and
bowel disease, or mucoid and hemorrhagic, consistent
the clinical situation. However, the best elimination
with colitis. The true incidence of GI signs associated
diet is a diet containing a single, novel protein
with food sensitivity is unknown.
source (turkey, venison, duck, rabbit, ostrich, kanga-
Signs tend to occur suddenly after the animal has roo, crocodile, whitefish, etc.) and a single, novel car-
been on a particular diet for months or years. bohydrate source (rice, potato, etc.), with no other
additives except a pet vitamin. Use either a commer-

FOOD INTOLERANCE***
cial hypoallergenic diet or a homemade diet (see
page 741, Food intolerance, for details).
Classical signs
Intestinal biopsies will have mild to severe infiltrates
● Signs may range from intermittent
of inflammatory cells, which may be lymphocytic,
vomiting or diarrhea to pruritus, dermatitis
plasmacytic or eosinophilic or a combination of those
and other dermatologic signs.
cell types. There is currently no way to differentiate
the inflammatory infiltrates present in cats with
See main reference on page 669, Food sensitivity in
food allergy from those typically seen in cats with
“The Cat With Signs of Chronic Vomiting” for details.
IBD.
Clinical signs
Adverse reactions to foods may be dermatologic or
The presence of dermatologic signs suggests that gastrointestinal and the percentage of signs associated
atopy and flea allergy as well as other dermatologic with either component is unknown.
conditions should be considered.
Intermittent to persistent vomiting (usually < 1 day)
Some cats will have GI signs only, and thus other dif- or diarrhea are the most common GI signs. Flatulence
ferentials such as food intolerance, parasites, and meta- and weight loss may occur.
bolic or neoplastic diseases should be considered.
Dermatologic signs may include pruritus, dermatitis or
Inflammatory bowel disease is also a disease that
alopecia.
mimics food allergy and is very difficult to differenti-
ate from it. In contrast to food allergy, food intolerance is a non-
immunologic reaction, and can occur on the first
exposure to the offending food or additive. A wide
Treatment variety of food ingredients may be responsible.
Once an elimination diet has been identified that suc- The relative occurrence of GI versus dermatologic
cessfully relieves the clinical signs, the cat should signs and the importance of one or the other in the diag-
remain on that diet indefinitely. However, it is best nosis of food intolerance is unknown. However, a com-
to try to identify a commercial diet that most bination of dermatologic and GI signs should raise the
closely resembles the elimination diet so that the cat index of suspicion of a food-related problem.
receives a nutritionally complete and balanced
diet. Most homemade elimination diets are not nutri-
tionally balanced and are not suitable for long-term Diagnosis
maintenance. There is no diagnostic test for this problem other than
Cats may develop a hypersensitivity to any diet, to observe a beneficial response to an appropriate
including the so-called hypoallergenic diet, and in that dietary trial for 1 week. Resolution of clinical signs is
situation, another novel protein source will need to be often apparent within 4 days.
selected. The best elimination diet to obtain a diagnosis is made
Most cats with food allergy only respond partially or do from a single novel protein and novel carbohydrate
not respond at all to prednisolone therapy or anti- source with no added colors or preservatives. For the
histamines. homemade diet, boiled white rice or potato (1/3 cup)
and a novel meat source that the cat has not previously
The importance of preventing access to any food eaten (2/3 cups venison, rabbit, duck, ostrich, crocodile,
other than the elimination diet should be emphasized kangaroo, tofu, turkey, whitefish, etc.) are good options.
to the owners. Use food intended for human consumption, not pet meat.
Alternatively, a commercially available hypoaller- Classical signs—Cont’d

genic diet made from a single novel protein or protein
hydrolysate is also a useful test diet. Once a diagnosis ● Weight loss, anorexia and dehydration may
of food sensitivity (food intolerance or food allergy) occur if severely affected.
has been made, a commercial hypoallergenic diet con- ● Most adult cats will be asymptomatic or
taining novel protein and carbohydrate sources should have subclinical infections.
be used for long-term maintenance, as homemade diets
are rarely balanced and complete. See main reference on page 705 for details (The Cat
Intestinal biopsies from cats with food intolerance
may be normal, or may have mild to moderate infil-
trates of lymphocytes, plasma cells or eosinophils, Clinical signs
depending on the duration of intolerance and severity The principal clinical sign of coccidiosis is acute
of clinical signs. small bowel diarrhea, which may be bloody, mucoid
or watery. It usually occurs in young cats or kittens
Differential diagnosis as acute diarrhea, but may persist and present as
chronic diarrhea. In severely affected kittens, weight
Intermittent but unrelenting vomiting in an other- loss, anorexia and dehydration may also occur.
wise healthy cat suggests gastrointestinal motility dis-
turbance, gastric parasites, early inflammatory bowel Other signs that may be observed include vomiting,
disease or antral pyloric hypertrophy. weight loss, lethargy and dehydration.
In cats where diarrhea is the presenting sign or Adult cats that are infected with coccidian parasites
occurs in addition to vomiting, hyperthyroidism, (including cryptosporidia) are typically asymptomatic.
chronic pancreatitis, early renal or liver disease, and Young or immunocompromised cats with cryp-
other primary GI abnormalities such as neoplasia or tosporidiosis will have profuse, watery diarrhea and
intermittent intussusception, must be considered. mesenteric lymphadenopathy due to intestinal hyper-
secretion and malabsorption.
Treatment Toxoplasma infections are also rarely associated with
Change to a diet that does not contain the offending diarrhea, but in cats with immunocompromise or other
substance. This may be as simple as changing from significant bowel conditions (e.g. IBD), quiescent toxo-
a grocery store brand to a premium brand food (or vice plasmosis may be re-activated and cause clinical signs.
versa), but also may require changing to a hypoaller-
genic food diet (e.g. IVD’s Limited Antigen diets, Hill’s
d/d or z/d, Eukanuba Response formula, Royal Canin Diagnosis
Select Protein) or in some cases, formulating a home- Diagnosis is made by identification of isosporoid
made diet that is complete and nutritionally balanced. oocysts in fresh feces.
Since the abnormal gastrointestinal response is non- The oocysts of cryptosporidia are 1/10th the size of
immunologic, use of oral prednisolone is not likely to Isospora (smaller than RBCs and 1/16th the size of
be beneficial. a Toxocara cyst). Toxoplasma oocysts are only
slightly larger.
COCCIDIOSIS (ISOSPOROSIS,
CRYPTOSPORIDIOSIS, TOXOPLASMOSIS)** Special flotation media (Sheather’s sugar or zinc sul-
fate flotation) is required along with special staining
Classical signs (Kinyoun’s carbolfuchsin negative) or phase contrast
microscopy, to identify cryptosporidia.
● In young cats or kittens acute small bowel
diarrhea occurs. Other methods of identification of fecal cryp-
tosporidia include an ELISA test, but its effectiveness
in identifying feline species of cryptosporidia is hypercalcemia or abnormal electrolytes due to vomit-

unknown. A PCR test for Cryptosporidium DNA in ing or diarrhea.
the feces, or electron microscopy of intestinal biopsy
Imaging studies, especially abdominal ultrasound, are
samples may also be used.
important in identifying and localizing intestinal abnor-
Fecal samples submitted to the laboratory for identifi- malities. Fine-needle aspirates of lymph nodes or affected
cation of cryptosporidia should be preserved in for- segments of bowel may point toward the diagnosis.
malin to minimize the risk of human infection.
The key to diagnosis is identification of neoplastic
Toxoplasma titers (both IgG and IgM) can be submit- lymphocytes in the intestinal mucosa or wall. This
ted to determine the presence of acute, chronic or pre- may be achieved by fine-needle aspirates, endoscopic
vious infections. See main reference on page 958. brush cytology or histopathology. Endoscopic biopsies
are an excellent method of obtaining tissue for diagno-
sis, but the biopsies must be of good quality to be use-
ALIMENTARY LYMPHOSARCOMA*
ful. Samples must include mucosa and muscularis
layers, and extend to the submucosa to be diagnostic.
Classical signs
In cats with early, or very well-differentiated lym-
● Chronic, progressive weight loss, anorexia,
phosarcoma, it may be impossible to distinguish lym-
diarrhea and/or vomiting.
phoma from severe IBD, even with full-thickness
● More common in middle aged to older cats.
biopsy samples. In these cases, immunohistochemistry
will be required to separate monoclonal neoplastic cells
from the polyclonal cell of IBD. Unfortunately, this tech-
nique is currently available at only a few institutions.
Clinical signs
Chronic, progressive weight loss, anorexia, diarrhea
and/or vomiting are the most common signs. The primary differential for alimentary lymphoma,
both clinically and diagnostically, is lymphocytic plas-
Lymphoma commonly causes diffuse intestinal thick-
macytic inflammatory bowel disease. However, other
ening due to infiltrative disease, but sometimes there
important differentials include food intolerance/allergy
are focal areas of intestinal constriction due to mass
and severe giardiasis, and systemic diseases such as
lesions or luminal constriction.
cholangitis and hyperthyroidism.
Palpable thickening or mesenteric lymphadenopa-
thy may be important clues to the problem.
Treatment
The best approach is to use multiple-agent chemother-
Diagnosis
apy, using a treatment regimen of stages: (1) induction
The history and clinical signs may be too non-specific of remission, (2) intensification, (3) maintenance and
to be of particular help. (4) rescue.
Palpable intestinal thickening or mesenteric lym- Cats treated with prednisolone alone may improve
phadenopathy is suggestive of neoplasia, but does initially, but once the tumor escapes remission, it is
not rule out other possible causes, such as inflamma- very difficult to re-induce remission.
tory bowel disease, alimentary histoplasmosis or
There are several protocols available, but the COAP pro-
other infectious intestinal diseases (FIP, FIV, severe
tocol is commonly used to induce remission. C =
giardiasis).
cyclophosphamide, O = vincristine (oncovin), A = cyto-
Hemogram and chemistry profile results may be sine arabinoside, P = prednisolone. The induction proto-
normal or will reveal non-specific abnormalities such col generally takes 6–8 weeks, and side effects with this
as chronic non-regenerative anemia, hyper- or hypopro- protocol are minimal. The dose-limiting toxicity is
teinemia, elevations in liver enzyme concentrations, hematologic, and thus, weekly hemograms are required
before each treatment. Specific dosing protocols are Clinical signs

described in detail under alimentary lymphoma in the
chronic vomiting section. Weight loss despite a good to ravenous appetite and
hyperactivity are the most common signs.
Intensification is only used if the induction phase does
not result in complete remission of the tumor. Polyuria/polydipsia, poor coat condition, vomiting,
diarrhea or voluminous feces individually occur in
The most common agents used for intensification in 30–50% of cats.
cats are doxorubricin or mitoxantrone.
Gastrointestinal signs associated with hyperthy-
The COAP protocol is also used for maintenance in roidism are often intermittent or relatively mild, with
cats, but the treatments are spread out to every other the exception of weight loss and appetite changes.
week or every third week for six treatments, with the About 90% of cats have increased appetite, but
goal to be able to maintain the cat with treatment once a small number are depressed and have a reduced
every 4 weeks. Maintenance therapy is continued appetite (apathetic hyperthyroidism).
until the tumor relapses.
Some cats will have tachycardia, a gallop rhythm or
Rescue, or re-induction of remission, is necessary in other signs associated with congestive heart failure
almost all cats and generally occurs 6–8 months after (coughing, increased respiratory rate, weakness) sec-
the start of induction. Rescue protocols are not as suc- ondary to thyrotoxic heart disease.
cessful in cats as they are in dogs. There have been
a wide variety of protocols recommended, and the reader
is referred to an oncology text for further details. In most Diagnosis
cases, the rescue protocol will involve mitoxantrone,
doxorubicin and the other COAP drugs. See the ali- The definitive diagnosis is an elevated serum total
mentary lymphoma section under chronic vomiting for thyroxine concentration (total T4). Other non-specific
specific protocol details. abnormalities of the hemogram or chemistry profile
may include hemoconcentration, mild anemia, elevated
Prognosis serum alanine aminotransferase activity, or hyper-
glycemia.
Most (80%) cats with lymphoma treated with multiple-
agent chemotherapy protocols are expected to live 3–9 A thorough assessment of renal function should be
months. As many as 20% will live for longer than undertaken (BUN, creatinine, urinalysis) before initiat-
1 year. ing treatment of hyperthyroidism because the increased
renal blood flow associated with hyperthyroidism may
Cats that are not treated will live for 4–8 weeks. result in acute renal decompensation when the
Feline leukemia-positive cats have a shorter survival thyroid disease is treated (especially with surgical or
time, not because they do not respond to chemotherapy, radioactive iodine therapy).
but due to development of other feline leukemia- Many cats will have a palpable thyroid nodule.
associated disorders.
Cats with signs of hyperthyroidism but serum T4
concentrations in the upper 1⁄2 of the normal range
HYPERTHYROIDISM*
should be tested using free (unbound) T4 levels, as
false lowering of the T4 level may occur due to non-
Classical signs
thyroidal illness.
● Weight loss despite a good to ravenous
In cats with suspected hyperthyroidism, but normal
appetite.
total or free T4 levels, radioactive thyroid scan can be
● Vomiting, diarrhea or voluminous feces.
performed to confirm the diagnosis. See page 305.
● Poor coat condition. Cats with tachycardia or an abnormal rhythm should
● Hyperactivity. also have thoracic radiographs and an echocardio-
gram performed to determine the extent of thyrotoxic
See main reference on page 304 for details. heart disease and evaluate the need for therapy.
Differential diagnosis Vomiting, dehydration, lethargy and anorexia may

be observed in severe cases, but are uncommon.
The major differentials for an older cat with weight
loss, vomiting or diarrhea include neoplasia, hepatic or Occasionally, chronic small bowel diarrhea with
renal disease, inflammatory bowel disease and chronic weight loss and poor body condition are observed.
pancreatitis. However, the presence of cardiovascular Cats are more likely to also have evidence of acute
signs, a ravenous appetite or hyperactive behavior with or chronic large bowel diarrhea (with hematochezia,
the GI signs should point to hyperthyroidism first. increased mucus and tenesmus) than are other species
affected.
Treatment
Treatment for hyperthyroidism includes both control of Diagnosis
the over-secretion of thyroid hormone as well as its The diagnosis is made by appropriate fecal examina-
effects on the remainder of the body (e.g. thyrotoxic tion techniques. Zinc sulfate flotation is considered
heart disease). to be the most accurate and practical test. Three
There are three commonly used therapeutic consecutive zinc sulfate flotations will identify 95%
approaches to treatment of the hyperthyroid condition of infected animals.
in cats: (1) medical management with methimazole or Other methods include examination of fresh fecal
carbimazole, (2) surgical removal of the adenomatous saline smears for trophozoites (only 40% of infected
thyroid, and (3) radioactive iodine treatment of the animals will be identified), duodenal aspiration of
cat to destroy thyroid follicular cells. fluid for examination for trophozoites (requires
See pages 305 and 671 for details (in The Cat With endoscopy or laparotomy, but is 88% effective), or fecal
Weight Loss and a good Appetite and The Cat with Signs ELISA testing for Giardia-specific antigens (good sen-
of Chronic Vomiting). sitivity, but not specificity).
Fecal ELISA testing is highly sensitive (93% sensitiv-
ity) but has low specificity (60% specificity).
GIARDIASIS*

● Liquid, to semiformed, diarrhea with Many other infectious, parasitic, dietary, toxic and idio-
increased frequency and urgency. pathic causes of small bowel diarrhea must be consid-
● Most cats are bright, alert and afebrile. ered since many cats will have mild signs and be
● Many cats are asymptomatic. otherwise healthy.

With Signs of Acute Small Bowel Diarrhea). Treatment
Metronidazole (25 mg/kg/q 12 h PO for 5 days) con-
Clinical signs tinues to be recommended for treatment of giardiasis in
cats. However, resistant strains of the protozoan are
Most adult cats infected with Giardia spp. remain
increasingly being reported, and thus this therapy may
asymptomatic.
not be effective in all cases.
The most common signs observed are the presence
Side effects associated with metronidazole therapy
of liquid to semi-formed diarrhea, associated with
include gastrointestinal upset and neurologic signs,
increased frequency and quantity of defecation, in
such as seizures, coma and behavioral changes. All of
an otherwise healthy cat.
these are less common in cats than in dogs and are
Most cats remain bright, alert and afebrile. reversible with discontinuation of treatment.
Other drugs that have been recommended for treatment Diagnosis

of giardiasis are quinacrine and furazolidine, but
these drugs may not eliminate the infection, only IBD is a diagnosis of exclusion, that requires two
improve the clinical signs. steps: (1) the histopathologic confirmation of an
excessive inflammatory response in the intestinal
Fenbendazole has been shown to be effective in treat- mucosa, and (2) the elimination of the multitude of
ment of giardiasis in cats and dogs. Another benzi- potential causes for GI inflammation.
madizole, albendazole, is not approved for use in cats
in the United States and it may be teratogenic, hepa- The majority of cats with IBD will have a normal
totoxic or cause bone marrow toxicity. Fenbendazole hemogram and serum chemistry profile. However,
(50 mg/kg/day × 5 days) has been recommended for abnormalities are not uncommon, but they are not
treatment of giardiasis in cats, and especially those specific for IBD. These include leukocytosis, mild non-
with other concurrent parasitic infections. regenerative anemia, increases in liver enzyme concentra-
tions, mild hypoalbuminemia and mild hyperglycemia.
Proper disposal of feces and good sanitation is
essential to remove any environmental contamination. Fecal examination (flotation, direct exam, cytology) is
essential to rule out parasitism, especially giardiasis.
Ultrasound examination is very important, not only
IDIOPATHIC INFLAMMATORY BOWEL in evaluation of the abdomen for structural abnormali-
DISEASE (IBD)* ties, but especially for assessing bowel wall thickness
and lymph node enlargement, which have recently
Classical signs been shown to correlate well with the severity of IBD.
Ultrasound is also important, as it may allow fine-
● Vomiting, anorexia and weight loss are the needle aspiration of abnormalities which facilitate
most common signs of upper GI IBD. diagnosis, but also will help determine the best
● Diarrhea can occur, but is more prevalent approach to take when obtaining the biopsies (full
with colonic disease. thickness vs. endoscopic).
● Affected cats are usually middle-aged or
older, with no particular sex or breed Radiography, including contrast studies, has not been
predisposition. shown to be helpful in differentiating cats with IBD
and those with other diseases.
See main reference on page 768 for details. Ultimately, endoscopic examination or a surgical
exploratory will be necessary to obtain biopsies of the
Clinical signs GI tract. Endoscopy is less invasive and allows visuali-
Vomiting, which may be intermittent or severe, weight zation of the mucosal surface, which may help obtain
loss and anorexia are the most common signs. more diagnostic biopsy samples. Multiple (6–8) biop-
sies should be taken from various sites including the
Diarrhea is also observed in some cats, but is more stomach, duodenum, ileum and colon, even if there is
prevalent with disease affecting the distal small intes- no visible evidence of disease.
tine or colon.
Since there are no simple, easy tests for food intoler-
Most cats with IBD have intermittent, chronic signs ance or allergy, dietary elimination trials should be
of GI disease, and with time, the signs progress to conducted in all cats with signs of IBD or that have
become more persistent and severe. inflammatory infiltrates of the GI tract.
The disease is most prevalent in middle-aged to older
cats, but the range is from 6 months to 17 years. Differential diagnosis
There appears to be no breed or sex predisposition to The list of diseases that may mimic, cause or compli-
IBD in most studies, but purebred cats and males cate IBD (e.g. cause GI inflammation and similar clin-
appear to be over-represented in some studies. ical signs) is extensive:
● Systemic diseases (hyperthyroidism, pancreatic cyclosporine therapy must be monitored by checking

disease, liver disease, feline viral diseases, toxo- trough and peak drug levels.
plasmosis).
Cats with a poor response to treatment or recurrent
● Parasitic diseases (nematodes, Giardia, Crypto-
disease should be carefully re-evaluated, including -
sporidia, other parasites such as coccidia,
re-biopsy if indicated. Lymphoplasmacytic enteritis
Entamoeba).
can be mistaken for lymphoma in the early stage.
● Bacterial infection (Helicobacter, Campylobacter,
Cats with IBD have been reported to have concurrent
Salmonella, Clostridia, etc.).
reactivation of toxoplasmosis. Food allergy/intoler-
● Metabolic diseases (EPI, serum cobalamin or folate
ance is extremely difficult to differentiate from IBD
deficiency).
and in some cats finding the appropriate diet is a true
● Nutritional disorders (food intolerance/allergy).
challenge.
● Neoplasia (lymphoma, adenocarcinoma, mast cell
tumor).
INFLAMMATORY HEPATOBILIARY
Treatment
DISEASE (CHOLANGOHEPATITIS)
The first key to successful treatment of IBD is to have
a correct diagnosis, and that is a real challenge. Classical signs
Even if food allergy/intolerance has been ruled out, ● With lymphoplasmacytic forms, chronic
a highly digestible, hypoallergenic or elimination weight loss, anorexia, vomiting and icterus
diet is important in the treatment of IBD. Cats with are common signs.
IBD have an abnormal gut immune system, thus the ● In neutrophilic cholangitis, the disease is
presence of additional dietary antigens may serve to more acute in nature, and fever, depression
exacerbate the inflammatory response. A “sacrificial” and icterus are typical.
protein source may have to be used first, while the
bowel is still subject to a strong inflammatory response, See main reference on page 427 for details (The Yellow
before moving onto a more permanent food choice. Cat or Cat With Elevated Liver Enzymes).
The mainstay of treatment of IBD in cats is immuno-
suppressive doses of prednisolone (2–4 mg/kg/day
PO).
Clinical signs
Metronidazole (10–15 mg/kg q 12 h PO) is also very
Weight loss (often dramatic), anorexia, intermit-
effective, and in some cats, may be as effective as
tent vomiting, and icterus are the most common
steroid therapy. Many clinicians start with metronida-
signs in cats with lymphocytic cholangitis. These
zole and dietary therapy, and then add prednisolone if
cats often are middle aged, there is no breed or sex
the response to treatment is incomplete.
predisposition, and they have hepatomegaly. Con-
In cats with severe IBD that is not responsive to current pancreatitis and/or IBD is seen in some cats
metronidazole, prednisolone and dietary therapy, cyto- and their illness is more chronic and subacute. In
toxic drugs may be considered. However, most cats some cats, there is a waxing and waning course with
with IBD do not require additional cytotoxic periods of normalcy and a good appetite following
drug therapy to manage their disease, so a careful re- episodes of signs.
evaluation of the patient is indicated to be sure you
Ascites (high protein content) is more likely with the
have the correct diagnosis. Drugs that may be consid-
lymphoplasmacytic form, but it is rare.
ered include chlorambucil (2 mg/m2), azathioprine
(0.3 mg/kg EOD) and cyclosporine (5 mg/cat/day). Cats with neutrophilic cholangitis are more often
Hemograms should be monitored every 2–3 weeks male, febrile, depressed, icteric and have an acute
to detect myelosuppression, and if cyclosporine is used, onset of illness that is rapidly progressive.
The diarrhea may be mild, with soft to unformed feces In addition to liver histopathology, samples of hepatic
in cats with lymphocytic cholangitis, to severe, liquid tissue should also be submitted for aerobic and anaer-
diarrhea in cats with neutrophilic cholangitis. obic culture.
Diagnosis
Cats that have vomiting, diarrhea, and weight loss in
The presence of icterus helps to narrow the differen-
addition to icterus, the list of differentials is narrowed
tials list to hepatic, pre-hepatic and post-hepatic
to pre-hepatic causes (hemolysis), hepatic causes
diseases.
(hepatic lipidosis, hepatic necrosis, hepatic failure,
The hemogram in cats with hepatic disease is often etc.), and post-hepatic causes (pancreatitis, neoplasia
abnormal (e.g. mild, non-regenerative anemia, with of stomach, pancreas, duodenum or bile duct, and com-
RBC morphology having schistocytes, leptocytes or mon bile duct obstruction).
target cells present), but the changes are not specific
In cats that are not icteric, the list of potential causes
for liver disease. However, it does help rule out pre-
broadens extensively to include the spectrum of meta-
hepatic causes of icterus.
bolic, neoplastic, toxic and infectious causes of both
Serum chemistry abnormalities may include elevated systemic and primary gastrointestinal origin.
liver enzyme activities (sometimes dramatically),
hyperbilirubinemia, hypocholesterolemia, hypoal-
buminemia, decreased BUN, and electrolyte alter-
Treatment
ations consistent with vomiting or dehydration, e.g.
hypokalemia, hypernatremia. Therapy for cats with cholangitis is largely support-
ive, but the histopathologic findings are crucial in
Bilirubinemia and bilirubinuria are both common.
determining severity, the type of inflammatory infil-
Serum bile acid assay (pre- and 2 hours post-prandial) trate (which is essential to choosing appropriate ther-
may show mild to moderate elevations. apy), and the overall prognosis for the disease.
Urine sulfated bile acids is a new test of hepatic func- Most cats with severe liver disease will require fluid
tion that may also become useful in the diagnosis of therapy to replace deficits, provide maintenance fluid
liver disease. support during the recovery period, and induce diuresis
to assist removal of hepatotoxins and prevent tubular
Coagulation function (platelet numbers and function,
sludging from bilirubinuria and casts.
and coagulation factors) should be evaluated since liver
disease often adversely affects these functions. The fluids should be isotonic, balanced electrolyte
solutions, but preferably not containing lactate which
Ultrasonography is the most useful imaging modal-
is not converted to bicarbonate in cats with liver failure
ity, because it can also be used to obtain fine-needle
and thus serves as an additional source of acid
aspirates or biopsies. However, needle biopsies are
(Ringers solution and Normosol-R are replacement
only accurate for diagnosis of cholangitis < 40% of
electrolyte solutions without lactate).
the time. In cats with cholangitis, the liver may be
normal, decreased or increased in size, but typically Vomiting should be controlled with a combination
will have a hyperechoic pattern due to the presence of of anti-emetic therapy (e.g. metoclopramide or
inflammatory infiltrates. dolasetron) and acid-blocking therapy (H2 antago-
nists such as famotidine, ranitidine or cimetidine),
Liver biopsies taken via surgical exploratory or
since cats with liver disease are prone to the develop-
laparoscopy are more accurate, and will also allow
ment of hypergastrinemic gastritis.
placement of a feeding tube (gastrostomy or jejunos-
tomy tube) during the procedure, which is essential for Diarrhea is rarely severe enough to require therapy and
any cat that has not eaten for 3–5 days. often resolves as the anorexia worsens.
Cholerectic agents (ursodeoxycholic acid) should be Anti-oxidant therapy with S-adenosylmethionine

used to reduce bile sludging and improve bile salt (SAMe) 20 mg/kg/day PO should be instituted for
flow. hepato protection.
Cats with neutrophilic cholangitis should be given
broad-spectrum parenteral antibiotics. Penicillin or CLOSTRIDIUM PERFRINGENS
metronidazole, and fluorinated quinolones or amino- ENTEROCOLITIS
glycosides combined together provide a good spectrum
of activity for enteric pathogens. Ideally, the antibiotic Classical signs
choice should be based upon culture results, but if the
● Typically, there is acute small bowel
culture is negative or the cat is systemically ill,
diarrhea with or without anorexia or
antimicrobial chemotherapy should be initiated and is
lethargy.
continued for 3–6 months.
● Some cats develop chronic, intermittent
Lymphocytic cholangitis is believed to be an diarrhea.
immune-mediated phenomenon and has recently
been shown to occur in association with inflamma- See main reference on page 721 for details (The Cat
tory bowel disease, inflammatory renal disease and With Signs of Acute Small Bowel Diarrhea).
pancreatitis. Prednisolone therapy (2–4 mg/kg/day)
is indicated in cats with lymphocytic plasmacytic
Clinical signs
hepatic infiltrates. The decision of when to decrease
the dose to 1 mg/kg/day or eventually every other The most common clinical sign is severe, watery to
day depends entirely on the cat, its clinical response mucohemorrhagic diarrhea.
to treatment and clinicopathologic evidence of
In most cats, the diarrhea only lasts a few days, but
improvement.
in some, it may persist and become chronic. Animals
Metronidazole (10–15 mg/kg/day PO) for 2–4 weeks that have severe diarrhea will become dehydrated,
or indefinitely is also used, especially in cats with con- lethargic and may be anorexic.
current IBD.
There is no breed, sex or age predisposition, but cats
Ursodeoxycholic acid supplementation is also rec- from catteries or in stressed environments are at
ommended (10–15 mg/kg/day PO) indefinitely for its increased risk.
choleretic activity.
Nutritional support must be provided, and in the Diagnosis
short term (1–3 days) nasoesophageal feeding tubes
The history and physical examination findings help
work well, but for longer periods, esophageal feeding
to focus the diagnostic approach toward infectious, par-
tubes or a percutaneous endoscopic gastrostomy
asitic and dietary causes of diarrhea.
(PEG) tube should be placed to allow larger amounts
of food per feeding, as well as feeding a blenderized cat The presence of the organism can be confirmed by cul-
food rather than liquid enteral diets. ture of fresh fecal specimens. However, because this
bacterium is part of the normal flora, this is not
Most anorectic or ill cats will benefit from addition of
definitive.
B vitamins to the fluids. However, fat-soluble vitamin
deficiency may also develop in cats that are anorectic or Similar to the dog, the presence of spores in large
have malabsorption. Supplementation with vitamin K numbers (> 5/hpf) on a stained fecal smear does not
(2.5–5 mg SC q 2 weeks) and in some cases, vitamin E correlate with the presence of enterotoxin.
should be considered in those cats.
Reverse passive latex agglutination (RPLA) tests for
In some cats with evidence of concurrent lipidosis, clostridial enterotoxin are available and have been
supplemental taurine (250–500 mg PO q 24 h) and used in dogs and humans, but have not been evaluated
carnitine (250 mg PO q 24 h) should be given. in cats. In dogs, the test does not differentiate dogs
with clostridial diarrhea from normal dogs. A positive Most cats with enteric coronavirus have subclinical
enterotoxin assay determined by ELISA (Techlab, infections or only develop mild, self-limiting diarrhea.
Inc., Blacksburg, VA) in the context of clinical signs
consistent with clostridial infection is strongly support-
Diagnosis
ive of clostridial-associated diarrhea in dogs. The clin-
ical utility of this assay in cats has not been The definitive diagnosis of FIP in cats is quite diffi-
evaluated. cult, especially in cases of focal or non-fulminant FIP.
PCR tests are also utilized for testing feces for entero- Serologic tests are not useful, because most are not
toxin, but are not universally available. specific for FIP rather than coronavirus infection.
The ELISA for the 7B protein of the FIP virus gener-
ates a relatively high number of false-negative and
FELINE CORONAVIRUS INFECTIONS
false-positive results. Polymerase chain reaction
(FELINE ENTERIC CORONAVIRUS/FELINE
(PCR) testing is the best hope for a definitive test, but
INFECTIOUS PERITONITIS)
at present is only definitive for confirmation that
a cat does not have FIP. The PCR test still has
Classical signs
false positives that prevent it from being a good screen-
● Variable and vague clinical signs including ing/diagnostic test.
weight loss, fever and anorexia.
Currently, the definitive test for FIP remains
● Vomiting or diarrhea are less common.
histopathologic examination and virus isolation.
See main references on page 372 for details.
FELINE IMMUNODEFICIENCY VIRUS

The clinical signs are quite variable and depend ● Variable clinical signs which depend on the
a great deal upon the stage when the cat presents for stage of the disease and its presentation
evaluation and whether they have enteric coronavirus (immunodeficiency disease, neoplasia,
infection or FIP. CNS disease, etc.).
● Chronic diarrhea sometimes occurs.
Cats with fulminant FIP will likely be severely
depressed, pyrectic, anorectic, and have significant
weight loss. Respiratory distress from pleural effusion
is also common, as is the presence of ascites.
Clinical signs
Cats with so-called non-effusive, or “dry” FIP, will
have more vague clinical signs, including reduced The most common signs in cats with FIV are
appetite, fever, mild weight loss and general malaise. immunodeficiency diseases such as chronic or recur-
Some cats will have mild abdominal discomfort, respi- rent infections, especially of the oral cavity (gingivi-
ratory signs and granulomatous retinal lesions. tis/stomatitis), skin (dermatitis, neoplasia), ears
(chronic otitis), urinary tract (cystitis) and GI tract.
In some cats, FIP granulomas will cause more focal
signs associated with the body system that is affected. Chronic enteritis or enterocolitis are associated with
chronic diarrhea, weight loss, anorexia and lethargy.
Vomiting and/or diarrhea are usually secondary to
the systemic effects of infection or due to granuloma In severe cases, the diarrhea is persistent and unrespon-
formation in the GI tract. sive to therapy.
Central nervous system signs range from ataxia to Other clinical signs are associated with development
seizures, and behavior changes, are common in cats of CNS disease, neoplasia or secondary infections that
with the non-effusive form of FIP. result in systemic illness.
FIV is most prevalent in middle-aged, male cats that Diagnosis

live outdoors or are allowed to roam, and are prone to
fighting. A history of persistent lethargy, weight loss or
anorexia in an older cat, especially a Siamese, should
raise suspicions of chronic GI disease and the need for
Diagnosis further evaluation.
The history and physical examination findings are Abdominal palpation may reveal a thickened region
often suggestive of chronic immunodeficiency disease. of bowel or a firm mass.
Hemogram and serum chemistry abnormalities are not A routine hemogram and chemistry profile is often
specific, but lymphopenia is a common finding. unremarkable or has non-specific abnormalities
Diagnosis is made by determining the presence of FIV associated with chronic disease, such as mild non-
antibody on a commercially available ELISA test, as regenerative anemia, hypoproteinemia, or elevated liver
long as the cat has not been previously vaccinated with enzyme concentrations.
the FIV vaccine. Imaging studies such as contrast radiography or
A western blot analysis or PCR test can be used to con- ultrasound examinations are useful in identifying and
firm the presence of the virus. localizing the lesion. Ultrasound can also be used to
obtain a fine-needle aspirate of the mass or regional
In cases where FIV is confirmed, a further search for lymph nodes. A thoracic radiograph to check for
other infectious or parasitic causes (Cryptosporidia, metastasis is also indicated.
Toxoplasma, Giardia, Campylobacter, Salmonella,
etc.) should be pursued because concurrent infections Ultimately, the definitive diagnosis is by histopatho-
with other agents are common with FIV. logic examination of the tissue obtained either by
endoscopic or surgical biopsies.
INTESTINAL ADENOCARCINOMA Surgical exploratory is often the best approach for

both obtaining tissue for diagnosis, as well as allowing
Classical signs for surgical removal of the affected tissue. In addition,
biopsies of regional lymph nodes can also be obtained.
● Weight loss, anorexia and vague signs of
malaise. CAMPYLOBACTERIOSIS
● Vomiting is the more common than
diarrhea. Classical signs
● Most common in older, Siamese cats.
● Abdominal distention, colicky abdominal
See main reference on page 677 for details. pain, and diarrhea are most common.
● Kittens are generally in poor body
Clinical signs condition, or have other concurrent
infections.
The most common clinical signs are anorexia,
weight loss and vague signs of malaise. See main reference on page 726 for details.
Vomiting is more common than diarrhea because of
the tendency of the tumor to produce an annular, Clinical signs
obstructive lesion in the distal small intestine, however,
Campylobacter was isolated from 21% of cats with
diarrhea is not unusual. In general, the GI signs occur
diarrhea and 4% of healthy cats in one study. Other
late in the course of the disease.
studies with and without diarrhea have reported isola-
Abdominal pain may also occur, especially in cats tion rates varying from 0–50%.
with metastatic disease.
In cats, clinical signs of campylobacteriosis are
The disease is most common in older, Siamese cats. uncommon, as most infections are asymptomatic in the
absence of other pathogens. Concurrent infections the effectiveness of antibiotics for treatment of this dis-
with other intestinal pathogens, such as Giardia or ease is unknown.
Salmonella may exacerbate signs.
Several antibiotics appear to be effective in eliminat-
Affected cats are usually less than 6 months of age. ing the organism, including erythromycin (10 mg/kg q
8 h PO), metronidazole (5–10 mg/kg q 12 h PO),
The primary clinical sign of infection is diarrhea,
cephalosporins (20 mg/kg q 12 h PO), and fluorinated
which may be watery, bloody, mucoid or a combina-
quinolones (5 mg/kg q 12 h PO).
tion.
Some kittens will become systemically ill with
EXOCRINE PANCREATIC INSUFFICIENCY
lethargy, dehydration and anorexia observed.
Most kittens will have acute diarrhea, but in some cats, Classical signs
chronic, recurrent bouts of diarrhea are observed.
● Weight loss despite a vigorous appetite,
which may include pica and coprophagy.
● Fecal characteristics may be normal, soft
Diagnosis
and voluminous or watery diarrhea.
History and physical examination findings are ● Poor haircoat and greasy, flakey seborrhea
important to rule out other causes, but may be unre- are also common.
markable. ● Very rare in cats.
Routine hematology, chemistry profiles and imaging
studies are typically within normal limits. Pathogenesis
Diagnosis can be confirmed by culturing freshly The most common cause of exocrine pancreatic insuf-
obtained fecal samples. Samples can be transported at ficiency (EPI) in the cat is chronic pancreatitis.
room temperature without special handling, but must
A less common cause of EPI is infestation with the
be cultured in a microaerophilic atmosphere.
feline pancreatic fluke, Eurytrema procyonis.
A specific request for culture of Campylobacter
Other, possible causes of EPI in cats include pancre-
should be submitted if it is suspected.
atic adenocarcinoma, and congenital pancreatic acinar
Dark-field or phase contrast microscopy can also be hypoplasia or aplasia.
used to identify the motile, curved bacteria on fresh
Idiopathic pancreatic acinar atrophy, the most com-
fecal samples. Gram-stained samples can also be used
mon cause of EPI in dogs, has not been reported in
to identify the gull wing-shaped rods in the feces.
cats.
However, these approaches are less sensitive and
require more technical skill. In humans with EPI caused by chronic pancreatitis, dia-
betes mellitus occurs concurrently. It is unknown
whether cats with chronic pancreatitis and EPI will
also progress to develop diabetes mellitus as well,
however, diabetes mellitus has been reported in a cat
Infectious (Salmonella, Clostridium), parasitic with EPI.
(Giardia, Cryptosporidia, etc.), and dietary (food
EPI is believed to develop when > 90% of the enzymes
intolerance or dietary indiscretion) agents should all be
of the exocrine pancreas are destroyed. These
considered.
enzymes play an integral role in assimilating the major
food components: proteins, lipids and carbohydrates.
Treatment
Pancreatic enzymes increase the efficiency of break-
Since most cats with Campylobacter infections are down of macromolecules in the digestive tract and
asymptomatic, or it is associated with other infections, enhance the transport mechanisms for sugars, amino
acids and fatty acids. Thus, without pancreatic Severely decreased fTLI concentrations (< 8 ug/L)
enzymes, food substances are inefficiently broken are diagnostic for EPI in cats.
down and cannot be readily transported across the
All cats with EPI should have a serum cobalamin and
intestinal lumen.
folate assay, since many cats with EPI are cobalamin
Diarrhea occurs due to the presence of large quanti- deficient or have concurrent small bowel disease (folate
ties of fats, protein and carbohydrates, which are levels will be low).
osmotically active.
Maldigestion of these important nutrients leads to Differential diagnosis
weight loss and may also cause deficiencies of vita-
The clinical signs are so non-specific that many other
mins, fatty acids or other essential nutrients.
diseases that cause polyphagia, weight loss and diar-
rhea must be considered. Hyperthyroidism, diabetes
mellitus, corticosteroid treatment or hyperadrenocorti-
Clinical signs cism, chronic renal failure, heart failure, liver disease,
dental disease, neoplasia, and chronic intestinal dis-
This is a rare disease in cats.
eases such as inflammatory bowel disease are the
The most common clinical signs are polyphagia, main differentials.
diarrhea and weight loss.
Vomiting and anorexia are also occasionally reported. Treatment
The feces are typically pale, loose, voluminous, and Most cats with EPI can be successfully treated by
they may be quite malodorous. dietary supplementation with pancreatic enzymes.
The powder products (1 tsp per meal) appear to be
Cats often have a greasy, flaky haircoat due to the fat
more clinically effective than tablets.
malabsorption.
If the cat refuses to eat the food with pancreatic extract,
Deficiencies of fat-soluble vitamins can result in
raw pancreas can be offered, but it is essential to
a bleeding disorder (vitamin K-responsive coagu-
use bovine pancreas to prevent transmission of
lopathy), which may present as excessive bleeding
Aujeszky’s disease in porcine pancreas.
from venipuncture sites or spontaneous hemorrhage
(nose bleeds, hematuria, melena, etc.). A diet that contains low amounts of insoluble fiber
should be fed, since insoluble fibers may interfere with
pancreatic enzyme activity.
Diagnosis Some cats will not respond to enzyme supplementa-
tion alone, and this may be due to concurrent cobal-
Results from routine hematology and chemistry
amin deficiency or small intestinal disease. Cobalamin
profiles will be normal in most cats. Occasionally,
supplementation should be given parenterally (100–250
elevations in hepatic enzymes or neutrophilia will be
μg SC once weekly for 6–8 weeks, then monthly or
observed.
bimonthly as needed).
Routine abdominal radiography and ultrasonogra-
In cats with suspected vitamin K deficiency, supple-
phy is usually normal, and is not diagnostic.
mentation should also be initiated (vitamin K1
Fecal proteolytic activity testing will reveal unde- 1 mg/kg/day PO).
tectable levels of enzymes, which is diagnostic for
It is unknown whether or not cats develop small
EPI, but the test is very labile, so false-positive results
intestinal bacterial overgrowth as a complication of
may occur due to improper sample handling.
EPI (as is common in dogs). However, in cats that do
A recently validated radioimmunoassay for feline not respond as anticipated to pancreatic enzyme sup-
trypsin-like immunoreactivity (fTLI) is available, plementation, addition of metronidazole or tetracycline
much like the TLI test available for use in dogs. to the treatment regime is indicated.
Prognosis Treatment
Because EPI is associated with the irreversible loss of There is no known effective treatment for this condi-
pancreatic acinar tissue, complete recovery is not pos- tion, but it appears to be self-limiting as the kitten
sible. reaches adult age. The reason for this is unknown, but
may be due to development of an adult, fully competent
However, with appropriate management, cats with EPI
immune system.
will gain weight, pass normal feces and can live a nor-
mal life.
Prognosis
Prevention Good once the kitten reaches adult age.
There is no known way to prevent the development
of EPI, however, if cats with chronic pancreatitis can
be recognized and appropriately managed, it may be INTESTINAL MAST CELL TUMOR
possible to prevent the consequences of chronic pan-
creatitis and the development of EPI. Classical signs
● Weight loss, decreased appetite or
IDIOPATHIC JUVENILE DIARRHEA anorexia and chronic diarrhea.
Classical signs See main reference on page 687 for details.

● The only presenting sign is chronic
diarrhea.
Clinical signs
Pathogenesis Systemic mast cell tumors produce GI tract signs
through release of histamine and other vasoactive sub-
Unknown pathogenesis.
stances, which result in gastroduodenal ulceration.
Clinical signs Intestinal mast cell tumors are typically poorly differ-
entiated, highly malignant tumors that appear to consist
Disorder occurs in kittens and young cats under
of degranulated (e.g. non-functional) neoplastic mast
a year of age.
cells. However, they produce GI tract signs through
The only clinical sign is presence of chronic small local effects (e.g. obstruction) or surface ulceration
bowel diarrhea. (bleeding) rather than through the release of vasoactive
substances, as is the case with systemic mast cell
Kittens are otherwise healthy, active and gain weight.
tumors.
Diagnosis The most common clinical signs are weight loss,
anorexia or decreased appetite, and chronic diar-
The diagnosis is one of exclusion. Thus, infectious,
rhea. Other signs include lethargy, vomiting or acute
parasitic, dietary and mechanical disorders must all be
abdominal pain.
ruled out.
Melena or chronic asymptomatic blood loss may
Cats with this syndrome are often purebred cats, and
result in anemia, and sometimes is severe enough to
the diarrhea is self-limiting once they reach adult age.
cause weakness or lethargy.
Differential diagnosis In some cats, a palpable thickened intestinal segment
or a mass will be present.
Because this is a disease of kittens, bacterial, viral, par-
asitic, protozoal, dietary and toxic causes of diarrhea Intestinal mast cell tumors are very small, difficult to
must all be carefully considered. palpate until late, and tend to be solitary. They occur as
an infiltrating mass, but metastasize early in the Surgical removal of the affected segment of bowel
course of the disease. with wide surgical margins is the only therapy
reported to be effective in prolonging survival.
Intestinal mast cell tumors are not generally associ-
Mesenteric, hepatic and splenic metastasis are com-
ated with development of massive splenomegaly
monly observed by the time the tumor is diagnosed.
or systemic mast cell infiltration like systemic mas-
tocytosis. Chemotherapy has not been shown to increase sur-
vival time in cats with this disease, although pred-
nisolone (2–4 mg/kg/day) and histamine2 blockers
Diagnosis
(cimetidine, ranitidine, famotidine) are advocated to
A chronic history of weight loss or anorexia in a mid- reduce secondary clinical signs associated with mast
dle-aged or older cat should raise the suspicion of intes- cell disease.
tinal neoplasia.
Nutritional support may be required in cats that refuse
Routine hemogram and serum chemistry profiles to eat, as they will develop hepatic lipidosis and protein
will often be normal, but non-specific abnormalities calorie malnutrition.
such as mild non-regenerative anemia, hypoproteine-
The prognosis is poor, as the average survival time fol-
mia or hypoalbuminemia, and electrolyte disturbances
lowing diagnosis with this tumor is 4 months.
associated with chronic vomiting or diarrhea can be
seen.
HYPOADRENOCORTICISM
Other tests of GI function (e.g. fTLI, fecal alpha-1
protease inhibitor, cobalamin/folate assays, fecal analy-
Classical signs
ses for parasites) should be considered or performed,
but will not be diagnostic. ● Typically, lethargy, weakness and vomiting.
● Regurgitation (megaesophagus), diarrhea
Imaging studies, especially ultrasound examination,
and abdominal pain may occur.
will be the most helpful in localizing the lesion (which
can be easily missed because they are often extremely
small or focal). Fine-needle aspirates of focal masses
can be obtained which will often help direct further
diagnostic and treatment plans. Clinical signs
Endoscopy may be helpful, but in many cases, these Lethargy, weakness and vomiting are the classic pre-
tumors are present in the jejunum, and are unreachable senting signs, but diarrhea and abdominal pain may
by the endoscope. also be observed.
If imaging studies are unavailable, or fine-needle aspi- Megaesophagus, with resultant regurgitation, may
rates are non-diagnostic, an exploratory laparotomy occur due to muscle weakness, but it is very uncom-
is indicated. mon in cats.
Hypoadrenal crisis is associated with an acute episode
Differential diagnosis of collapse due to severe alterations in sodium and
potassium that result in severe muscle weakness and
The primary differentials for cats with chronic weight
cardiovascular collapse. This is a rare occurrence in
loss, anorexia and chronic diarrhea are IBD, neoplasia,
cats compared to dogs, but requires rapid recognition
lymphangiectasia, and systemic organ failure or dys-
and response to stabilize the patient.
function (renal disease, liver failure, etc.).
Diagnosis
Treatment
The history and clinical signs are often too non-
Treatment is palliative and supportive for cats with specific to be helpful, but are still important in devel-
intestinal mast cell tumors. opment of a diagnostic approach.
The classic hemogram and biochemical changes Therapy for cats with this disease will be lifelong,
include eosinophilia, lymphopenia, azotemia, hypercal- and frequent rechecks to allow dose adjustments will
cemia, hyperkalemia, hyponatremia and low or isos- be required. Most cats will have a good quality of life
thenuric urine specific gravity. with proper management of this disease.
However, some cats will not have mineralocorticoid
deficiency, thus, no electrolyte changes will be evi-
dent on the chemistry profile. HISTOPLASMOSIS
Cats with severe hyperkalemia (> 7 mEq/L) will have
Classical signs
characteristic ECG abnormalities and bradycardia.
● Signs may indicate respiratory, eye, CNS,
Definitive diagnosis is by performing an ACTH
bone marrow or GI tract involvement.
stimulation test. Cortisol levels will be low and will
● Typically, respiratory signs such as
not respond to ACTH administration.
wheezing, coughing or dyspnea
predominate.
● GI signs are usually associated with
protracted, watery diarrhea, that may
Because the clinical signs and routine blood work are contain blood or mucus.
non-specific, a wide variety of metabolic, neoplastic,
infectious and idiopathic conditions must be consid-
Pathogenesis
ered. In many cats, the ACTH stimulation test is per-
formed based on clinical suspicion, not clear physical or Histoplasma capsulatum is a soil-borne fungus, which
biochemical findings that suggest hypoadrenocorticism. is found in many temperate and subtropical areas of the
world, especially where it is moist and humid. The
organism grows particularly well if there is bird or bat
Treatment excrement in the soil.
In cats that are clinically dehydrated, have pre-renal In the States, it is most frequent in Southern and
azotemia or in an acute adrenal crisis, fluid therapy Central USA around the Ohio, Missouri and
with isotonic saline is the initial treatment of choice. If Mississippi Rivers.
there are cardiac arrhythmias or ECG abnormalities
The majority of infections are subclinical or cause
associated with severe hyperkalemia, regular insulin
only mild, transient clinical signs.
(0.2–0.5 U/kg IV) and dextrose therapy (0.5–1.0 g/kg
IV slowly), intravenous bicarbonate (body weight Cats are equally susceptible as dogs, and the majority
(kg) × 0.5 × base deficit, or 0.5–1.0 mEq/kg over 6 h), of symptomatic cats are young (< 4 years of age).
or intravenous calcium gluconate therapy (0.5–1.0
Infection is contracted via inhalation, although the
ml/kg, IV slowly) may be administered to rapidly lower
GIT may also be a route of infection. Signs occur
extracellular potassium levels.
approximately 12–16 days after exposure.
Parenteral corticosteroids (dexamethasone, methyl
Initial infection is confined to the respiratory tract, but
prednisolone, which have some mineralocorticoid
dissemination often occurs resulting in chronic dis-
effects as well) should be administered in physiologic
ease over months or years with signs referable to spleen
doses (0.2–0.4 mg/kg) initially, and continued daily
(splenomegaly), liver (hepatomegaly, icterus, ascites),
(oral or injectable) as replacement therapy until the cat
GIT (chronic diarrhea and weight loss), peritoneum
is stable.
(omental or mesenteric masses); lymph nodes (periph-
Once the cat is in stable condition, replacement of eral or abdominal lymphadenopathy), bone marrow
mineralocorticoid hormones can be achieved orally (anemia, thrombocytopenia, leukopenia), bones (lame-
(fluorinef) or with repository forms of the hormone, ness and proliferative or lytic boney lesions), eyes (con-
such as desoxycorticosterone pivalate (DOCP). junctivitis, exudative anterior uveitis, multifocal
granulomatous chorioretinitis, optic neuritis), central Treatment

nervous system (ataxia, seizures, circling, disorienta-
tion, anisocoria, paresis, decreased conscious proprio- Itraconazole (10 mg/kg PO q 24 h) is the drug of
ception), and occasionally skin (nodular or ulcerated choice for initial therapy. It is highly effective and has
lesions). minimal toxicity, but is relatively expensive and treat-
ment must be continued for 1 month (at least) beyond
Clinical signs the resolution of clinical signs and evidence of disease
The most common clinical signs of histoplasmosis in (typically 6–9 months).
cats are multisystemic, including depression, weight Other treatment options include fluconazole, keto-
loss, anorexia, dyspnea or lameness. conazole and amphotericin B.
Other signs may include fever, pale mucous mem- The success rate with itraconazole therapy is
branes, peripheral lymphadenopathy, icterus, hepato- reported to be anywhere from 33% to >90%, but this
megaly, skin nodules or splenomegaly. depends in large measure on the severity of the infec-
The organism can be most commonly found in the res- tion at the time of diagnosis.
piratory tract, bone, bone marrow, skin and GI tract.
GI signs are not common in cats (as they are in dogs), INTUSSUSCEPTION
but when they occur chronic diarrhea, mesenteric
lymphadenopathy and anorexia are common. Classical signs
Ocular changes may include conjunctivitis, anterior

● Abdominal pain, anorexia and vomiting.
uveitis, retinal detachment or chorioretinitis.
● Diarrhea, weight loss, and lethargy occur
in long-standing cases.
Diagnosis ● Intussusceptions are usually seen in young
cats or kittens.
The clinical signs of disseminated histoplasmosis are
consistent with systemic illness and are associated with See main reference on page 643 for details.
a wide variety of non-specific clinical and laboratory
changes.
Clinical signs
Anemia of chronic disease is the most common
hematologic abnormality. With high intussusceptions, vomiting, abdominal dis-
comfort, anorexia, lethargy, dehydration and hypovolemia
Occasionally histoplasma organisms can be found in leading to shock are the most common clinical signs.
circulating mononuclear cells and eosinophils.
Low intussusceptions (at the iliocolic junction) typi-
Thrombocytopenia is also a common abnormality. cally present with bloody, mucoid diarrhea, tenesmus,
Diagnosis of histoplasmosis by serology is unreliable intermittent vomiting and weight loss. In many of these
as the sensitivity and specificity for the organism is poor. cases, the intussusception can be palpated.
The best method of diagnosis is to identify the organ- Most intussusceptions are associated with acute dis-
ism in cytologic or histopathologic examinations. ease, but sliding intussusceptions may result in
The best tissues for diagnosis of histoplasmosis in the chronic, intermittent signs.
cat are bone marrow, lymph nodes, lung, liver or A palpable mass in the abdomen may be evident,
skin nodules if present. especially with low intussusceptions.
Diagnosis
There are a wide variety of potential differentials due
to the different clinical presentation that may occur Hemogram and serum biochemistry profiles will be
depending on the organ system affected. variable depending on the severity and location of the
intussusception, however, dehydration, electrolyte Motility-enhancing drugs, such as metoclopramide,

abnormalities, anemia and leukocyte changes have all are contraindicated in patients with GI obstruction
been observed depending on the site, severity and pre- and should not be used.
cipitating cause of the intussusception.
After surgical correction, if gastric ulceration is not
Radiographs and/or ultrasound examination of the a complicating factor, oral alimentation should be
gastrointestinal tract are the best means of confirming instituted in the first 24 hours, to enhance the return
the diagnosis. Radiographs may not be definitive, but in of normal motility and reduce the possibility of post-
most cases, an obstructive pattern (dilated loops of operative ileus.
bowel, different bowel loop sizes) will be apparent.
However, an ultrasound of the abdomen will often
definitively identify the intussusception. Contrast
OTHER SMALL INTESTINAL NEOPLASIA
studies may be used but should not be done at the
(FIBROSARCOMA, CARCINOIDS,
expense of delaying treatment in severely ill cases. In
PLASMACYTOMA)
the case of sliding intussusceptions, the diagnostic pro-
cedures should be performed when the clinical signs
Classical signs
are most prominent.
● Weight loss.
used to obtain a diagnosis, especially with low intus-
● Anorexia.
susceptions.
● Vomiting and/or diarrhea.
Exploratory laparotomy may be required to obtain
a definitive diagnosis, and is essential for treatment, so
in cats with evidence of intestinal obstruction, or in Clinical signs
cats with acute abdomen and shock, surgery should
The clinical signs observed will depend upon the
be performed early.
tumor location in the GI tract.
In cats, anorexia, weight loss and lethargy are the most
Differential diagnosis common clinical signs of any gastrointestinal neoplas-
Many diseases that can precipitate an intussuscep- tic disease.
tion (e.g. viral enteritis, foreign bodies, gastroenteritis, Vomiting and/or diarrhea may be observed, but will be
intestinal parasitism, etc.) also have clinical signs that variable depending on whether the tumor is in the small
mimic it. Thus, a thorough physical examination, diag- intestine or colon, and whether it is diffuse or solitary
nostic evaluation, and close patient monitoring are in extent.
essential. Mesenteric volvulus is a very difficult con-
dition to differentiate from intussusception, both clini-
cally and radiographically. Diagnosis
Palpation of an intestinal mass is an important diag-
Treatment nostic tool, since many of these tumors are solitary and
produce strictures or obstructions.
Intussusception must be considered a surgical emer-
gency. Cats with signs of shock or endotoxemia should Hematology and serum biochemistry profiles may be
be prepared for surgery by correcting fluid and elec- within normal limits in cats with intestinal neoplasia.
trolyte imbalances, administration of broad-spec-
Abnormalities associated with secondary effects of the
trum, parenteral antibiotics (combinations such as
tumor include dehydration, electrolyte imbalances,
ampicillin or cefazolin and enrofloxain, amikacin,
anemia of chronic disease, etc.
cefoxitin or imipenam), and use of histamine-2 block-
ers (ranitidine or famotidine) or protectants if gastric Radiographs of both the thorax and abdomen are
erosions or ulceration is suspected. an important, but sometimes non-diagnostic, tool.
Radiographs are best for assessment of pulmonary Some of these tumors (insulinoma, gastrinoma) can be
metastasis. presumptively diagnosed by measuring the level of
the hormone they produce, but most APUDomas do
Ultrasound is an invaluable tool for lesion localiza-
not secrete hormones that are routinely measured.
tion, determination of lesion extent and in some
cases, obtaining a fine-needle aspirate or biopsy of
the lesion. Differential diagnosis
Definitive diagnosis is by histopathologic evalua- Because these tumors are so rare, all other causes of
tion of a biopsy or tissue obtained after surgical chronic diarrhea should be considered before pursu-
resection. ing the APUD tumors as the cause of diarrhea.
APUDOMAS Treatment
The treatment of choice is to find and surgically excise
Classical signs
the tumor. However, because the tumors are often
● Severe and in some cases intractable microscopic or extremely small, they are often over-
small bowel diarrhea. looked during an exploratory. In addition, by the time
the tumor is large enough to find, it has often already
metastasized.
Pathogenesis
Supportive care and symptomatic therapy are often
Amine precursor uptake and decarboxylation the only avenue. For example, in cats with gastrinomas,
(APUD) cells are a diffuse system of endocrine cells in histamine2 blockers and proton pump inhibitors are
the body (primarily associated with the GI tract and used to help control the excessive secretion of acid.
other endocrine organs) that are able to secrete bio-
genic amines from amino acid precursors.
Prognosis
APUD cells are responsible for the potent secretory
Guarded to poor. These tumors are usually malignant,
functions that APUD tumors display (e.g. insulinomas,
surgical excision is rarely curative and metastatic
gastrinomas, pheochromocytomas and carcinoid
tumors are poorly responsive to chemotherapy.
tumors of the gut).
Clinical signs HYPEREOSINOPHILIC SYNDROME

The clinical signs are dependent on the tumor and
Classical signs
effects, for example carcinoid tumors of the GI tract
may produce secretory diarrhea in affected cats ● Severe and in some cases intractable
because of the vasoactive amines they produce. small bowel diarrhea.
● Peripheral eosinophilia and infiltration of
These are rare tumors, and most tumors reported to
the bone marrow, spleen, liver, lymph
date have been clinically silent.
nodes and other organs with eosinophils.
Gastrinomas are also rare neoplasms that secrete
gastrin, causing excessive secretion of hydrochloric
acid by the stomach and resulting in gastric and duo- Pathogenesis
denal ulcer disease.
Hypereosinophilic syndrome is a relatively common
variant of eosinophilic enteritis in the cat, but is dis-
Diagnosis tinct from eosinophilic leukemia.
These are rare neoplasms that are extremely difficult The disease is characterized by infiltration of
to diagnose (because they are very difficult to find). eosinophils in bowel, lymph nodes, spleen, liver and
other organs, and peripheral eosinophilia, which sep- Cats with hypereosinophilic syndrome often have
arates this disease from eosinophilic IBD. severe diarrhea, and may require nutritional or fluid
support until the disease is brought under control.
The etiopathogenesis of this disorder is unknown,
but may be due to extensive antigenic dissemination
or aberrant regulation of the normal eosinophilic Prognosis
response.
The prognosis is guarded to poor.
The disease is most common in middle-aged to older
cats, and there is no breed or sex predisposition.
INTESTINAL DIVERTICULOSIS
Classical signs
Clinical signs
● Moderate to severe, small or large bowel
The clinical signs are similar to those of cats with IBD
diarrhea, and weight loss, depending on
except the intestinal wall thickening is more pro-
the location and number of diverticuli.
nounced, hepatosplenomegaly is common, and
bloody diarrhea is common.
Pathogenesis
Some cats will cough, have skin lesions (miliary der-
matitis) and have peripheral lymphadenopathy, but Diverticuli may be congenital or occur secondary
these clinical signs are less common. to intussusception or other intestinal obstructive
processes.
Most clinical disease is associated with the diverticuli-
Diagnosis
tis and infection occurring at the site.
The diagnosis is made by histopathologic examina-
tion of liver, spleen, lymph node or intestinal biop-
Clinical signs
sies which will reveal infiltration of large numbers of
normal eosinophils. Many intestinal diverticuli are clinically silent and are
only found incidentally.
Diverticulitis may result in the development of diar-
rhea, abdominal pain, lethargy or anorexia.
The primary differentials are eosinophilic IBD and
eosinophilic leukemia. Eosinophilic leukemia is dif-
Diagnosis
ferentiated from hypereosinophilic syndrome by its
localization of eosinophils to the peripheral circula- The definitive diagnosis is made by imaging studies
tion and bone marrow. In eosinophilic IBD, (ultrasound, contrast rads) or by visualization
eosinophils are found only in the lamina propria of (endoscopy or exploratory surgery).
the intestine and do not infiltrate other abdominal
organs and lymph nodes.
The rarity of this problem should suggest that all
Treatment other possible causes of diarrhea and lethargy are ruled
out before consideration of this condition.
High-dose prednisolone therapy (3–6 mg/kg/day PO)
is most commonly used, but relapses are common,
even if the high doses of steroids are maintained. Treatment
An alternative therapy is with hydroxyurea (7.5 Surgical resection of the affected bowel segment in
mg/kg q 12 h PO) for 3–14-day courses, as required to clinically affected patients. Cats with diverticuli but
maintain the cat in remission. without signs of disease do not require surgery.
lymphangiectasia or idiopathic PLE as is reported in

PROTEIN-LOSING ENTEROPATHY
dogs.
Classical signs Other causes for low albumin and serum protein
levels must be considered when this abnormality is dis-
● Weight loss, poor hair coat, inappetance,
covered, e.g. renal protein loss, severe hepatic disease,
and chronic (may be intermittent) diarrhea.
third space loss, and severe protein calorie malnutri-
tion.
Pathogenesis
Primary lymphangiectasia is rare as a cause of Treatment
protein-losing enteropathy (PLE) in cats. Most cats
Treatment of PLE is directed solely at correction of
have PLE secondary to IBD or lymphosarcoma.
the primary disease process. Specific therapy for lym-
PLE in cats may be associated with other severe mal- phoma or IBD will correct or at least control the cause
absorptive or infiltrative diseases (e.g. histoplasmo- of the protein loss.
sis, exocrine pancreatic insufficiency), but these are
Symptomatic therapy for severe intestinal protein loss
rare causes of protein loss in cats.
includes a highly digestible diet. Alternative sources
of protein for inclusion in the diet are hydrolyzed pro-
Clinical signs tein diets (Hill’s z/d) and elemental diets (e.g.
Vivonex).
The clinical signs are dependent on the primary
cause of the PLE. Cat may have anorexia and weight Medium chain triglyceride (MCT) oil is not recom-
loss only, or have chronic unrelenting diarrhea, along mended for use in cats, as it is in dogs, because of the
with inappetance. increased risk of hepatic lipidosis.
Most cats are middle-aged to older, typical of the age
range for IBD or lymphoma. PLE is simply another Prognosis
complication of the primary process and is not
Guarded, as most cats with PLE have a disease that is
a diagnostic entity in cats.
difficult if not impossible to cure.
Diagnosis
SHORT BOWEL SYNDROME
Cats with PLE will have decreased serum total pro-
tein and albumin levels, in addition to other abnor- Classical signs
malities consistent with their primary disease.
● Severe and in some cases intractable
Urinary protein loss, third space loss, lack of ade- small bowel diarrhea.
quate intake and severe hepatic disease must all be
ruled out before considering a diagnosis of PLE. Fecal
Pathogenesis
alpha-1 protease inhibitor levels, a test for abnormal
GI protein loss available for dogs, have not yet been Short bowel syndrome is classically due to surgical resec-
validated for use in cats. tion of a large segment of the small intestine that results
in fluid overload to the colon and resultant diarrhea.
As for many other GI conditions, the definitive diag-
nosis of the inciting cause of PLE is obtained by biopsy. Other causes include ischemic intestinal diseases
such as intussusception, bowel strangulation and
intestinal volvulus.
Intestinal adaptation occurs in the large bowel,
Since PLE is not a definitive diagnosis, a search for which ultimately results in a return to a soft or semi-
the primary cause is essential. Cats rarely develop formed fecal specimen, usually within 2–6 weeks.
If greater than 85% of the small intestine has been Treatment

removed the chance for adaptation is poor.
Tincture of time will allow the bowel to adapt.
Clinical signs Broad-spectrum antibiotics may be needed.
Diarrhea, dehydration and weight loss all occur as Low-fat, highly digestible diets are necessary to max-
a result of short bowel syndrome. imize absorption of nutrients.
Other signs are related to intestinal malabsorption, Administration of vitamins and minerals is usually
such as deficiencies of essential amino acids, vitamins needed. Monitoring prothrombin time and serum
or clotting factors. cobalamin levels will help determine whether supple-
mentation is needed. (Vitamin K1 5 mg/kg once, then
Small intestinal bacterial overgrowth may also 2.5 mg/kg q 12–24 h, cobalamin or multi-B complex
occur, resulting in vomiting or anorexia as well. injection weekly).
Parenteral nutrition may be required in some cats in
Diagnosis the early stages to support them until bowel function
The diagnosis is presumptive if surgical resection is returns.
the cause.
Cats are often hypoproteinemic, may be hypocholes- Prognosis
terolemic, and have other non-specific hemogram or The prognosis is guarded in cats in which diarrhea per-
chemistry abnormalities. sists for longer than 2 months after the resection, as by
Imaging studies can be used to confirm the diagnosis. that time, the chances of a return to normal function are
poor.
Other diseases that may cause similar signs include
severe intestinal strangulation, intussusception and
intestinal volvulus, which is rare in cats.
RECOMMENDED READING
August JR. Consultations in Feline Internal Medicine, 2001, WB Saunders, Philadelphia, PA.
Guilford W, Jones B, Markwell P, Arthur D, Collett M, Harte J. Food sensitivity in cats with chronic idiopathic gastro-
intestinal problems. J Vet Intern Med 2001; 15: 7–13.
Guilford WG, Center SA, Strombeck DR, Williams DA, (eds). Strombeck’s Small Animal Gastroenterology,
1996,WB Saunders, Philadelphia, PA.
Marks SL, Kather EJ. Bacterial-associated diarrhea in the dog: a critical appraisal. Vet Clin North Am Small Anim
Pract 2003; 33: 1029–1060.
Simpson KW. Vet Clin North Am 1999; 29(2).
34. The cat with signs of large bowel
diarrhea (acute and chronic)
Debra L Zoran
KEY SIGNS
● Soft, mucoid, formed to semi-formed feces.
● + Fresh blood or straining.
MECHANISM?
● Large bowel diarrhea is induced by increased secretion of water and electrolytes by
colonic epithelial cells, overload of substrate (from small bowel) or by altered motility
(e.g. decreased motility, loss of segmentation).
● Increased fermentable substrate (e.g. carbohydrates such as soluble fibers, lactulose, etc.)
may increase fecal water and create a softer fecal mass.
Signs of large bowel diarrhea:
● Soft, mucoid, formed to semi-formed feces.
● Hematochezia.
● Straining to defecate.
● Increased urgency to defecate.
● Small volume of fecal material expelled.
● Vomiting or weight loss not typically observed.
WHERE?
● Acute, large bowel diarrhea is uncommon in cats and is less likely to be associated with
parasites (e.g. whipworms) or clostridial enterocolitis compared to dogs.
● Chronic or recurrent large bowel diarrhea may be caused by local (e.g. large bowel) or sys-
temic disease, and thus a thorough evaluation that includes a minimum database, imaging
studies (radiographs, ultrasound, etc.), or endoscopy with collection of biopsies is required to
determine the cause.
● Irritant colitis secondary to ingestion of hair, feathers or other foreign material is a com-
mon cause of acute large bowel diarrhea.
● Cats usually do not lose weight or have vomiting episodes in association with large
bowel diarrhea unless a systemic disease is the cause of the problem.
WHAT?
● The most common causes of large bowel diarrhea are inflammatory (inflammatory
bowel disease), neoplasia, metabolic diseases (hyperthyroidism) and mechanical (hair,
feathers or bone-induced colitis).
● Food intolerance may be a common cause of colitis, but is not well documented in cats.
● Clostridial enterocolitis is the most common infectious cause of colitis in adult cats, but
the incidence in cats is low compared to other causes of large bowel diarrhea.
762
34 – THE CAT WITH SIGNS OF LARGE BOWEL DIARRHEA 763

Diseases causing signs of large bowel diarrhea
ANOMALY
● Congenital malformations (e.g. diverticulum, short colon syndrome, vascular ectasia) (p 779)
All are rare conditions that are observed in young cats or kittens, with the severity depending on
the anomaly (e.g. short colon syndrome causes severe signs, while vascular ectasia and diverticular
formations may initially be clinically silent.
MECHANICAL
● Irritant (foreign body) colitis** (p 765)
This is the acute development of colitis manifest by the presence of mucoid- to blood-streaked
feces resulting from ingestion of hair, bones, string, feathers or other foreign material.
● Perineal hernia (p 776)
Perineal hernias cause perineal swelling associated with a mucoid- or blood-streaked fecal mass
and straining to defecate. In long-standing cases, constipation may occur.
● Perianal tumors (p 777)
The tumor mass may cause straining to defecate and other signs of large bowel disease, or it may
obstruct the passage of feces and cause constipation.
METABOLIC
Hyperthyroidism may cause voluminous, soft and mucoid feces due to increased intake and reduced
GI transit time, changes in metabolism (malassimilation of food) and motility disturbances.
● Pseudomembraneous colitis (antibiotic-induced colitis) (p 777)
Acute or chronic large bowel diarrhea may be caused by the use of anaerobic antibiotics
resulting in overgrowth of pathogenic species that may be resistant to many or most antibiotics.
Severe forms of this disease are rare in cats, but diarrhea due to antibiotic use is not
uncommon.
NEOPLASTIC
● Colonic adenocarcinoma* (p 774)
This is the most common non-hematopoietic tumor of the GI tract and the most common colonic
tumor in cats. It typically affects old cats (>10 years) and vomiting, weight loss and lethargy are
more common signs than diarrhea.
● Lymphosarcoma* (p 773)
Lymphosarcoma tends to cause infiltrative disease that affects both the large and small intestine,
but may be localized to the colon in some cases causing only signs of large bowel disease.
● Colorectal polyps (p 778)
These are benign growths that are clinically silent until they grow large enough to prevent normal
fecal passage and cause large bowel diarrhea or constipation. Most cases reported in Siamese
cats.
continued
continued
NUTRITIONAL
● Food intolerance** (p 766)
Food intolerance is a non-immune-mediated condition associated with intermittent diarrhea or
vomiting, with no pattern or association with eating, and it resolves when the food source is
changed to omit the offending substance from the diet. The clinical significance of food intoler-
ance is unknown relative to other causes of diarrhea because of the difficulty in obtaining a
definitive diagnosis.
IMMUNOLOGIC
● Food allergy (dietary hypersensitivity)* (p 767)
Chronic vomiting appears to be more common than diarrhea in cats with food allergy, and cuta-
neous signs may also be present.
This is a chronic inflammatory disease of the feline GI tract that has no known cause. Depending
on the extent of the disease, the diarrhea may be entirely of large bowel character, small bowel
character or may be a combination of both. Weight loss and vomiting are also frequently observed
clinical signs.
INFECTIOUS
● Infectious colitis (Clostridium spp., E. coli, Campylobacter spp.)* (p 770)
Clostridial spp. cause an enterocolitis characterized by acute onset of soft, mucoid- or blood-
streaked feces that may become liquid, unformed small bowel diarrhea. Diarrhea is caused by
overgrowth of clostridial spp. followed by subsequent sporulation and enterotoxin formation.
E. coli is an uncommon cause of enterocolitis and large bowel diarrhea in cats.
●Parasitic infections (Giardia, Tritrichomonas, Cryptosporidia, Isospora, Toxoplasma,
Balantidium and Trichuris) * (p 775)
Diarrhea is the primary clinical sign with Tritrichomonas, Cryptosporidia and Cystoisosporidia
infections. Infections are inapparent except in young kittens and debilitated or immunocompro-
mised adult cats. Trichuris vulpis is a rare cause of colitis or large bowel diarrhea in cats, but is
occasionally found on fecal examination in cats from a contaminated environment.
Inflammatory:
● Chronic pancreatitis (p 776)
This disease is most often associated with vague, non-localizing signs, but hematochezia and diar-
rhea with a large bowel character are not unusual.
both for effective therapy to be initiated and for pro-

INTRODUCTION viding an accurate prognosis.
● The minimum database should include a CBC,
MECHANISM panel, urinalysis and complete fecal examination
(fecal flotation, direct, cytology).
The signs of large bowel disease include: ● Other diagnostic approaches that may be required
● Increased mucus.
include radiography, ultrasonography, endoscopic
● Hematochezia.
examination (especially for biopsy).
● Straining or increased urgency to defecate.
● Surgery on the colon is difficult, but in some neo-
● Soft to semi-formed feces.
plastic conditions or obstructive diseases, it will be
● Normal or increased frequency of defecation but
required.
not increased volume.
● It is rarely associated with weight loss or vomiting.
The colon responds to inflammatory conditions by pro- DISEASES CAUSING SIGNS OF

ducing increased amounts of mucus. LARGE BOWEL DIARRHEA
Blood streaks or fresh blood is also a common pre-
senting sign due to the proximity to the anus. IRRITANT (FOREIGN BODY) COLITIS**
Classical signs
WHERE
● Mucus- or blood-streaked, soft (semi-
Large bowel disease can result from disorders of ileo-
formed) stools.
cecal region, colon or rectum.
● History of ingestion of feathers, hair, bones
Historical and physical examination signs are impor- or other foreign objects (e.g. string, plants).
tant in localizing the problem to the large intestine.
Pathogenesis
Rectal examination is an especially important com-
ponent of the physical examination when evaluating Colitis and large bowel diarrhea that is caused by the
a cat for large bowel disease. presence of foreign objects (e.g. hair, bones, feathers) is
primarily due to the irritation of the colonic epithelium.
This results in motility disturbances and release of
WHAT
local inflammatory mediators that cause secretory or
Large bowel diarrhea can be caused by a variety of motility changes and ultimately, diarrhea.
infectious, dietary, metabolic, mechanical, neoplastic
Ingested hair, or a trichobezoar, is a common cause of
or idiopathic disorders.
irritant colitis in cats, especially in cats with long hair
● Acute large bowel diarrhea is often managed by
coats or with dermatologic disorders that result in
empirical therapy with anthelminitics, antibiotics
excessive grooming.
or a diet change.
● The most common causes of acute large bowel
diarrhea are parasites, dietary or infectious agents. Clinical signs
Chronic large bowel diarrhea is defined as the pres- Irritant colitis causes large bowel diarrhea that is inter-
ence of signs for more than 3 weeks. mittent and generally not severe in nature. Mucus- or
● Cats with chronic large bowel diarrhea should be blood-streaked, soft (semi-formed) stools are the
thoroughly evaluated to determine the diagnosis, most common presenting signs.
The history typically supports the presumptive diag- Prevention

nosis (e.g. cat consumes prey, feces contains large
amounts of hair or other foreign material). Prevention is most successful if the cause of the irri-
tation is identified and removed.
Removal of excess hair (grooming, brushing, clipping)
Diagnosis from long-haired cats, reduction of causes of excessive
A good history and visual examination of the feces is grooming (management of pruritus, behavioral ther-
especially helpful in making this diagnosis in cats with apy), prevention of prey consumption or ingestion of
irritant colitis. foreign objects (e.g. string, rubber bands, etc.) are
important measures in controlling foreign body colitis.
The physical exam and minimum database are usu-
ally unremarkable in these cats.
FOOD INTOLERANCE**
Survey radiographs may be helpful if there is bony
material present in the colon, but otherwise, imaging Classical signs
studies are not helpful.
● Dietary indiscretion: Vomiting, small or
Fecal exams are not diagnostic, but may be helpful to large bowel diarrhea, inappetance.
reveal the presence of large amounts of foreign ● Food intolerance: Vomiting, small or large
material in the fecal material. bowel diarrhea.
Because the episodes are typically intermittent, short
lived (few days at the most) and the cat is normal in See main reference on page 669 (The Cat With Signs of
the intervening periods, more aggressive diagnostic Chronic Vomiting) for details.
evaluations are rarely indicated.
Clinical signs
Differential diagnosis Dietary indiscretion is more commonly associated
with vomiting, but colitis (hematochezia, large
Other important differentials are infectious (clostridial
bowel diarrhea, mucus-covered feces) may occur if
enterocolitis), dietary indiscretion or food intolerance,
the substance ingested reaches the colon intact (hair,
and parasitic causes of large bowel diarrhea.
feathers, bones) or changes the colonic microflora due
to bacterial overgrowth of E. coli or other pathogens.
Treatment The signs are acute, and often include vomiting or
Identification and removal of the offending sub- inappetance in addition to diarrhea.
stance is curative. Food intolerance is an adverse reaction to a food or
In cats in which the cause cannot be identified or food substance that is not immunologic in nature (e.g.
removed: reaction to protein, preservative, flavoring, etc.).
● Addition of bulk-forming laxatives (e.g. psyllium, The signs of food intolerance may be acute, but often
methylcellulose). are chronic and intermittent, and can involve vomit-
● Lubricant laxatives (petroleum-based laxatives ing alone, diarrhea alone, or a combination.
found in hair ball remedies).
● Foods that contain increased fiber (canned pump-
kin, coarse wheat bran) may be helpful. Diagnosis
Alternatively, feeding the cat a diet that is high in The diagnosis of food intolerance is based on cessa-
insoluble dietary fiber to increase segmentation and tion of clinical signs upon elimination of the offend-
propulsion movements in the colon, may also be ing substance from the diet, and recurrence of signs
effective in decreasing occurrences of irritant colitis. when the substance or diet is re-introduced to the cats.
A response should be seen with the non-offending diet, Clinical signs

whether commercial or homemade, within 4 days if
there is total compliance with the diet. Food allergy is an adverse reaction to food (usually
protein, but may also be carbohydrate) that is immuno-
Dietary indiscretion is a presumptive diagnosis made logic (i.e. food allergy, hypersensitivity, delayed hyper-
based upon the history of eating lizards, beetles, plants, sensitivity).
etc., lack of other physical examination or diagnostic
(fecal examinations negative for parasites, normal fecal The signs are acute, and often include vomiting or
cytology, normal blood work and radiographs) findings. inappetance in addition to diarrhea.
The GI signs of food allergy are usually chronic and
Differential diagnosis may be intermittent. They can involve vomiting
alone, diarrhea alone, or a combination.
Food allergy is the major differential diagnosis for cats
with food intolerance and it is very difficult to distin- Clinical signs of food allergy may also involve the
guish the two conditions clinically. Since the treat- skin around the head and neck (pruritus, alopecia, der-
ment for both food intolerance and food allergy is the matitis, otitis) as well as the GI tract, and vomiting or
same and the response to treatment should be identi- diarrhea is reported.
cal, it is probably unnecessary in clinical practice to Those cats that develop GI signs usually have vomiting
differentiate the two conditions. or small bowel diarrhea, however, some cats will
develop colitis due to food allergy and have large bowel
Treatment diarrhea, or episodes of mucoid feces.
In most cats, treatment of dietary indiscretion is symp-

tomatic (e.g. feeding a high-fiber diet for cats with large
Diagnosis
bowel signs, low-residue diet if both large and small Diagnosis of food allergy is based on cessation of clin-
bowel signs are present), with judicious use of antibiotics ical signs upon elimination of the offending sub-
(for bacterial flora manipulation) and fluid support if stance from the diet, and recurrence of signs when the
needed. Prevent access to the offending material. substance or diet is re-introduced to the cats.
Treatment of food intolerance involves the removal A response should be seen with the hypoallergenic
of the offending substance from the diet, which is diet, whether commercial or homemade, within 4 days
usually achieved by changing to a commercial diet con- if there is total compliance with the diet and the cat
taining different protein or carbohydrate sources, and no has not been previously sensitized to ingredients in
additives, flavorings, colorings, etc. the diet.
Intradermal skin testing and measurement of food-
FOOD ALLERGY (DIETARY specific IgE in the serum have been advocated by
HYPERSENSITIVITY)* some, but are fraught with both false-negative and
false-positive results since most food allergies are not
Classical signs mediated by IgE. Also, IgE present in the skin does not
correlate to IgE in the GI tract.
● GI signs (vomiting, diarrhea, weight loss,
inappetance) are most commonly Gastroscopic food sensitivity testing has not been
associated with this condition. reported to be useful in cats.
● Dermatologic signs (pruritus, alopecia,
papules) may accompany the GI signs in
some cases.
Colonic IBD is the major differential for cats with
See main reference on page 667 (The Cat With Signs of severe or persistent signs, and endoscopic biopsy will
Chronic Vomiting) for details. not distinguish between eosinophilia or inflammation
due to food allergy and that due to other causes. Cats A diagnosis of colonic IBD is based on exclusion of
with food allergy usually have signs that resolve within all other causes of colitis in conjunction with the histo-
4 days on an appropriate hypoallergenic diet. Signs of logic presence of an increased number of inflamma-
IBD do not usually resolve solely with a change in diet, tory cells in the lamina of the crypts.
although they may improve.
The histopathologic changes associated with colonic
IBD are quite variable and include infiltration of the
Treatment lamina with lymphocytes and plasma cells (most
common), eosinophils, macrophages, neutrophils, or
Food allergy is diagnosed and treated by feeding an
a combination of these cells.
elimination diet for the dietary trial period.
An immunologic mechanism is suspected primarily
Homemade diets allow the use of a single novel
because of the response to immunosuppressive therapy,
protein source (turkey, duck, venison, etc.) and a
but this has not been proven.
novel, highly digestible carbohydrate source (rice,
potato) without preservatives, flavorings, or other The disease in cats is so heterogeneous (compared to
additives that may be cause of the problem. human IBD) that it likely represents a combination of
Alternatively, use a commercial hypoallergenic diet genetic (purebred cats have a higher incidence), envi-
containing protein and carbohydrate the cat has been ronmental, infectious (bacterial), dietary and
previously exposed to. immunologic components.
However, homemade diets are not recommended for
long-term management of food allergy as they are not Clinical signs
balanced or nutritionally complete.
Hematochezia is the most commonly observed clinical
There are a number of commercial diets that have sign in colonic IBD.
been formulated as “hypoallergenic” or limited
When large bowel diarrhea occurs, it may be either mild
antigen diets. Many of these diets (Hill’s, Innovative
and intermittent or persistent and severe in character.
Veterinary Diets, Royal Canin, Iams, Nature’s Recipe,
Nutro, and Wysong to name just a few) will be quite Most cats with the colonic form of IBD do not have
effective and should be used for long-term dietary vomiting, weight loss or decreased appetite, but it
management of intolerance or allergy to prevent nutri- can occur in cats with severe disease or disease affect-
tional deficiencies or excesses. ing the small and large bowel together.
The presence or severity of diarrhea or hema-
IDIOPATHIC INFLAMMATORY BOWEL tochezia does not correlate with the histologic grade
DISEASE (IBD)* of disease.
Classical signs
Diagnosis
● Diarrhea ranges from soft, mucoid blood-
Hematologic abnormalities are uncommon, but are
streaked feces to liquid diarrhea (more
consistently associated with severe colonic IBD and
characteristic of small bowel disease).
usually represent a typical stress response.
● Other signs may include vomiting,
anorexia, weight loss and lethargy. The most common biochemical abnormalities (when
they occur) are elevated hepatic enzyme activities and
hypokalemia. Hyperglobinemia may also occur.
Pathogenesis
Fecal floatation should be performed to rule out intes-
The etiopathogenesis of colitis or IBD is unknown. tinal parasitism, including giardiasis and coccidia.
Fecal cultures are rarely indicated in acute colitis, the duration of the elimination diet in cats with GI dis-
but in chronic or recurrent colitis they should be per- ease need not exceed 7 days as signs in most cats
formed. resolve within 3–4 days. A single novel protein and car-
bohydrate source diet is the best choice.
Imaging studies may reveal a thickened colonic wall
or abnormal gas patterns, but these findings are non- Clostridial enterocolitis or overgrowth of other
specific. intestinal flora are important infectious causes of
colitis. Testing for clostridial toxin or culture for
The definitive diagnosis is achieved by histopatho-
specific pathogen is the best means of diagnosis.
logic evaluation of the colonic mucosa from biopsies
obtained via endoscopy. Campylobacter spp. are more common in young kit-
tens or immunocompromised adult cats and can be
Endoscopic biopsies are less invasive, and are an accu-
identified on fecal cytology (motile, “seagull”-shaped
rate and rapid means of obtaining the diagnosis (if the
bacteria) or via culture (the definitive means of making
biopsies are adequate), and they also allow examination
the diagnosis).
of the mucosal surface.
Metabolic diseases should also be considered, as they
Mild or moderate infiltrations of lymphocytes or
may mimic or complicate IBD. The metabolic dis-
plasma cells in the lamina of the colon are normal,
eases that should be ruled out include hyperthyroidism
or suggest inflammation that is due to normal response
and chronic pancreatitis.
to a lumenal pathogen.
The amount of infiltration should be carefully
graded and the presence of other alterations in crypt Treatment
architecture should be found before concluding that
The best approach is to use a combination of dietary
the inflammatory cells present are pathologic or sug-
(increased fiber, hypoallergenic or low-residue) and
gestive of IBD.
pharmacologic therapy.
There is no single diet that will be effective in all
cases, and sometimes dietary trials using different diet
A major differential for lymphoplasmacytic colitis is types is necessary.
gastrointestinal lymphoma. Lymphocytic infiltration
Diets with increased insoluble fiber (Hill’s r/d, Purina’s
in the GI tract may be very difficult to distinguish from
OM formula, IVD’s hifactor diet) increase normal seg-
a well-differentiated neoplastic infiltration.
mentation, reduce fecal water and dilute luminal toxins,
Differentiating lymphoma from IBD is an important thus normalizing motility and reducing the stimulus for
step in the diagnostic process, both for appropriate release of inflammatory mediators. In some cats signs
treatment planning as well as for giving an accurate are improved using high insoluble fiber and in others
prognosis. signs are worsened. High-fiber diets tend to be less palat-
able to cats and may cause constipation in some cats.
The presence of inflammatory cells in the lamina
propria is not diagnostic for IBD, because almost all Diets that are highly digestible, and hypoallergenic,
other causes of colitis can result in the influx of inflam- are also recommended for treatment of colonic IBD.
matory cells. By minimizing the opportunity to react to proteins in
the diet, the response to therapy is often more pre-
Another differential for colonic IBD is food sensitiv-
dictable.
ity (food intolerance and food allergy). Some cats will
have an eosinophilic infiltrate, but this is not consis- The best hypoallergenic diet for ruling out food sen-
tent. Dietary trials must be instituted to investigate the sitivity is a homemade diet (1/3 cup boiled rice or
possibility of food intolerance or food allergy. In con- potato and 2/3 cup venison, rabbit, duck, ostrich, croco-
trast to elimination diets used for dermatological trials, dile, kangaroo). For long-term management of IBD,
commercial diets are recommended because they are Pathogenesis

nutritionally complete and balanced.
Disease is induced by changes in the diet, antibiotic
Low-residue diets are usually more appropriate for therapy, ingestion of carrion or contaminated
cats with small bowel IBD, but in some cases, provid- food, or stress that results in alteration of the nor-
ing a diet that will result in reduced colonic residue is mal colonic bacterial flora and changes in colonic
more effective. motility.
The key to choosing a diet is recognizing that not all These changes allow pathogens normally present
cats respond the same and a willingness to try a differ- (Clostridia, Campylobacter, E. coli, etc.) to overgrow
ent approach is necessary. or begin to secrete toxins that change permeability,
● Initial pharmacologic therapy includes pred- increase secretions, or cause release of inflammatory
nisolone (2–4 mg/kg q 12 h) and metronidazole mediators.
(10–15 mg/kg q 12 h).
● In cases that do not respond to these drugs,
Campylobacter is much more common in young cats,
tylosin (5–100 mg/kg q 12 h), sulfasalazine (11–22 while clostridial overgrowth is more commonly seen
mg/kg q 12–24 h) or olsalazine (no dose established in adults.
in cats, but 5–10 mg/kg may be reasonable), may be
added.
● Chlorambucil and azathioprine have been used in Clinical signs
refractory cases of small bowel IBD, but usually
are not required in colonic IBD. Cats are particu- Hematochezia and large bowel diarrhea that is
larly sensitive to the myelosuppressive side effects mucoid, soft and self-limiting is common.
of azathioprine. Diarrhea may become more liquid with time and
Most cats will respond to a combination of dietary severity, and is more common with E. coli infections.
and prednisolone or metronidazole therapy and Vomiting may occur, but is uncommon.
eventually can be maintained with dietary management
alone. Anorexia or lethargy are variably present, depend-
ing on the severity.
Prognosis Fever and other signs of infectious disease rarely

occur with infectious colonic diseases.
The prognosis for complete remission is only guarded
to fair. Weight loss is uncommon due to the acute nature of
the condition.
However, most cats with colonic IBD can be success-
fully managed with a combination of dietary and Historical information is very important in estab-
pharmacologic therapy, and thus, the prognosis for lishing the presumptive diagnosis.
control is very good.
INFECTIOUS COLITIS* (CLOSTRIDIUM Diagnosis

SPP., E. COLI, CAMPYLOBACTER SPP.) A definitive diagnosis is difficult, because identification
of these organisms in feces is not necessarily abnormal.
Classical signs ● Clostridium perfringens enterotoxicosis is best
● Diarrhea ranges from soft, mucoid blood- diagnosed by positively identifying the presence
streaked feces to liquid diarrhea (more of enterotoxin in the feces (ELISA or RPLA
characteristic of small bowel disease). assays are commercially available). Note: these
● Other signs may include vomiting, anorexia assays have not been evaluated in cats, but the
and lethargy. ELISA assay appears to be more specific in dogs.
A positive enterotoxin test determined by ELISA
(regardless of spore numbers) in the context of clin- Dietary management should include feeding a high-
ical signs consistent with C. perfringens is strongly fiber diet, unless the signs also involve the small
supportive of clostridial-associated diarrhea. In intestine. In those cases, a low-residue diet is recom-
dogs, the RPLA test does not differentiate dogs mended.
with clostridial diarrhea from normal dogs and 25%
Most cases in adults are self-limiting, but respond
of normal dogs have positive test results. In both
rapidly to antibiotics and dietary intervention. In
cats and dogs, there appears to be poor correlation
neonates or debilitated cats, additional supportive
between the presence of fecal endospores and the
care (e.g. fluid therapy) may be required in severe
presence of enterotoxin.
cases.
Campylobacter is also a normal inhabitant of the
feline colon and thus, a pure culture along with detec-
tion of the presence of enterotoxin is recommended Prognosis
for diagnosis.
Good to excellent, especially with appropriate antibi-
Pathogenic and nonpathogenic strains of E. coli can otic therapy.
be cultured from feces and thus before a diagnosis can
be based upon the culture results and clinical pres-
entation, the results should be confirmed by PCR Prevention
testing for specific pathogenic strains.
In kittens or colonies of cats that have recurrent prob-
Once the diagnosis has been made, affected cats should lems with infectious colitis, minimizing stress,
be tested for FIV/FeLV, in case the condition is sec- improving sanitation, and maximizing nutrition will
ondary to immunocompromise by viral disease. all help to reduce the occurrence of these stress-related
diseases.
Differential diagnosis All cats should be tested to be sure that they are
FeLV/FIV negative.
Dietary indiscretion.
Parasitic enterocolitis (e.g. protozoal agents such as
Giardia, Tritrichomonas, etc.), and mechanical diseases
HYPERTHYROIDISM*
of the large bowel (e.g. intussusception, cecal inver-
sion, foreign bodies) should all be considered when for-
Classical signs
mulating a differential diagnosis.
● Weight loss despite a good appetite.
● GI signs (vomiting or diarrhea).
Treatment
● Unkempt hair coat and increased dander
Clostridial enterocolitis: ampicillin (22–33 mg/kg PO are common.
q 8 h), amoxicillin (10–22 mg/kg PO q 12 h), metroni- ● Tachycardia secondary to thyrotoxic heart
dazole (5–15 mg/kg PO q 12 h), tylosin 5–20 mg/kg PO disease.
q 12–24 h), clindamycin (5–10 mg/kg q 12 h). ● Hyperactivity or restlessness.
Campylobacteriosis: tetracycline (20 mg/kg q 8 h PO)
tylosin (20 mg/kg PO q 12 h) or fluorinated quinolones
(e.g. enrofloxacin).
E. colibacillosis: trimethoprim-sulfonamide (15 mg/kg Clinical signs
PO q 12 h), cephalosporins (10–30 mg/kg PO q 12 h),
This disease is most commonly observed in middle-
doxycycline (5–10 mg/kg PO q 12–24 h), or fluorinated
aged to old cats (> 8 years).
quinolones (e.g. enrofloxacin, orbifloxacin, ciprofloxacin,
etc.). Weight loss is a very common feature of the disease.
Polyphagia, normal or decreased appetite, are all Major differentials associated with the systemic
observed, but ravenous appetite is the classic presen- signs of hyperthyroidism are diabetes mellitus,
tation. chronic renal failure, neoplasia, IBD and hyper-
trophic or restrictive cardiomyopathy.
Hyperthyroidism may cause hyperactive or restless
behavior and some cats are also irritable.
Decreased grooming habits, unkempt hair coat and
Treatment
increased dander are often reported.
Anti-thyroid drug therapy includes methimazole
Vomiting or diarrhea may be observed. Feces are usu-
(2.5–5 mg/cat q 12–24 h), with a maximum dose of 15
ally voluminous due to increased intake and decreased
mg/day. Occasionally, side effects such as anorexia,
gut transit time.
vomiting, lethargy, pruritus, hepatotoxicity and hema-
Tachycardia, and sometimes a gallop rhythm are tologic changes may be observed, but will resolve if the
present secondary to thyrotoxic effects on the drug is stopped. Carbimazole (5 mg PO q 8–12 h) is
myocardium that leads to thyrotoxic heart disease and metabolized to methimazole.
heart failure.
Radioactive iodine therapy: if available is the treat-
ment of choice. Iodine-131 is concentrated in adeno-
Diagnosis matous thyroid but spares normal tissue. Note:
Use with extreme caution if the cat has concurrent
This is confirmed by presence of elevated serum total
renal disease as reduced renal perfusion post-treatment
thyroxine (T4) levels.
may worsen the condition, or unmask subclinical renal
Other diagnostic methods that may be used if the failure.
serum total T4 is in the upper half of the normal range,
Cats treated with I-131 must be isolated for a variable
but the cat has clinical signs of hyperthyroidism include
period (up to 3 weeks) of time (depending on local
radionuclide scanning, serum free T4 test, or a T3
laws) following treatment.
suppression test.
Surgical removal of a hyperplastic or neoplastic thy-
Abnormalities may be observed in routine blood
roid nodule is only indicated if the disease is unilat-
screening tests (e.g. erthyrocytosis, elevated liver
eral (70% of cats have bilateral disease).
enzyme activities) but these are not specific for thyroid
disease. The risk of anesthesia is reduced by prior treatment
with methimazole to make the cat euthyroid and also
If the cat has an elevated heart rate or gallop rhythm
by careful selection of anesthetic agents. Xylazine,
consistent with heart disease, thoracic radiographs
ketamine or other arrhythmogenic agents should not be
and echocardiography are indicated to assess the
used.
severity.
Bilateral thyroidectomy should be staged to mini-
mize risk of hypoparathyroidism.
Management of thyrotoxic heart disease with beta-
Other metabolic diseases and extra-intestinal causes
adrenergic antagonists (atenolol, 6.25–12.5 mg PO q
of GI signs, weight loss or tachycardia that affect
12–24 h) may be necessary in some cases, although
older cats should be considered carefully.
cardiac complications usually resolve when the hyper-
Differentials for chronic large bowel diarrhea thyroidism is treated. Other agents that may be consid-
include IBD, neoplasia and food intolerance or food ered include calcium channel blockers e.g. diltiazem
allergy. (1.5–2.5 mg/kg q 8–12 h).
LYMPHOSARCOMA* Differential diagnosis

The primary differential for lymphoma in cats is
Classical signs severe lymphocytic plasmacytic IBD, and it is sus-
● Vomiting, small bowel diarrhea, weight pected that this may be a precursor lesion to lymphoma
loss and anorexia are the most common in some cats.
presenting signs. Other extra-intestinal causes of weight loss and vomit-
● Large bowel diarrhea alone is rarely ing must also be considered, including pancreatitis, renal
observed because the tumor is typically or liver disease, hyperthyroidism, diabetes mellitus, etc.
infiltrative throughout the GI tract.
Other less-common neoplastic diseases to consider in
See main reference on page 317 for details. cats are mast cell tumors, leiomyosarcomas and carci-
noids.
Clinical signs
Treatment
Vomiting, small bowel diarrhea, weight loss and
anorexia are the most common presenting signs. Combination chemotherapy with cyclophosphamide,
vincristine and prednisolone (COP protocol) is the
Large bowel diarrhea alone is rarely observed most commonly recommended regimen. Most cats
because the tumor is typically infiltrative throughout treated with this protocol are expected to live 6–9
the GI tract. months, with 20% living longer than 1 year. Asparaginase
Palpation may reveal thickened loops of bowel. or doxyrubricin can be added to increase the remission
times or serve as the rescue.
Most cats with alimentary lymphoma are FeLV nega- ● Cyclophosphamide (300 mg/m2 PO q 3 weeks).
tive so associated clinical disease is uncommon. ● Vincristine (0.75 mg/m2 IV weekly for 4 weeks).
● Prednisone (2 mg/kg/day).
Occasionally, lymphoma will present as a solitary
● Doxyrubricin (25 mg/m2 IV q 3 wk).
mass in the small intestine or colon, which obstructs
● L-Asparaginase (10 000 IU/m2 IM).
the GI tract and must be differentiated from adenocar-
cinoma and other neoplastic or granulomatous diseases. Other protocols exist for induction, maintenance
and rescue, but the reader is referred to oncology texts
Diagnosis for additional information.
Routine hematology and chemistry profiles are often Supportive care in the form of nutrition is essential
within normal limits. for cats with alimentary lymphoma because they tend
not to eat and often vomiting precludes oral alimenta-
Survey radiographs of the abdomen may reveal thick- tion.
ened bowel loops or abnormal gas patterns, but they
also may be interpreted as normal. Placement of jejunostomy tubes may be required in
these cats.
Ultrasound examination of the abdomen is especially
helpful in identifying enlarged lymph nodes, liver or
splenic changes in echogenicity, and measurement of Prognosis
intestinal wall thickness. Guarded to poor. Survival times are shorter for cats
● Fine-needle aspirates may be obtained via ultra- with alimentary lymphoma than other forms of lym-
sound guidance that will facilitate a definitive phoma (e.g. multicentric or mediastinal), primarily
diagnosis and staging. because response to chemotherapy is more variable
Endoscopy is also an important diagnostic tool in mak- with these tumors.
ing a definitive diagnosis, because multiple samples In one recent report, mean survival was 230 days, but
can be obtained for histopathologic examination. median survival was only 50 days.
Late changes may include hypoproteinemia, hypoal-

COLONIC ADENOCARCINOMA*
buminemia, electrolyte disturbances due to vomiting
or elevations in liver enzyme activities due to metasta-
Classical signs
sis.
● Vomiting, weight loss and anorexia are
Imaging studies (radiography, ultrasound) are useful
classical signs.
in identifying the abdominal mass and a preliminary
● Hematochezia, tenesmus or large bowel
diagnosis can be made via ultrasound-guided fine-nee-
diarrhea occur with a distal location.
dle aspiration of the mass in many cases.
Ultrasonography is also especially useful in assessing
Pathogenesis regional lymph nodes and liver for evidence of
metastatic disease.
Adenocarcinoma is the most common tumor of the
feline colon and most common non-hematopoietic The definitive diagnosis is obtained by histopathology.
tumor of the GI tract.
Endoscopy may be used to obtain biopsies, but
It usually occurs in old cats (>10 years) and has exploratory surgery with resection of the affected
a higher incidence in Siamese cats. area and biopsy of regional lymph nodes or liver is
diagnostic, prognostic and therapeutic.
It most commonly occurs as a solitary lesion causing
signs of bowel obstruction due to a large mass or
annular growth around the circumference of the Differential diagnosis
bowel.
Other intestinal diseases such as IBD, lymphoma,
Malignant behavior with metastasis to regional lymph other tumors, or intussusception may have a similar
nodes, mesentery, liver and other abdominal organs is clinical presentation.
typical of this neoplasm.
Extra-intestinal diseases should also be considered
However, it rarely metastasizes to the lungs. when the clinical signs are vague. These include pan-
creatitis, hyperthyroidism, chronic renal failure, hepatic
Clinical signs disease and neoplasia in other locations.
Vomiting, weight loss and anorexia are the classical
signs.
Treatment
Hematochezia, tenesmus or large bowel diarrhea are
The treatment of choice for colonic adenocarcinoma is
observed the more distal the tumor location.
wide surgical excision, even if the tumor has metasta-
Some cats may only have lethargy, decreased appetite sized, which it usually has at the time of surgery.
or weight loss without GI signs, so history and sig-
Chemotherapy for metastatic disease has not been
nalment (old, Siamese cat) are important clues.
reported, but would not be expected to be success-
Physical examination may reveal an abdominal mass ful.
or abdominal discomfort upon palpation.
Mean survival time following surgical resection is
generally less than one year but this is not corre-
Diagnosis
lated with the presence of metastatic disease.
Careful abdominal palpation may reveal a mass or Survival time is shorter without treatment.
thickened bowel loop.
Extensive surgical removal of the colon will require
Routine hematology and serum chemistry profile are that the cat be fed a highly digestible, low-residue
often within normal limits in the early stages of diet to minimize clinical signs of short bowel syn-
disease. drome.
Prognosis Tritrichomonas is the exception, as kittens or young

cats with Tritrichomonas infection will have persistent
Long-term prognosis is poor. However, many cats foul-smelling diarrhea.
will have lengthy (up to 15 months) periods of good-
quality life following surgical resection. Hematochezia, mucoid stools, large bowel diarrhea
and flatulence have all been infrequently reported in
cats with these parasites, but are secondary to the pri-
PARASITIC INFECTIONS (GIARDIA, mary disease (often FIV).
TRITRICHOMONAS, CRYPTOSPORIDIA,
ISOSPORA, TOXOPLASMA, BALANTIDIUM
AND TRICHURIS)* Diagnosis
Fecal floatation, direct smears of feces, and fecal
Classical signs cytology have all been used to identify these parasites.
● Mucus- or blood-streaked, soft (semi- Multiple (at least three) zinc sulfate solutions on
formed) feces. consecutive days are best to float Giardia and
● Rarely, overt large bowel diarrhea in Cryptospordia oocyts.
immunocompromised or very young cats.
Cryptosporidia are so small that identification is diffi-
cult without special stains or advanced microscopy
Pathogenesis techniques.
There are no major parasitic causes of large bowel Cryptosporidia can also be identified by use of a fecal
diarrhea in the cat. ELISA test (human test but effective in cat feces).
However, occasional infections with Giardia, Tritri- Toxoplasma will float in salt solution but are very
chomonas, Cryptosporidia, Isospora, Toxoplasma, and small (< 5 micron) and may be missed without careful
Balantidium may be observed. examination of the slide.
Each of these parasites has a different life cycle and Diagnosis of Tritrichomonas is best confirmed by PCR
degree of pathogenicity in the host, but none of these is testing or culture of the organism in feces using a spe-
a strictly large bowel parasite and most cause disease cial technique.
only in the very young, the very old, or sick, debili-
tated cats (especially FIV- or FeLV-positive cats).
Whipworm eggs (Trichuris serrate and T. campanula)
Because these are rare causes of large bowel disease
are occasionally observed in cats, but do not cause
in cats, all other, more common, causes of colitis
clinical disease and are believed to be either mis-diag-
should be ruled out first.
nosed (e.g. Capillaria spp.) or are present because the
cat ingested rodent or canine whipworm eggs in the If these parasites are found in the feces of an adult cat
environment. that is symptomatic, an immediate search for an
immunosuppressive disease should be initiated (ie.
Most of these protozoan parasites (e.g. Giardia,
rule out FeLV, FIV, FIP, etc.).
Toxoplasma, Cryptosporidia) are pathogenic (zoonotic)
to humans.
Treatment
Clinical signs Tritrichomonas: Ronidazole (30–50 mg/kg PO q 12h)
Most infections of these parasites in cats are asympto- Giardia: Metronidazole (10–25 mg/kg PO q 12 h for
matic and are accidentally found on a routine fecal 5–10 days) or fenbendazole (25–50 mg/kg PO q 24 h
examination. for 5–7 days)
Isospora: Sulfadimethoxine (25 mg/kg PO q 24 h for Ultrasonographic examination of the pancreas is

10–14 days) a good method of detecting pancreatic abnormali-
ties. However, this is still not a specific or sensitive
Cryptosporidia: Azithromycin (5 mg/kg q 24 h PO for
test for pancreatitis.
5 days then q 48 h)
Elevations in serum trypsin-like immunoreactivity
Toxoplasmosis: Clindamycin (10–25 mg/kg PO q 12 h)
(TLI) have been used as a screening test, but caution is
(high dose recommended but often causes GI side
advised because the assay often has false-negative and
effects), or azithromycin 5 mg/kg q 24 h for 5 days
-positive results.
then q 48 h.
Feline pancreatic lipase immunoreactivity (fPLI) is
the most specific and sensitive serum test for pan-
CHRONIC PANCREATITIS
creatitis currently available. fPLI is 100% specific for
pancreatitis.
Classical signs
fPLI and ultrasound examination, when used together,
● Clinical signs are vague and non-localizing
have a sensitivity of >90%.
in cats (e.g. lethargy, anorexia).
● Vomiting or diarrhea are less common.
● Hematochezia or large bowel diarrhea
occur more often with chronic pancreatitis. PERINEAL HERNIA
See main reference on page 318 for details. Classical signs

Clinical signs ● Large bowel diarrhea.
● Irritation or perineal swelling.
Anorexia and lethargy are the most common signs
associated with feline pancreatitis.
Vomiting is less common (< 50% of cats vomit) and Pathogenesis
thus, dehydration is less common.
Perineal hernia occurs when there is failure of the
Chronic pancreatitis is also associated with vague clin- pelvic diaphragm musculature to support the rectal
ical signs, but hematochezia or large bowel diarrhea wall. A peritoneum-lined sac protrudes through the
may be observed. defect and may contain pelvic and abdominal contents.
The rectal wall stretches and deviates into the sac.
Diagnosis
Feces are retained in the divided section of the rectal
There is no single, definitive test for pancreatitis in wall resulting in straining and difficulty defecating.
cats.
Weakness of the pelvic diaphragm musculature and
Non-specific abnormalities on the hemogram may herniation is often idiopathic but may be associated
include neutrophilia or mild, non-regenerative anemia. with previous perineal urethrostomy, megacolon, per-
ineal mass or chronic colitis.
Serum chemistry abnormalities may include elevated
liver enzyme activities and/or hyperbilirubinemia.
Serum amylase and lipase are of no use in the cat
Clinical signs
for diagnosis of pancreatitis due to false-negative and
-positive results. Straining to defecate, constipation or less com-
monly, large bowel diarrhea, irritation or perineal
Loss of visceral detail or increased duodenal gas are
swelling are all typical signs of perineal hernia.
sometimes observed on survey radiographs, but this is
not consistent. Usually older cats are affected.
On rectal examination there are impacted feces in a rec- Cats often will lick at the area frequently which may
tal dilation or sacculation, and evidence of a defect in draw attention to the region.
the pelvic diaphragm musculature.
Diagnosis
Diagnosis In the majority of cases, the presence of a perianal mass
The diagnosis may be suggested by the history or will be the obvious cause of the intestinal disturbance.
appearance of the perineal area and a rectal exami- Perianal tumors may metastasize locally (to regional
nation will confirm the problem in many cases. lymph nodes or bones) or to distant sites (liver, lung or
In cases where the diagnosis is in doubt, a barium abdominal sites) and so, a routine database, radio-
enema will outline the herniated rectal tissue. graphs and ultrasound, and fine-needle aspirates of
regional or enlarged lymph nodes should be per-
These hernias are rare in cats compared to dogs. formed.
Fine-needle aspirates of the tumor can be used to iden-
Treatment tify the tumor type prior to surgical biopsy.
Medical management using low-residue food and fecal
softeners (e.g. lactulose) or enemas may help in cats Differential diagnosis
with small hernias.
The primary differential for this problem is anal sac-
Surgery is considered the preferred treatment and culitis or abscess, which are more common problems,
several herniorrhaphy techniques have been described, but generally are less likely to cause problems with
although recurrence rates can be high (10–50%). In cats fecal passage.
with megacolon, subtotal colectomy may resolve the
constipation and tenesmus. Herniorraphy can be
Treatment
performed in cats that do not improve with medical
therapy. Surgical resection of tumor with wide margins to
prevent recurrence.
PERIANAL TUMORS Histopathologic examination of the tumor as well as
biopsies of regional lymph nodes is recommended for
Classical signs confirmation of the diagnosis and determination of
the prognosis.
● Large bowel diarrhea or constipation. Fecal softeners (e.g. lactulose or docusate sodium) may
● Perineal swelling. be helpful if fecal material is difficult or painful to pass.
● Licking excessively at the perineum.
PSEUDOMEMBRANEOUS COLITIS
(ANTIBIOTIC-INDUCED COLITIS)
Pathogenesis
These tumors occur more commonly in older cats. Classical signs
Tumors of the perianal region in cats, unlike those in ● Mucus- or blood-streaked, soft (semi-
dogs, are usually adenocarcinomas. Perianal tumors formed) feces.
are very rare in cats compared to dogs. ● Progression to severe large bowel
diarrhea.
Clinical signs
Pathogenesis
Straining to defecate, large bowel diarrhea, perineal
swelling, or constipation may all occur due to large This disease is caused by the use of antibiotics (espe-
perianal mass(es). cially clindamycin or cephalosporins) that disturb the
normal bacterial flora of the colon resulting in over- Prevention

growth of antibiotic-resistant, pathogenic species.
Cautious use of antibiotics that have an anaerobic
Diarrhea due to clostridial spp. is not uncommon, but it spectrum over a long period (weeks).
is usually due to Clostridium perfringens. Clostridium
difficile are not common inhabitants of the feline
colon, but may populate and overgrow in the right cir- COLORECTAL POLYPS
cumstances (primarily chronic antibiotic use).
Classical signs
This is a very uncommon problem in cats.
● Mucus- or blood-streaked, soft (semi-
formed) feces.
Clinical signs
Mucus- or blood-streaked feces which may progress
to severe large bowel diarrhea. Pathogenesis
In some cases, the diarrhea is poorly responsive to Benign growths of the colonic epithelium.
treatment. Rare in cats, but reported occasionally.
Most are found in the upper duodenum, near the pylorus
Diagnosis or in the ileum or proximal colon, and Siamese cats are
Historical correlation between the development of over-represented.
mucoid diarrhea and the use of antibiotics that have
an anaerobic spectrum. Clinical signs
Confirmation of the diagnosis requires fecal culture May be clinically silent.
(requiring special handling) or colonic biopsies that
confirm the presence of pseudomembrane formation. May cause intermittent large bowel signs: increased
tenesmus, mucus- or blood-streaked feces, or diffi-
Fecal analysis for Clostridial toxins A and B is very culty in passing feces (constipation is possible).
important for confirmation.
Diagnosis
No changes in hematology or serum chemistries will
Clostridial enterocolitis due to Clostridium perfrin- occur.
gens is the primary differential, but simple diarrhea
due to antibiotic therapy, diet changes or infectious or Contrast radiography or ultrasound examination
parasitic agents should be considered carefully. will delineate them, but colonoscopy is the best
diagnostic method, and will allow visualization,
biopsy and in some cases assist removal (if distal
Treatment enough).
The choice of antibiotic should be based upon cul-
ture results due to resistance. Metronidazole has been
used successfully in some cases.
Other neoplastic diseases of the large bowel: i.e. ade-
Non-specific therapy for this disorder includes use of
nocarcinoma, focal lymphoma, mast cell tumors, carci-
a high-fiber diet (or addition of insoluble fiber to the
noids, etc.
diet) to normalize colonic function (secretion and
motility). Sliding or intermittent intussusception.
In severe cases, long-term (weeks) antibiotic therapy Granuloma due to fungal or infectious disease (e.g.
will be required to achieve control. FIP).

Surgical removal is curative. Large bowel diarrhea and flatulence.
Recurrence is unusual. Constipation.
Abdominal pain (due to typhilitis or gas distention).
Prognosis
Diagnosis
Excellent.
These are rare congenital diseases.
CONGENITAL MALFORMATIONS (SHORT Kittens are usually presented at just weeks of age.
COLON SYNDROME, VASCULAR ECTASIA,
Blood work (CBC, profile) will usually be completely
DIVERTICULUM)
normal.
Classical signs Survey radiographs will generally not be helpful,
except in cases of short colon syndrome, where the
● Signs depend on the location of the
colon may be visibly abnormal.
anomaly.
● Large bowel diarrhea, constipation or Contrast radiographs may be very helpful in identi-
abdominal pain (typhilitis). fying short colon syndrome.
● Young cats or kittens, and do not worsen
Ultrasonography is very useful in identifying an
with age, except with short colon
abnormal enterocyst, but colonoscopy or surgical
syndrome.
exploration may be required to make the definitive
diagnosis.
Pathogenesis Differential diagnosis

The etiopathogenesis of the congenital malformations The differentials are usually limited to those things
affecting the large bowel is unknown. causing colonic disease in kittens, e.g. parasites,
infectious, mechanical (foreign objects) and dietary
The most frequently reported malformations affect-
indiscretion or food intolerance.
ing the large bowel are vascular ectasia, short colon
syndrome and enterocyst formation.
Treatment
Vascular ectasia is a syndrome of abnormal blood
Treatment of vascular ectasia and enterocysts is via
vessel formations that results in abnormal bowel func-
surgical resection of the affected area(s).
tion (especially motility) due to the lack of a normal
blood supply. Short colon syndrome must be managed medically
by providing a low-residue diet (e.g. Hill’s i/d diet,
Short colon syndrome can be congenital or iatro-
Iam’s low residue diet or IVD neutral formula), use of
genic (secondary to surgical removal of the colon due
motility-modifying drugs as needed (e.g. lomotil,
to neoplasia or other disease). Cats with short colon
loperamide), and antibiotics when they are indicated.
syndrome are unable to reabsorb water and elec-
trolytes and thus, are not able to form normal feces
Prognosis
without providing very highly digestible diets that
reduce the amount of ingesta that reaches the colon. The prognosis is guarded to good, depending on the
anomaly that is present.
Diverticular formations are also found, however, they
can be congenital or secondary to chronic disease. Cats with vascular ectasia or enterocysts that can be
corrected surgically have a very good prognosis.
Many diverticular formations are incidental findings
and are not associated with abnormal colon function Cats with short bowel syndrome have a very guarded
unless they are large or become diseased. prognosis and will require life-long therapy.
RECOMMENDED READING
Guilford WG. The gastrointestinal tract and adverse reactions to food. Consult Feline Intern Med 2001; 4.
Guilford W, Jones B, Markwell P, Arthur D, Collett M, Harte J. Food sensitivity in cats with chronic idiopathic gastro-
intestinal problems. J Vet Intern Med 2001; 15: 7–13.
Guilford WG, Center SA, Strombeck DR, Williams DA, (eds) Strombeck’s Small Animal Gastroenterology, 3rd edn
2000, WB Saunders, Philadelphia, PA.
Jergens AE. Feline idiopathic inflammatory bowel disease. Comp Cont Ed 1992; 14(4): 509–520.
Simpson, KW. Vet Clin North Am Small Anim Pract 1999; 29(2): 441–470, 501–522, 577–588.
Steiner J. Diagnosis of pancreatitis. Vet Clin North Am Small Anim Pract 2003; 33: 1181–1195.
35. The constipated or straining cat
Albert E Jergens and Annette Litster
KEY SIGNS
● Reduced frequency of defecation.
● Tenesmus or painful defecation.
● Hard, dry, low-volume feces, sometimes with mucus.
MECHANISM?
● Constipation denotes infrequent or difficult defecation and is a common problem in cats.
Straining (tenesmus) occurs when there is ineffectual defecation or urination, or irritation of
the bowel or bladder wall.
● Straining may also be associated with conditions affecting the lower urinary tract. Refer to p. @
(The Cat Straining to Urinate).
WHERE?
● Disorders of the large intestine are the most common causes of constipation.
WHAT?
● Constipated cats may have underlying orthopedic or neurologic diseases which cause fecal
impaction and clinical signs.

Diseases causing a constipated or straining cat
DEGENERATIVE
● Constipation (including idiopathic megacolon)***(p 783)
The hallmarks are reduced, painful, or absent defecation +/− tenesmus. Idiopathic megacolon
denotes diffuse colonic dilatation with colonic hypomotility.
This is a rare cause of constipation, and associated clinical signs include sudden onset of depression
and anorexia coupled with a variety of signs including regurgitation, mydriasis, constipation, brady-
cardia and dysuria. Dysautonomia was of regional importance in the UK in the early 1980s and
more recently in the USA.
781
MECHANICAL
● Hair matting* (p 789)
Matting of the hair around the anus with feces is associated with poor grooming, and may cause
perianal dermatitis and discomfort with defecation. It may also obstruct fecal passage through the
anus. It occurs more often in obese cats, and long-haired cats.
METABOLIC
● Dehydration and hypokalemia* (p 787)
Metabolic conditions such as dehydration or hypokalemia can predispose to constipation by reducing
fecal moisture and colonic muscle activity. Signs of dehydration, inability to jump, or ventroflexion of
the neck may be evident.
NEOPLASIA
Intraluminal or extraluminal tumors may cause mechanical obstruction to the passage of feces.
Signs may include straining to defecate and evidence of fresh blood on the feces.
PSYCHOLOGICAL
● Litter box dissatisfaction* (p 789)
Litterbox dissatisfaction, caused by poor litterbox hygiene or inadequate litterbox access, may dis-
courage regular defecation and result in constipation.
INFLAMMATION
● Acute non-specific colitis** (p 786)
This condition presents with an abrupt onset of large bowel diarrhea which is usually self-limiting.
Signs include tenesmus, mucoid feces and hematochezia. Vomiting may occur.
● Chronic colitis** (p 787)
Chronic colitis causes hematochezia, large bowel diarrhea, and tenesmus, which are attributable to
infectious, inflammatory, neoplastic and benign infiltrative mucosal diseases.
● Perineal inflammation/infection (p 792)
Conditions such as perineal abscesses, perianal fistulae and anorectal foreign bodies may cause
pain, discouraging regular defecation and lead to constipation and/or tenesmus.
● Lower urinary tract disease* (p 790)
Hematuria, strangiuria and pollakiuria caused by lower urinary tract disorders must be differenti-
ated from constipation by history and physical examination.
IATROGENIC
● Drugs (p 791)
Drugs such as opioid agonists, cholinergic antagonists, diuretics, phenothiazines and barium sul-
fate can cause constipation.
TRAUMA
● Pelvic fractures* (p 788)
Pelvic fractures may reduce the size of the pelvic canal, causing obstruction. In the acute phase
following trauma, painful defecation may lead to constipation.
35 – THE CONSTIPATED OR STRAINING CAT 783
a high squat with an arched tail, while urination

INTRODUCTION posture is a low squat with a straight tail.
● Other signs suggesting a urinary tract problem
MECHANISM? include a small or large firm bladder, normal
amounts of fecal material on abdominal palpation,
Constipation may be suspected when a cat has chronic and a history of small amounts of urine being pro-
difficulty or pain while defecating; defecation is duced associated with tenesmus. The urine may be
reduced in frequency; or reduced amounts of hard dry discolored; typically there is hematuria.
feces are passed. The proximal colon in cats is par-
Abdominal radiography and routine urinalysis most
ticularly efficient at water reabsorption, so pro-
readily differentiate constipation from lower urinary
longed transit times predispose to constipation.
tract disorders.
Common signs of constipation include:
● Reduced or absent defecation.
● Marked tenesmus. WHAT?
● Painful defecation may be evidenced by crying
Causes for constipation are diverse and may include
out on defecation, numerous aborted attempts to
orthopedic, neoplastic, pharmacologic, metabolic
defecate, or prolonged attempts to defecate.
and neurologic etiologies or they may be idiopathic in
● Reduced amounts of hard, dry feces which may
origin.
have a mucus covering.
● Anorexia, lethargy, vomiting and weight loss are Abnormal evacuation of feces leads to constipation,
systemic manifestations observed in cats with colonic impaction and clinical signs.
severe constipation.
The most common causes of straining to urinate include
Obstipation is the presence of chronic intractable lower urinary tract disease or idiopathic cystitis, bacter-
constipation with massive fecal impaction and ial cystitis in older cats, neoplasia and uroliths.
inability to defecate.
Diagnosis of the constipated/straining cat is based on
Idiopathic megacolon denotes severe generalized history, physical examination findings, radiogra-
colonic dilatation which is irreversible and poorly phy, urinalysis and histopathology of colonic
responsive to aggressive medical therapy. biopsy specimens.
Tenesmus (straining) may also be associated with other

colonic disorders that cause inflammation and diarrhea. DISEASES CAUSING CONSTIPATION
Cats with tenesmus may be straining to urinate, and
OR STRAINING
if signs or physical examination findings suggest a uri-
nary tract problem, the reader is referred to page 173 CONSTIPATION*** (INCLUDING
(The Cat Straining to Urinate). IDIOPATHIC MEGACOLON)
WHERE? Classical signs
Signs of constipation and straining result from prob-

● Most common in middle-aged male cats,
lems involving the following sites: but may occur in any age, or gender.
● Colonic lumen and mucosa.
● Reduced, painful, or absent defecation +/-
● Urinary bladder and/or urethra.
tenesmus.
● Feces are hard, dry and low-volume, with
Physical examination (especially abdominal palpation) or without mucus.
and history help localize the cause. Posture while ● +/- Anorexia, lethargy, weight loss, and
straining often differentiates a problem with defecation vomiting with chronicity.
from a urinary tract problem. Defecation posture is
Pathogenesis breed. Burmese cats are over-represented with idio-

pathic megacolon.
Etiologies for constipation are diverse. While the
majority of cases are idiopathic, pelvic canal stenosis, Reduced, absent or painful defecation occurs over
nerve injury and Manx sacral spinal cord deformity are days to weeks.
also regularly diagnosed. Tenesmus is frequently noted.
● Idiopathic megacolon is likely a generalized dys-
function of colonic smooth muscle. The disorder Feces are hard, dry and low-volume, with or without
involves a disturbance in the intracellular activa- mucus.
tion of smooth muscle myofilaments, and affects Systemic signs including lethargy, dehydration,
both longitudinal and circular smooth muscle from anorexia, weight loss, vomiting, and mild to moderate
both the proximal and distal colon. Histologic eval- mesenteric lymphadenopathy, are often seen in chronic
uation is unhelpful in the diagnosis of this condition. cases.
Burmese are over-represented with idiopathic
megacolon. Occasionally, small amounts of brown mucoid liquid
● Orthopedic causes for constipation include pelvic are passed and can be mistaken for diarrhea.
fractures and pelvic canal stenosis.
● Mechanical (extraluminal) obstruction may be
caused by intra-abdominal tumors. Diagnosis
● Anal inflammation may discourage defecation
because of pain. Cats with megacolon often have a previous history of
● Perineal hair–fecal mats may impede fecal pas- episodes of constipation.
sage, especially in obese cats that are unable to Careful history taking is necessary to identify any
groom effectively. Long-standing mats are associ- underlying causes. Check the frequency of litterbox
ated with perianal dermatitis which may contribute cleaning, litterbox accessibility, drug administration,
to the discomfort of defecating. diet, and history of previous injuries. Details of pos-
● Nerve injury may manifest as spinal cord injury or
ture while straining are often helpful in differentiat-
sacral spinal cord deformities (e.g. Manx cats). ing problems of defecation and urination.
Affected cats usually present with accompanying
clinical signs of nerve injury, such as urinary incon- Abdominal palpation reveals firm fecal masses in con-
tinence, poor anal sphincter tone, reduced perineal stipation, or severe, generalized colonic distention with
sensation or poor tail sensation, with reduced motor impacted feces if megacolon is present. The perineal area
function of the tail in more severe cases. should be checked for inflammation or hair matting.
● Constipation may be one manifestation of feline
Abdominal radiography serves to delineate the sever-
dysautonomia. ity of fecal impaction.
Abnormal evacuation of feces leads to constipation, Abdominal ultrasound examination may identify
colonic impaction and associated clinical signs. intra-abdominal tumors.
Idiopathic megacolon in some cats has been reported in Digital rectal examination should be performed to
association with either intestinal pyogranuloma due to detect/rule out intraluminal and pelvic causes for con-
feline infectious peritonitis virus infection, or intestinal stipation.
lymphosarcoma. Refer to the main references for these
conditions. Neurologic examination is completed to assess caudal
spinal cord integrity and function.
● A diminished or absent perineal reflex with
reduced anal sphincter tone is found with lower
Clinical signs
motor neuron lesions involving S1–S3 spinal cord
Constipation is most common in middle-aged male segments, or pudendal nerve and/or pelvic nerve
cats, but may be observed in cats of any age, gender or disorders.
Serum biochemistry analysis may detect electrolyte lactulose on a daily basis for the prevention of con-
disturbances (e.g. hypokalemia) contributing to stipation.
reduced evacuation of feces. ● Emollient laxatives act as anionic detergents to
increase the miscibility of water and lipid in the
bowel contents, enhancing lipid absorption but
impairing water absorption. Dioctyl sodium sulfos-
Constipation can usually be easily differentiated from uccinate (Colace, 50 mg PO q 24 h) and dioctyl cal-
other causes of straining, such as lower urinary tract ium sulfosuccinate (Surfax, 50 mg PO q 12–24 h)
disorders, by physical examination. are two examples of this class of drugs. Care
should be taken that the cat is well hydrated
prior to the administration of these agents, as
Treatment
they retard the absorption of water from the intes-
Therapy is dependent on the severity of constipation tine.
and the underlying cause. Any underlying causes ● Lubricant laxatives act by easing fecal passage
such as litterbox problems, intraluminal or extraluminal and decreasing water absorption from the colon by
obstructions, orthopedic disorders, anal inflammation creating a coating layer on the mucosa. These
or perineal hair matting should be corrected. agents (e.g. mineral oil or petrolatum products such
as Laxatone or Kat-A-Lax) are suitable only for
Animals with mild to moderate constipation may be
mild constipation, or for regular use to prevent
treated as outpatients.
constipation in mildly affected cats.
● Tepid water enemas (5–10 ml/kg q 8–24 h)
or commercially available pediatric enemas If there is obstipation, manual extraction of feces
(Microlax, 1–2 tubes/cat) should be administered as under general anesthesia is usually required to treat
needed to facilitate fecal breakdown and passage. obstipation, as the condition is too severe to respond to
● Dietary fiber serves to enhance fecal bulk, and has enemas alone.
laxative effects. These effects are due to increased ● Balanced fluids (e.g. Lactated Ringer’s Solution,
fecal water content, decreased intestinal transit time Plasma-Lyte A or Normisol-R) should be adminis-
and increased frequency of defecation. A number of tered to rehydrate and correct fluid deficits. This is
fiber supplements are available, including psillium particularly important in older cats or if general
(Metamucil, 1–4 tsp mixed with food at each meal), anesthesia is required for treatment. An endotra-
or wheat bran (1–2 tsp mixed with food at each cheal tube should be placed to prevent inhalation
meal). Some cats find the sweetness of canned pneumonia as manipulation of the colon may
pumpkin or canned creamed corn (1–4 tbsp induce vomiting.
mixed with food at each meal) makes a more palat- ● After the distal colon has been lubricated by a warm
able fiber supplement. water or saline infusion, forceps are inserted and
● Lactulose (0.5 ml/kg PO q 8–12 h) is a hyperos- used to carefully grasp or break down fecal mate-
motic laxative which softens feces by reducing rial. A constantly twisting motion, clockwise and
water absorption in the colon. Milk may be a more counterclockwise, should be used to prevent the
palatable alternative, as the lactose in milk is indi- forceps accidentally grasping the colonic
gestible in most cats, causing it to act as a hyperos- mucosa. Alternatively, a spoon-shaped instrument,
motic agent. specifically designed for the purpose, may be used
● Cisapride (2.5 mg PO q 12 h) is a gastrointestinal to gradually break down the fecal mass, while con-
prokinetic agent, which stimulates colonic motility nected to a faucet to provide a steady trickle of
from the gastroesophageal sphincter to the descend- warm water into the colon.
ing colon. It is believed to enhance cholinergic ● If any bleeding is noted on manual fecal extrac-
neurotransmission in the gastrointestinal tract tion, the procedure should be aborted to mini-
via stimulation of enteric neuronal serotonin mize the risk of intestinal perforation or
receptors. Cisapride may be used alone for the devitalization of the colonic mucosa. It may be
treatment of mild to moderate constipation, or with preferable to perform manual extraction over
short periods on consecutive days, rather than risk Pathogenesis

prolonged anesthesia and intestinal mucosal dam-
age. Acute colitis may be caused by hair ingestion, infec-
tious agents, dietary factors (indiscretion, additives)
Severe constipation or megacolon is usually non- and/or parasites.
responsive to aggressive medical management.
Colotomy may be required if manual fecal extraction is The cause is rarely identified as most animals sponta-
unsuccessful. Recurrent severe obstipation, refractory neously resolve or respond to symptomatic therapy.
to dietary therapy, enemas or manual extraction, may
be treated by subtotal colectomy. Clinical signs
Assessment of serum electrolyte status and adminis- There is an acute onset of large bowel diarrhea char-
tration of intravenous fluid therapy are particularly acterized by small-volume, high-frequency feces,
important in severely affected cats and in older cats. sometimes accompanied by mucus or blood.
Subtotal colectomy is the preferred therapy in severe
chronic constipation or megacolon. Straining to defecate is a common clinical sign.
While subtotal colectomy is a major surgical proce- Vomiting may accompany diarrheic episodes.
dure, it provides a permanent cure for idiopathic Signs are usually mild and often self-limiting.
megacolon. Postoperative diarrhea should be
expected and usually lasts for about 2 weeks,
although it may persist for 4–6 weeks in some cases. Diagnosis
Post-operative diarrhea is less likely to occur if the
An underlying cause for gastrointestinal signs is
ileocolic junction is not removed during the surgical
rarely identified.
procedure (i.e. subtotal colectomy rather than total
colectomy). Signs tend to be self-limiting or they respond to
symptomatic therapy in 3–5 days.
Perform fecal flotation and direct fecal examinations
Prognosis
for intestinal parasites.
Generally good to excellent in cats with mild to mod-
Fecal cytology is useful in identification of infectious
erate constipation.
agents (bacteria) and leukocytes may be seen with
Cats with severe constipation or megacolon have acute mucosal inflammation.
a favorable long-term prognosis following total or
Culture feces if infectious (bacterial) colitis is suspected.
subtotal colectomy.
ACUTE NON-SPECIFIC COLITIS** The history and clinical features of acute non-specific
colitis make most other diseases unlikely.
Classical signs
● Acute onset of large bowel diarrhea
Treatment
(tenesmus, mucoid feces, hematochezia)
predominates. Provide intravenous or subcutaneous fluids lactated
● +/- Vomiting with diarrheic episodes. ringers solution if dehydration is evident.
● Signs are usually mild and often self-
Feed small but frequent meals of an easily digested
limiting.
food.
See main reference on page 762 (The Cat With Signs of Administer an appropriate broad-spectrum anthel-
Large Bowel Diarrhea) for details. mintic to eliminate parasitic infestations.
Antibiotics are only used in culture-proven cases of Differential diagnosis

infectious colitis.
Chronic colitis should be differentiated from more
If the cat is long-haired or over-grooms, consider acute causes of tenesmus, such as acute non-specific
clipping the coat if other causes of colitis cannot be colitis, and conditions causing small intestinal diar-
identified. rhea, because some causes of chronic colitis also
involve the small intestine, resulting in signs of both
Prognosis large and small bowel involvement.
The prognosis for full recovery is excellent in most

instances. Treatment
Treatment for this condition is based on treating
CHRONIC COLITIS** (INFECTIOUS, the primary cause. Lymphocytic-plasmacytic coli-
NEOPLASTIC, AND BENIGN INFILTRATIVE tis may require a food trial to investigate a dietary
MUCOSAL DISEASE) etiology, combined with oral prednisolone ther-
apy at immunosuppressive dose rates (2–4 mg/kg/
Classical signs day).
● Chronic large bowel diarrhea (tenesmus,
small-volume mucoid feces, DEHYDRATION AND HYPOKALEMIA*
hematochezia).
● +/- Systemic signs (lymphadenopathy, Classical signs
anorexia, weight loss, +/- fever) if
● Skin tenting, tacky mucus membranes,
infectious cause.
increased plasma protein and PCV.
● ± Muscular weakness, reluctance to jump,
See main reference on page 762 (The Cat With Signs of
ventroflexion of the neck associated with
Large Bowel Diarrhea) for details.
hypokalemia.
● Reduced, painful or absent defecation +/-
Clinical signs tenesmus.
● Feces are hard, dry with or without mucus.
Hematochezia, small-volume, high-frequency feces,
● +/- Anorexia, lethargy, weight loss and
and straining are observed.
vomiting depending on the cause.
Systemic signs (lymphadenopathy, anorexia, weight
loss, +/− fever) may be seen with infectious viral dis- See main reference on page 557 (The Polycythemic Cat
eases (FeLV and FIV) and systemic mycoses. (for dehydration)) and page 945 (The Cat With
Generalized Weakness) and page 893 (The Cat With
Cats with benign infiltrative mucosal disease (e.g. lym-
Neck Ventroflexion) for hypokalemia)) for details.
phocytic-plasmacytic colitis) rarely have systemic signs
except with concurrent small intestinal involvement.
Pathogenesis
Diagnosis Both dehydration and hypokalemia may be caused by
either reduced intake in anorexia, or by increased losses,
Laboratory testing detects evidence of infectious viral
or by a combination of both. This most commonly
diseases.
occurs in chronic renal failure in older cats. Other causes
Screen susceptible cats for FeLV antigenemia and of vomiting and/or diarrhea may also result in dehydra-
serum antibodies to FIV. tion and/or hypokalemia and constipation.
Mucosal biopsies are required for definitive diagnosis Dehydration exacerbates the already efficient reabsorption
of neoplastic, mycotic and benign infiltrative mucosal of water from the feline colon, and hypokalemia results in
diseases causing chronic colitis. weakness of the colonic smooth muscle, slowing the
passage of fecal material to the rectum. The increased Treatment

fecal volume that occurs over the extended time in the
colon, and fecal dryness, worsen the condition. Treatment of dehydration is by administration of fluid
therapy to correct hydration, electrolyte and acid–base
The differential diagnosis of dehydration depends on status.
the primary cause. Hypokalemia may be caused by
any condition which causes reduced intake from Potassium deficits can be corrected by oral and/or IV
anorexia, or increased losses via the urinary or gas- supplementation, depending on the severity of the
trointestinal tract. Conditions commonly associated problem. Fluid therapy may initially worsen
with increased loss of potassium include chronic hypokalemia because of expansion of blood volume and
renal failure, and any causes of vomiting and/or diuresis, so it may be beneficial to supply oral K+ con-
diarrhea. currently. Oral potassium should ideally be supplied
as gluconate or citrate, as KCl may worsen concurrent
metabolic acidosis. Please refer to the main reference
Clinical signs
for correction of K+ deficits in dehydration on page 557.
Depending on the severity of dehydration, signs
Maintainence fluid rates are 70 ml/kg/day. Fluid
progress from subtle loss of skin tenting to dry
deficits and ongoing losses should be estimated and
mucous membranes and sunken eyeballs. There are
added to maintenance rates so that the deficit can be cor-
signs of shock in advanced cases.
rected over the first 12–24 hours. Please refer to the main
Hypokalemic cats are weak, and may show a reluc- reference for treatment of dehydration on page 558.
tance to jump or climb stairs, ventroflexion of the
head and poor limb tone. Prognosis
Reduced, absent or painful defecation may be pres- The prognosis for constipation from dehydration and
ent, and tenesmus is frequently noted. hypokalemia depends on the primary cause of the
problem.
Feces are hard, dry and may or may not be covered in
mucus.
PELVIC FRACTURES*
Systemic signs including lethargy, anorexia, weight
loss and vomiting may be present, depending on the
Classical signs
underlying cause.
● Inability to walk and severe pain on
Diagnosis palpation of the pelvic area in a cat with
a recent history of trauma.
Clinical signs of loss of skin elasticity and tacky ● Dry hard feces and straining to defecate in
mucous membranes, accompanied by elevations in a cat with evidence of healed pelvic
PCV and total protein are indicative of dehydration, fractures.
together with evidence of constipation (hard, dry
feces and tenesmus).
Clinical signs
Serum potassium concentration is low, determined
by in-house or laboratory analysis. Cats with recent pelvic fractures may be able to sit up,
but are rarely able to walk normally. Attempts at
Differential diagnosis abdominal and especially pelvic palpation elicit a pain
response. When the tuber ischii are palpated from
Severe constipation or megacolon can result in behind, there may be asymmetric movement in an
depression, anorexia and dehydration. Constipation anteroposterior direction. Attempts to defecate may be
resulting from dehydration and hypokalemia is more absent.
likely when an underlying disease with the potential to
cause dehydration and hypokalemia is detected, and the Cats with old healed pelvic fractures may have asym-
constipation or megacolon is not severe. metry on pelvic palpation, and differences in length of
pelvic limbs when they are compared with each other in cats should normally be able to groom well enough to
full extension. prevent this happening.
Constipation may result either from pain associated Morbidly obese cats frequently are unable to groom
with defecation, or obstruction from a narrowed effectively around the anal region and may develop
pelvic cavity. mats of feces adhered to hair. These result in perianal
dermatitis if they are not removed. The discomfort and
obstruction to defecation promote constipation.
Diagnosis
Concurrent signs of constipation or obstipation are
The pelvis should be radiographed in two views (lat-
present including tenesmus and infrequent passage of
eral and DV or VD) to detect fractures and gauge pelvic
hard dry feces.
narrowing.
Diagnosis
The diagnosis is made by an inspection of the perineal
Any conditions that cause pain in the hindquarters and region. More information should be obtained to investi-
lumbosacral region, such as severe bruising, should be gate an underlying cause by performing a general phys-
considered. ical examination and neurological examination, and
Conditions causing hindlimb paresis or paralysis may if indicated, more specific blood and/or fecal tests.
present as a refusal to move, as do pelvic fractures. The perineum should also be clipped and inspected.
A physical and neurological examination should be
performed to differentiate these conditions. Differential diagnosis
This condition is self-evident on perineal examina-
Treatment tion, but should be differentiated from other conditions
that cause inability to groom and reluctance to defe-
Pelvic fractures often require surgical repair, but
cate, such as pelvic fractures and perineal abscesses.
depending on the position and degree of distraction of
the bone fragments, some may heal with extended
cage rest (4–6 weeks). Treatment
Laxatives and/or dietary fiber supplements should be The perineum should be clipped and cleaned.
provided to produce a soft stool that is easy to pass. See Corticosteroid/antibiotic cream may be applied
page 785 (Constipation) for details. morning and night if there are signs of perineal inflam-
mation. Purulent skin infections should be treated with
oral antibiotics such as doxycycline (5 mg/kg PO q 12
HAIR MATTING*
h 8 days).
Classical signs Any underlying cause should be treated appropriately.
● Hair is matted with feces over the perineal
region, usually in a long-haired or obese cat.
LITTERBOX DISSATISFACTION*
● Constipation or obstipation.
Classical signs
Clinical signs
● Cats may urinate and defecate in
Long-haired cats in unkempt condition may be pre- inappropriate places.
sented with hair matted with feces over the perineal ● History of poorly cleaned litter box or
region. An underlying cause should be established for insufficient litter boxes for the number of
this lack of grooming, such as inability to reach the cats.
perineal region because of severe obesity, or an under- ● Straining, hard dry feces.
lying condition causing diarrhea or lethargy, because
Clinical signs Classical signs—Cont’d

Litterbox dissatisfaction often results in both defeca- ● Affected cats may urinate in inappropriate
tion and urination in inappropriate places. places.
Because of reluctance to use the litter tray, the cat may ● Anorexia, weakness and anuria with
defecate infrequently, predisposing it to chronic con- urinary obstruction.
stipation.
See main reference on page 176 (The Cat Straining to
On close questioning of the owner, litterbox hygiene Urinate) for details.
may be unacceptable. Alternatively, the position of
the litterbox may be unacceptable to the cat because
Clinical signs
of noise or accessibility by other animals.
Pollakiuria, hematuria, stranguria and inappropri-
ate urination are the most common signs. The bladder
Diagnosis is typically small on palpation.
The owner must be questioned closely but tactfully
Anorexia, depression, vomiting and anuria occur
about the frequency and method of litterbox cleaning,
with urinary obstruction. Typically the bladder is
and the position of the litter tray, especially in relation
distended and firm on palpation.
to noise levels and accessibility by other animals. Type
of litter material and the cat’s previous history in this
regard should also be determined, as some cats do not Diagnosis
accept a change in litter material readily. A house call The diagnosis of non-obstructive LUTD is often based
may be required to fully assess the situation. on relevant history and a normal physical examina-
tion. The majority (55–69%) of cats with signs of lower
Differential diagnosis urinary tract disease have idiopathic cystitis; some
have struvite or calcium oxalate uroliths (20%); and
Litterbox dissatisfaction must be differentiated from the remainder have a variety of conditions including
other conditions causing reluctance to defecate, such anatomical defects, urethral obstruction, tumors and
as painful pelvic or perineal conditions. bacterial infection.
Urinalysis reveals hematuria, and is usually sterile.
Treatment Depending on the cause, struvite crystalluria, bacteria
The litterbox must be placed in a quiet, secluded area or neoplastic cells may be evident.
easily accessed by the cat, but not by other animals A diagnosis of obstructive LUTD is based on history
such as dogs. There should be at least one litter tray and palpation of a turgid, distended bladder, which is
provided per cat in the household. The litter should difficult or impossible to express. Radiography, includ-
be completely changed and the tray scrubbed every ing contrast radiographs, and ultrasonography will help
day. Just a small amount of the type of litter accept- to identify uroliths, neoplasia, anatomical defects and
able to the cat should be placed in the tray, to facilitate urethral obstruction.
frequent cleaning during the day. Automatic litter
trays may also be helpful.
Distinguish LUTD from other causes of straining
LOWER URINARY TRACT DISEASE*
associated with the gastrointestinal tract.
Classical signs
Treatment
● Pollakiuria, dysuria and hematuria if non-
obstructed. Non-obstructive LUTD generally resolves sponta-
neously or with symptomatic therapy in 5–7 days.
● Modify the diet to minimize urine concentration by Abdominal radiographs may also be useful in visual-
using canned food or add water to dry food. If urine izing the mass. The obstruction may be caused by
pH is > 6.5 and there is struvite crystalluria, maxi- intraluminal or extraluminal masses.
mize urine acidity, and minimize magnesium intake
using a diet designed to reduce struvite formation.
● Amitriptyline (2.5–12.5 mg/cat PO q 24 h) may be
effective in reducing clinical signs in cats with idio- Abdominal neoplasia must be differentiated from other
pathic cystitis. causes of abdominal masses such as an obstructed
● Empirical use of antibiotics, anti-inflammatory bladder or trichobezoars (hairballs). This can be done
agents and antispasmodics is controversial. by abdominal ultrasonography or radiographs, and
clinical signs.
Obstructive LUTD is a medical emergency.
● Therapeutic strategies are directed at relief of the
obstruction and supportive therapy as needed. Treatment
For prevention, use specific diets for struvite and
Treatment of abdominal neoplasia depends on the
calcium oxalate uroliths, and maximize dietary
type of tumor identified on histopathology. Surgical
water intake.
excision should be performed, sometimes followed by
See a detailed discussion on obstructive LUTD see a chemotherapeutic protocol, depending on the
page 179 (The Cat Straining to Urinate). histopathological diagnosis.
DRUGS
NEOPLASIA
Classical signs
Classical signs
● History of drug use, such as opiates or
● ± Palpable abdominal mass. kaolin/pectin.
● Straining, hard, dry feces. ● Signs of constipation.

Abdominal neoplasms may obstruct the passage of There are signs of constipation, such as reduced fre-
feces along the large intestine. quency of defecation, and straining, with an appro-
priate drug history, such as the administration of
Signs of neoplasia, such as weight loss and a palpable
opiates or kaolin/pectin.
abdominal mass, may accompany the clinical signs of
constipation and straining. Overzealous use of furosemide promotes dehydra-
tion which predisposes to constipation.
An abdominal mass may be palpable.
The abdominal neoplasms that have the potential to
Diagnosis
cause constipation because of their anatomical position
and prevalence in cats are lymphosarcoma of the intes- The diagnosis is made by a thorough drug history and
tine or abdominal lymph nodes, intestinal adenosar- evidence of constipation on abdominal palpation or
coma and intestinal mast cell tumor. radiographs.
Diagnosis
Abdominal neoplasms are most readily diagnosed by
abdominal ultrasound followed by fine-needle aspi- Drug-related causes of constipation should be differ-
rate biopsy or surgical biopsy and histopathology. entiated from other causes of constipation that do
not have overt accompanying clinical signs on Treatment

physical examination, such as idiopathic megacolon,
acute or chronic colitis, and litterbox dissatisfaction. The perineal area should be clipped and cleaned.
This is done by taking a thorough drug and litterbox Wounds and/or abscesses should be debrided and
history. flushed with saline or an aqueous iodine solution.
Feces should be kept soft by the use of laxatives
and/or dietary fiber supplements until healing has
Treatment occurred. See page 785 (Constipation (including idio-
pathic megacolon)).
The condition resolves once the causative drug is
withdrawn. Oral antibiotics, such as doxycycline (5 mg/kg q 12 h
8 days) should be prescribed.
PERINEAL INFLAMMATION/INFECTION DYSAUTONOMIA

● History of pain or sensitivity in the perianal ● Mostly young adult cats (< 3 years of age).
region or evidence of perianal wound or ● Acute onset of depression and anorexia
abscess. over 48 h.
● Signs of constipation. ● Constellation of signs including
regurgitation, constipation, mydriasis and
dry eyes.
Clinical signs ● ± Protrusion of the third eyelids,
Cats are presented with a history of pain or sensitivity bradycardia and dysuria.
in the hindquarters, and sometimes a reluctance to sit or
an unusual sitting posture. On inspection of the per- Pathogenesis
ineum, there may be hair loss and/or matting, and
Dysautonomia is an idiopathic condition character-
wounds or abscessation. Sometimes, an abscess is asso-
ized by widespread degeneration of the autonomic
ciated with one of the anal sacs.
ganglia.
Signs or history of constipation are present because
The condition was originally reported in the UK and
pain associated with defecation promotes fecal
Europe, but is rarely recognized at this time. There are
retention.
rare reports of affected cats in the USA. While some of
these cats were imported from the UK, a small number
were bred in USA.
Diagnosis
Recent evidence suggests that Clostridium botulinum
The condition is self-evident, but in some cats, heavy
type C neurotoxin may be involved. The toxin was
sedation or general anesthesia may be required to
detected in the feces or ileum contents in affected cats,
thoroughly inspect the area.
and also in their dry food, but not in healthy control
cats. Fourteen weeks after the outbreak, IgA antibodies
to the toxin and organism were significantly higher in
the feces of affected cats compared to unaffected cats.
Perineal inflammation or infection should be differenti-
Both sympathetic and parasympathetic nervous sys-
ated from other conditions causing matting of the
tems are affected.
perineal hair, such as chronic diarrhea or conditions
causing poor grooming. This is done by performing The predominance of gastrointestinal signs relates to
a thorough physical examination including the per- failure of parasympathetic stimulation of esophageal,
ineal region. gastric and colonic motility.
Loss of autonomic control to the eye and heart result in to a normal position in a cat with dysautonomia,
dilated fixed pupils and a fixed heart rate. but will have no effect on a normal cat.
– This results from the phenomenon of denerva-
Tenesmus is attributable to constipation and/or
tion hypersensitivity in the dysautonomic cat,
dysuria.
causing an enhanced response to direct-acting
agents.
Clinical signs ● By contrast, topical physostigmine is an indirect-
acting parasympathomimetic agent, which acts by
Dysautonomia is primarily seen in young cats (< 3 years
inhibiting cholinesterase to prevent local degrada-
old).
tion of acetylcholine, causing rapid miosis in
Outbreaks in multicat households and single isolated a normal cat, but no response in a cat with
cases have been reported. dysautonomia.
Signs often develop acutely over 48 h, with nearly all Determination of plasma and urinary catecholamine
cats showing depression and anorexia. In some cats, concentrations may also be useful. Plasma epinephrine
signs develop over several weeks, and weight loss may and norepinephrine concentrations and urinary cate-
be evident. cholamine levels are reduced in cats with dysautono-
mia compared to normal cats.
Regurgitation associated with megaesophagus, vom-
iting, constipation, weakness and dry mucous mem-
branes of the mouth, nose and eye, are the most Differential diagnosis
commonly reported clinical signs.
The clinical features of classical feline dysautonomia
Pupils are dilated and fixed, but the cat is visual. make most other diseases unlikely.
There is protrusion of the third eyelids in more than
Atypical cats may present with constipation or obstipa-
90% of affected cats, and the eyes appear dry.
tion as the major sign. Careful physical examination,
Braycardia of 90–120 beats per minute occurs in and an index of suspicion for dysautonomia are
about 60% of cats. required to make a diagnosis in these cats.
Loss of anal tone and fecal incontinence may be evident.
Treatment
Dysuria and a distended bladder are less common
signs. Urinary incontinence may also occur. Treatment is supportive but palliative in most
instances. Approximately 20–40% recover with sup-
Occasionally constipation or obstipation is the major
portive therapy. Recovery is over 2–12 months, and
presenting sign, and the other signs are less obvious.
may not be complete.
Diagnosis Correct dehydration if present.
A presumptive diagnosis is usually made based on the Prolonged nutritional support should be provided via
characteristic clinical presentation. parenteral or enteral means if there is persistent vomit-
ing or regurgitation.
Survey and/or contrast radiography demonstrate
megaesophagus, delayed gastrointestinal transit Parasympathomimetic drugs may be administered to
and/or bladder distention. improve oronasal secretion, and treat the ocular mani-
festations of the condition, especially decreased
Confirmation of abnormal autonomic function tests
lacrimation.
may be pursued if indicated. Ocular (pupillary)
● Pilocarpine drops (0.25–1% solution 1 drop q
response tests to 0.1% pilocarpine and 0.25%
6–8 h).
physostigmine may be performed.
● Physostigmine drops (0.5% 1 drop q 12 h).
● Pilocarpine is a direct-acting parasympath-
omimetic agent, which when applied topically will Metoclopramide (Reglan, 0.2–0.4 mg/kg PO or SC q
result in miosis and retraction of the third eyelid 8 h) enhances gastrointestinal motility. The aim is
to decrease esophageal dilation and increase gastric Relieve constipation using laxatives and enemas. See
emptying, and hence reduce vomiting and regurgi- page 785 (Constipation (including idiopathic mega-
tation. oesphagus)).
● Cisapride (Propulsid, 2.5–5 mg/cat q 8–12 h) is
Manual emptying of the bladder and colon may be
thought to be more effective than metoclopramide,
required if drug therapy is ineffective. Urine should be
and can be combined with metoclopramide to
monitored for bacterial infection, and infection treated
improve gastric emptying and small intestinal
promptly.
motility. Cisapride is indicated in cats with
esophagitis from vomiting. Cisapride is currently
unavailable in the USA. Nizatadine (2.5–5 mg/kg Prognosis
PO once daily) or ranitidine (1–2 mg/kg PO q
Initial severity of clinical signs is not necessarily corre-
8–12 h) may be used instead as colonic prokinetic
lated with survival, and response to treatment is a bet-
agents.
ter indication of prognosis.
Dysuria, urinary bladder emptying, and gastrointestinal
The prognosis is guarded to poor, especially in cats
motility may be improved with bethanecol (2.5–5.0
with megaesophagus. If cats continue to regurgitate flu-
mg PO q 8–12 h, or 0.0375 mg/kg SC q 8–12 h). Start
ids after 1–2 weeks of treatment, consider euthanasia.
with the lower dose and increase if necessary, but
beware of adverse effects such as bradycardia and The mortality rate is approximately 60%, and surviving
arrhythmias). cats may have residual signs.
RECOMMENDED READING
Firth M, Fondacaro JV, Greco DS. Challenging cases in internal medicine: What’s your diagnosis? Vet Med 2000;
95(8): 606–614.
Grauer GF. Feline lower urinary tract inflammation. In: Nelson RW, Couto CG (eds) Small Animal Internal
Medicine, 3rd edn. Missouri, Mosby, 2003, pp. 642–649.
Washabau RJ, Hasler AH. Constipation, obstipation and megacolon. In: August JR (ed) Consultations in Feline
Internal Medicine, 3rd edn. Philadelphia, PA, W.B. Saunders, 1997, pp. 104–112.
White RN. Surgical management of constipation. J Feline Med Surg 2002; 4(3): 129–138.
PART 10
Cat with signs of neurological
disease
36. The cat with seizures, circling

and/or changed behavior
Andrée D Quesnel † and Joane M Parent
KEY SIGNS
● Compulsive circling without a head tilt or loss of balance, accompanied by
mental confusion.
● Personality changes, dementia, depression, staring into space, confusion, pacing,
head pressing, frantic vocalization, aggression or running fits.
● Loss of consciousness, generalized, symmetrical and usually violent tonic and/or
clonic motor activity resulting in complete recumbency, often with thrashing and
limb paddling, accompanied by jaw champing, facial twitching and autonomic
signs (e.g. mydriasis, hypersalivation, piloerection, micturition).
● Generalized seizures may be preceded or followed by localizing or lateralizing
signs.
● Partial seizures have localizing signs to one part or side of the body, or are
generalized but do not cause lateral recumbency.
MECHANISM?
● Seizures occur when a forebrain lesion irritates the surrounding neurons or when there is dif-
fuse neuronal hyperexcitability as a result of a genetic predisposition (primary epilepsy), meta-
bolic disturbance (e.g. hypoglycemia) or intoxication.
● Circling may occur with forebrain disease and is compulsive and obsessive in nature.
● Changed behavior arises from intellectual dysfunction, psychic perturbations, learning disabil-
ities and memory losses.
continued
795
796 PART 10 CAT WITH SIGNS OF NEUROLOGICAL DISEASE
continued
WHERE?
● Most cats with seizures, compulsive circling or changed behavior from neurological disease
have a forebrain (thalamocortex) lesion.
WHAT?
● Seizures are most often associated with tumors, encephalitides and inactive lesions (e.g. glial
scar), while extracranial causes (metabolic and toxic) and idiopathic epilepsy are rare.
● Compulsive circling is caused by any kind of lesion located in the frontal lobe or rostral thala-
mus, although trauma, tumors and ischemic encephalopathy are the most common causes.
Circling is usually toward the side of the lesion.
● Changed or abnormal behavior usually consists of subtle personality changes, and is most
often associated with tumors, head trauma, ischemic encephalopathy, congenital and inherited
forebrain anomalies, hepatic encephalopathy, feline infectious peritonitis, and feline immunod-
eficiency encephalopathy.

Diseases causing seizures, circling and/or changed behavior
DEGENERATIVE
● Likely symptomatic epilepsy*** (p 800)
Recurrent seizures typically beginning as single seizures at intervals of several weeks to months.
Frequency may remain low or progressively increase over time. Seizures are partial in onset (±
aura, unilateral or localized motor activity, ± localized post-ictal motor deficits) with or without
secondary generalization (to violent tonic-clonic motor activity involving the whole body) which
may obscure the partial signs.
● Feline ischemic encephalopathy*** (p 804)
Peracute onset of unilateral forebrain signs (mental depression and confusion, compulsive circling,
hemiparesis) and rarely, severe cluster seizures or status epilepticus. Personality changes and/or
post-ischemic epilepsy may be the only manifestation of the milder atypical form.
● Cerebrovascular accidents** (p 808)
Peracute onset of focal cerebral signs attributable to the forebrain (confusion, circling, pacing) or
brainstem (depression, head tilt, loss of balance, nystagmus, facial paresis) or cerebellum (hyper-
metria, intentional tremors). Occasionally, seizures occur either as immediate cluster seizures or
status epilepticus, or later as secondary epilepsy.
ANOMALY
● Congenital and inherited forebrain anomalies*** (p 805)
Developmental abnormalities, such as mental retardation, learning disability or loss of training are
often evident historically in kittens and young adult cats (< 2 years old) presenting with abnormal
mentation and behavior, central visual deficits and occasionally, secondary epilepsy.
36 – THE CAT WITH SEIZURES, CIRCLING AND/OR CHANGED BEHAVIOR 797
METABOLIC
● Hepatic encephalopathy*** (p 806)
Episodes of mental alteration including depression, confusion, agitation, dementia or stupor
occur together with bizarre behavior, hypersalivation and rarely, seizures. Mostly in young animals
(< 1–2 years of age) with congenital portosystemic shunt.
● Hypoglycemia** (p 809)
Mental confusion, muscles tremors, weakness, ataxia and occasionally, seizures or coma.
Typically, there is history of a diabetic cat receiving insulin therapy or hypoglycemic drugs.
● Hypocalcemia* (p 817)
Progressive neuromuscular hyperexcitability evidenced as muscle fasciculation, tremors or gener-
alized tetany. Rarely culminates in terminal convulsive status epilepticus.
● Uremia (p 819)
CNS depression; occasionally, seizures. Typically, there are other signs of severe acute or chronic
renal failure, for example anorexia, vomiting, dehydration, polydipsia, polyuria or anuria.
NEOPLASTIC
● Forebrain tumors** (p 810)
Typically middle-aged and older cats with progressive focal forebrain signs such as personality
changes, mental depression, confusion, pacing, compulsive circling and subtle hemiparesis.
Seizures may also occur.
NUTRITIONAL
● Thiamine deficiency*** (p 808)
Central vestibular signs (head tilt, loss of balance), mydriasis, spasmodic ventroflexion of the neck
with whole-body contorsions, which may be misinterpreted as seizures. Terminally, opisthotonos,
coma and death.
INFLAMMATORY
● Feline non-suppurative meningoencephalitis*** (p 803)
Focal or multifocal neurological signs attributable to any portion of the CNS (hindlimb paresis and
ataxia, head tilt and loss of balance, seizures) ± systemic (fever, inappetence, lymphadenopathy)
and/or ocular (chorioretinitis) signs.
INFECTIOUS:
VIRAL
● Feline infectious peritonitis** (p 811)
CNS signs (typically head tilt, balance losses, intentional tremors) accompanied by systemic (fever,
lethargy, inappetence, weight loss) ± ocular signs (anterior uveitis, chorioretinitis) in cats usually
younger than 3 years of age.
● Rabies (p 819)
Variable prodromal signs progressing often to a furious phase characterized by vicious and aggres-
sive behavior +/− dysphagia, paralysis, convulsions, coma and death.
continued
continued
● Feline immunodeficiency virus encephalopathy (p 819)

Usually asymptomatic, but may cause subtle and non-specific behavioral changes such as depres-
sion, social withdrawal and roaming.
PROTOZOAL
● Toxoplasmosis** (p 815)
Focal or multifocal CNS signs are rare signs accompanying the more common systemic signs such
as fever, or dyspnea or ocular manifestations (anterior uveitis, chorioretinitis) of the disease.
FUNGAL
● Cryptococcosis** (p 812)
Cerebral signs such as depression, circling and ataxia are often accompanied by chronic nasal dis-
charge, cutaneous nodules or ulcers, or ocular signs including chorioretinitis, retinal detachment
and panophthalmitis.
IDIOPATHIC
● Idiopathic epilepsy* (p 816)
Rare in cats and occurs as recurrent generalized motor seizures starting with single seizures at sev-
eral week intervals in a young adult animal that has no other neurological signs or deficits.
TRAUMA
● Head trauma (p 806)
Peracute onset of cerebral signs such as confusion to dementia, pacing, circling or hemiparesis.
Immediate onset of seizures and/or post-traumatic epilepsy may occur.
TOXIC
● Intoxications** (p 812)
Typically present with signs of depression or stimulation of the CNS (depression, agitation),
together with autonomic system signs (miosis, hypersalivation) and neuromuscular signs (weak-
ness, muscle tremors). Occasionally, convulsive status epilepticus.
● In idiopathic epilepsy, no causes other than a genetic

INTRODUCTION predisposition underlie the intrinsic neuronal distur-
bances.
MECHANISM? ● Extracranial causes of seizures (metabolic and
toxic) diffusely affect the brain.
Seizures are generated by paroxysmal excessive dis-
The clinical appearance of seizures varies a great deal,
charge of thalamocortical neurons which are rendered
depending on the origin and extent of spreading of the
focally or diffusely hyperexcitable by several mechanisms:
seizure discharge within the brain.
● Structural brain lesions, either active (e.g.
encephalitis, tumor) or inactive (e.g. glial scar), irritate Primary generalized seizures have a diffuse onset
the surrounding neurons and transform them into within both cerebral hemispheres.
transient or permanent epileptic foci; some areas of ● They manifest with a complete loss of consciousness
the brain are more likely to generate seizures (e.g. and generalized, symmetrical and usually violent
frontal and temporal lobes) than others (e.g. occip- tonic and/or clonic motor activity that results in com-
ital lobe). plete recumbency often with thrashing and limb pad-
dling. This is often accompanied by jaw champing, Seizures must be differentiated from seizure-like
facial twitching and autonomic signs (e.g. mydriasis, events such as syncopes, sleep disorders (e.g. excessive
hypersalivation, piloerection, micturition). dream-like movements), movement disorders (e.g.
● In partial (focal) seizures with secondary general- myoclonia, tremors-tetany), narcolepsy-cataplexy,
ization, the seizure is preceded by behavioral episodic behavioral disorders (e.g. fly catching, feline
change (aura) or localized or lateralized motor signs hyperesthesia), dysphoric and agitated anesthetic
or followed by motor deficits. recovery, and paddling associated with decerebration.
Partial (focal) seizures have a focal onset in one cere- Compulsive circling is usually accompanied by men-
bral hemisphere and a limited propagation within one tal confusion with either depression or agitation. It is
or both hemispheres. often associated with wandering, pacing and sometimes
● They manifest with variable degrees of alteration of with an abnormal posture (head and eye deviation or
consciousness ranging from normal to totally turning, leaning).
absent awareness and responsiveness. ● Compulsive circling must be differentiated from
● Partial (focal) seizures have motor signs that may vestibular circling which is due to marked loss of
be either lateralized to one side of the body, local- balance.
ized to one part of the body, or may even be gener- – The cat with compulsive circling does not have
alized but not violent enough to cause complete a head tilt (its head may however be turned), loss
recumbency (e.g. mild tremors of the whole body). of balance, nystagmus and other vestibular signs.
– Lateralized signs include unilateral facial It usually has a normal gait (no detectable ataxia
twitching, tonic or clonic movements of one or nor paresis) and often can walk in a straight line
both limbs on one side, and spasmodic turning when it is motivated to do so (e.g. reach a spe-
of the head to one side. cific goal such as a food plate).
– Signs localized to one part of the body include
Personality and behavioral changes due to forebrain
hindlimb weakness causing difficulty or inabil-
diseases must be differentiated from pure behavioral
ity walking, and bilateral facial twitching with or
disorders.
without spasmodic head bobbing.
● Partial (focal) seizures of cats are often subtle
WHERE?
and/or bizarre and may be difficult to recognize as
being seizure activity. Forebrain (thalamocortex) diseases can cause any of
● Some partial (focal) seizures previously called psy- the following signs:
chomotor seizures mainly manifest with bizarre ● Mentation abnormalities ranging from depression
stereotypical and behavioral activities (e.g. halluci- to semi-stupor, or confusion.
natory prey or predator behavior with running fits). ● Subtle personality changes (e.g. loss of good or
● Seizures preceded by an aura (behavioral changes bad habits) to obvious behavioral abnormalities
within a few seconds or minutes of the ictus onset) or (e.g. dementia, aggression).
followed by localized post-ictal motor deficits (e.g. ● Abnormal activities such as wandering, propulsive
hemiparesis) are partial in onset, even if they appear pacing, head pressing and compulsive circling.
to be generalized from the beginning of the ictus. ● Seizures.
● Partial (focal) seizures may secondarily general- ● Mild contralateral hemiparesis and proprioceptive
ize to tonic-clonic generalized seizures and this may loss causes either subtle gait abnormalities (e.g.
occur so quickly that their initial partial phase may knuckling) or is only detected as postural reaction
not be observed clinically; most generalized deficits (e.g. proprioceptive positioning, hopping,
seizures of cats are probably within that category. lateral tactile limb placing).
● The occurrence of partial seizures usually indicates ● Central visual loss either causes the cat to bump
that there is a focal forebrain lesion which into things, or is only detected by a deficit in the
excludes the possibility of idiopathic (genetic) menace response together with normal pupillary
epilepsy and extracranial (metabolic and toxic) light reflexes in the contralateral eye when the
causes of seizures. affected eye is tested.
● Impaired facial sensation is detected by decreased Pathogenesis

head withdrawal when the contralateral nasal sep-
tum, upper lip or whiskers are touched. Likely symptomatic epilepsy is common in cats.
Large or diffuse forebrain lesions (e.g. tumors, edema) It is most often caused by an acquired focal thalamo-
may cause signs of increased intracranial pressure cortical lesion that is no longer active but has trans-
(e.g. marked depression, bilateral miosis); this may formed into an epileptic focus by irritating the
evolve to tentorial herniation with signs of brainstem surrounding neurons.
● Following an insult to the brain such as trauma,
compression (e.g. coma, unresponsive mydriasis, abnor-
mal respiratory patterns and death by respiratory arrest). encephalitis or ischemia, the glial reaction may result
in a persistent glial focus, which irritates the sur-
rounding neurons.
● Seizure onset is usually delayed by a few to several
WHAT?
months from an initial brain insult. The insult
Most cats with seizures have a structural forebrain may have occurred in utero (e.g. porencephalic
lesion that may be active (e.g. encephalitis, tumor, [cystic] lesions due to fetal encephalitis), at birth
ischemic encephalopathy) or inactive (e.g. post- (e.g. dystocia-related cerebrovascular accidents) or
ischemic glial scar). Extracranial causes of seizures later in life at any age. Post-natal diseases may have
(e.g. metabolic, toxic) and idiopathic epilepsy are rare. been symptomatic (e.g. encephalitis, ischemic
Compulsive circling may be caused by lesions affect- encephalopathy, head trauma) or asymptomatic
ing the rostral thalamus or frontal lobe and is usually (e.g. atypical form of ischemic encephalopathy,
toward the side of the lesion. Most common causes are non-suppurative meningoencephalitis).
● Symptomatic seizures occurring during the active
neoplasia, trauma and ischemic encephalopathy.
phase of a cerebral disease may or may not lead to
Personality and behavioral changes result from lesions likely symptomatic epilepsy, depending on the
affecting the limbic system and associated areas of extent of secondary gliosis.
frontal and temporal lobes. Most common causes are neo-
plasia, trauma, ischemic encephalopathy, feline infectious Other rare congenital or inherited focal cerebral
peritonitis and hepatic encephalopathy. anomalies may also act as epileptic foci. These include
lesions associated with surrounding gliosis (e.g. vascu-
Diagnosis is based on history, clinical examinations, lar malformations such as angiomas and arteriovenous
CSF analysis (reference values in cats are a protein malformations) or with intrinsic neuronal hyper-
concentration ≤ 0.36 g/L (0.036 mg/dl) and a leukocyte excitability (e.g. disorders of neuronal migration such
count ≤ 0.002 cells/109(2/μl) with the majority of cells as cortical dysplasia and heterotopias).
being mononuclear cells), brain imaging and other ● Seizures usually start during adolescence or young
ancillary tests. adulthood.
DISEASES CAUSING SEIZURES, Clinical signs

CIRCLING AND/OR CHANGED
The initial seizure frequency usually is low with single
BEHAVIOR seizures occurring at intervals of several weeks to
months. The subsequent seizure frequency often
LIKELY SYMPTOMATIC EPILEPSY*** remains low but may progressively increase over
months or years due to a self-perpetuating electrical
Classical signs kindling-like phenomenon. This sometimes leads to
intractable seizures with frequent and severe cluster
● Recurrent seizures are the only problem. seizures and status epilepticus.
● The initial seizure frequency is low but
may increase over time. Seizures are partial (focal) with or without secondary
● Seizures are partial in onset with or generalization. Secondary generalization may some-
without secondary generalization. times occur so quickly that no features of partial
seizures may be detected clinically.
● Seizures preceded by an aura (behavioral changes or months. A regressive course may occur with self-
a few seconds or minutes before the onset of ictus) limiting conditions. Other progressive (or regres-
or followed by localized post-ictal motor deficits sive) neurological signs and deficits, and abnormal
(e.g. hemiparesis) are partial, even if they appear to CSF and/or brain imaging findings reflecting an
be generalized from their onset. active disease process are also likely to be present.
● Idiopathic (genetic) epilepsy causes primary gener-
Other static neurological signs (e.g. personality
alized seizures that begin in young adult cats that have
changes) and/or thalamocortical deficits (e.g. menace,
no other neurological signs and deficits (see page
facial sensation, postural reactions) may or may not be
816).
present, depending on the size and location of the
● Intoxications typically cause an acute onset of severe
lesion.
convulsive status epilepticus or cluster seizures that is
usually preceded by signs of other body systems (e.g.
Diagnosis vomiting) as well as diffuse neurological signs (e.g.
mental depression, hyperexcitability, tremors). There
There may be a history of neurological signs a few to
are no periods of normalcy in between the seizures,
several months before the seizure onset (initial cerebral
which continue until appropriate treatment is provided
insult). These signs should have improved or resolved;
or until death occurs (see page 812).
if not, an active brain disease is likely.
● Metabolic causes produce a high initial seizure fre-
Neurological examination may be normal or reveal quency. Metabolic causes may be excluded when
thalamocortical deficits that are often subtle; the there are no other signs of metabolic disorders pre-
responses obtained from both sides of the body must be ceding and following the seizures (e.g. severe and
carefully compared. classical signs of hepatoencephalopathy, hypocal-
cemic tremors – tetany, hypoglycemic weakness and
CSF analysis is usually normal. Mild non-specific
confusion). They can also be excluded when there are
degenerative changes such as an increased proportion of
partial seizures or focal (unilateral, asymmetrical)
macrophages despite a normal leukocyte count may
neurological signs or deficits. Metabolic diseases, like
sometimes persist for months after the initial cerebral
intoxications, produce generalized seizures and bilat-
insult (e.g. trauma, ischemic encephalopathy).
eral and symmetrical neurological dysfunction.
Brain imaging may identify an inactive lesion; mag-
netic resonance imaging (MRI) is more sensitive than
Treatment
computed tomography.
Aggressive but rational anti-epileptic drug therapy is
In many cases with clinical evidence of likely sympto-
mandatory if there is more than one single seizure
matic epilepsy (e.g. partial seizures, non-progressive
every 6–8 weeks.
focal thalamocortical deficits), the underlying cause
● Start phenobarbital 1.5–2.5 mg/kg PO q 12 h.
remains unknown because the CSF analysis and brain
– Measure serum phenobarbital concentration 14
MRI are normal. Such epilepsy previously classified as
days after treatment initiation and after any
cryptogenic (hidden cause) is now called “likely symp-
dosage modification. Measure trough level, that
tomatic” epilepsy.
is, just prior to next treatment. Adjust the dosage
to obtain an optimal phenobarbital concentration
of 100–130 μmol/ml (23–32 μg/ml) using the
Exclusion of other causes of seizures is often possible formula: optimal dosage = optimal phenobarbi-
based on the history and clinical examination, even tal concentration ÷ actual phenobarbital concen-
before any ancillary tests are performed. tration × actual dosage.
● Active brain diseases often cause a higher initial ● Add diazepam (0.5–1.0 mg/kg q 12 h) if seizures
seizure frequency, including cluster seizures and are not well controlled (if > 1 seizure/6–8 weeks)
status epilepticus, and a rapid progression toward despite an optimal phenobarbital concentrations 14
high-frequency seizures within the first few weeks days after treatment initiation or change in drug dose.
sion (to 0.75–1.0 mg/kg/h), or give a pheno-

● Measure serum benzodiazepine concentration at
barbital IV bolus (2–5 mg/kg) and add pheno-
steady state (reached within 4–5 days) and adjust
barbital to the diazepam infusion (0.5–1
the dosage to obtain at least 500–700 nmol/L
mg/kg/h) for at least 4–6 hours before attempt-
(ng/L); use the same formula as for phenobarbital.
ing to decrease it. Because it takes at least 20
– Also measure liver enzymes to detect rare idio-
minutes for a phenobarbital IV bolus to exert its
syncratic acute hepatic necrosis induced by
anticonvulsant effect, sustained seizure activity
diazepam in cats.
must be controlled with diazepam in the mean
● Add gabapentin 10–40 mg/cat q 8 h if seizures are
time.
still not well controlled despite optimal phenobar-
– If phenobarbital is to be started as a mainte-
bital concentrations and benzodiazepine concentra-
nance anti-epileptic drug, a loading dose of
tions.
15–20 mg/kg (slow IV bolus) may be given to
– Potassium bromide (KBr) is contraindicated
immediately achieve a therapeutic serum con-
in cats; in a study of 26 cats treated with KBr,
centration of 60–110 μmol/L (15–25 μg/ml).
42% developed respiratory signs from 7 weeks
Maintenance dosing should be continued after-
to 14 months after onset of therapy. Two cats
wards (2.5 mg/kg q 12 h PO or IM if the cat is
died of their airway disease. The safety of
sedated to the point it is unable to safely swal-
potassium bromide use in the cat remains
low). Phenobarbital is potentiated by diazepam.
a serious issue. If there are no other options,
Close monitoring of the patient must be done
monitoring monthly by way of thoracic radi-
when adding phenobarbital to diazepam.
ographs should be done. The clinical signs
– If the cat is already treated with chronic oral
resolve with the arrest of treatment (up to 17
phenobarbital therapy and its phenobarbital con-
months are required for full recovery).
centration is known to be sub-therapeutic, it can
Anti-epileptic drug therapy is likely to be required for be immediately increased by administering an
life. Only if the cat remains seizure-free for longer than IV bolus; each 1 mg/kg IV bolus will increase
6–12 months should slow weaning from drugs be the phenobarbital concentrations by 5 μmol/L
attempted. Weaning should occur over a few months with (1 μg/ml).
one drug at a time. If more than one seizure/8 weeks ● If seizures are not adequately controlled, propo-
recurs during or after drug withdrawal, resume treatment. fol at sub-anesthetic dosage can be administered.
● Status epilepticus and cluster seizures require Use an IV bolus of 1.0–3.5 mg/kg plus a continuous
emergency treatment. IV infusion of 0.01–0.25 mg/kg/min, to effect, for
– First give a diazepam bolus of 0.5 mg/kg IV. several hours (up to 12–48 hours, if necessary)
Repeat if the seizure has not stopped within 1–2 before attempting weaning.
minutes or if another one begins. ● If high-frequency or sustained convulsive
– Immediately start a diazepam constant rate seizures persist despite the above treatment,
IV infusion of 0.5 mg/kg/h to prevent seizure proceed to general anesthesia with pentobarbital
recurrence. (5–15 mg/kg slow IV over several minutes, to effect;
– Mix the diazepam in an in-line burette with wait 10 minutes to see maximal effect before giving
maintenance fluids. Prepare only 1–2 hour sup- more).
ply at a time as diazepam is rapidly adsorbed – Add an IV continuous rate infusion of 5 mg/kg/h
into the plastic tubing and is inactivated by expo- for at least 6 hours if other seizures occur after-
sure to light. wards.
– When no seizures have occurred after 4–6 hours, – Intubation and ventilation are recommended
slowly decrease the infusion rate (25% steps as well as close anesthetic monitoring (tempera-
every 4–6 hours). ture, blood pressure, etc.).
– If > 2 seizures occur during the diazepam – Isoflurane anesthesia is the last resort for
infusion, either give another diazepam bolus refractory seizures. It should be done for at least
(0.5 mg/kg) and increase the diazepam infu- a few hours.
Prognosis ● Seizures may occur alone or with other signs dur-

ing the active phase of the disease. They may pres-
Good seizure control is often obtained with appropriate ent with the full spectrum of severity.
anti-epileptic drug therapy. Progression toward ● Delayed onset post-encephalitic secondary epilepsy
intractability may however occur despite adequate may also occur after a symptomatic or an asympto-
treatment and indicates a poor prognosis. matic course of the disease.
A steroid-responsive “shaker cat syndrome” similar
FELINE NON-SUPPURATIVE to the “little white dog shaker syndrome” has been
MENINGOENCEPHALITIS*** observed as the only clinical manifestation of the dis-
ease in a few cats.
Classical signs Systemic signs including fever, inappetence, lym-
● Focal or multifocal CNS signs. phadenopathy and mild hematological abnormalities
● Seizures. (e.g. leukopenia, lymphocytosis, anemia) may some-
● Occasionally, generalized tremors (“shaker times precede or accompany the neurological signs.
cat syndrome”). Ocular signs (e.g. chorioretinitis) may also be seen.
A viral infection is suspected even though the condi- CSF analysis may be normal or reveal a mild increase
tion does not appear to be contagious. Signs are usually of the protein concentration (< 0.70 g/L) and/or
confined to a single cat in a household. a mononuclear pleocytosis (< 50 cells/μl) with numer-
● Several feline (e.g. herpesvirus type I) and non- ous small lymphocytes and/or large foamy mononu-
feline (e.g. arboviruses) viruses may infect the clear cells.
CNS of cats and produce a subclinical or clinical
meningoencephalitis. Brain imaging (MRI) may be normal or show
inflammatory lesions with contrast uptake. Obstructive
An immune-mediated process is also possible. This or compensatory hydrocephalus and porencephalic
can be primary (idiopathic autoimmune) or secondary (cystic) lesions may sometimes be seen.
to various antigenic stimulation such as vaccination,
CNS infection with a non-pathogenic virus or infection
in another system. Differential diagnosis
Cats of any age and with or without outdoor access Other infectious encephalitis (e.g. FIP, toxoplasmo-
may be affected. sis, cryptococcosis) when there are other systemic
signs, ocular involvement or a progressive course.
● CSF analysis is the best test to differentiate the dis-
Clinical signs ease from FIP. Cats with FIP usually have a higher
CSF protein concentration and cell count with a pre-
The clinical course is variable with an acute or insid- dominance of neutrophils (see page 844). Toxoplas-
ious onset and a static, progressive or regressive mosis can however produce similar CSF changes.
course. Rarely, cryptococcosis may produce only mild CSF
The disease can produce focal or multifocal signs of inflammation but culture and titers help with diagno-
variable severity attributable to any portion of the sis when the organism is not visible in the CSF.
CNS; central vestibular (head tilt, balance losses, Usually signs are rapidly progressive with crypto-
mental depression, postural reaction deficits), spinal coccosis.
cord (hindlimb proprioceptive ataxia and paresis), Other causes of seizures in cats should be considered
cerebellar and cranial nerve signs are most common when seizures are the only sign of the disease (e.g. idio-
and may occur alone or in any combination. pathic and likely symptomatic epilepsies).

Treatment is generally supportive to ensure fluid, The classical form of the disease is seen with large
electrolyte and nutritional requirements are met. ischemic lesions that may involve up to two thirds of an
hemisphere.
Symptomatic anti-epileptic drug therapy should be
instituted in cats with seizures (see Likely symptomatic Typically, there is peracute onset of severe and uni-
epilepsy, page 802). lateral forebrain signs usually including mental
depression, pacing, circling, hemiparesis, and deficits
Glucocorticosteroids such as dexamethasone (0.25
in the menace response, facial sensation and postural
mg/kg q 24 h to be decreased over a few weeks to
reactions.
months) may be beneficial in immune-mediated cases,
● Rarely, seizures occur and may initially be difficult
but could be deleterious if a pathogenic virus is
to control (e.g. cluster seizures or status epilepticus).
involved.
● Rapid neurological improvement occurs in the
first 24–72 hours. Good recovery and minimal
residual signs and deficits occur within a few
Prognosis weeks in most cases.
– Rare complications that lead to neurological
The prognosis is often excellent as signs resolve sponta-
deterioration in the first 24 hours and sometimes
neously over weeks or months. Sometimes it is poor
to death or euthanasia include hemorrhage,
because of progressive deterioration leading to death or
increased intracranial pressure, tentorial hernia-
euthanasia.
tion and intractable seizures.
– Personality changes, especially a more or less
affectionate behavior and tolerant attitude
FELINE ISCHEMIC ENCEPHALOPATHY*** towards other animals, or for grooming, nail
cliping, etc., may become apparent as the initial
Classical signs signs resolve.
– Persistent seizures or delayed onset of post-
● Peracute onset unilateral forebrain signs
ischemic secondary epilepsy may occur, but
(mental depression/confusion, compulsive
appear to be unusual.
circling, hemiparesis) ± seizures.
● Personality changes and/or post-ischemic The atypical form of the disease is caused by small
epilepsy several months later. and superficial ischemic lesions that often do not cause
any clinical signs at the time of the infarction.
● A few seizures and/or personality changes may
however occur.
Pathogenesis
● Delayed onset post-ischemic secondary epilepsy
An ischemic cerebral infarction typically occurs in may be the only clinical manifestation. This may be
the parietal-temporal field of one cerebral hemisphere a common cause of seizure disorders in cats.
which controls contralateral sensorial (proprioceptive, – The seizures are usually of low to moderate fre-
nociceptive) and motor function as well as behavior. quency initially and subsequently.
Secondary edema and necrosis lead to atrophy and gliosis. ● No or only subtle unilateral or occasionally asym-
● The lesion is usually unilateral, although it can be metric bilateral thalamocortical deficits may be
bilateral but markedly asymmetrical. detected in these cats.
● A vasospasm phenomenon of the middle cerebral
artery is suspected but its pathogenesis remains
unknown. Cuterebra larval migration has been Diagnosis
incriminated as a cause.
CSF analysis may be normal or reveal mild non-
Young adults to middle-aged cats are usually affected. specific degenerative changes (increased proportion
of large foamy mononuclear cells) that may persist – Mannitol 25% (0.5–2.0 g/kg slow IV over
for several months after the infarction. 20–30 minutes) may be indicated in severe
cases (semi-stupor, pinpoint pupils).
Brain imaging (MRI is optimal) is the only means of
● To control seizures, give anti-epileptic drugs (see
antemortem diagnosis. It typically reveals the lesion in
Likely symptomatic epilepsy, page 802).
the parietal-temporal field of one cerebral hemisphere.
A similar but much milder lesion may be seen in the
other hemisphere. Prognosis
The prognosis is excellent in most cases.
● Persistent personality changes are usually mild,
Differential diagnosis but rarely they may make the animal unsuitable as
The typical form of the disease must be differentiated a pet, for example severe aggression.
from the following: ● Post-ischemic epilepsy is usually well controlled
● Cerebrovascular accidents are rare in cats and with adequate anti-epileptic drug therapy.
older animals are at greater risk. They may be asso- Recurrences of infarction are not reported to occur.
ciated with hypertension due to renal insufficiency,
hyperthyroidism or blood hyperviscosity due to
polycythemia vera. CONGENITAL AND INHERITED FOREBRAIN
● Head trauma is differentiated by the history and ANOMALIES***
external signs of trauma to the head and face area.
● Sudden decompensation or hemorrhage associ- Classical signs
ated with a cerebral tumor is usually seen in older ● Focal or diffuse forebrain signs (mentation
cats with other preceding neurological signs, espe- depression and confusion, central visual
cially mentation and behavioral changes. A pro- deficits with normal pupillary light
gressive rather than a regressive course would be reflexes, proprioceptive positioning and
expected afterwards. hopping deficits).
● Acute and severe encephalitides (infectious and ● Abnormal development and behavior.
non-infectious) are more likely to produce initially ● Occasionally, seizures.
progressive multifocal or diffuse signs.
In cats with the atypical form of ischemic encephalopa-
Pathogenesis
thy with personality changes or seizures as the only
sign, behavioral disorders and other intracranial Congenital hydrocephalus is uncommon and rarely
causes of seizures such as idiopathic epilepsy, active symptomatic in cats. It may be primary (e.g. inherited)
brain diseases must be investigated. or secondary, for example obstructive and/or compen-
satory following fetal encephalitis. Signs are diffuse
and mainly due to a lack of formation or loss of cerebral
Treatment
tissue, although intracranial pressure elevation may
Treatment is symptomatic. sometimes contribute to the signs.
● To reduce cerebral edema and intracranial pressure
Lysosomal storage diseases are inherited, progressive
in the typical form of ischemic encephalopathy,
and lethal multisystemic degenerative disorders that
give:
often involve the CNS of young to adolescent kittens
– Glucocorticosteroids (methylprednisolone
under 1 year of age. Initial signs are often attributable
sodium succinate [SoluMedrol®] 30 mg/kg IV
to cerebellar dysfunction.
or dexamethasone phosphate 0.25 mg/kg IV).
– Furosemide (0.5–2.0 mg/kg IV) may be pre- Lissencephaly-pachygyria is due to an abnormal
ferred to or combined with glucocorticosteroids migration of cerebrocortical neurons. It usually causes
when neurological signs are mild (mental learning disabilities, sometimes with behavioral abnor-
depression/confusion, miotic pupils). malities and seizures.
Dermoid cysts and other tumors of embryonic ori- Other specific tests, for example, ultrasonography
gin, for example teratomas and germ cell tumors, pro- through open fontanelles for hydrocephalus, enzymatic
duce progressive focal forebrain signs that often assays and biopsies of peripheral nerves or other organs
become complicated by an increased intracranial pres- for some lysosomal storage diseases are useful for
sure and/or secondary obstructive hydrocephalus. obtaining a definitive diagnosis.
Likely symptomatic epilepsy may be the only neuro-
logical sign in cats with small focal and inactive brain Differential diagnosis
lesions (e.g. cysts, cortical dysplasia) (see Likely symp- Acquired forebrain diseases affecting young cats such
tomatic epilepsy, page 801). as FIP and non-suppurative meningoencephalitis usu-
ally have a subacute onset and a rapidly progressive (or
Clinical signs regressive) clinical course.
Forebrain signs including mentation abnormalities, Hepatoencephalopathy due to portosystemic shunting
compulsive pacing or circling, central visual deficits would be distinguished by its episodic nature.
with normal pupillary light reflexes and hemiparesis
are present since birth, young kittenhood or early adult Treatment
life. Neurological deficits and signs can be focal or dif-
fuse, and static or progressive, depending on the under- Anti-epileptic drug therapy should be instituted for
lying pathological process. likely symptomatic epilepsy (see Likely symptomatic
● Extensive or diffuse forebrain anomalies such as epilepsy, page 802).
hydrocephalus or lissencephaly-pachygyria may Symptomatic medical treatment including glucocor-
manifest with retarded development, learning ticosteroids and surgical shunting for hydrocephalus is
disability, loss of training, mental depression, poorly documented in cats.
abnormal behavior and visual deficits.
– Severe hydrocephalus may also cause gait abnor- Lysosomal storage diseases are currently untreatable.
malities as a result of cerebellar and brainstem
distortion, as well as pacing and head pressing, Prognosis
especially when the intracranial pressure is ele-
Prognosis is usually guarded to poor, with the excep-
vated.
tion of secondary epilepsy, which may be successfully
Symptomatic seizures may occasionally occur but controlled with anti-epileptic drugs.
usually are preceded by other signs of the anomaly (e.g.
of hydrocephalus, tumors of embryonic origin, lysoso- HEPATIC ENCEPHALOPATHY***
mal storage diseases, lissencephaly-pachygyria).
Likely symptomatic epilepsy may occur. Seizures typ- Classical signs
ically are initially of low frequency and are partial in ● Episodes of hypersalivation, abnormal
origin, but can secondarily generalize to tonic-clonic mentation and bizarre behavior.
seizures (see Secondary epilepsy, page 800).
Pathogenesis
Diagnosis
Hepatic encephalopathy results when endogenous
Facial and head deformities may be apparent with
toxins produced by the action of the gut microflora on
hydrocephalus, for example a domed calvaria with
alimentary proteins are not removed from the systemic
open suture lines and fontanelles.
circulation by the liver. When a critical toxin level is
CSF analysis is likely to be normal or only reveal reached, diffuse cerebral dysfunction ensues.
mild non-specific degenerative changes.
Hepatic encephalopathy is most often due to a con-
Brain MRI will often show the underlying anomaly, for genital portosystemic vascular shunt and signs are
example porencephalic lesions. usually noticed during the first year of life.
Severe acquired liver diseases also very occa- Diagnosis

sionally cause hepatic encephalopathy in cats of any
age. Other signs of liver disease will usually predom- Pre- and post-prandial bile acids are usually
inate including anorexia, weight loss and sometimes markedly increased.
jaundice. Laboratory abnormalities may include microcytic
non-regenerative anemia, low albumin, urea and cho-
lesterol concentrations, and urinary ammonium biurate
Clinical signs crystals.
Neurological signs are episodic. They develop then Fasting blood ammonia is markedly elevated in most
regress progressively over periods of a few to several (90%) cats with a portosystemic vascular shunt, espe-
hours. cially during episodes of hepatoencephalopathy. This
● Episodes may be precipitated by feeding, espe- test is however inconvenient in most practices because
cially when a high-protein diet is ingested in blood samples must be drawn in cold heparinized tubes
large amounts. Several (up to 8–10) hours may and immediately transported to an appropriate labora-
however elapse between meal times and onset of tory on ice for refrigerated centrifugation and assay,
signs. Signs do not follow each meal, especially preferably within an hour of collection. False blood
early in the course of the disease. Several days ammonia values may occur with hemolysis, prolonged
and sometimes a few weeks may elapse between venous occlusion and struggling at the time of
episodes. venipuncture.
● An ammonia tolerance test identifies virtually all
Neurological signs are of diffuse thalamocortical
dysfunction: cats with a portosystemic vascular shunt but may
● Mentation abnormalities include depression, con-
precipitate severe signs of hepatoencephalopathy.
fusion, staring into space. Cats with a shunt have a blood ammonia concentra-
● Bizarre behavioral activities may occur, for exam-
tion 30 minutes post-challenge that is > three times
ple pacing, head pressing, dementia with running higher than the fasting values.
fits, frantic vocalization and aggression. Abdominal radiographs may show a small liver in
● Profuse salivation is common. This may last for cats with congenital portosystemic shunt.
several minutes to hours and may be the first and
only sign early in the course of the disease. Abdominal echography may allow visualization of
● Fine generalized muscle tremors (shivering).
a congenital portosystemic shunt or may detect diffuse
● Central blindness and ultimately stupor and coma
liver disease.
may develop in the advanced stage of hepatic
encephalopathy. Differential diagnosis
● Episodes of dementia with frantic behavioral activ-
ities such as running fits, attacking inanimate Cats presented for bouts of hypersalivation are often
objects and profuse salivation sometimes are misin- erroneously diagnosed with a stomatitis, even though
terpreted as being seizure activity. True seizures they may have no oral lesions. Ingestion of irritant
are rare and usually occur as clustered seizures substances or plants is another common misdiagnosis.
after the other classical and severe signs of hepatic Some intoxications may produce signs similar to those
encephalopathy have developed. of hepatic encephalopathy including depression or agi-
Systemic signs may include polyuria, polydipsia, vom- tation, but are not recurrent unless re-exposure to the
iting, diarrhea, dysuria with hematuria (due to urate toxin occurs.
calculi) and delayed anesthetic recovery.
● Cats with congenital portosystemic shunts may be Treatment
thin and small for their age.
Medical treatment is aimed at reducing the production
Other physical and laboratory signs of liver failure will and absorption of endogenous colonic toxins.
be obvious in cats with severe liver pathology. Maintenance therapy includes a low-protein diet (e.g.
Prescription Diet feline k/d, Hill’s Pet Nutrition), with Clinical signs
added carnitine, taurine and arginine, antibiotics (e.g.
metronidazole 7.5 mg/kg PO q 12 h, or neomycin 22 History of feeding all-fish diets (containing thiamin-
mg/kg PO q 8–12 h, or amoxicillin 22 mg/kg PO q 12 ase), diets consisting of entirely cooked meat (thiamine
h) and lactulose (0.25–0.5 ml/kg PO q 8–12 h). See page destruction by heating), poor-quality, thiamine-deficient
821, The Cat With Stupor or Coma, for further details. commercial diets, commercial food stored for long
periods of time or in excessively hot conditions or, pet
Surgical treatment including ligation or use of an meat preserved with sulfur dioxide which destroys
occlusive device offers the best chance for long-term thiamine.
control of clinical signs. This must be performed by an
experienced surgeon to decrease the risk of excessive Depression and inappetence are initial signs. Later
ligation which may cause rapid post-operative death mydriasis with poor pupillary light response, but usu-
due to portal hypertension and bowel ischemia. Like in ally without blindness and central vestibular dysfunc-
dogs, severe seizures may develop in the first few post- tion occur with head tilt, loss of balance, spastic gait
operative days, and some cats have remained epileptic and tremors. Terminally, semicoma, crying, opisthotonos
for months and years afterwards. with limb spasticity and death result.
True seizures are uncommon and must be differen-
tiated from periods of opisthotonic posturing with
Prognosis paddling, and from the spasmodic ventroflexion of
the neck and body contorsions that may be induced
Prognosis is good if surgical treatment is feasible, for when the cat is picked from the ground. These are
example with a single extrahepatic shunt, and is not likely due to marked spatial disorientation because
complicated by portal hypertension. Recurrence of of the bilateral vestibular dysfunction.
signs appears to be more common in cats than in dogs
and occurs in more than 40–50% after a few years. It
may be due to the persistence of shunting through Diagnosis
a partially ligated vessel or the development of mul- Diagnosis is based on a history of dietary deficiency
tiple secondary shunts because of chronic portal and response to thiamine supplementation (10–20
hypertension. mg thiamine IM q 8– 12 h, then orally).
Prognosis is guarded with medical treatment as the
condition often worsens over time.
CEREBROVASCULAR ACCIDENTS**
Classical signs
THIAMINE DEFICIENCY***
● Peracute and rapidly resolving cerebral
Classical signs signs.
● Inappetence, depression, intermittent
vomiting. Pathogenesis
● Central vestibular signs (reluctance to
Cerebrovascular accidents are rare in cats.
walk, nystagmus, loss of balance).
● Mydriasis with poor pupillary light Vascular events result in acute ischemic lesions.
reflexes. Vascular events include spontaneous hemorrhage from
● Spasmodic ventroflexion of the neck or coagulopathies, thrombocytopenia and hypertension
opisthotonos. associated with chronic renal failure and hyperthy-
roidism. They also include thrombosis (e.g. poly-
See main references on page 848 (The Cat With Head cythemia hyperviscosity syndrome) and embolization
Tilt, Vestibular Ataxia or Nystagmus) and page 899 including septic and metastatic from rapidly growing
(The Cat With Neck Ventroflexion). cell type tumors.
Clinical signs Recurrences may occur if the underlying cause per-

sists (e.g. hypertension). The lesion localization is how-
Peracute onset of non-progressive and rapidly ever likely to be different from one event to another.
regressive focal cerebral signs, including seizures
alone or with other signs. Post-ischemic gliosis may result in epilepsy.
● Slight deterioration may occur over the first 24
hours as a result of edema or increased intracranial HYPOGLYCEMIA**
pressure before the condition improves. A rapidly
progressive course is expected with septic and Classical signs
metastatic embolization.
● Mental alteration, weakness, ataxia, visual
Diagnosis loss.
● Seizures.
Diagnosis is based on a clinical course suggestive of
a vascular event, that is, a peracute, onset of signs that
improve rapidly. PATHOGENESIS
Neurological signs and deficits are attributable to Because blood glucose is the primary energy source for
a focal CNS lesion. Multifocal lesions are however pos- the CNS, hypoglycemia causes diffuse CNS dysfunc-
sible, for example, hemorrhage due to coagulation dis- tion. The nature and severity of the neurological signs
orders or thrombocytopenia, or multiple metastasis. depend on the rate of blood glucose decrease, level of
glucose attained and duration of hypoglycemia.
Evidence of historical, clinical, laboratory and imaging
findings related to the underlying cause such as poly- Severe and symptomatic hypoglycemia is rare in cats
cythemia, hypertensive retinal changes, hyperthy- except as a result of insulin over-dosage in diabetic
roidism, abdominal tumor increase the index of cats. Rarely reported causes include insulin-secreting
suspicion when neurological findings are consistent tumors, other tumors secreting insulin-like growth fac-
with a vascular accident. tor (IGF), sepsis and terminal hepatic disease.

The classical form of the feline ischemic encephalopa- Signs may be episodic or persistent and include men-
thy is a cerebrovascular accident that occurs in young tation abnormalities (e.g. depression, confusion, stu-
adult to middle-aged healthy cats. por), weakness, ataxia, central visual impairment and
generalized seizures. Nervousness, muscle fascicula-
Acutely decompensated brain tumor as occurs fol-
tions and tremors may also occur.
lowing spontaneous hemorrhage, or tentorial herniation
● Seizures more often occur when there is a sudden
may appear clinically similar.
and marked decrease in the glucose concentration,
and are usually preceded by other more subtle signs
Treatment
of hypoglycemia such as confusion and weakness.
Treatment is specific if the cause is known and treatable.
Severe and sustained hypoglycemia may cause diffuse
Supportive and symptomatic therapy is indicated to cerebral anoxic injuries resulting in stupor-coma,
control secondary brain edema and increased intracra- decerebrate rigidity and miotic pupils. This may
nial pressure (see Feline ischemic encephalopathy, progress to irreversible damage (cortical necrosis) and
page 805 and Head trauma, page 818). permanent neurological sequela including blindness
and secondary epilepsy.
Prognosis
Diagnosis
The prognosis depends on the severity of the neuro-
logical signs and the underlying cause and whether it is Serum glucose concentration is usually < 2.2 mmol/L
treatable or not. (40 mg/dl).
Other historical, clinical and laboratory abnormalities extension of nasal cavity and paranasal sinus neo-
may be evident, depending on the underlying cause. plasms and metastatic brain tumors.
More commonly, there is a history of diabetes mellitus
Clinical signs
treated with insulin or hypoglycemic drugs.
Initial signs often include subtle personality and
behavioral changes, mental depression, pacing and
circling.
Other episodic or peracute conditions such as meta-
Seizures may manifest as the first and only sign, occur
bolic disturbances, intoxications and encephalo-
concurrently with other signs or develop later. The initial
myelitis should be considered depending on the
seizure frequency is variable but is inevitably progressive.
clinical presentation.
Focal signs such as contralateral hemiparesis with
postural reaction deficits, visual loss and decreased
Treatment
facial sensation are often detected upon examination.
Treatment involves glucose administration (food, sugar
Tumors complicated with obstructive hydro-
water, corn syrup or dextrose 50% IV [1/2–4 ml/kg],
cephalus and increased intracranial pressure cause
according to the severity of hypoglycemic signs) and
more diffuse signs (e.g. profound depression, bilat-
specific treatment of the underlying cause. See page
eral miosis). This may also lead to tentorial herniation
956 (The Cat With Generalized Weakness) and
which often develops slowly and remains asympto-
page 832 (The Cat With Stupor or Coma).
matic until an acute decompensation is triggered by
Diabetic cats need re-evaluation of their treatment further tumor growth, spontaneous hemorrhage in or
regime. Some cats presenting with hypoglycemia are in around the tumor, concomitant disease or stress, anes-
diabetic remission and do not require further insulin or thesia and CSF collection.
oral treatment. ● Tentorial herniation resulting in brainstem com-
pression produces coma, unresponsive mydriasis,
abnormal respiratory patterns and death from
Prognosis
respiratory arrest.
Prognosis is good unless the underlying cause is asso-
ciated with a poor prognosis (e.g. neoplasia) or signifi- Diagnosis
cant structural cerebral damage has occurred.
Skull radiographs are likely to be unrewarding except
for some meningiomas which may result in thinning or
FOREBRAIN TUMORS** thickening of the adjacent calvaria and increased den-
sity of adjacent soft tissue, and neoplasms of the nasal
Classical signs cavity and paranasal sinus which produce soft tissue
density, osteolysis and bone proliferation.
● Progressive forebrain signs (personality
changes, circling, pacing) in middle-aged CSF analysis may reveal mild to moderate increase
and older cats. of the protein concentration and/or pleocytosis (ele-
● Seizures. vated leukocyte count); CSF may be normal with
small and deeply seated tumors.
● CSF collection is contraindicated in cats with
signs of increased intracranial pressure (marked
PATHOGENESIS mental depression, inappropriate miosis) because it
may cause or exacerbate a tentorial herniation lead-
Forebrain neoplasms cause progressive focal neuro-
ing to death.
logical signs, the nature and severity of which depend
on the tumor location and growth rate. Brain imaging is essential to confirm the diagnosis and
● Meningiomas are the most common. Other brain to localize the tumor when surgical or radiation therapy
tumors of cats include gliomas, pituitary tumors, is considered.

Other focal and slowly progressive brain diseases FIP causes multifocal or focal neurological signs
are uncommon in cats (e.g. toxoplasma granuloma, attributable to any portion of the CNS. Central
cerebral abscess). vestibular signs (head tilt, balance losses, nystagmus,
mental depression, postural reaction deficits) are the
Multiples tumors (e.g. meningiomas, metastases) may
most common and are often accompanied by cerebel-
cause multifocal signs and must be differentiated from
lar signs (intentional tremors, hypermetria).
encephalitides.
● Seizures are unusual and do not occur as the only
sign.
Treatment
Affected cats usually have other clinical and labora-
Surgical excision may be possible if the tumor is surgi- tory evidence of systemic involvement (e.g. lethargy,
cally accessible. Meningiomas on the dorsal surface of inappetence, weight loss, fever, anemia, renal and
the cerebral hemispheres can be successfully removed. hepatic signs).
Radiation therapy is a useful adjunct to surgical Ocular signs are also common (e.g. chorioretinitis,
debulking, or can be used alone when surgical excision anterior uveitis).
is not possible.
Typically, there is an insidious onset and a slowly pro-
Chemotherapy is poorly documented for brain tumors gressive course over weeks.
of cats. Lomustine (a nitrosourea) has been safely used
in the cat. Usually, cats are less than 3 years old and were
obtained from a large multiple-cat household,
Palliative medical treatment using dexamethasone breeder or pet store.
(0.12–0.25 mg/kg q 24–48 h) to decrease peritumoral
edema. Diagnosis
Symptomatic anti-epileptic drug therapy should be CSF analysis is the most useful test when there are
instituted in cats with seizures (see Secondary epilepsy, CNS signs; typically, there is a marked increase of the
page 801). protein concentration (> 1 g/L; 100 mg/dl and often >
2 g/L; 200 mg/dl) and leukocyte count (> 100 cells/μl)
Prognosis with a large proportion of non-lytic neutrophils.
Long-term prognosis is poor except for convexity Serological testing has been of little diagnostic value
meningiomas (located on the dorsal surface of the except that a negative test suggests the disease is
cerebral hemispheres), which can often be completely unlikely to be FIP. However, negative test results do
excised with good survival, rapid recovery and low occur rarely in cats with FIP, especially in the terminal
incidence of recurrence. stages.
The ELISA that detects antibody to the 7B protein,
FELINE INFECTIOUS PERITONITIS** which is specific to the coronavirus strains causing
FIP has not been shown to improve accuracy of diag-
Classical signs nosis in clinical practice. Newer PCR methods may be
● Multifocal CNS signs (head tilt, nystagmus, useful.
intentional tremors, ataxia, paresis).
● Systemic signs (fever, lethargy,
inappetence, weight loss) +/- ocular signs.
Other infectious and non-infectious encephalitides,
See main references on page 844 (The Cat With Head for example non-suppurative meningoencephalitis and
Tilt, Vestibular Ataxia or Nystagmus) and page 352 toxoplasmosis need to be differentiated from FIP. CSF
(The Thin, Inappetent Cat). analysis may help to differentiate theses diseases.
Treatment Serology from blood, CSF, aqueous humor and urine is

highly specific and sensitive.
No treatment is effective once neurological signs are
present. Glucocorticosteroid may temporarily improve Identification of the organism may be made by cytol-
the neurological signs. ogy, histology or culture of various body fluids and tis-
sues including CSF, nasal discharge and polyp-like
masses, skin lesions, enlarged lymph nodes.
CRYPTOCOCCOSIS**
Classical signs
Other infectious encephalitides such as FIP and toxo-
● Chronic nasal discharge, often with nasal plasmosis need to be differentiated from cryptococco-
distortion. sis. With cryptococcosis the organism is usually
● Cutaneous lesions – nodules or ulcers. evident in CSF, although occasionally culture may be
● Occasionally, ocular and CNS signs. required to demonstrate it.

With Signs of Chronic Nasal Disease). Treatment
Fluconazole (2.5–10 mg/kg PO q 12 h) is best for CNS
infections, or itraconazole (5 mg/kg PO q 12 h). See
Pathogenesis main reference on page 26 for treatment details.
Infection is by inhalation of the organism contained
in high concentration in soil contaminated by pigeon Prognosis
droppings or eucalyptus tree debris.
The prognosis is guarded once CNS involvement
CNS infection occurs by direct extension through the occurs.
cribriform plate or by hematogenous spread. A diffuse
or focal granulomatous meningoencephalitis results.
INTOXICATIONS**
Clinical signs
Classical signs
CNS signs can occur alone or with other signs (e.g.
rhinitis, cutaneous lesions) and are usually rapidly pro-
● Signs of CNS, autonomic or neuromuscular
gressive. stimulation or depression.
● Most commonly, cats exhibit cerebral signs such
● Rarely and terminally, convulsive status
as mental depression, behavioral changes, cir- epilepticus.
cling, head pressing and ataxia; seizures may occur
with forebrain involvement but are unlikely to be Pathogenesis
the only sign.
● Blindness with dilated and unresponsive pupils may
Signs of intoxications usually occur shortly after acute
occur due to optic neuritis. and accidental ingestion or topical contact. Cats’ selec-
tive eating behavior is protective but their grooming
Ocular signs including chorioretinitis, panophthalmi- habits may increase exposure.
tis, and retinal detachment are often associated with
CNS involvement. Most intoxicants cause functional disturbances for
example conduction failure or neurotransmitter imbal-
ance in various portions of the nervous system,
Diagnosis although others cause structural damage.
CSF analysis may reveal mild to marked inflammatory Intoxicants that may cause seizures include the fol-
changes, often with numerous cryptococcal organisms. lowing:
● Pyrethrins and pyrethroids (e.g. fenvalerate, ● Neurological signs vary according to the intoxi-
allethrin, tetramethrin, deltamethrin). Signs of intox- cant and include various combinations of CNS
ication usually occur a few minutes to hours after signs (e.g. mental depression to coma, hyperex-
excessive topical application of anti-flea and tick citability, tremors, ataxia, paresis), autonomic
sprays, powders, foam, dips and shampoos. signs (e.g. hypersalivation, miosis, diarrhea) and
● Organochlorines are used for pest control (e.g. lin- neuromuscular signs (e.g. muscle fasciculations-
dane, methoxychlor, endosulfan, DDT, aldrin, tremors, LMN signs).
chlordane, dieldrin, heptachlor, dicofol, endrin, ● True seizures are less common than generally
perthane, toxaphen) and may contaminate water or believed and must be differentiated from other
food, or be absorbed through the skin and the seizure-like features of poisoning such as tremors,
mucous membranes. tetany or hysterical behavior. Seizures usually man-
● Organophosphates (e.g. dichlorvos, malathion, ifest as convulsive status epilepticus that continues
chlorpyrifos, fenthion, parathion, phoxime, until treatment is provided or until death ensues.
cythioate, diazinon, safrotin, phosmet, tetrachlorv- – Pyrethrins and pyrethroids intoxications are
inphos, diazinon) and carbamates (e.g. propoxur, usually mild and resolve in most cases within
carbaryl, bendiocarb, chlorprophane, buphame 24–72 hours. Signs include depression, saliva-
methomyl) are insecticides used in various formu- tion, anorexia, vomiting, muscle tremors (ear
lations to control fleas, ticks and mites on pets, in flicking, contractions of the cutaneous muscles,
the house and yard, on crops, stored grains, soils, paw shaking), hyperexcitability or hyperactivity,
and have also been used as fly, ant and roach baits. disorientation, weakness, ataxia, dyspnea and
Intoxication occurs by ingestion, dermal exposure rarely, seizures and death.
and after inhalation. – Organochlorines produce progressive or explo-
● Bromethalin is a non-anticoagulant rodenticide sive onset of hyperesthesia, nervousness, agitation,
available in bait form. Secondary intoxication due hyperexcitability, salivation, vomiting, tremors,
to the ingestion of bromethalin-poisoned rodents ataxia, nystagmus, blindness, opisthotonos, convul-
may occur. sive seizures, depression, coma and death.
● Strychnine is a rodenticide marketed as pellets or – Organophosphates and carbamates inactivate
treated seeds. acetylcholinesterase resulting in excessive activ-
● Methaldehyde is a molluscicide often mixed with ity and fatigue of cholinergic end-organs and
bran flakes or pellets. muscles. This includes muscarinic signs (mio-
● Lead is ingested in old paint flakes or paint dust from sis, bradycardia, vomiting, diarrhea, hypersaliva-
sanding, linoleums, roofing materials, plaster board, tion, lacrimation, dyspnea due to excessive
putty, artist paint, lead objects (drapery and fishing bronchosecretions and bronchoconstriction,
weights, sinkers, bullets), used motor oils from leaded anorexia), nicotinic signs (muscle tremors,
gasoline-burning engines, greases leaded gazoline, weakness), as well as CNS signs depression,
eating or drinking from improperly glazed bowls. behavioral changes, ataxia, hyperactivity,
● Other intoxicants potentially dangerous for cats seizures).
include penitrem mycotoxins (produced in spoiled – Strychnine toxicity results in anxiousness and
dairy products such as cottage cheese), nicotine nervousness, extreme sensitivity to external
(gum and skin patches), caffeine, chocolate (theo- stimuli (e.g. noise, bright light), muscle tremors,
bromine) and illicit drugs (e.g. cocaine). intermittent then sustained extensor rigidity with
opisthotonos and tetany (pseudo-convulsions),
hyperthermia and death by respiratory apnea and
Clinical signs
hypoxia.
Most intoxications are acute and produce diffuse and – Methaldehyde causes anxiety, restlessness,
rapidly progressive neurological signs. These may be ataxia, tremors, salivation, vomiting, diarrhea,
accompanied by signs of stimulation of other body sys- mydriasis, nystagmus, opisthotonos, tetanic con-
tems, for example gastrointestinal with vomiting and/or vulsions, hyperthermia and death from respira-
diarrhea. tory muscle spastic paralysis.
– Lead poisoning induces gastrointestinal (anorexia, cats are rare. Hypoglycemia is typically associated
vomiting, diarrhea, constipation), renal (polyuria, with insulin overdose in a diabetic patient, hypocal-
polydipsia) and neurological (depression, central cemia is mainly seen after bilateral thyroidectomy,
blindness, hyperexcitability, running fits, seizures, and hepatoencephalopathy causes episodic signs,
vocalization, ataxia, head pressing, opisthotonos, which rarely occur in intoxications.
paraparesis) signs. Megaesophagus with regurgita-
Inflammatory conditions (e.g. encephalitides,
tion and pharyngeal/laryngeal paresis has been
polyneuropathies) need to be ruled out. Usually his-
observed with chronic lead poisoning in cats.
tory and physical examination findings differentiate
– Bromethalin acute toxicity causes tremors,
these from intoxications.
hyperexcitability, hyperesthesia, depression,
fever, anisocoria, positional nystagmus, extensor
rigidity, opisthotonos and seizures (running fits Treatment
and generalized). Death may sometimes be
With dermal exposure it is important to bath the cat
delayed up to 2–3 weeks in cats. Chronic intox-
with soap or detergent to remove the toxin from the hair
ication with lower dosages causes occasional
and skin. Intoxication with anti-flea and -tick sprays,
vomiting, ascending paresis and ataxia with pro-
dips, and aerosols containing insecticides such as
prioceptive deficits, depressed spinal reflexes
pyrethrins, carbamates, organophosphates often occurs
(patellar and withdrawal), tremors, depression
via dermal exposure.
and lateral recumbency. Recovery is possible
after exposure is discontinued. When ingestion has occurred within the previous
– Penitrem mycotoxins. 2 hours, emesis may be indicated or contraindicated,
according to the specific toxin and formulation that was
ingested. Emesis may be induced with hydrogen perox-
Diagnosis
ide 3% (2 ml/kg PO) or apomorphine (0.03–0.04 mg IV
Diagnosis is based on a history of exposure to a toxin or 0.04–0.08 mg/kg IM). Gastric lavage performed
capable of producing the observed signs within the doc- under general anesthesia may be beneficial if emesis is
umented time for exposure. not effective. Enemas also may be useful. Activated
charcoal (0.1–1.0 mg/kg q 8–12 h) preferably adminis-
Toxicologic analysis may be diagnostic when per-
tered with a cathartic such as magnesium sulfate (250
formed on the following:
mg/kg) or 70% sorbitol (3 ml/kg) is also indicated to
● Tissues (e.g. liver, kidney, fat, brain) for organochlo-
reduce gastrointestinal absorption.
rines, organophosphates, strychnine, lead, etc.
● Vomitus and stomach content (for bromethalin, Atropine sulfate (0.02–0.04 mg/kg IM or SC) will
strychnine, methaldehyde). decrease salivation and muscarinic signs associated
● Urine (for strychnine). with organophosphate and other poisoning, but because
● Blood for lead concentration and acethyl- of the risk of fatal bronchospasm it is only recom-
cholinesterase activity (organophosphate poisoning). mended if marked bradycardia is present.
Toxicity as a cause of seizures can be excluded when Pralidoxime chloride (2-PAM, Protopam chloride) is
(a) there are no other diffuse neurological signs preced- useful to reactivate cholinesterase (10–15 mg/kg IM or
ing the seizure onset (e.g. tremors, hyperexcitability), (b) SC q 8–12 h) and control nicotinic signs of organophos-
when partial seizures occur, (c) when isolated seizures phate poisoning. It is most effective if exposure was
are interspersed with periods of normalcy, or (d) when within the previous 24–48 hours, if exposure was by the
focal neurological signs or deficits are present. dermal route and if a slowly eliminated compound was
involved (e.g. fenthion, chlorpyrifos).
Differential diagnosis Diphenhydramine also has antinicotinic activity.
Metabolic disturbances that are severe enough to Chelation therapy (e.g. calcium EDTA and/or penicil-
cause obvious neurological signs including seizures in lamine) is indicated for lead poisoning.
Treat cerebral edema (e.g. bromethalin, lead) with man- The enteroepithelial cycle with oocyst shedding almost
nitol and/or glucorticosteroids, and control seizures or exclusively occurs in young weanling kittens and rarely
pseudo-seizures with diazepam, phenobarbital, propo- results in gastrointestinal signs.
fol and pentobarbital. See page 801 (Likely sympto-
Sudden death associated with acute Toxoplasma
matic epilepsy) for treatment details.
encephalitis may occur in approximately 30% of kit-
Provide supportive care including fluids, which also tens infected at 6–12 weeks of age.
promote excretion of the toxin.
Ocular signs such as anterior uveitis and chorioretini-
tis are also common.
Prognosis Neurological signs manifest rarely even though the
Prognosis is variable and depends on the severity of the organism is frequently found in the CNS.
signs and time between intoxication and treatment. ● Acute to subacute multifocal or focal cerebral signs
are more common. Seizures are unlikely to occur as
the only sign.
TOXOPLASMOSIS**

● Pneumonia, hepatitis, pancreatitis, The antemortem diagnosis of clinical toxoplasmosis
myositis. is difficult; it relies on serological demonstration of
● Often, uveitis or chorioretinitis. previous exposure and perhaps of recent or active infec-
● Occasionally, focal or multifocal tion, exclusion of other causes, and positive response to
neurological signs. treatment.
See main reference on page 705 for details (The Cat CSF analysis may reveal a mild to moderate increase
With Signs of Acute Small Bowel Diarrhea). of the protein concentration (< 1.0 g/L) with normal
or only slightly elevated leukocyte count (<50/μl).
Organisms are only rarely seen on cytologic examina-
Pathogenesis tion of CSF and other body fluids.
Toxoplasma gondii is an opportunistic pathogen. Demonstration of the organism in tissue biopsy sec-
Although subclinical infection is common in cats, clin- tions will confirm the diagnosis only if inflammation is
ical disease rarely develops. present.
● Clinical toxoplasmosis causing neurological signs
Fecal examination is likely to be unrewarding
in adult cats is believed to be mainly associated
because of the short period of oocyst shedding that
with concurrent stress, illness or immunosuppres-
occurs for only a few weeks after infection.
sion that reactivate a latent infection acquired
at a young age by carnivorism associated with Serologic testing often cannot distinguish latent
hunting. asymptomatic from active clinical infection. A posi-
tive IgM titer or a 4-fold increase in IgA or IgG titer
Toxoplasma gondii causes a non-suppurative encep-
suggests recent infection. However, in some cats, IgM
halomyelitis that may be widely scattered throughout
titers remain positive for months to years after infec-
the CNS or localized in one area as a granuloma.
tion, and 20% of cats may not develop IgM titers. IgG
titers may take 4–6 weeks to develop and high
IgG titers (> 30 000) are commonly detected 6 years
Clinical signs
after infection. Positive titers occur in 30–60% of cats.
Systemic signs including lethargy, anorexia, fever are Many adult cats with neurological signs are believed to
most often related to pneumonia, dyspnea, tachypnea. have reactivation of a latent infection, rather than
Hepatitis, pancreatitis, myositis and myocarditis may a newly acquired infection, which is typically detected
also occur. by a positive 1 IgM titer or rising IgG titer.

Other infectious and non-infectious causes of Recurrent primary generalized tonic-clonic seizures
encephalomyelitis including FIP and non-suppurative should be the only sign.
meningoencephalitis should be considered. ● There is no aura, no localized or unilateral signs
during the ictus and in the post-ictal phase.
The initial seizure frequency should be low with iso-
Treatment
lated single seizures at more than 6–8 week intervals.
Clindamycin 12.5 mg/kg PO q 12 h doses for a mini- ● The subsequent seizure frequency could remain
mum of 4 weeks. low or progressively increase, perhaps to the point of
intractability, but this should not occur before several
Clarithromycin (7.5 mg/kg PO q 12 h) and azithro-
months to a few years from the seizure onset.
mycin (7–15 mg/kg q 12 h) are newer macrolides which
may be useful. Onset of seizures should be during adolescence or
young adulthood (probably between 6 months and
5 years).
Prognosis
Prognosis is guarded with CNS involvement. Diagnosis
Clinical signs of systemic illness usually begin to
Diagnosis is by exclusion of other causes.
resolve within 24–48 h of beginning therapy but neu-
rological signs may take weeks to improve and major Physical and ophthalmological examinations should
neurological abnormalities may remain. Response be normal. Abnormal findings would indicate the pres-
may be poor, slow, incomplete, and recurrence may ence of another pathological process possibly related to
occur. the seizure disorder (e.g. fever, chorioretinitis).
Neurological examination should be normal. Other
neurological signs or deficits would indicate that an
IDIOPATHIC EPILEPSY* active or inactive structural brain lesion is present.
Classical signs CSF analysis should be normal. Abnormalities would

reveal the presence of an active or a resolving brain
● Recurrent primary generalized tonic-clonic
disease.
seizures.
● The initial seizure frequency is low (< 1 Brain imaging (MRI) should be normal. Any abnor-
single seizure every 6–8 weeks) but may mality could be related to the seizure disorder (e.g.
later increase. active or inactive lesions).
● Seizures begin in young adult cats
Idiopathic epilepsy should be excluded when there
(6 months to 5 years of age) that
are partial seizures (including seizures that appear to
have no other neurological signs and
be generalized from their onset but that are preceded by
deficits.
an aura or followed by localized post-ictal signs),
a seizure onset before 6 months or after 5 years of
age, an initially high seizure frequency, a rapid
Pathogenesis increase of the seizure frequency within the first few
This is believed to result from a diffuse imbalance weeks or months, other neurological signs or deficits,
between neuronal excitatory and inhibitory mecha- CSF changes or MRI abnormalities.
nisms that has no underlying cause other than a genetic
predisposition. Differential diagnosis
Idiopathic epilepsy is rare and poorly documented in Extracranial causes of seizures such as metabolic,
cats. toxic and hypoxic causes usually produce a sudden
onset of high-frequency seizures, often cluster seizures Diagnosis

or status epilepticus, and other diffuse neurological
and/or systemic signs before and in between the Diagnosis is based on finding a total serum calcium
seizures. concentration < 1.6 mmol/L (6.5 mg/dl) and ionized
calcium level < 0.6 mmol/L (2.5 mg/dl).
Active brain diseases often cause a higher seizure fre-
quency, interictal neurological signs and deficits, and Other historical, clinical and laboratory abnormalities
abnormal findings upon CSF analysis or brain imaging. may reflect the underlying cause, including idiopathic
or post-thyroidectomy hypoparathyroidism, puerperal
Likely symptomatic epilepsy may sometimes be distin- tetany, renal failure and phosphate enema.
guished from idiopathic epilepsy only by the occur-
rence of partial seizures and/or the presence of focal Differential diagnosis
neurological deficits because CSF analysis and MRI
may also be normal. Other causes of neuromuscular hyperexcitability such
as intoxications should be considered. With organophos-
phate toxicity, muscarinic signs are usually present
Treatment (miosis, salivation, vomiting, bradycardia). Fenthion
Symptomatic anti-epileptic drug therapy for life has few muscarinic signs and mainly produces muscle
(see Likely symptomatic epilepsy, page 801). weakness.
Tetany must be differentiated from convulsive status
Prognosis epilepticus of hypocalcemia. The cat with tetany is con-
scious although it is very anxious.
Good seizure control should be obtained in most cases,
although some cats can progress toward refractoriness, Treatment
despite adequate anti-epileptic drug treatment.
Calcium supplementation and specific treatment of
the underlying cause is required.
HYPOCALCEMIA* ● Use 0.5–1.5 ml/kg IV of 10% calcium gluconate.
Infuse slowly over 10 minutes while monitoring
Classical signs heart rate. Stop if bradycardia develops. See
● Muscle fasciculation, especially involving Hypocalcemia, page 962 in “The Cat With
the head and ears. Generalized Weakness” for treatment.
● Generalized weakness.
● Stiffness, tremors, tetany. HEAD TRAUMA
● Rarely, convulsive status epilepticus.
● Vomiting. Classical signs
● Peracute onset of cerebral signs ±
See main reference on page 962 for details (The Cat seizures.
With Generalized Weakness). ● Signs of head trauma, including
hemorrhage in eyes, ears, nose.
● Delayed onset epilepsy.
Clinical signs
Symptomatic hypocalcemia is rare in cats. It is usu-
ally iatrogenic following bilateral thyroidectomy. Clinical signs
Signs are episodic or persistent and include multi- Concussion manifests with immediate and brief (a few
focal muscle fasciculations, which often involves the seconds to minutes) mental confusion or loss of con-
face and ears. This may progress to generalized weak- sciousness. Recovery is rapid and complete with no
ness with stiffness, panting, tremors and tetany. residual neurological signs as there are no parenchymal
Terminally, convulsive status epilepticus may occur. lesions.
Contusions and lacerations produce parenchymal – Hetastarch 6%, 10–20 ml/kg to effect, to be
lesions and signs that may worsen over the initial 24 given in 5 ml/kg increments over 5–10 minutes
hours because of edema and increased intracranial to avoid nausea and vomiting,
pressure, but improve afterwards. OR
● Forebrain signs include mentation abnor- – Hypertonic saline (NaCl 7%), 4–5 ml/kg slow
malities such as depression to semi-stupor and IV over 3–5 minutes.
confusion, behavioral manifestations such as ● If volume replacement fluids are not available, give
agitation and dementia, compulsive activities isotonic crystalloid fluids (e.g. NaCl 0.9%, LRS),
including restlessness with propulsive pacing and 40–60 ml/kg/h IV, to effect administering just
circling. Hemiparesis and central blindness may enough to re-establish euvolemia and mean arterial
also occur. blood pressure.
● Whole blood transfusion or plasma administra-
Seizure onset is often with cluster seizures or status
tion may be indicated when significant blood loss
epilepticus occurring immediately or within the first
has occurred.
12–24 hours after trauma. These may initially be diffi-
● Administer supplemental oxygen via a nasal or
cult to control.
transtracheal catheter. If the cat is unconscious,
Delayed onset post-traumatic epilepsy (see Likely intubate and ventilate at 10–20 breaths/minute to
symptomatic epilepsy, page 800) may occur a few to keep PaCO2 around 30–35 mmHg.
several months later.
Control secondary brain edema to prevent or reduce
intracranial hypertension.
Diagnosis ● If shock treatment has not sufficiently improved the
cat’s neurological status, if the cat is mentally very
History and external signs of severe head trauma as
depressed or stuporous, or if its neurological status
a result of a road accident, fall from several stories or
deteriorates (mental status, pinpoint pupils or pro-
mistreatment by humans.
gression to mydriatic and non-responsive pupils):
Post-traumatic epilepsy should be excluded if there – Give furosemide 0.5–2 mg/kg IV.
were no serious forebrain signs and deficits at the time – A few minutes later, give mannitol 0.5–1.0 g/kg
of a reported trauma, as well as when the seizure onset IV slowly over 10–20 minutes. A dramatic
occurs more than 2 or 3 years after trauma. decrease of the intracranial pressure and neuro-
● Brain imaging may demonstrate a parenchymal logical improvement usually occurs within 15
lesion. A skull fracture may or may not be present. minutes and lasts for 2–5 hours. If neurological
deterioration occurs afterwards, mannitol can be
repeated for a maximum of three doses over a
24-hour period. Careful monitoring of serum
Cerebrovascular accident may also manifest with an osmolality and electrolytes is mandatory.
acute onset of severe focal cerebral signs but there are ● Keep the head elevated at 15–30 degrees, avoid
no history or external signs of trauma. pressure on the jugular veins from IV lines, band-
age and bedding, and monitor mental status and
Onset of seizures with low to moderate frequency a few
pupil size continuously.
to several months after major head trauma has occurred
is highly suggestive of post-traumatic epilepsy but Glucocorticosteroid administration in the head
other causes of seizures must be ruled-out. trauma patient is controversial because of few docu-
mented beneficial effects and potential deleterious
effects, etc. If the patient does not respond adequately
Treatment
to appropriate fluid, oxygen and mannitol administra-
Re-establish or maintain adequate cerebral perfusion. tion, methylprednisolone (Solu-Medrol) may be given
● First treat hypotension and systemic shock, if if hyperglycemia is not already present (30 mg/kg at
present, by giving volume replacement fluids: time 0, and 15 mg/kg at 2 and 6 hours, followed or not
with a continuous intravenous infusion of 2.5 mg/kg/h

UREMIA
for 24 hours).
Control cluster seizures and status epilepticus with Classical signs
anti-epileptic drugs (see Likely symptomatic epilepsy,
● Mental alterations, abnormal motor
page 801).
function and occasionally, seizures.
Emergency craniectomy may be indicated when ● Depression, anorexia.
aggressive medical treatment has not succeeded in sta- ● Polyuria, polydipsia, weight loss.
bilizing a patient with a depressed skull fracture, cal-
varial penetration with contaminated bone fragments or See main reference on page 334 (The Thin, Inappetent
foreign material, and focal hemorrhage as documented Cat) and page 231 (The Cat With Polyuria and Polydip-
by brain imaging (CT scan or MRI). Craniectomy with sia).
durotomy solely as a decompressive procedure may
also be attempted.
Clinical signs
RABIES Neurological signs occur mainly in severely ill
patients with advanced stage of acute or chronic renal
Classical signs failure.
● Progression from mild behavioral changes, Signs are often vague and include mental distur-
to aggression and vicious behavior, to bances such as depression, confusion, restlessness,
paralysis and death. hyper-reactivity to various stimuli, delirium. Weakness
may be evident sometimes with muscle spasms,
myoclonia or tremors. Ataxia, head-bobbing and mus-
Clinical signs cle fasciculations may also occur. The signs are likely
caused by the debilitating effects of renal failure, ure-
The development of the disease often follows three
mic encephalopathy and associated metabolic distur-
stages; an early short prodromal phase (1–2 days) char-
bances including hypocalcemia, hypoglycemia, acid–
acterized by a non-specific change in mental status; the
base disturbances, anemia.
cat may become shy and withdrawn or affectionate and
● Seizures occur in severely ill cats and more often
unpredictable. This progresses into an aggressive and
with acute than chronic renal failure.
furious form (2–4 days) where the cat may viciously
attack anything in sight. This may be accompanied by
excessive drooling secondary to dysphagia. Convulsions Diagnosis
may also occur. In the later stage (1–4 days) of the ill-
ness, the animal develops paralysis, coma and death. Other historical, clinical and laboratory abnormalities
consistent with severe renal failure and perhaps related
to the underlying cause (e.g. ethylene glycol intoxica-
Diagnosis tion) are present. There is no correlation between the
Any cat presented with an acute onset of aggression or degree of azotemia and the severity of the neurolog-
with unusually fractious behavior, should be considered ical signs.
as a rabies suspect and handled with caution.
The diagnosis is made on post-mortem tissue using
immunofluorescence antibody (IFA), ELISA and more
ENCEPHALOPATHY
recently polymerase chain reaction (PCR) testing.
Classical signs
The strain of rabies can be further diagnosed using
● Usually asymptomatic.
monoclonal antibody testing.
● Rarely, behavioral abnormalities.
Routine laboratory tests are unrewarding.
Clinical signs CSF analysis may reveal a mild non-specific

mononuclear pleocytosis (5–10/μl) with normal pro-
Subtle and non-specific changes in behavior includ- tein concentration. A positive antibody test on a CSF
ing depression, social withdrawal, compulsive roaming sample not contaminated with blood indicates CNS
and psychotic behavior have been attributed to FIV infection.
encephalopathy. Signs have mainly been observed in
the advanced stage of infection. Unrelated CNS pathologies and secondary opportunis-
tic infections (e.g. FIP, toxoplasmosis) would likely be
responsible for neurological signs other than behavioral
Diagnosis changes in FIV-positive cats.
Other systemic signs of FIV infection for example,
weight loss, fewer immunodeficiency-related infections
Treatment
of the skin, respiratory or gastrointestinal tracts should
have manifested by the time neurological signs develop. No effective treatment is known.
RECOMMENDED READING
Parent JM, Quesnel AD. Seizures in cats. Vet Clin North Am 1996; 26: 811–825.
Quesnel AD. Seizures. In: Ettinger JE, Feldman EC (eds) Textbook of Veterinary Internal Medicine – Diseases of
the Dog and Cat, 5th edn. Philadelphia, WB Saunders Co., 2000, pp. 148–152.
Quesnel AD, Parent JM. Diagnostic approach and medical treatment of seizure disorders. In: August T (ed)
Consultations in feline internal medicine 3. Philadelphia, WB Saunders Co., 1997, pp. 389–402.
Quesnel AD, Parent JM, McDonell W, Percy D, Lumsden JH. Diagnostic evaluation of cats with seizure disorders:
30 cases (1990–1993). J Am Vet Med Assoc 1997; 210: 65–71.
Quesnel AD, Parent JM, McDonell W. Clinical management and outcome of cats with seizure disorders: 30 cases
(1991–1993). J Am Vet Med Assoc 1997; 210: 72–77.
37. The cat with stupor or coma
Rodney S Bagley
KEY SIGNS
● Moderate to marked decrease in consciousness and wakefulness.
● Reduced or absent response to external stimuli.
MECHANISM?
● Stupor and coma result from diseases that alter consciousness and wakefulness.
WHERE?
● Disease of the intracranial nervous system including the supratentorial structures (cerebral
cortex, thalamus) and the brain stem (midbrain, pons or medulla oblongata) may result in
stupor or coma.
● Systemic (metabolic) disease may affect these areas secondarily and result in stupor or coma.
WHAT?
● Diseases of the intracranial nervous system resulting in coma include head trauma, brain
tumor, encephalitis, vascular-based diseases and severe hypoglycemia.
● Many of these diseases result in increased intracranial pressure that perpetuates the
clinical signs.
● These diseases are often severe.

Diseases causing stupor or coma
ANOMALY
● Hydrocephalus** (p 826)
If hydrocephalus is congenital, cats may have an enlarged, “dome-shaped” skull. A fontanelle that
persists during maturation may be palpable. Acquired hydrocephalus in adults will show no out-
ward anatomical signs. Clinical signs include seizures, poor learning ability, behavior changes,
paresis, cranial nerve deficits and changes in consciousness.
continued
821
continued
METABOLIC
● Metabolic encephalopathy* (p 830)
Metabolic encephalopathies secondary to hypoglycemia, hepatic or renal disease may be associated
with signs of cerebrocortical dysfunction including seizures, behavior abnormalities and limb dys-
function. Neurological signs tend to be symmetrical. Other signs of a polysystemic disease such as
vomiting and diarrhea may be present. Hypoglycemia results in a dazed cat with a drunken, wobbly
gait and muscle trembling, which may progress to seizures and coma if severe and untreated.
● Feline ischemic encephalopathy* (p 828)
Clinical signs begin acutely and rapidly evolve. Clinical signs usually include circling, blindness
and seizures.
NEOPLASTIC
● Brain tumor*** (p 824)
Tumors occur most often in older cats. Clinical signs may be acute in onset or slowly progressive.
Seizures, circling, paresis, head tilts and nystagmus are most common.
NUTRITIONAL
● Thiamine deficiency* (p 832)
Decreased thiamine can result in brain stem disease in cats. Clinical signs initially begin with
lethargy, inappetence and reluctance to walk. Later there is vestibular ataxia and episodes of spas-
tic ventroflexion of the neck or opisthotonus, dilated pupils, stupor and coma.
INFLAMMATORY (INFECTIOUS)
● Encephalitis* (p 829)
Clinical signs are often diffuse and may not localize to a single area within the nervous system.
Fever and leukocytosis are inconsistent findings. Systemic signs of disease such as fever, cough-
ing, vomiting and diarrhea may accompany the neurologic signs. Feline infectious peritonitis, tox-
oplasmosis and Cryptococcus are more common causes of encephalitis. The systemic signs are
consistent with the disease process.
TRAUMA
● Head trauma*** (p 823)
Usually associated with an acute onset of clinical signs reflective of an intracranial problem. Signs
present often include alterations in consciousness, paresis and cranial nerve abnormalities. Fresh
blood from lacerations on or around the head, skull fractures, blood in the ear canals, and scleral
hemorrhage may be clues to a previous traumatic incident.
TOXICITY
● Lead toxicity* (p 833)
Rare in cats because of eating behavior, but they may be exposed through aerosolized paint dust
during house renovations. Inappetence and weight loss are early signs. In addition to central nerv-
ous system signs of behavioral abnormalities and alterations in mentation, blindness, vomiting,
diarrhea and hematologic abnormalities may be found.
37 – THE CAT WITH STUPOR OR COMA 823
INTRODUCTION Classical signs—Cont’d

● Evidence of external trauma to the head
MECHANISM? and face such as facial lacerations,
bleeding from the nose and mouth,
Stupor and coma result from diseases that primarily bruising, retinal hemorrhage or
or secondarily affect the cerebral cortex and thala- hemorrhage in the external ear canals.
mus and/or the reticular activating system of the
brain stem responsible for consciousness and wake-
fulness. Pathogenesis
Systemic (metabolic) disease may affect these areas Traumatic injury to the brain occurs most commonly
indirectly and result in stupor or coma. from automobile trauma, although gunshot wounds and
falls may also occur.
All of these disease processes result in mechanical dis-
WHERE?
ruption of intracranial tissues (primary injury) such as
Disease of the intracranial nervous system including axonal shearing.
the supratentorial structures (cerebral cortex, thalamus)
Primary injuries to the brain may initiate a number of
and the brain stem (midbrain, pons or medulla oblon-
secondary pathophysiological sequelae such as meta-
gata) may result in stupor or coma.
bolic alterations in neuronal or glial cells, impairment
of vascular supply to normal tissue (ischemia), impair-
ment of cerebrovascular autoregulation, hemorrhage
WHAT?
(intraparenchymal, intraventricular, extradural or sub-
Diseases of the intracranial nervous system resulting in dural), irritation (seizure generation), obstruction of the
coma include head trauma, brain tumor, encephalitis ventricular system; edema formation, production of
and vascular-based diseases. physiologically active products, and finally, increased
intracranial pressure (ICP).
Many of these diseases result in increased intracranial
pressure that perpetuates the clinical signs. Hemorrhage, either within or around the brain, may
result in rapid cerebral dysfunction.
These diseases are often severe.
In an experimental study of blunt craniocerebral trauma
The most common metabolic diseases producing
in cats, all had some degree of subarachnoid hemor-
stupor or coma are hypoglycemia secondary to
rhage, and many had subdural hemorrhage. Fifteen per-
insulin overdose in a diabetic cat and hepatic ence-
cent of cats had subdural hematomas that displaced the
phalopathy secondary to a congenital portosystem-
corresponding cerebral hemisphere.
atic shunt.
● Many also had cortical contusion. Intraparenchymal
hemorrhage and petechiation were common, most
DISEASES CAUSING STUPOR often in the hemisphere directly receiving the blunt
OR COMA force.
● One-fifth of the cats had tentorial herniation.
HEAD TRAUMA***
Clinical signs
Classical signs
Signs usually begin acutely after trauma.
● Acute onset of signs including stupor,
coma, paresis, gait abnormalities and Intracranial signs most commonly seen include stupor
cranial nerve deficits, especially those and coma, paresis and gait abnormalities, and cranial
involving pupillary responses. nerve deficits, especially those involving pupillary
responses.
Evidence of external trauma to the head and face such Mannitol is used to decrease cerebral edema and ICP.
as facial lacerations, bleeding from the nose and mouth, Mannitol has been thought to decrease cerebral edema
bruising, or hemorrhage in the external ear canals may primarily through its associated osmotic effects,
be clues to the traumatic etiology. although other effects such as concurrent decreases in
blood viscosity and free-radical scavenging may, in
Diagnosis fact, be more beneficial. By decreasing blood viscosity,
cerebral perfusion will be increased at the same level of
The diagnosis of trauma is usually straightforward systemic blood pressure. Vasoconstriction will result,
when the trauma is witnessed. lowering cerebral blood volume and concurrently low-
In some instances, when animals are presented with an ering ICP. Mannitol is administered at 1 g/kg IV over
acute onset of neurological signs and an unknown his- 5–10 minutes. Maximal lowering of ICP most often
tory, examining for external signs of trauma such as occurs in 10–20 minutes.
lacerations or skull fractures is important. Furosemide (0.7 mg/kg IV) is a loop diuretic that may
Evaluating the retinas and external ear canals for help to lower ICP primarily or may potentiate the
acute hemorrhage may also provide clues to the diag- effects of mannitol. Furosemide given 15 minutes after
nosis. mannitol administration potentiates the intracranial
pressure-lowering effects of the latter.
Advanced imaging studies such as CT or MR imaging
are useful, primarily for determining structural damage The antioxidant drug, desferoxamine mesylate has
to the brain. been shown to reduce cold-induced brain edema in cats.
Surgical treatment centers on evacuation of sub-
Differential diagnosis dural hematomas, removal of depressed skull frac-
External evidence of a traumatic incident is helpful to tures, or debridement of damaged tissue and foreign
separate traumatic causes of stupor and coma from material.
● Craniectomy and durotomy has been shown to
other intracranial diseases.
lower ICP acutely by 15–65%, respectively, in cats,
Sometimes cats with intracranial disease are unbal- however, long-term benefits are uncertain.
anced, weak or have seizures and fall. This may result
in external injuries being misconstrued as the actual
cause of the intracranial signs. Prognosis
Prognosis for life is good if signs are not severe.
Treatment
Cerebrocortical and cerebellar injuries are more readily
Basic life support measures may be necessary includ- recoverable from than brain stem injuries.
ing blood or isotonic fluid administration.
Corticosteroid administration for treatment of head Prevention
trauma is commonly used but efficacy is often based
Keep cats in a controlled environment and prevent free-
upon anecdotal evidence. Beneficial effects of methyl-
roaming.
prednisolone sodium succinate (30 mg/kg IV slowly)
in nervous system injury include inhibition of lipid per-
oxidation and its associated detrimental effects. The BRAIN TUMOR***
role of corticosteroids in the treatment of head trauma,
however, is unclear and are currently not recommended Classical signs
in humans suffering from head trauma.
● Middle-aged to older cats.
Hyperventilation keeping PaCO2 concentrations ● Signs include seizures, circling, blindness,
between 28 and 32 mmHg can decrease ICP due to behavior changes, and may progress to
the established effects of PaCO2 concentrations on stupor and coma.
cerebral blood flow.
Pathogenesis Hyperostosis of the skull is occasionally present on

survey radiographs of the skull, especially with menin-
Neoplasia can arise from structures within or surround- giomas. A “sky-line” view may be necessary to image
ing the brain (primary brain tumors). this abnormality.
Neoplasia secondarily involves the brain via metasta- Diagnosis of a structural intracranial abnormality in the
sis or via direct extension from extraneural sites. brain is most readily accomplished with magnetic res-
Primary tumors within the skull, nasal cavity or onance (MR) imaging or computed tomography
frontal sinuses can extend directly into the brain. (CT) of the brain.
Meningioma is the most common brain tumor in ● A broad-based, extra-axial (arising outside and push-
cats. Meningiomas arise from the arachnoid layer of the ing into the parenchyma) contrast-enhancing mass
meninges. Meningiomas are usually histologically on CT or MR imaging is found in most instances of
benign, but occasionally are malignant. meningioma.
● The CT and MR appearance of gliomas is varied
Some younger cats with mucopolysaccharidosis have and enhancement after contrast administration may
a high incidence of meningiomas. not be present. As these tumors arise from brain
Gliomas arise from cells of the brain parenchyma. parenchymal cells, they are found within the neu-
These include astrocytes and oligdendrogliocytes. roaxis (intra-axial).
● Choroid plexus tumors, because of the increased
Choroid plexus tumors arise from areas where the concentration of blood vessels within the tumor,
choroid plexus is concentrated (the lateral, third and often enhance markedly after contrast adminis-
fourth ventricles). tration. Because of their association with the ven-
Signs reflect either primary nervous parenchymal dam- tricular system, associated hydrocephalus is
age from the tumor, or secondary pathophysiological common.
sequelae such as hemorrhage and edema. Frequently, Cerebrospinal fluid often contains elevations in pro-
these secondary sequelae are more devastating to tein content but this finding is not pathognomonic for
intracranial function than the primary disease itself. brain tumors.
● Cerebrospinal fluid can contain evidence of
inflammation (contains elevations in nucleated
Clinical signs cells and protein content). If CSF is the only assess-
Middle-aged to older cats are most commonly ment made, an erroneous diagnosis of encephalitis
affected. Cats are usually older than 5 years of age with may be made.
a median age of onset of clinical signs at 9 years of age. ● Cerebrospinal fluid collection may be associated
with an increased mortality in cats with space-
Clinical signs are often slowly progressive, however, occupying mass lesions within the intracranial
they can also occasionally begin acutely and be rapidly space, because of the sudden decrease in pressure at
progressive. the cisterna magna.
Signs reflect the intracranial location of the lesion.
● Signs include seizures, circling, blindness, behavior Differential diagnosis
changes, cranial nerve abnormalities, and may
progress to stupor and coma. Cats with intracranial tumors may present with signs
● If the brain stem is involved, head tilt, nystagmus
similar to other intracranial diseases.
and paresis are most common. There are no pathognomonic clinical signs for intracra-
nial tumor.
Congenital hydrocephalus may be associated with
Diagnosis
changes in the skull (“Dome-shaped” skull, persistent
Routine laboratory evaluations (CBC, biochemistry fontanelle), but these will not be present with acquired
profile) are not affected by intracranial neoplasia. hydrocephalus.
Feline ischemic encephalopathy is usually associated Pathogenesis

with an acute onset of clinical signs localizing to the
cerebral cortex. Hydrocephalus is the term commonly used to describe
a condition of abnormal dilation of the ventricular
Encephalitis may be associated with systemic diseases system within the brain.
causing chorioretinitis, fever and leukocytosis.
Hydrocephalus can result from obstruction of the ven-
tricular system, irritation of the ventricular lining (from
Treatment inflammation or hemorrhage), loss of brain parenchyma
Corticosteroids (prednisolone 1–2 mg/kg q 12 h) may (hydrocephalus ex vacuo), be present without an obvi-
reduce peritumoral edema and improve clinical signs. ous cause (congenital), or rarely, be the result of over-
production of CSF associated with a choroid plexus
Surgical removal of primary brain tumors may be tumor.
accomplished, especially with meningioma.
If the ventricular system is obstructed, CSF will be
A well-encapsulated, firm whitish mass is most often trapped behind the level of obstruction.
encountered at surgery in cats. Cortical parenchyma is
usually not infiltrated but rather compressed in cats, Anatomically smaller areas of the ventricular system
leaving indentations in the nervous tissue parenchyma are common sites of obstruction. These include the
after resection. interventricular foramen and the mesencephalic
aqueduct.
Radiation therapy at a total dose of 45–48 GY may
control tumor growth. Obstruction can result from tumor, granuloma, hem-
orrhage or inflammation.
● With infectious diseases that affect the ventricular
Prognosis system, the ependymal layer may be damaged pre-

disposing the underlying parenchyma to be pene-
Prognosis for life is good (22–27 months median sur- trated by the agent or associated products.
vival) after surgical removal of meningiomas in cats. ● An inflammatory reaction ensues, further damaging
Uncontrolled or untreated brain tumors usually result local tissues.

● The ependymal cells may be lost and replaced by
in death of the cat in less than 6 months, however,
the natural course of affected cats has not been accu- subependymal microgliacytes or astrocytes. The
rately determined. end stage is a granular ependymitis.
● Feline infectious peritonitis virus infection is a
common cause.
Prevention
In Siamese cats hereditary hydrocephalus in trans-
There is no known way to prevent these diseases. mitted as an autosomal recessive trait.
The cause of congenital hydrocephalus, however, is not
HYDROCEPHALUS** always apparent. Speculation suggests that this abnor-
mality may be due to an obstruction of the ventricu-
Classical signs lar system during a critical stage in development and
subsequent damage to the vulnerable maturing nervous
● Young cats may have a dome-shaped or parenchyma.
bossed appearance to the head or
persistent fontanelles. Feline cerebellar hypoplasia is caused by in utero infec-
● Other signs of hydrocephalus include tion with the panleukopenia virus (parvovirus), which
seizures, poor learning ability, behavior affects the external germinal layer of the cerebellum
changes, paresis, cranial nerve deficits and and prevents the formation of the granular layer. Some
changes in consciousness. affected cats have a concurrent hydrocephalus and
hydranencephaly.
Hydrocephalus can result in clinical signs due to loss Classically, slow-frequency, high-voltage (amplitude)
of neurons or neuronal function, alterations in activity is noted. This pattern, however, can be seen
intracranial pressure, or the associated pathophysio- with other encephalopathies that destroy cortical
logical effects of intracranial disease. parenchyma. Because of this, EEG is rarely used as the
sole means of diagnosing hydrocephalus.
Clinical signs Ultrasound can be used to diagnosis hydrocephalus.
● This is most readily accomplished when a fontanelle
In young cats prior to ossification of the cranial
is present providing an “acoustic window” as ultra-
sutures, hydrocephalus may contribute to abnormalities
sound waves do not usually penetrate the skull well
of skull development such as a thinning of the bone
enough.
structure, a dome-shaped or bossed appearance to the
● If the bone is intact, a craniotomy defect can be cre-
head or persistent fontanelles.
ated.
Clinical signs of hydrocephalus reflect the anatomical ● For imaging of the lateral and third ventricles, the
level of disease involvement. bregmatic fontanelle may be used.
● Often, ultrasound can be performed in awake cats
Supratentorial, vestibular and cerebellar signs are
as a screening test to determine ventriculomegaly.
most common.
● Depending upon the size of the fontanelle, the lat-
As the supratentorial structures are often involved with eral and third ventricles as well as the mesen-
hydrocephalus, alterations in awareness and cogni- cephalic aqueduct are usually easily identified.
tion are common.
Computed tomography (CT), as a non-invasive
Many animals affected congenitally may appear to be intracranial imaging modality, is often useful in defin-
less intelligent than normal. ing ventricular size.
Circling, paresis and seizure may also be seen. Magnetic resonance (MR) imaging also affords evalu-
ation of the ventricular system. This modality provides
Severity of clinical signs is not dependent upon the
better parenchyma resolution than CT, and is especially
degree of ventricular dilation, but rather on a host of
useful for evaluation of the infratentorial structures.
concurrent abnormalities including the underlying dis-
ease process, associated intracranial pressure changes, Diffuse ventricular enlargement suggests congenital
intraventricular hemorrhage, and the acuity of ventric- ventricular dilation or obstruction at the level of the lat-
ular obstruction. eral apertures or foramen magnum. Focal ventricular
enlargement suggests focal obstruction or parenchy-
mal cell loss.
Diagnosis
Animals with an asymmetric appearance of the ven-
Routine laboratory evaluations are normal.
tricles should be critically evaluated for focal obstruc-
Historical, invasive techniques for diagnosis of hydro- tion of or impingement on the ventricular system due to
cephalus such as pneumo- or contrast ventriculography mass effect.
have been replaced by non-invasive diagnostic modalities.
Survey radiographs may suggest the presence of hydro-
cephalus, however, are usually not helpful for definitive Congenital hydrocephalus may be associated with
diagnosis. Findings associated with congenital hydro- changes in the skull (“dome-shaped” skull, persistent
cephalus include loss of gyral striations, separation of fontenelle), but these will not be present with acquired
cranial sutures (diastasis), and persistent fontanelles. If hydrocephalus.
hydrocephalus is acquired after the skull has formed,
Cats with hydrocephlaus may present with signs
abnormalities are rarely encountered.
similar to other intracranial diseases. Rule out other
Electroencephalography has been used to diagnosis inflammatory, neoplastic and traumatic causes of
hydrocephalus, primarily prior to advanced imaging. intracranial disease.
There are no pathognomonic clinical signs for acquired Pathogenesis

hydrocephalus in adult animals.
Feline ischemic encephalopathy is an ischemic necro-
Correlation of degree of ventricular enlargement and sis of the cerebral hemisphere of cats.
clinical signs is poor.
The distribution of the vascular change is usually in the
area supplied by the middle cerebral artery.
Treatment
Vascular lesions, however, are infrequently found at
Medical treatment may include general supportive care, necropsy.
and medications to limit CSF production and reduce
intracranial pressure. Some authors have speculated that this disease is the
result of a Cuterebra migration.
Glucocorticoids are used to decrease CSF produc-
tion, thereby, limiting intracranial pressure and further One 7-year-old Siamese cat has been reported with an
neurologic injury. Prednisone at 0.25–0.5 mg/kg is intravascular malignant T-cell lymphoma occluding the
given orally twice daily. The dose is gradually reduced middle cerebral artery.
at weekly intervals to 0.1 mg/kg every other day. This
dose is continued for at least one month. Then the med-
ication is discontinued if possible. Clinical signs
Alternatively, dexamethasone may be given orally at Clinical signs begin acutely.

0.25 mg/kg every 6–8 hours. The dose can be gradually Signs often reflect a unilateral cerebrocortical abnor-
reduced over 2–4 weeks. mality.
Some animals can be adequately managed with long- Signs include seizures, circling, blindness, behavior
term glucocorticoid administration at low doses. changes and may progress to stupor and coma.
If no clinical benefits are observed within 2 weeks, or
if side effects develop, other forms of therapy should be
tried. Diagnosis
Surgical procedures where a shunt is placed in the Routine laboratory evaluations are normal.
ventricle are designed to provide controlled CSF flow Cerebrospinal fluid often contains elevations in pro-
from the ventricles of the brain to the peritoneal cavity. tein content but this finding is not pathognomonic for
Commercial pediatric ventriculoperitoneal shunts are this disease.
available for thus purpose.
CSF may contain mild increases in nucleated cells
Prognosis (usually < 10 cells/μl). Neurophils, macrophages and
mononuclear cells are possible.
Generally poor unless definitive surgical correction is
successful. In some cats, clinical signs can be managed Diagnosis of a structural intracranial abnormality in the
on a long-term basis with medication therapy alone. cerebral hemisphere is most readily accomplished with
magnetic resonance imaging of the brain. Minimal
changes, however, may be seen on MR studies with this
FELINE ISCHEMIC ENCEPHALOPATHY* disease.
Classical signs Cerebral angiography would theoretically aid in the

diagnosis of this disease, but is rarely performed.
● Signs occur acutely and reflect a unilateral
cerebrocortical abnormality.
● Signs include seizures, circling, blindness, Differential diagnosis
behavior changes and may progress
rapidly to stupor and coma. Rule out brain tumor, encephalitis, head trauma and
hydrocephalus.
Treatment Clinical signs are often diffuse or multifocal and may

not localize to a single area within the nervous system.
No treatment has been shown to be effective. Clinical signs often reflect multiple levels of neurolog-
ical involvement
Prognosis Cervical pain can be present.
Prognosis for life is good after the first 48 hours as Fever is an inconsistent finding.
this is a non-progressive disorder.
Fundic examination is important to look for clues of
Residual neurologic deficits, most notably seizures, systemic inflammatory disease, as chorioretinitis is
may persist throughout life. Behavioral changes, such often present.
as aggression or irritability may persist and make the
cat less acceptable as a pet. Other signs of a polysystemic disease process such as
inappetence, weight loss, nasal discharge, coughing,
vomiting, and diarrhea may be associated.
Prevention
None.
Diagnosis
Complete blood cell count may show evidence of sys-
ENCEPHALITIS*
temic inflammation (e.g. leukocytosis).
Classical signs Serum biochemical analysis may show evidence of
systemic abnormalities if the disease diffusely affects
● Neurological signs are often diffuse or
the body (e.g. vasculitis) such as elevated globulin, CK,
multifocal.
liver enzymes or creatinine.
● Cervical pain can be present.
● Fever is an inconsistent finding. Evaluation of titers for the infectious diseases often
● Chorioretinitis is often present on fundic helps to rule in or out the diseases.
examination.
Cerebrospinal fluid analysis (CSF) will usually show
● Other signs of polysystemic disease such
evidence of increased nucleated cells and/or elevated
as coughing, vomiting and diarrhea may be
protein content. Occasionally, CSF will be normal.
associated.
● Evidence of inflammation on CSF evaluation alone,
however, is not specific for primary encephalitis as
other CNS disease (e.g. neoplasia) may result in
With Tremor or Twitching).
a CSF pleocytosis and protein increases.
● With feline infectious peritonitis (FIP), cere-
Clinical signs brospinal fluid analysis may show a pleocytosis,
with either mononuclear or non-lytic neutrophils
Numerous infectious agents have been incriminated,
as the predominant cell type and elevated protein
with the incidence of infectious agents causing menin-
concentration, often > 1 g/L (0.1 g/dl).
gitis varying with geographic location. Systemic signs
● With toxoplasmosis, cerebrospinal fluid frequently
reflect the specific agent.
contains a pleocytosis, usually with mononuclear
● Infectious agents causing brain disease include
cells, and occasionally, eosinophils. Increasing IgG
viral (feline infectious peritonitis), fungal
or a single positive IgM serum antibody titer is sug-
(cryptococcosis, blastomycosis, histoplasmosis,
gestive of active infection. Animals with neuro-
coccidioidomycosis, aspergillosis), protozoal
logic signs and positive IgM titers warrant
(toxoplasmosis, neosporosis), bacterial, rick-
treatment for the disease.
ettsial, and unclassified organisms (protothecosis).
● Involvement of the intracranial nervous system can With cryptococcosis, identification of the organism
occur with parasites such as Cuterebra larvae, from cytological evaluation of samples such as CSF,
toxocara, and aberrant heartworm migration. nasal discharge, and skin lesions supports the diagnosis.
A neurophilic pleocytosis, and occasionally an With feline infectious peritonitis (FIP), no specific
eosinophilic pleocytosis may be found on CSF analysis. treatment is effective. Immunosuppressive therapy may
If positive, detection of the cryptococcal capsular anti- result in short-term improvement of clinical signs.
gen in serum is usually diagnostic. Tissue biopsy and
With toxoplasmosis, treatment includes clindamycin
fungal culture or fungal culture of CSF may be more
and trimethoprim sulfa antibiotics.
definitive in the diagnosis as occasionally the serum titer
is negative. For cryptococcosis, treatments that have had some suc-
cess for cryptococcosis in cats include amphotericin B,
With parasites such as Cuterebra larvae, toxocara and
fluconazole, itraconazole, and flucytosine. See page 26
aberrant heartworm migration, CSF may show inflam-
(The Cat With Signs of Chronic Nasal Disease for
mation with eosinophils is some instances.
treatment details).
Imaging studies (CT and MR) are helpful for defining
With CNS parasites, treatment has not been attempted
structural lesions. Multifocal, contrast-enhancing
uniformly and treatment recommendations are anec-
lesions are usually seen. Occasionally, non-contrast-
dotal.
enhancing lesions are present, especially with toxoplas-
mosis.
Prognosis
Many of the encephalities are poorly responsive to treat-
Differential diagnosis ment, and therefore morbidity and mortality is > 50%.
Multifocal signs are more suggestive of encephalitis. Some infectious encephalities (e.g. toxoplasmosis)
Cats with encephalitis may present with signs similar to may be cured with appropriate treatment.
other intracranial diseases such as brain tumor, trauma,
hydrocephalus and cerebrovascular disease. METABOLIC ENCEPHALOPATHY*
Classical signs
Treatment
● Hepatic encephalopathy usually occurs in
Treatment is directed at a specific infectious cause if younger cats. Clinical signs include
found. seizures, ptyalism and mentation changes.
Without a definable cause of the encephalitis, the author ● Cats with diabetic ketoacidosis may have
uses trimethoprim-sulfadiazine (30 mg/kg PO q 12 h), cerebral signs (depression).
clindamycin (25 mg/kg q 12 h), and corticosteroids ● Cats with hypoglycemia may show
(prednisone 1–2 mg/kg PO q 12 h) in combination. depression, seizures and tremors.
While corticosteroids are contraindicated with infec-

Pathogenesis
tious diseases, they are often beneficial in the acute
treatment of brain inflammation and edema. These Various metabolic imbalances within the body may
associated pathophysiological events often lead to more produce physiologic alterations, toxins or by-products
neurologic deterioration than the organism itself. that effect nervous system functions.
If rickettsial diseases are endemic, chloramphenicol or Hepatic encephalopathy (HE) results when numerous
doxocycline can be substituted or added to the regime. putative neurotoxins reach the brain unmetabolized as
they pass through an abnormally functioning liver or
If the animal is receiving phenobarbital, do not use
bypass hepatic detoxification.
chloramphenicol as this drug will decrease the metab-
olism of the barbiturate and the animal will become Younger animals with HE usually have congenital por-
comatose and possible die. Also, chloramphenicol may tosystemic shunts, however, some animals do not have
result in bone-marrow suppression in cats. clinical signs of this disease until later into adulthood.
Hepatic encephalopathy in older animals can be associ- ● Weakness and seizures are most common. Affected
ated with liver failure such as with cirrhosis. animals may be depressed, and have intermittent
twitches or tremors.
Hypoglycemia can occur secondary to some endocrine
disorders such as hypoadrenocorticism and insulinoma Clinical signs of hypernatremia include adipsia, depres-
or from lack of production by the liver in young kittens sion, seizures progressing to stupor and coma.
or in cats with liver failure, and some tumors. However,
Uremic encephalopathy may result in depression, stu-
it is most common following overdose of insulin in
por, myoclonic movements, generalized weakness and
diabetic cats.
partial or generalized seizures.
Because the central nervous system (CNS) requires
a constant supply of glucose, clinical signs of hypo-
Diagnosis
glycemia relate to CNS dysfunction and activation of
the sympathetic nervous system and include depres- Diagnosis of metabolic encehalopathy is suggested by
sion, seizures and tremors. metabolic abnormalities on routine physical examina-
tion or laboratory evaluations (CBC, serum biochemi-
Cats with diabetic ketoacidosis may have cerebral
cal analysis, urinalysis).
signs (depression), but whether these changes relate to
the hyperglycemia or other physiologic derangements Diagnosis of hepatic encephalopathy is supported by
such as hyperosmolality is unknown. abnormal liver function studies such as elevated pre-
or post-prandial bile acids or elevated fasting ammo-
Hypernatremia can result in abnormal mentation pro-
nia. Ammonia chloride challenge is rarely required in
gressing to stupor and coma.
cats to make a diagnosis.
● Hypernatremia usually results from inadequate
● Abdominal ultrasound may show abnormal liver
drinking. This may occur due to alterations in
vasculature.
awareness of thirst or inability to physically move
● Portal vein angiography or direct visualization at
to water.
surgery may be needed for accurate diagnosis.
● Idiopathic adipsia can occur, usually in younger
cats. Diagnosis of hypoglycemia is based upon finding
hypoglycemia (blood glucose < 3.3 mmol/l: 60 mg/dl)
Hypernatremia and adipsia in an older animal should
in the face of clinical signs.
warrant an evaluation for structural intracranial disease
● Concurrent measurement of serum insulin concen-
such as hydrocephalus and brain tumor.
tration will help identify an insulin-secreting
Renal failure and pancreatitis may affect cerebral func- tumor, by demonstrating inappropriately high
tion if severe, producing depression, stupor, tetany or insulin concentration in the presence of hypoglycemia.
seizures. Non-beta cell tumors producing hypoglycemia have
low to undetectable insulin concentration during
hypoglycemia.
● Insulin-treated diabetic cats with clinical hypo-
Clinical signs
glycemia need re-evaluation. Some cats will be in
Neurologic signs often include seizure, alterations in diabetic remission and do not need insulin. Other
mentation, behavior abnormalities and paresis. cats have accidentally received a higher than nor-
mal dose. This may occur when insulin syringes are
Neurologic signs are often symmetrical and may be
changed from U100 to U40 or from 0.5 ml to 1 ml
episodic.
syringes. Accidental overdose may also occur when
Clinical signs of hepatic encephalopathy include someone other than the owner gives the insulin.
seizures, ptyalism and mentation changes. Careful history taking will identify these problems.
In hypoglycemia, clinical signs occur due to decreased Diagnosis of hypernatremia is based upon finding
CNS glucose supply (neuroglycopenic signs) or elevated serum sodium (> 165 mmol/l: 165 mEq/l) in
because of sympathetic nervous system activity. the face of clinical signs.
● Diagnosis of a structural intracranial abnormality in (1/2–2 ml IV, 20–50% dextrose) to effect. The insulin
the hypothalamus or pituitary region is most readily dose should be decreased by 50% or stopped if the cat
accomplished with computed tomography or mag- is in remission. Accidental causes of overdose should
netic resonance imaging of the brain. be resolved.
Cats with hypoglycemia associated with neoplasia,
Differential diagnosis including insulinoma should be managed with fre-
quent feeding and corticosteroids (0.5–6 mg/kg/day in
Rule out other inflammatory, neoplastic and traumatic
divided doses) to antagonize insulin action. See page
causes of intracranial disease.
962 (The Cat With Generalized Weakness) for further
treatment details. Surgical removal of a pancreatic
Treatment insulin-secreting tumor may normalize serum glucose
concentrations.
Treatments should be directed at the underlying meta-
bolic abnormality. Treatment for hypernatremia centers on slowly
decreasing serum sodium through fluid administra-
Medical treatment of hepatic encephalopathy cen-
tion. This is most safely accomplished with oral
ters on frequent small meals of a low-protein diet,
administration of water. If the hypernatremia has
antibiotics (metronidazole 7.5 mg/kg PO q 12 h and
evolved slowly, extreme caution should be exercised
neomycin sulfate 20 mg/kg PO q 8–12 h), l-carnitine
when attempting to decrease serum sodium with fluid
(250–500 mg/cat/day PO as aqueous solution), tau-
therapy. As a rule, slowly decreasing serum sodium
rine (250–500 mg/cat/day in food), arginine (250 mg
concentrations (over 2–3 days) is safe, however,
q 12 h in food), vitamins B, Kl and E and lactulose
serum sodium should be measured frequently to avoid
(1–3 ml/cat PO q 8–12 h to produce a soft stool,
rapid decreases in sodium which can result in life-
beginning at the lowest dose and increasing as neces-
threatening cerebral edema. Do not decrease serum
sary). If the cat is severely depressed, lactulose should
sodium by more than 0.5 mmol (mEq)/L/h (12
be given as a retention enema for the first 1–2 days. A
mmol/L/day) if the hypernatremia is chronic.
solution of three parts lactulose to seven parts water is
dosed at 18 ml/kg q 4–6 h. The solution is instilled via If metabolic encephalopathy results in cerebral edema,
a Foley catheter as cranially in the colon as possible. mannitol (1 g/kg IV bolus) and furosemide (0.7 mg/kg
The solution must be aspirated after 15–20 minutes. IV) can be given provided the cat is not dehydrated.
Fluid and electrolyte status should be monitored care- Indications for therapy are severe signs or lack of
fully to avoid dehydration and hypernatremia. improvement after 4–6 hours of appropriate medical
Benzodiazepine receptor antagonists (e.g. flumazenil) treatment.
may be useful in cats with severe encephalopathy, but
are unproven. Prognosis
If the clinical signs of hepatic encephalopathy are Prognosis depends upon the ability to treat the underly-
severe, or do not improve within 4–6 hours after insti- ing disease process.
tution of medical treatment, and if the animal is not
dehydrated, mannitol (1–2 g/kg IV) followed by
THIAMINE DEFICIENCY*
furosemide (0.7 mg/kg IV) can be administered as
a treatment for possible secondary cerebral edema.
Classical signs
Surgical correction of a congenital portosystemic shunt
● Initially, lethargy, inappetence and ataxia.
may result in a permanent cure.
● Later signs include weakness, ventral
Diabetic cats with marked signs of hypoglycemia flexion of the neck, dilated pupils, stupor,
should be treated initially at home with honey or and coma.
a sugar-solution designed for human diabetics
poured on the owner’s finger and rubbed on the cat’s See main reference on page 848 for details (The Cat
buccal mucosa. In hospital, treatment is with dextrose With a Head Tilt, Vestibular Ataxia or Nystagmus).
Pathogenesis Dysautonomia is a consideration in countries where it

occurs. The bilateral non-responsive pupils and ven-
Occurs in anorexic cats or cats that are fed all-fish troflexion of the neck may appear similar to thiamine
diets containing thiaminase. deficiency, but there is no response to thiamine.
This deficiency results in polioencephalomalacia of the Hypokalemic myopathy, myasthenia gravis, poly-
oculomotor and vestibular nuclei, the caudal colliculus myositis and organophosphate toxicity can all cause
and the lateral geniculate body. ventral flexion of the neck. However, ventral neck
flexion in thiamine deficiency is the result of active
Clinical signs muscle contraction associated with increased muscle
Early non-specific signs are typically lethargy and tone rather than passive ventroflexion from weakness.
inappetence. Thiamine deficiency responds to thiamine supplemen-
tation unless in terminal stages.
The earliest localizing sign is bilateral vestibular
ataxia, which appears as an abnormal broad-based
Treatment
stance, loss of balance and vertigo.
Treatment is administration of thiamine dosed typi-
There is weakness and an inability or reluctance to
cally at 5–30 mg/cat/day per os. Maximum dose up to
walk. The cat sits crouched with ventral flexion of
50 mg/cat/day.
the neck.
Severely affected cats should receive at least 1 mg par-
Pupils are dilated and non-responsive or poorly
enterally.
responsive to light reflexes.
Change the diet to one with adequate thiamine and sup-
If untreated, signs progress to semi-coma, persistent
plement with thiamine for at least a week.
vocalization, opisthotonus and death.
Episodes of spastic opisthotonus or ventroflexion of Prognosis
the neck and generalized muscle spasm may occur
especially when the cat is lifted or stressed. They may Mildly affected cats usually recover rapidly following
be interpreted as seizures, but true seizure activity administration of thiamine.
rarely occurs. Cats that have progressed to a comatose state have
a poor prognosis.
Diagnosis
No antemortem diagnostic test is available. LEAD TOXICITY*
Diagnosis is based on clinical signs and rapid
Classical signs
response to thiamine.
● Rare in cats compared to dogs.
Differential diagnosis ● Nervous system signs include mentation
changes, seizures, ataxia, blindness.
Other encephalopathies and encephalitis are differen-
● Gastrointestinal signs and hematologic
tiated on history, CSF findings and lack of response to
abnormalities may accompany the CNS
thiamine.
signs.
Head trauma may appear similar to late signs of thi-
amine deficiency, but can usually be differentiated on
Pathogenesis
history and evidence of trauma. Thiamine-deficient
cats are lethargic and inappetant days and weeks before Lead toxicity usually results from ingestion of lead-
signs are severe. containing products.
Hydrocephalus can present with central blindness and Removal of lead-containing paint via sanding may
ataxia, but there is no response to thiamine. allow for lead-laden dust to be produced. If this dust
contaminates the cat’s fur or adheres to the feet, enough Differential diagnosis
lead may be ingested during normal grooming to cause
toxicity. Rule out other encephalopathies, encephalitis, head
trauma, hydrocephalus and tumor.
Clinical signs
Treatment
Early signs are lethargy, inappetence and weight loss.
Chelation therapy with calcium EDTA (25 mg/kg SC,
Gastrointestinal signs (vomiting, diarrhea) and hema- IM or IV q 6 h for 2–5 days) or penicillamine (10–15
tologic abnormalities (obvious basophilic stippling or mg/kg PO q 12 h) may be necessary to improve clinical
nucleated red cells occur in less than 50% of cats with signs.
lead poisoning) may accompany the CNS signs.
Nervous system signs include depression, behavioral Prognosis
changes, tremors, seizures, ataxia, blindness and weight
loss. Variable depending upon the degree of toxicity.
Diagnosis Prevention
Increased lead levels in the cat’s blood best supports Prevent exposure to the toxin.
a diagnosis.
RECOMMENDED READING
Braund KG. Clinical Syndromes in Veterinary Neurology, 2nd edn. St. Louis, Mosby, 1994.
Bunch SE. Acute hepatic disorders and systematic disorders that involve the liver. In: Textbook of Veterinary Internal
Medicine, 5th edn. WB Saunders, Philadelphia, 2000, pp. 1326–1340.
Chrisman CL. Problems in Small Animal Neurology, 2nd edn. Philadelphia, Lea & Fabiger. 1991.
deLahunta A. Veterinary Neuroanatomy and Clinical Neurology, 2nd edn. Philadelphia, WB Saunders, 1983.
Greene CE (ed) Infectious Diseases of the Dog and Cat, 2nd edn. Philadelphia, WB Saunders, 1998.
Oliver JE, Hoerlein BF, Mayhew IG. Veterinary Neurology. Philadelphia, WB Saunders, 1987.
Oliver JE Jr, Lorenz MD. Handbook of Veterinary Neurologic Diagnosis. Philadelphia, WB Saunders, 1993.
Wheeler SJ. Manual of Small Animal Neurology. West Sussex, British Small Animal Veterinary Association, 1989.
38. The cat with a head tilt, vestibular
ataxia or nystagmus
Joane M Parent
KEY SIGNS
● Cat leans, drifts, falls or rolls to the side of the head tilt.
● Rapid eyeball movement, either horizontally, vertically or rotatory.
● Reluctance to walk, crouched stance, exaggerated swaying of head, poor to
absent normal nystagmus.
MECHANISM?
● Any disease affecting the vestibular system, peripherally or centrally, results in a head tilt that
may or may not be associated with vestibular ataxia and nystagmus.
● Pendular (described as oscillatory) nystagmus is not vestibular in origin. It is the result of a
defect in the visual pathways. It is always congenital.
WHERE?
● The vestibular system is affected either peripherally, in the inner ear within the petrosal bone,
or centrally, within the cranial vault, in the brainstem, at the level of the rostral medulla.
WHAT?
● The diseases of the peripheral vestibular apparatus are the most common. They include idio-
pathic vestibular disease and otitis media-interna.
● Involvement of the central vestibular system occurs less frequently. The meningoen-
cephalomyelitides, including principally feline infectious peritonitis and fungal conditions, are
the most common causes.

Diseases causing head tilt, vestibular ataxia or nystagmus
ANOMALY
● Congenital vestibular disease (p 848)
Varying degrees of head tilt, falling and rolling are present from birth. Reported in Siamese and
Burmese kittens.
continued
835
continued
● Congenital pendular nystagmus (p 848)

Nystagmus is due to a congenital defect in the visual pathways observed mainly in Siamese and
Himalayan cats. Nystagmus persists for life and is oscillatory in character.
NEOPLASTIC
Chronic and progressive onset of a head tilt. The head tilt may be associated with facial nerve
paralysis, decreased lacrimation and/or Horner’s syndrome if the tumor is invading the tympanic
bulla (squamous cell carcinoma is the most common tumor of the middle ear), or with somno-
lence, +/− ipsilateral proprioceptive deficits, +/− trigeminal and facial nerve deficits may occur if
the tumor is intracranial at the level of the brainstem.
NUTRITIONAL
● Thiamine deficiency (p 848)
Acute onset of bilateral central vestibular signs (lethargy, pupillary dilatation, poor to absent physi-
ological nystagmus, reluctance to move, and side-to-side exaggerated head movements), in cats fed
a fish-based diet containing thiaminase or pet mince containing the preservative sulfur dioxide.
Signs may also occur following a period of anorexia. A characteristic posture with ventro-flexion
of the neck is present.
INFLAMMATORY (INFECTIOUS)
● Otitis media-interna (p 840)
Ipsilateral head tilt, with or without nystagmus, and with varying degrees of ataxia. Unilateral
deafness may result. Neurological structures in the middle ear may also be affected leading to an
ipsilateral facial paresis/paralysis, decreased lacrimation and/or a Horner’s syndrome. Signs may
appear 48–72 hours after an ear flush. Very rarely extension of the infection to the central nervous
system occurs.
● Feline infectious peritonitis (FIP) (p 844)
History of chronic illness (fever, inappetence, weight loss, lethargy) that has been unresponsive to
antibiotics. Ocular lesions may be present. The neurological disease is variable and depends on the
location and extent of the central nervous system lesion. Seizures, changed behavior and head
tremor are common. If head tilt is present it is always associated with somnolence, with or without
cerebellar signs.
Head tilt and altered mental status are associated with systemic manifestations such as anorexia,
upper respiratory tract disease or skin disease. Chorioretinitis and optic neuritis often observed.
The neurological disease is variable and depends on the location and extent of the central nervous
system lesion.
INFLAMMATORY (NON-INFECTIOUS)
● Middle ear polyps (p 842)
Chronic, progressive onset of a head tilt, facial paresis/paralysis, decreased lacrimation, Horner’s
syndrome and unilateral deafness. Polyps can occur bilaterally. Upper respiratory signs may be
present. A mass may be visualized in the external ear canal or the oropharynx.
38 – THE CAT WITH A HEAD TILT, VESTIBULAR ATAXIA OR NYSTAGMUS 837
IDIOPATHIC
● Idiopathic vestibular syndrome (p 839)
Acute to peracute non-progressive onset of a head tilt with ipsilateral falling or rolling in an other-
wise healthy cat. The disorientation may be severe. If the disease is bilateral, the head tilt is not
evident, the physiological nystagmus is poor to absent, and the cat moves in a crouched posture,
low to the ground. The head swings from side to side in exaggerated motions.
IATROGENIC
● Aminoglycosides (p 849)
Acute onset of peripheral vestibular signs uni- or bilaterally following systemic or topical therapy
with aminoglycosides. Deafness may accompany the vestibular signs.
● Ear flush (p 846)
Peripheral vestibular signs that appear immediately or in the 72 hours following an ear flush.
TOXIC
● Blue-tailed lizard ingestion (p 848)
In southeastern United States, ingestion of a blue-tailed lizard is thought to be the cause of an
acute unilateral peripheral vestibular syndrome.
TRAUMA
● Fracture of the petrous temporal bone or tympanic bulla, and ethmoid fracture
(base of the skull) (p 848)
Peripheral and central vestibular signs following a road accident.
exaggerated motions of the head and neck and the

INTRODUCTION cat moves in a crouched posture close to the ground.
Physiological nystagmus is poor to absent. In these
MECHANISM? instances, a head tilt may not be present, or if present,
is subtle on the most affected side.
The presence of a head tilt, ipsilateral to the lesion, is
Circling is not a feature of vestibular disease but is
the salient feature of vestibular disease. Nystagmus
frequent with thalamic and cerebral diseases.
and/or vestibular ataxia may accompany the head
tilt. The more acute the disease process, the more likely The most important diagnostic step is to differenti-
that nystagmus and ataxia are present. In vestibular ate if the disease involves the peripheral OR the cen-
ataxia, the animal leans, drifts, falls or rolls toward the tral portion of the vestibular system.
side of the lesion. The nystagmus can be resting or
Peripheral vestibular disease:
positional (induced by holding the head in full exten-
● The head tilt is toward the side of the lesion. The
sion), and, vertical, horizontal or rotatory in direction.
nystagmus is horizontal or rotatory but never verti-
The direction may change in time. Pendular nystag-
cal, and never changes in direction. The ataxia, if
mus (oscillatory with rapid, short excursions) is not
present, is on the side of the head tilt.
a sign of vestibular disease.
● By close proximity, the neurological structures
Occasionally, there is bilateral vestibular disease. The associated with the middle ear may be affected
animal may be reluctant to move because of severe dis- leading to facial nerve paresis/paralysis, dry eye
orientation. If able to walk, there are characteristic from decreased to absent lacrimation, and/or
Horner’s syndrome, partial or complete. The postural reaction deficits ipsilateral to the lesion but
cochlear part of the vestibulo-cochlear nerve may contralateral to the head tilt.
be affected leading to ipsilateral deafness.
● If the disease is bilateral, there is no head tilt or
only a mild one on the side that is the most
WHERE?
severely affected. The more acute the disease, the
more severe the disorientation. The cat is reluc- Peripheral vestibular disease results from a problem
tant to walk and has a crouched posture, low to in the petrosal bone or tympanic bulla.
the ground. The head characteristically moves ● The peripheral part of the vestibular apparatus
from side to side in exaggerated motions and (receptors and nerve) is situated in the inner ear,
there is often ventroflexion of the head and neck. in close proximity to the middle ear. The inner and
The physiological nystagmus (normal involuntary middle ear are located within the petrosal bone or
rhythmic typewriter-like movements of the eyes tympanic bulla. The facial nerve, the parasympa-
initiated by side-to-side movements of the head) thetic innervation of the lacrimal glands and
is poor to absent. the sympathetic nerve for pupillary dilatation
are the neurological structures associated with the
Central vestibular disease:
middle ear.
● The most consistent feature indicating central
● Diseases of the inner ear can by extension reach the
vestibular disease is the concomitant presence
middle ear and vice versa.
of somnolence, or quietness of the animal. This
● The neurologic structures of the middle ear are
may or may not be obvious at time of exami-
more resilient to insult than the receptors in the
nation, but will be evident with good history
inner ear (receptors vs axons). As a result, middle
taking.
ear disease may be present without neurological
● The head tilt is toward the side of the lesion. The
deficits. With time, facial paresis/paralysis and/or
nystagmus is horizontal, rotatory or vertical and
Horner’s syndrome may appear.
may change in direction.
● The auditory receptors are situated in the inner
● Due to their close proximity, other central nerv-
ear as well. Unilateral deafness goes unnoticed
ous system structures may be involved ipsilater-
clinically but is diagnosed with electrodiagnostic
ally. These include the ascending reticular
testing (brain auditory-evoked potentials).
activating system or ARAS (somnolence) and the
ipsilateral trigeminal nerve (loss of facial sensation Central vestibular disease results from an intracranial
and/or masticatory muscle atrophy), abducent nerve problem in the brainstem, at the level of the rostral
(strabismus), facial nerve (facial paresis/paraly- medulla. This area is in close proximity to the cerebel-
sis), cerebellum (tremors, hypermetria), ascend- lum and pons. This anatomical location is called the
ing sensory pathways (proprioceptive deficits) and cerebello-ponto-medullary angle.
descending motor pathways (upper motor neuron
weakness).
WHAT?
● Bilateral involvement of the central vestibular
system appears clinically similar to bilateral The most common causes of vestibular disease are
peripheral vestibular disorders in the early phase, peripheral and include:
except that the animal is more quiet or somnolent. ● Idiopathic vestibular disease.
If the cause is not corrected, involvement of other ● Otitis media-interna.
structures of the brainstem and/or cerebellum ● Less common causes are the middle ear polyps and
ensues. tumors.
Paradoxical vestibular syndrome. Central vestibular diseases are not as frequent as
● In this rare syndrome of central vestibular disease, peripheral diseases.
the head tilt is contralateral to the lesion. The diag- ● Inflammatory diseases are the most common, with
nosis is made on the presence of cerebellar signs or the clinical signs directly related to the location and
severity of the inflammation. Although inflamma-

tory diseases are multifocal or diffuse pathologi- DISEASES CAUSING A HEAD TILT,
cally, this is often not the case clinically, where the VESTIBULAR ATAXIA OR
neurological deficits in most cases can be assigned NYSTAGMUS
to one location.
Diagnosis is based on careful history taking (to dis- IDIOPATHIC VESTIBULAR SYNDROME***
close if there is somnolence or quietness of the ani-
mal), physical, neurological, otoscopic and Classical signs
ophthalmoscopic (including Schirmer tear test) ● Acute to subacute onset of a head tilt,
examinations, serum protein concentration, cere- falling, rolling and nystagmus.
brospinal fluid analysis (CSF), CSF anti-coronavirus ● Disorientation can be severe with the cat
IgG titer, electrodiagnostic testing (brain auditory- unwilling to move and crying out with
evoked responses), bullae radiography, computed anxiety.
tomography (CT) and magnetic resonance imaging ● Otherwise healthy cat.
(MRI) scan.
Reference ranges for feline CSF. Pathogenesis
● RBC < 0.030 × 109/L (30/μl)
● WBC ≤ 0.002 × 109/L (2/μl) Unknown.
● Cytology (%)
– Monocytoid cells 69–100% Clinical signs
– Lymphocytes 0–27% Possibly higher incidence in July and August in north-
– Neutrophils 0–9% east United States.
– Eosinophils 0
– Macrophages (large foamy mononuclear cells) Cats of any age or sex, median age is 4 years old.
0–3% Acute, non-progressive, unilateral and occasionally
● Protein 0.036 g/L (36 mg/dl)
bilateral, peripheral vestibular disturbance.
It is good practice to request electrodiagnostic testing The head tilt, ataxia and nystagmus (most often hori-
(BAER) to evaluate for deafness. If deafness is con- zontal) can be severe with the animal crying out with
comitantly present, it is an indication of a more aggres- anxiety, reluctant to walk, remaining in a crouched pos-
sive disorder and a thorough diagnostic work up should ture or with wide abduction of the limbs.
be pursued.
Rarely, can be bilateral.
When a head tilt is present, or when there is facial
Vomiting occasionally occurs, usually soon after onset
paresis/paralysis or a Horner’s syndrome, bulla radi-
of signs.
ography is recommended to evaluate the middle
ear cavities. An open mouth view is best to compare Affected cats are otherwise healthy.
the density between the bullae. Bulla radiography is
not a sensitive tool. It may be normal despite the pres- Diagnosis
ence of disease. Computed tomography (CT) scan of
History of an acute to subacute onset, in a previously
the bullae is superior and should be done when avail-
healthy cat, of severe disorientation, falling and rolling,
able.
that improves rapidly (a few days to 2 weeks) and with-
Regardless of the cause of the vestibular signs, nystag- out treatment.
mus and vestibular ataxia usually resolve, but the head
The cat is otherwise healthy and has no other neurolog-
tilt usually persists for the life of the animal. It may
ical signs.
be barely noticeable but may be exacerbated after
a general anesthetic or when the cat is ill. The otoscopic examination is unremarkable.
Diagnosis is usually by exclusion of other diseases Prognosis

causing similar acute signs.
Excellent.
With currently available diagnostic techniques it may
not be possible initially to differentiate this syndrome Rapid improvement of the clinical signs within the first
from otitis media-interna, but the vestibular signs in 2 weeks in all cats.
otitis media-interna do not usually occur so acutely Most cats recover entirely but frequently have a mild
and severely. residual head tilt.
It is advisable to perform BAERs. If there is concomi-
tant deafness, the idiopathic syndrome is ruled out as OTITIS MEDIA-INTERNA***
only the vestibular system should be affected.
Classical signs
● Acute to chronic history.
Otitis media-interna usually has a more progressive ● Variable degree of peripheral vestibular
history. On otoscopic examination there may be otitis disturbance.
externa, mite infestation and/or a ruptured tympanic ● Signs of otitis externa often present.
membrane. Signs of middle ear disease such as facial ● Facial paresis/paralysis, decreased
paresis/paralysis, decreased lacrimation and/or lacrimation and/or Horner’s syndrome
Horner’s syndrome are often present. Radiographic often present.
changes in the tympanic bulla are rarely observed.
Computed tomography and MRI scans are more sensi-
tive for detecting changes. Pathogenesis
Middle ear polyps can cause peripheral vestibular dis- The infection extends from an otitis externa or from
turbance uni- or bilaterally but since the polyps origi- the oro- and nasopharynx by way of the eustachian
nate from the middle ear, facial and/or sympathetic tubes, or hematogenously.
nerve deficits are present. The onset is mild and pro-
gressive. Blue-tailed lizard ingestion is believed to Most infections are caused by Staphylococcus spp.,
cause similar signs in the southeastern United States. Streptococcus spp., Proteus spp., Pseudomonas spp. or
Vomiting, salivation, irritability and trembling are also Escherichia coli.
observed. Signs may be indistinguishable from idio- Frequently, mites are the instigating factor for the otitis
pathic vestibular syndrome. externa, which leads to secondary microbial infection
Aminoglycoside toxicity, especially topical strepto- with spread to the middle ear.
mycin, can cause uni- or bilateral peripheral vestibular
disturbance but the history reveals use of the drug.
Clinical signs
The diagnosis of otitis media-interna is difficult as,
Treatment
except for surgical exploration of the tympanic bulla,
Supportive. In a few cats, fluid therapy, intravenously the tests performed have a low diagnostic yield.
or subcutaneously, may be necessary initially.
The cat may have a history of chronic otitis externa.
Sedation (acepromazine 0.05–0.10 mg/kg IM, SC, IV The ear may be sore to touch. There may be head shak-
to a maximum of 1 mg) may occasionally be required ing or scratching and frequent pawing at the ear.
if the rolling is severe.
There may be difficulty in prehension or chewing
Antibiotics such as amoxicillin or cephalosporine for food due to pressure on the petrosal bone region upon
10 days are indicated if otitis media-interna cannot be jaw opening as the temporo-mandibular joint is in the
ruled out. vicinity of the petrosal bone.
Glucocorticoids are not indicated. The corner of the mouth may be wet with saliva.
On otoscopic examination, the external ear canal may cation that a more thorough diagnostic work up
be red and inflamed with a brownish discharge. Mites should be performed.
may be present. The tympanic membrane may be red ● Normal hearing does not rule out middle-inner ear
and bulging or perforated. infection because the auditory receptors are in the
inner ear.
The onset and the neurological deficits depend on the
extension and severity of the infection. The onset of the Bullae radiographs have a low sensitivity:
vestibular signs may be acute with a marked head tilt, ● It is important to obtain an open mouth view to visu-
disorientation and nystagmus, or, chronic with nothing alize both bullae simultaneously for comparison.
else other than a mild head tilt. ● A normal study does not rule out middle-inner ear
disease.
The concomitant presence of facial nerve paresis/
● The tympanic bulla may appear denser if there is an
paralysis, decreased lacrimation and/or Horner’s
effusion.
syndrome confirms involvement of the middle ear.
● Thickening of the bulla or bone lysis may be
The facial weakness may be subtle. Look for a com-
observed in more severe and chronic infections.
plete closure of the lids following a single stroke of the
finger on both lids at once. Look for saliva-stained hair Cytological examination and culture with sensitivity
at the commissure of the lips or for a droop of the lips testing of the middle ear fluid is indicated when an
on the side affected. The symmetry of the pupils is best effusion is suspected:
assessed in a dark room to evaluate for the presence of ● The myringotomy is done using an otoscope to
a partial Horner’s syndrome. guide a 21⁄2” spinal needle through the tympanic
membrane.
Facial nerve paralysis may be accompanied by kerato-
conjunctivitis sicca because innervation of the CT or MRI scans are superior to radiographs to con-
lacrimal glands is carried by the facial nerve. firm tympanic bulla disease, but the changes detected
A Schirmer tear test should be routinely done in these are not specific for infection.
cases to avoid the formation of corneal ulcer.
Surgical exploration of the middle ear with cytologi-
Unilateral deafness is often present, but can be sub- cal examination and culture with sensitivity testing is
stantiated only with electrodiagnostic testing (BAER). the only definitive diagnostic tool in middle-inner ear
disease.
Diagnosis
Otoscopic examination may disclose an otitis externa, Differential diagnosis
mite infestation or tympanic membrane bulging/perfo- Idiopathic vestibular disease has an acute to per-acute
ration. onset in a cat that is otherwise healthy. There is no
If there is an otitis externa, cytology and culture with facial paresis/paralysis, decreased lacrimation, deaf-
sensitivity testing should be done. The same organism ness or Horner’s syndrome because the disease is lim-
may be causing the middle-inner ear infection. ited to the vestibular part of the inner ear. Signs resolve
over 1–2 weeks without treatment.
The presence of facial paresis/paralysis, decreased to
absence of lacrimation or Horner’s syndrome is a Neoplasia and middle ear polyps can be difficult to
strong indicator of concomitant middle ear disease, but differentiate from middle-inner ear infection without an
is not specific for infection. exploratory bulla osteotomy. If a polyp is visible in the
external ear canal or in the oro-nasopharynx, a diagno-
On physical examination, there may be pain on opening sis of middle ear polyp is likely.
the mouth or pain upon manipulation of the head.
Hearing should be evaluated with BAERs:
Treatment
● Concomitant deafness indicates a more significant
disease process such as in middle-inner ear infec- If a bacterial middle-inner infection is suspected, early
tion, but is not specific for the disease. It is an indi- and aggressive treatment with antibiotics is best. If cul-
ture and sensitivity are not available, a broad-spectrum Prevention

antibiotic is chosen such as trimethoprim-sulfa,
cephalosporin or a penicillinase-resistant penicillin Treat otitis externa effectively when it occurs.
(enrofloxacin). Treat ear mites.
Antibiotic treatment should be continued for 6–8
weeks.
MIDDLE EAR POLYPS**
If otitis externa is present, the antibiotic is chosen
based on the culture and sensitivity of the external ear Classical signs
canal. The otitis externa should be treated as well.
Systemic treatment is preferable if the tympanic
● Mild and slowly progressive head tilt.
membrane is perforated or cannot be visualized.
● +/- respiratory signs.
Avoid topical drugs that are toxic for the vestibular
● +/- signs of otitis externa.
and/or auditory system (gentamycin, neomycin).
● +/- facial paresis/paralysis, +/- Horner’s
Selamectin (Revolution®) or systemic ivermectin syndrome +/- keratoconjunctivitis sicca,
(200–300 μg/kg IM, SC, PO) is preferable as a miticide +/- deafness.
rather than topical treatment.
Cats with radiographic changes in the bullae are treated Pathogenesis
with surgical curettage of the tympanic bulla to allow
The pathogenesis is incompletely understood.
drainage, followed by long-term antibiotherapy based
on the culture and sensitivity obtained from the sample The polyp originates from the middle ear cavity and
collected at time of surgery. If the culture is negative, is composed of inflammatory granulation tissue cov-
a broad-spectrum antibiotic as listed above is adminis- ered by respiratory epithelium.
tered for 2–4 weeks.
The instigating cause is not exactly known. Some
If there is chronic or recurrent otitis externa, ablation of believe that it is congenital, to explain its frequency in
the external ear canal is indicated. very young cats. Others postulate that it results from
chronic inflammatory middle ear disease, secondary to
In the presence of paralysis of the eyelids, artificial
upper respiratory infections. The respiratory infection
tears are unnecessary if tear secretion is normal as the
would create abnormalities in the eustachian tube
spread of the tear film is taken over by the third eyelid.
epithelium, resulting in poor middle ear ventilation and
Artificial tears should be administered 2–6 times daily
secondary inflammation.
in the affected eye, if the Schirmer tear test is abnor-
mal (< 10 mm/minute), to avoid development of a Most cats with middle ear polyps have a bacterial
corneal ulcer. infection. The most common bacterial isolates are
Pasteurella multocida, Streptococcus, Staphylococcus,
Bacteroides and Pseudomonas.
Prognosis The polypoid growth has a tendency to exit the mid-
dle ear cavity. It can do so by rupturing the tympanic
Facial paralysis and partial Horner’s syndrome
membrane and emerging into the external ear canal,
often remain, although the severity is much improved.
causing characteristic signs of otitis externa, or it
An ipsilateral mild deviation of the face occurs over
enters the eustachian tube to exit into the nasophar-
time.
ynx with subsequent upper respiratory signs. The fre-
The vestibular signs resolve in most cases, except for quency of each end location versus the other is
the head tilt, which frequently remains for the life of unknown.
the animal.
The polypoid growth within the middle ear cavity may
The cases managed medically may recur and require encroach on the inner ear leading to vestibular
surgical curettage at later date. signs.
Clinical signs When a head tilt is present and there is facial paresis/
paralysis, decreased lacrimation or a Horner’s syn-
Typically occurs in young cats, but any age can be affected drome, bulla radiography is recommended to evaluate
(mean age 1–5 years; range 6 months to 15 years). the middle ear cavities. An open mouth view is best to
The most common signs associated with a middle ear compare the density between the bullae. Bulla radiog-
polyp, which extends into the nasopharynx, are upper raphy is not a sensitive tool. It may be normal despite
respiratory signs including noisy breathing, dyspnea the presence of uni- or bilateral polyps. CT and MRI
with or without nasal discharge, sneezing or cough- scans are superior in the diagnosis of middle ear cavi-
ing and gagging. ties, and one of these scans should be performed if
available.
Less often are signs characteristic of otitis externa.
CT and MRI scans are the most sensitive imaging tech-
Rarely a head tilt may be present. The head tilt may niques to reach a diagnosis of middle ear disease, but
occur without other signs, or with upper respiratory are not specific for the type of disease.
signs, or with a visible external ear canal polyp.
The final diagnosis is obtained at the time of surgery.
Since the polyp originates within the middle ear cavity, Surgical exploration of the middle ear is the only
the neurological structures of the middle ear may be reliable test to reach a diagnosis. Cytology and cul-
affected causing facial paresis/paralysis, keratocon- ture and sensitivity of the curetted tissue should always
junctivitis sicca and/or partial or complete Horner’s be done.
syndrome. These can also occur without other signs.
Diagnosis
If the disease process involves the middle ear, otitis
A mild and transient head tilt may be the only abnor- media-interna, middle ear polyp and neoplasia of the
mality on neurological examination. middle ear cavity cannot be differentiated without
biopsies taken at the time of surgical bulla explo-
The concomitant presence of a fibrous mass in the
ration.
external ear canal, or upper respiratory signs, is
pathognomonic for middle ear polyp.
Treatment
The concomitant presence of facial paresis/paralysis,
decreased lacrimation and Horner’s syndrome with Removal of the polyp from its origin through a
a head tilt is indicative of middle and inner ear disease ventral bulla osteotomy is the best therapeutic
but is not diagnostic for the type of disease. approach to avoid recurrence. Removal by grasping
the polyp and cutting it at the base from the nasopha-
If there are upper respiratory signs, visualization of the
ryngeal or aural location leads to a high recurrence
polyp in the nasopharynx under anesthesia is the most
rate.
efficient way of reaching a diagnosis.
● A glistening, red or pinkish mass filling the Horner’s syndrome is a frequent complication of
nasopharynx, or originating from the eustachian bulla osteotomy. It resolves in most cases in 1–3 weeks,
tube may be found. but even if it remains, it does not alter the patient’s
quality of life.
Otoscopic examination, which may necessitate seda-
tion/anesthesia to evaluate both ear canals and tym- The head tilt, if present at onset, usually remains for the
panic membranes should be performed. life of the patient. Occasional transient vestibular ataxia
● Aural inflammation may be present. is rarely reported as a surgical sequella of polyp
● A pedunculated red, pink or grayish mass may be removal.
observed in the ear canal.
The cat should be treated for 6–8 weeks with an
The polyp may also affect hearing. Presence of deaf- antibiotherapy based on the culture and sensitivity
ness is evaluated by doing BAERs. done at the time of surgery.
Prognosis compulsive walking and decreased menace are some of

the signs that may be observed.
Removal of the polyp by a ventral bulla osteotomy
minimizes the risk of recurrence. Recurrence is fre- Clinically, the disease frequently appears to be focal,
quent using oral or aural access to the polyp. although this is not the case at postmortem.
The head tilt usually remains but the other vestibular The head tilt is always associated with somnolence,
signs (ataxia and nystagmus) usually resolve. with or without cerebellar signs, because the cerebel-
lum is closely situated.
If facial paralysis is present, ipsilateral deviation of the
face ensues. Chorioretinitis may be present (see The Blind Cat or
Cat with Retinal Lesions).
If a Horner’s syndrome is present, it usually improves
and the residual deficit (aniscoria) is of no clinical Diagnosis
significance.
The history of a young cat originating from a multi-
cat household or breeder, with a protracted disease,
FELINE INFECTIOUS PERITONITIS** vague systemic signs and neurological abnormalities
raises the index of suspicion for FIP.
Classical signs
The cerebrospinal fluid analysis on its own is not sen-
● Head tilt in a cat systemically ill for a few sitive for a diagnosis of FIP.
weeks. ● Cell counts and protein concentration can be within
● Non-specific systemic signs such as fever, reference range especially if the disease is focal.
weight loss and lethargy. Typically, there is a moderate to severe pleocytosis,
● Chronic progressive disease. with mononuclear cells or neutrophils as the pre-
● There may be neurological deficits other dominating cell type, and a marked increase in pro-
than a head tilt. tein concentration.
● Protein concentration > 2 g/L increases the like-
See main references on page 372 for details (The lihood of FIP.
Pyrexic Cat).
MRI scan of the brain is helpful, as frequently there is
periventricular enhancement suggestive of ependymi-
Pathogenesis tis, and hydrocephalus with ventricular dilatation. The
The causative virus is a macrophage-tropic mutant of MRI findings are more representative of the neu-
the ubiquitous feline enteric coronavirus. ropathological extent of the disease than is the clinical
presentation, which is often focal in nature.
The clinical disease results from an immune-mediated
response of the host to macrophage-infected feline infec- Hematology and chemistry abnormalities are non-
tious peritonitis virus (FIPV). The severity of the disease specific except for a high serum total protein concen-
is based on host susceptibility and strain virulence. tration, which is frequent.
The anti-coronavirus IgG titer in CSF is consistently
positive.
Clinical signs
The polymerase chain reaction (PCR) test detects the
Affected cats are usually less than 3 years of age and
presence of feline coronaviruses but is not specific to
from large multiple-cat households or breeders.
FIP coronavirus.
The most common non-specific systemic signs are
Immunohistochemistry and immunocytochemistry are
fever, weight loss and lethargy.
techniques which appear promising for diagnosis of
Thirty-five percent of the cats with FIP have neuro- FIP. They use monoclonal antibody targeted against
logical signs. These vary with the lesion location. feline coronavirus to demonstrate coronavirus within
Behavioral changes, head tremor, seizures, depression, macrophages in tissue or effusions. The concentration
of infected monocytes in CSF fluid may make the test Pathogenesis

less sensitive for diagnosis of FIP than if used for tissue
sections. The most common tumor affecting the middle-inner
ear is the squamous cell carcinoma. The tumor arises
At this point in time, no single test is diagnostic for the from the epithelial lining of the ear canal and is usually
neurological form of FIP, but when the history, signal- aggressive, invading the adjacent tissue (middle and
ment, serum protein concentration, CSF results, CSF inner ears) then the skull. Squamous cell carcinomas of
serology and MRI findings are combined, an ante- the ear canal are most commonly presented with neuro-
mortem diagnosis can be reached. logical signs.
Ceruminous gland adenocarcinomas are also
Differential diagnosis reported with some frequency in the middle-inner ear.
Other inflammatory infectious diseases of the central
nervous system may produce similar neurological
abnormalities. However, no other central nervous sys- Clinical signs
tem infections are typically presented with the gamut of
abnormalities mentioned above. Middle-aged to older cats.
Initially, the signs relate to otitis externa. There is
Treatment a more or less rapid progression depending on the tumor
type, to cause peripheral vestibular signs, i.e., a head
There is no effective treatment for FIP. Patients almost tilt, with or without nystagmus or vestibular ataxia.
invariably die. Therapy is based on supportive care.
Immunomodulating and antiviral agents seem promising Due to the invading nature of the squamous cell carci-
in vitro but have not shown good results in cats. noma and the ceruminous gland adenocarcinoma, the
facial nerve and the sympathetic chain in the middle ear
are involved leading to facial paralysis, decreased
Prognosis lacrimation and Horner’s syndrome.
Poor. Most cats die of their disease from 6 weeks to There is pain when the mouth is open, which may
6 months after the onset of the neurological signs. result from involvement of the temporo-mandibular
joint, soft tissue pain, microfractures (pathological),
Prevention bone pain from lysis or involvement of the bulla struc-
tures.
Since most cats with FIP are from a multiple-cat house-
hold or breeder, adequate cleanliness is essential to pre- The face may be swollen and firm on palpation.
vent fecal–oral spread of virus.
Vaccination may be preventive. Diagnosis
The history of an older cat presented with a rapid onset
of neurological signs relating to the inner (vestibular
NEOPLASIA* signs and deafness) and middle ear (facial paralysis,
decreased lacrimation and Horner’s syndrome) with
Classical signs pain upon jaw opening and a swollen face increases the
index of suspicion.
● Otitis externa initially.
● Subsequent development of peripheral In most cases, bulla radiography is diagnostic for the
vestibular signs. presence of a destructive process. There is opacity in
● Swollen face. the tympanic bulla with sclerosis and lysis of the bone.
● Facial nerve paresis/paralysis and Depending on the tumor and how invasive it is, adja-
Horner’s syndrome are frequent. cent bony tissue such as the temporo-mandibular joint
and the zygomatic arch may also be affected.
Differential diagnosis lar receptors by the product used to flush the ear (e.g.
chlorhexidine, quaternary ammonium compounds).
As in most cases of middle-inner ear disease, if there is
no swelling of the face, surgical exploration of the bulla If the peripheral vestibular signs develop 48–72
is the only reliable approach to reach a definitive diag- hours following an ear flush, an inner ear infection is
nosis. suspected. Bacteria may have been introduced through
a perforated tympanic membrane at the time of the
Middle ear polyp is usually in young cats, but can be flush. The ear flush may not be vigorous for this to
in older cats. Typically, the progression is slower. The occur because the tympanic membrane may have
polyp may be visible in the ear canal or oro-nasophar- already been ruptured secondary to an otitis externa.
ynx. There is no pain, and no swelling of the face. Alternatively, topical (e.g. gentamycin-containing ear
drops) or systemic treatment administered after the ear
Treatment flush may be toxic to the vestibular receptors.
Aggressive excision including ear canal ablation and

lateral bulla osteotomy is the treatment of choice for Clinical signs
malignant ear canal tumors. If excision is incom- Acute onset of peripheral vestibular signs in the 72
plete, radiation therapy can be a useful adjunct to hours following an ear flush. The flush may have been
surgery. an elective procedure or therapeutic for a severe otitis
externa.
Prognosis
Prognosis is guarded because of the invasive nature of Diagnosis
the tumor and advanced stage of the disease by the time Diagnosis is based on the history of acute vestibular
neurologic signs are present. signs following a recent ear flush.
Cats with ceruminous adenocarcinoma have a 75%
1-year survival rate following aggressive ear ablation Differential diagnosis
and bulla osteotomy compared to a 33% 1-year survival
after conservative surgical resection. The prognosis is Idiopathic vestibular syndrome cannot be differenti-
more guarded for squamous cell carcinoma. ated from the iatrogenic cause if the signs appear 2–3
days following the flush.
EAR FLUSH*
Treatment
Classical signs Whenever acute vestibular signs appear to be associ-
● Acute onset of peripheral vestibular signs ated with an ear flush, a broad-spectrum antibiotic
that develop immediately or in the such as trimethoprim-sulfa, a cephalosporine or amoxi-
72 hours following an ear flush. cillin should be administered for 2–6 weeks.
Prognosis
Pathogenesis
If the onset was immediate and due to a change in the
The exact pathogenesis is unknown, but several mech- temperature or flooding of the inner ear, then the signs
anisms have been postulated to be involved. An ear may disappear within a few hours.
flush that leads to such consequences is usually done
If the signs are the result of toxicity, the head tilt may
under anesthesia or heavy sedation. If the signs develop
remain.
immediately after the flush, it is possibly due to: (1) a
change in the temperature of the endolymph; (2) If the signs appeared 2–3 days later, most vestibular
flooding of the inner ear through a perforated tym- signs resolve except for the head tilt, which usually per-
panic membrane; or (3) a toxic effect on the vestibu- sists for the life of the animal.
Prevention upper respiratory tract signs and/or draining skin

lesions should raise the index of suspicion for this
If an elective ear flush is to be performed under anes- infection.
thesia or with heavy sedation, ensure the tympanic
membrane is intact prior to the procedure. A latex agglutination test measuring the cryptococ-
cal polysaccharide capsular antigen can be per-
If the tympanic membrane cannot be visualized, use formed on the serum, cerebrospinal fluid or urine.
only sterile normal saline, as most ear-cleaning solu- However, negative results do not exclude the possi-
tions contain components that are potentially ototoxic, bility of disease.
such as propylene glycol, salicylic acid, malic acid, lac-
tic acid detergents and dioctols. The CSF analysis is often diagnostic because the char-
acteristic budding yeast forms are visible. This is best
Perform ear flush with extreme care. Cleansing the seen using India ink, but new methylene blue, Diff
ear with rubber bulb syringes, plastic syringes or water- Quick, and Gram’s stain preparation are adequate.
jet appliances may rupture the tympanic membrane. Sometimes organisms are not evident, but grow when
If the ear needs cleaning in the consultation room, the CSF is cultured.
avoid using solutions that are acidic or potentially oto- ● The CSF inflammatory response associated with
toxic. Instead of removing the debris manually, let the Cryptococcus neoformans varies greatly. The CSF
animal shake its head and dislodge the debris itself after may be normal to grossly abnormal with WBC
the medication had been put and massaged into the counts ranging from 0 to > 500 cells × 106/L (0–0.5
external ear canal. × 109/L).
● In mild inflammation, lymphocytes and monocytes
CRYPTOCOCCOSIS* predominate. In severe inflammatory responses, neu-

trophils and occasionally eosinophils are present.
Classical signs ● The protein concentration varies from mildly to
markedly increased (> 2 g/L).
● Lethargic cat with a head tilt, +/- ataxia,
+/- nystagmus. If the disease is suspected, but the organism is not vis-
● Concomitant upper respiratory tract signs. ible in the CSF, CSF culture and/or serology may pro-
● Anorexia, weight loss. vide a definitive diagnosis.
Cats may be simultaneously positive for feline
See main reference on page 26 for details (The Cat leukemia virus (FeLV) and/or feline immunodefi-
With Signs of Chronic Nasal Disease). ciency virus (FIV), increasing their susceptibility to
infection.
Clinical signs
Typically, the cat has usually been ill for a few weeks Differential diagnosis
prior to the development of the neurological signs. Cryptococcosis cannot be differentiated from feline
The systemic signs may have been vague such as infectious peritonitis in cats presented with a pro-
decreased appetite, weight loss, lethargy, or signs tracted illness and vague systemic signs on history,
may relate to a specific system such as the upper respi- physical and neurological examination alone. If
ratory tract, the skin or a combination of both. Cryptococcus organisms are not visible, culture or
serology may be necessary to establish the diagnosis.
Chorioretinitis may be present (see The Blind Cat or
Cat With Retinal Lesions).
Treatment
Fluconazole is the drug of choice because of its broad
Diagnosis
antifungal spectrum, its meningeal penetration even in the
The development of central nervous system signs in absence of inflammation, and the fact that serious side
a cat systemically ill for a few weeks or having effects are uncommon. The recommended dose is 10
mg/kg/day divided twice daily for a period that extends Clinical signs
beyond the resolution of all signs by 2–3 months. The
drug should be given with food. Lethargy and decreased appetite, sometimes with
increased salivation, occur after 2–4 weeks on a defi-
Ketoconazole should not be used. It does not pene- cient diet.
trate the blood–brain barrier effectively and is hepa-
totoxic. The cat has an inability or a reluctance to walk and
therefore may appear weak. This is associated with a char-
See page 26 (The Cat With Signs of Chronic Nasal acteristic rigid ventro-flexion of the neck, a crouched
Disease) for further details on treatment of cryptococcosis. body posture and loss of righting responses.
There is bilateral mydriasis with poor light reflexes
from the involvement of the oculomotor and geniculate
THIAMINE DEFICIENCY* lateral nuclei.
Classical signs Physiologic nystagmus is poor to absent.
● Bilateral vestibular signs, i.e., a Brief episodes of opisthotonus or neck ventroflexing

characteristic ventro-flexion of the neck and muscle rigidity may appear like seizures.
associated with a crouched body posture Bradycardia, and marked sinus arrhythmia may also
and reluctance to move. occur.
● Bilateral pupillary dilatation with poor light
reflexes. If untreated, the cat becomes comatose and dies. The
time of death varies from 1 week to a few weeks to
months depending on the health status of the animal
Pathogenesis and the amount of thiamine in the diet.
Thiamine is a co-enzyme in the oxidative metabolism
for energy production in the central nervous system. Diagnosis
Thiamine deficiency typically produces lesions Diagnosis is based on a combination of a history that
(polioencephalomalacia) in the brainstem gray the cat has been quiet and anorexic, signs of a charac-
matter and more specifically in the vestibular, ocu- teristic posture with poor to absent physiologic nystag-
lomotor and lateral geniculate nuclei. Focal, bilater- mus indicative of bilateral vestibular disease and
ally symmetric hemorrhages are present in affected documentation of a thiamine-deficient diet (usually
areas. large quantities of uncooked fish).
The deficiency occurs in cats that are fed an uncooked Rapid response (within 24 hours) to treatment con-
all-fish diet (due to the thiaminase content of the vis- firms the diagnosis.
cera), diets entirely made of cooked meat (where
the thiamine is destroyed by heating), poor-quality
thiamine-deficient commercial diets, or commercial
food stored for long periods of time or in excessively In bilateral idiopathic vestibular syndrome, the cat is
hot conditions. In addition, the meat preserver sodium healthy just prior to the development of the clinical
metabisulfite releases sulfur dioxide, which destroys signs. Thiamine-deficient cats are typically lethargic
thiamine. Pet mince meat containing this preserver is and anorexic.
thiamine-deficient, and even when mixed with other
food may have sufficient preserver to destroy all dietary
Treatment
thiamine.
Injectable thiamine at 10–20 mg intramuscularly. For
Anorexia in a sick cat especially associated with
supplementation, give 5–30 mg/cat/day PO to a maxi-
polydipsia and polyuria or fluid diuresis may precipi-
mum of 50 mg/cat/day.
tate thiamine deficiency and complicate the primary
illness. Change diet.

Prognosis is good if treatment is given early when the Sudden onset of head tilt associated with somnolence
only clinical signs are bilateral vestibular signs. or stupor following a road accident or other trauma
that caused a fracture at the base of the skull affecting
Prognosis is poor in the late stage of the disease when
the petrosal and ethmoid bones.
the animal’s consciousness is significantly altered.
Facial paresis/paralysis and/or Horner’s syndrome
CONGENITAL PENDULAR NYSTAGMUS* may be present if there is hemorrhage in the middle ear.
If the injury is primarily intracranial, facial paresis/para-
Classical signs lysis and/or ipsilateral proprioceptive deficits may be
● Siamese, Himalayan and white tiger cats. present.
● Pendular nystagmus, i.e., the phase of the On otoscopic examination, blood may be observed in
nystagmus is equal on both sides. the ear canal.
● Present from birth.
Diagnosis
Clinical signs
History of a road accident.
Typically, the nystagmus has a rapid, short and oscil-
latory motion that is equal bilaterally. It is observed Brain auditory-evoked responses (BAER) may be
especially when the cat is fixing its gaze. helpful in localizing the lesion to mainly a peripheral or
central location.
The defect is within the visual pathways and not the
vestibular pathways. No obvious visual impairment is Survey radiographs of the skull are difficult to inter-
present. pret because of the juxtaposition of multiple structures.
The nystagmus is always congenital and is evident in

the first few weeks of life. DRUG-INDUCED
It occurs primarily in Siamese, Himalayan and white
tiger cats. Classical signs
Medial strabismus is usually simultaneously present. ● Unilateral or bilateral peripheral vestibular

signs, following the use of drugs that are
Diagnosis toxic for the vestibular receptors.
● Concomitant deafness is frequent.
Diagnosis is based on the characteristic oscillatory nys-
tagmus.
Pathogenesis
FRACTURES OF THE PETROUS TEMPORAL Multiple drugs cause damage to the vestibular and/or
BONE OR TYMPANIC BULLA, AND ETHMOID auditory receptors separately or simultaneously.
FRACTURE (BASE OF THE SKULL) Aminoglycosides especially streptomycin, chloram-
phenicol, chlorhexidine, cisplatin, furosemide, sal-
Classical signs icylates and ceruminolytic agents are a few of
● Altered consciousness and head tilt after a long list of agents that may cause damage to these
a recent accident. receptors.
● +/- Facial nerve paresis/paralysis and
Horner’s syndrome. Clinical signs
● +/- Signs of brainstem involvement such
as proprioceptive deficits. Toxicity occurs following systemic or topical admin-
istration.
The vestibular signs are peripheral and can be unilat- Head tilt with tipping, rolling or falling developing at
eral, or bilateral. birth or in the first 12 weeks of life. The head tilt can be
marked and may vary with time.
The signs may develop acutely following exposure to
a high dose or after prolonged administration (> 14 The clinical signs are non-progressive and decrease in
days). Cats with renal dysfunction are at risk because severity with time, but usually persist for life.
decreased renal excretion of many drugs results in
higher plasma concentrations.
Diagnosis
The vestibular signs may disappear following dis-
Diagnosis is based on characteristic signs in a kitten
continuation of the drug.
from a susceptible breed.
Diagnosis
BLUE-TAILED LIZARD INGESTION
The history of use of a drug potentially toxic for the
vestibular receptors, topically or systemically. Classical signs
The vestibular signs may appear immediately following ● Southeastern United States.
an ear flush, or following topical treatment with a toxic ● Unilateral peripheral vestibular signs
medication, in a cat that has a perforated tympanic following the ingestion of a blue-tailed
membrane. lizard.
● The cat also salivates, vomits, trembles
and is irritable.
Prevention
Avoid using any medication in the external ear canal if
Clinical signs
the tympanic membrane is perforated or cannot be visu-
alized. This includes ceruminolytic agents and deter-
Acute onset of unilateral peripheral vestibular dis-
gents.
turbance following ingestion of the blue-tailed lizard.
The syndrome has not been well substantiated.
CONGENITAL VESTIBULAR DISEASE
Varying degrees of vestibular signs associated with
salivation, vomiting, trembling and irritability.
Classical signs
Spontaneous recovery occurs in most cats.
● Unilateral or bilateral vestibular signs
present at birth or developing in the first Death may occur.
12 weeks of life.
● Siamese, Burmese and Tonkinese cats.
Diagnosis
● Head tilt and tipping or rolling.
Acute onset of unilateral peripheral vestibular signs in
Clinical signs a cat living in southeastern United States with access
to lizards. Signs are indistinguishable from the idio-
Reported in Siamese, Burmese and Tonkinese cats.
pathic vestibular syndrome although salivation, vom-
Usually unilateral vestibular signs, but can be iting and trembling are less common with the
bilateral. idiopathic disease.
RECOMMENDED READING
Burke EE, Moise NS, de Lahunta A, Erb HM. Review of idiopathic feline vestibular syndrome in 75 cats. J Am Vet
Med Assoc 1985; 187: 941–943.
Faulkner JE, Budsberg SC. Results of ventral bulla osteotomy for treatment of middle ear polyps in cats. J Am Anim
Hosp Assoc 1990; 26: 496–499.
Foley JE, Lapointe J, Koblik P, Poland A, Pedersen C. Diagnostic features of clinical neurologic feline infectious
peritonitis. J Vet Intern Med 1998; 12: 415–423.
Hammond GJC, Sullivan M, Weinrauch S, King AM. A comparison of the rostrocaudal open mouth and rostro 10˚
ventro-caudodorsal oblique radiographic views for imaging fluid in the feline tympanic bulla. Vet Radiol
Ultrasound 2005; 46: 205–209.
Little CJL. Nasopharyngeal polyps. In: August JR (ed) Consultations in Feline Medicine, 3rd edn. W.B. Saunders,
Philadelphia, 1997, pp. 310–316.
London CA, Dubilzeig RR, Vail DM, et al. Evaluation of dogs and cats with tumors of the ear canal: 145 cases
(1978–1992). J Am Vet Med Assoc 1996; 208: 1413–1418.
Rand JS, Parent J, Jacobs R, Percy D. Reference intervals for feline cerebrospinal fluid: Cell counts and cytologic
features. Am J Vet Res 1990; 51: 1044–1048.
Rand JS, Parent J, Jacobs R, Johnson R. Reference intervals for feline cerebrospinal fluid: Biochemical and serologic
variables, IgG concentration, and electrophoretic fractionation. Am J Vet Res 1990; 51: 1049–1054.
Remedios AM, Fowler JD, Pharr JW. A comparison of radiographic versus surgical diagnosis of otitis media. J Am
Anim Hosp Assoc 1991; 27: 183–191.
39. The cat with tremor or twitching
Rodney S Bagley
KEY SIGNS
● Head and/or body tremor.
● Twitching.
MECHANISM?
● Tremor is an involuntary, rhythmic, oscillatory movement of all or part of the body. It results
from the alternate or synchronous contraction of reciprocally innervated, antagonistic muscles.
WHERE?
● Disease of the nervous system (central and peripheral) and muscle may result in tremor, shak-
ing or twitching.
● Usually tremors with increased amplitudes and slower frequencies (coarse tremor) are associ-
ated with cerebellar disorders. Those tremors with decreased amplitudes and faster frequencies
(fine tremor) are associated with diffuse central nervous system disease or muscle weakness.
● Tremor can have differing amplitudes (the distance traveled during the movement) and fre-
quencies (how fast the tremor is).
WHAT?
● Disease of the nervous system that results in persistent, generalized (whole body) tremor is
usually diffuse (encephalitis).

Diseases causing tremor or twitching
COARSE TREMOR AND TWITCHING (INTENTIONAL)
DEGENERATIVE
● Degenerative cerebellar diseases (p 857)
Using storage diseases as an example, these diseases tend to be breed-associated. Clinical signs usu-
ally begin in cats less than 1 year of age. Slowly progressive signs are typical and there is no hyper-
esthesia. When the disease involves the cerebellum, ataxia and hypermetria are most common.
852
39 – THE CAT WITH TREMOR OR TWITCHING 853
NEOPLASIA
Tumors involving the cerebellum usually occur in middle-aged to older cats. Clinical signs of cere-
bella dysfunction may occur acutely or be more chronically progressive.
INFECTIOUS/INFLAMMATORY
● Cerebellar hypoplasia** (p 855)
Cats are born with or develop this disease immediately after birth. Clinical signs become apparent
when the cat begins moving and are most obvious when the animal begins walking (somewhere
between 4–8 weeks of age). Intention tremor, ataxia and hypermetria are often found.
● Encephalitis (p 859)
Viral, fungal, protozoan, bacterial, rickettsial and parasitic agents are potential causes. Multifocal
central nervous system signs are most common. Fever and leukocytosis are inconsistent findings.
Other signs of a polysystemic disease such as coughing, vomiting or diarrhea may be associated.
TRAUMA
● Head trauma* (p 856)
blood from lacerations on or around the head, skull fractures, blood in the ear canals and scleral
FINE TREMOR AND TWITCHING (UNINTENTIONAL)
DEGENERATIVE
● Degenerative diseases of the nervous system (p 867)
Some of these diseases are inherited with clinical signs beginning in cats less than 1 year of age.
Examples include hypomyelination or dysmyelination and motor neuronopathies. Affected animals
tend to have a “bouncy” movement. With other degenerative diseases, such as encephalomyelopa-
thy of young cats and spongiform encephalopathy, tremoring may be acquired in young to middle-
aged cats.
ANOMALY
● Myotonia (p 866)
Clinical signs are most often recognized in cats between 1–12 months of age. Classically affected
cats have a stiff-stilted gait with increased size of the muscles. Tremor, if present, is usually of
short duration and episodic.
METABOLIC
● Hypocalcemia* (p 862)
Most often occurs after thyroidectomy. Muscle weakness, tetany and tremors are typical.
Preparturient hypocalcemia presents as anorexia, lethargy, trembling, muscle twitching and weak-
ness. Primary hypoparathyroidism occurs in young to middle-aged cats and can result in similar
clinical signs.
continued
continued
● Hypokalemia (p 865)
Typically older cats or Burmese < 1 year of age. Signs include weakness, inability or reluctance to
walk or jump, stiff, stilted gait, neck ventroflexion and sensitivity to palpation of larger muscle
groups. A short duration tremor may be present episodically and usually when the cat attempts
purposeful movement.
NEOPLASTIC
A 2-year-old cat has been reported with diffuse tremor resulting from multiple meningiomas.
Clinical signs progressed to paresis and ataxia.
INFLAMMATORY
● Encephalomyelitis (p 864)
Clinical signs are often diffuse and may not localize to a single area within the nervous system.
Fever and leukocytosis may be present but are inconsistent findings. The associated tremor tends
to involve the entire body and is rapid and of low amplitude (fine).
● Myasthenia gravis (p 866)
Typically adult cats or Siamese < 1 year of age. Tremor usually is episodic and occurs during
movement. Generalized weakness, a stiff, stilted gait prior to collapse, ventral neck flexion and
decreased palpebral reflexes may also be seen. The gait improves with rest.
● Polioencephalomyelitis (p 868)
This is a diffuse nervous system disease that primarily affects the spinal cord. A viral cause is sus-
pected. Signs have a slow onset and are chronically progressive. They include pelvic limb ataxia,
paresis, hypermetria, intention tremors, decreased pupillary light reflexes, seizures and hyperesthe-
sia over the thoracolumbar area.
IDIOPATHIC
● Feline hyperesthesia syndrome* (p 862)
A syndrome in which cats become suddenly startled, agitated and often run madly, usually when
stimulated over the thoracolumbar area of the spine. Skin rippling and spasms occur usually over
the lumbar region and the cat may lick or bite this area.
TOXICITY
● Toxins* (p 861)
Toxins such as organophosphate, hexachlorophene and ivermectin can affect nervous system trans-
mission and result in tremor. Other signs such as miosis, salivation, urination, defecation and weak-
ness may be present with OP toxicity. Ivermectin resulted in ataxia, tremor and weakness in a kitten.
INTRODUCTION nate or synchronous contraction of reciprocally inner-

vated, antagonistic muscles.
MECHANISM? True tremor ceases with sleep.
Tremor is an involuntary, rhythmic, oscillatory move- Tremor can be localized to one body area or be gener-
ment of all or part of the body. It results from the alter- alized and involve the whole body.
Tremors usually have a characteristic distance of travel

(amplitude) and speed of travel (frequency). Tremors DISEASES CAUSING COURSE
can be categorized generally into those that have an TREMOR
increased amplitude with a slower frequency (coarse
tremor) or a decreased amplitude with a faster fre- CEREBELLAR HYPOPLASIA**
quency (fine tremor).
Classical signs
● Signs are present from the early prenatal
WHERE? period.
Disease of the nervous system (central and periph- ● Clinical signs usually remain unchanged or
eral) and muscle may result in involuntary tremor, may improve during life.
shaking or twitching. ● Coarse tremor that worsens when the cat
moves in a goal-oriented fashion (intention
Cerebellar disease usually results in a coarser tremor tremor).
that worsens (increases in frequency or amplitude) ● Other signs include ataxia, hypermetria,
when the animal moves in a goal-oriented fashion menace deficits, head tilt and nystagmus.
(intention tremor).
Other signs of cerebellar disease that accompany
cerebellar tremor include ataxia (incoordination; sway- Pathogenesis
ing from side to side), dysmetria (“goose-stepping”;
overflexing of the limbs when walking), menace Cerebellar hypoplasia results from in utero or imme-
deficits (with normal vision, palpebral, and pupillary diately postnatal infection with the panleukopenia
light reflexes), head tilt and nystagmus. virus (parvovirus).
Fine tremor (decreased amplitude and increased fre- Infection of the fetus may occur when a pregnant queen
quency) is more often associated with diffuse neuronal is vaccinated with a modified-live panleukopenia
disease or muscle weakness that result in involuntary virus vaccination.
muscle contraction. This virus destroys the external germinal layer of the
cerebellum and prevents the formation of the granular
layer.
WHAT?
Some affected cats have a concurrent hydrocephalus
Diseases of the intracranial nervous system (primarily and hydranencephaly.
the cerebellum) resulting in tremor include storage
diseases, brain tumor, encephalitis and vascular-
based diseases.
Clinical signs
Systemic metabolic diseases altering neuronal or
Clinical signs are most apparent when the animal
muscle membrane potentials (such as hypoglycemia,
begins purposeful movement and attempts to walk.
hypocalcemia, hypokalemia) can result in tremor.
Tremor accompanying the disease usually has a slower
Diseases that decrease neuronal impulse conduction
frequency (2–6 times/second) and larger amplitude.
via abnormalities of myelin (hypomyelination) often
The tremor worsens (increases in frequency or ampli-
result in tremor.
tude), when the cat moves in a goal-oriented way (e.g.
Diseases of the nervous system that result in persist- bends down to eat), which is termed an intention
ent, fine tremor are usually diffuse (encephalitis). tremor.
Other signs include ataxia (incoordination; swaying Prognosis

from side to side), hypermetria (“goose-stepping”;
overflexing of the limbs when walking), menace Clinical signs associated with previous panleukopenia
deficits (with normal vision and pupillary light virus infection of the developing cerebellum usually
reflexes), head tilt, and nystagmus (combination quick remain static or improve with growth, causing the
followed by slow movement of the eyes). tremor to become less apparent.
Clinical signs usually remain static or improve with

growth as the cat compensates, causing the tremor to Prevention
become less apparent. Do not vaccinate queens with modified live pan-
leukopenia virus vaccine.
Diagnosis
HEAD TRAUMA*
Antemortem testing for this disease often results in
negative or normal findings. Classical signs
Routine laboratory investigations are normal. ● Acute onset of signs following a traumatic
Definitive diagnosis is usually rendered only at event.
necropsy and histopathological examination of the
nervous tissue. and face such as facial lacerations,
In some instances of cerebellar atrophy, a smaller than bruising, retinal hemorrhage, or
normal cerebellum may be seen on magnetic reso- hemorrhage in the external ear canals.
nance imaging of the intracranial nervous system. This ● Cerebellar involvement may result in
is most readily seen on the sagittal view. intention tremor, decerebellate rigidity,
Occasionally, inflammatory cells may be present in ataxia, hypermetria, head tilt and
cerebrospinal fluid examination in cats with active nystagmus.
panleukopenia viral infection. Cerebrospinal fluid
with the other degenerative cerebellar conditions and See main reference on page 823 for details (The Cat
with previous panleukopenia infection is usually With Stupor or Coma).
normal.
Clinical signs
Exogenous injury to the brain occurs most commonly
Differential diagnosis from automobile trauma, although gunshot wounds and
In this age of cat, other inflammatory central nervous falls may also occur.
system abnormalities such as toxoplasmosis infection Cerebellar involvement may result in intention
is possible. tremor, decerebellate rigidity (extension of all four
Congenital anatomical defects of the cerebellar may limbs and the trunk), ataxia, hypermetria, head tilt and
be present. nystamus.
Trauma occurring at a young age may permanently Signs usually begin acutely after trauma.
damage the cerebellum. Intracranial signs most commonly seen include stupor
and coma, paresis and gait abnormalities, and cra-
nial nerve deficits.
Treatment Evidence of external trauma to the head and face
No treatment is currently helpful for cats affected with such as facial lacerations, bleeding from the nose and
this disease. mouth, bruising or hemorrhage in the external ear
canals may be clues to the traumatic etiology, however, cells physiologically or mechanically, resulting in cel-
some animals that are uncoordinated may fall and lular dysfunction, and hence, clinical signs. Examples
injure themselves secondarily. include gangliosidosis, sphingomyelinosis, globoid
cell leukodystrophy and mannosidosis.
Diagnosis
The diagnosis of trauma is usually straightforward
Clinical signs
when the trauma is witnessed.
Clinical signs usually begin between 3–12 months of
In some instances, animals are presented with an acute
age.
onset of neurological signs and an unknown history,
examining for external signs of trauma such as lacera- Cerebellar disease usually results in a coarse tremor
tions or skull fractures is important. that worsens (increases in frequency or amplitude)
when the animal moves in a goal-oriented fashion
Evaluating the retinas and external ear canals for acute
(intention tremor).
hemorrhage may also provide clues to the diagnosis.
Other signs of cerebellar disease that accompany cere-
Advanced imaging studies such as CT or MR imaging
bellar tremor include ataxia (incoordination; swaying
are useful, primarily for determining structural damage
from side to side), dysmetria (“goose-stepping”; over-
to the brain.
flexing of the limbs when walking), menace deficits
(with normal vision and pupillary light reflexes), head
DEGENERATIVE CEREBELLAR DISEASES tilt, and nystagmus (combination quickly followed by
slow movement of the eyes).
Classical signs
Clinical signs of the hereditary cerebellar degeneration
● Signs usually begin or are present in cats described in Japan in cats begin around 7–8 weeks of
less than 1 year of age. age and include head tremor along with ataxia, dysme-
● Signs usually are slowly progressive or tria, and intention tremor.
remain unchanged.
Cerebellar degeneration with neuroaxonal dystrophy
● Signs include coarse tremor, hypermetria,
in domestic tricolored cats results in head tremors
ataxia, intention tremor and menace
and shaking. Clinical signs begin at 5–6 weeks of age
deficits.
and progress to ataxia and hypermetria. Affected kit-
tens have a lilac color that darkens with age.
See main reference on pages 934 and 935 for details
(The Cat With Ataxia Without Weakness). In cats with sphingomyelinosis (Niemann–Pick type C
disease) clinical signs begin early in life (< 6 months)
and progress to ataxia and hypermetria, absent men-
Pathogenesis
ace responses, and occasionally positional nystagmus.
Cerebellar degeneration is usually an inherited disease. Death usually occurs by 8–10 months of age.
A hereditary cerebellar degeneration has been Niemann-Pick type A disease occurs in Siamese and
described in Japan in cats. An autosomal recessive Balinese cats. Head tremor, head bobbing and dysme-
mode of inheritance was presumed. tria begin at 3–4 months of age. Clinical signs progress
to ataxia and paresis, worse in the pelvic limbs.
Cerebellar degeneration with neuroaxonal dystro-
phy has been reported in domestic tricolored cats. This
is inherited as an autosomal-recessive trait.
Diagnosis
Storage diseases result from inherited (or less com-
Antemortem testing for these diseases often results in
monly, acquired) intracellular metabolic derangements
negative or normal findings.
that result in abnormal metabolism of cellular products.
Cellular products accumulate and afferent neuronal Routine laboratory investigations are normal.
Definitive diagnosis is often rendered only at

NEOPLASIA
nervous tissue.
Classical signs
In some instances of cerebellar atrophy, a smaller than
● Signs usually begin in cats 5 years of age
normal cerebellum may be seen on magnetic reso-
or older.
nance imaging of the intracranial nervous system. This
● Signs usually are progressive over weeks
is most readily seen on the sagittal view.
to months.
Cerebrospinal fluid with these degenerative cerebellar ● Occasionally, clinical signs begin acutely.
conditions is normal. ● Intention tremor is often associated with
other signs of cerebellar disease including
With hereditary cerebellar degeneration described in
ataxia, dysmetria, menace deficits, head tilt
Japan in cats there is marked loss of Purkinje cells upon
and nystagmus.
histologic evaluation of the cerebellum.
In cats with sphingomyelinosis (Niemann–Pick type C See main reference on page 824 for details (The Cat
disease) cerebellar atrophy, Purkinje cell loss, and With Stupor or Coma).
neuroaxonal dystrophy are the predominant patho-
logical changes.
Clinical signs
Differential diagnosis Signs reflect either primary nervous parenchymal
damage from the tumor or secondary pathophysiolog-
In this age of cat, other inflammatory central nervous
ical sequelae such as hemorrhage and edema.
system abnormalities such as toxoplasmosis infection
is possible. Meningiomas are the most common brain tumor in
cats and are usually histologically benign.
Congenital anatomical defects of the cerebellar may
be present. Less frequent tumors arise from astrocytes, oligden-
drogliocytes, ependymal cells and choroid plexus cells.
Trauma occurring at a young age may permanently
damage the cerebellum. Neoplasia may secondarily involve the brain via metas-
tasis or via direct extension from extraneural sites.
Clinical signs usually begin in cats 5 years of age or
Treatment
older.
No treatment is currently helpful for affected cats.
Clinical signs usually are progressive over weeks to
months.
Prognosis Occasionally, clinical signs begin acutely.
Clinical signs associated with degenerative cerebellar Intention tremor is often associated with other signs
diseases progressively worsen. of cerebellar disease including ataxia (incoordination;
swaying from side to side), dysmetria (“goose-step-
Animals are commonly euthanized due to the progres-
ping”; overflexing of the limbs when walking), menace
sive incapacitation.
deficits (with normal vision and pupillary light
reflexes), head tilt, and nystagmus (combination quick
followed by slow movement of the eyes).
Prevention
Do not breed cats affected that have produced kittens
Diagnosis
with a presumed genetic or congenital cerebellar
disease. Routine laboratory investigations are normal.
Diagnosis of a structural intracranial abnormality in the leaving indentations in the nervous tissue parenchyma
brain is most readily accomplished with magnetic res- after resection.
onance (MR) imaging or computed tomography
Radiation therapy (45–48 Gy) may control tumor
(CT) of the brain.
growth of some brain tumors.
A broad-based, extra-axial (arising outside and push-
ing into the parenchyma) contrast-enhancing mass on
ENCEPHALITIS
CT or MR imaging is found in most instances of
meningioma.
Classical signs
The CT and MR appearance of gliomas is varied and
● Diffuse or multifocal neurological signs.
enhancement after contrast administration may not be
● Cerebellar signs such as intention tremor,
present. As these tumors arise from brain parenchymal
ataxia, hypermetria, head tilt and
cells, they are found within the neuroaxis (intra-
nystagmus.
axial).
● Cervical pain can be present.
Choroid plexus tumors, because of the increased con- ● Fever is an inconsistent finding.
centration of blood vessels within the tumor, often ● Clues of systemic inflammatory disease
enhance markedly after contrast administration. such as chorioretinitis are often present.
Because of their association with the ventricular sys- ● Other signs of polysystemic disease such
tem, associated hydrocephalus is common. as coughing, vomiting or diarrhea may be
present.
Cerebrospinal fluid often has increased protein con-
centration but this finding is not pathognomonic for
neoplasia.
Pathogenesis
Cerebrospinal fluid can contain evidence of inflamma-
The source of the inflammatory reaction includes both
tion (contains elevations in nucleated cells and protein
infectious and non-infectious etiologies.
content). If CSF is the only assessment made, an erro-
neous diagnosis of encephalitis may be rendered. Numerous infectious agents have been incriminated,
with the incidence of infectious agents causing menin-
gitis varying with geographic location.
Differential diagnosis Infectious agents causing brain disease include viral
(feline infectious peritonitis), fungal (cryptococcosis,
Congenital and inherited cerebellar diseases occur in
blastomycosis, histoplasmosis, coccidioidomycosis,
younger animals.
aspergillosis), protozoal (toxoplasmosis), bacterial,
Cerebrovascular, traumatic and inflammatory condi- rickettsial and unclassified organisms (protothecosis).
tions can mimic the signs of a brain tumor.
Feline infectious peritonitis (FIP) is caused by a coro-
navirus infection in cats. This virus can involve various
areas of the nervous system including the intracranial
Treatment structures and spinal cord. Very young and, conversely,
very old cats seem predisposed. Of the two forms of
Corticosteroids (prednisolone 1–2 mg/kg q 12 h) may
FIP that exist in cats, the “dry” form commonly affects
reduce peritumoral edema and improve clinical signs.
the nervous system. This viral infection results in an
Surgical removal of primary brain tumors may be immune complex vasculitis, which is responsible for
accomplished, especially with meningioma. most of the pathological effects.
A well-encapsulated, firm whitish mass is most often Toxoplasmosis (Toxoplasma gondii) can affect the
encountered at surgery in cats. Cortical parenchyma is nervous system at any level including the brain and
usually not infiltrated but rather compressed in cats, spinal cord.
Neosporosis results in necrotizing encephalitis in cats Evaluation of titers for the infectious diseases often
experimentally inoculated with Neospora caninum. helps to rule in or out the diseases.
Only those cats that were concurrently immunosup-
Cerebrospinal fluid analysis (CSF) will usually show
pressed by administration of methylprednisolone had
severe histological brain lesions.
Of the fungal diseases of the brain in cats, cryptococcosis ● Evidence of inflammation on CSF evaluation alone,
caused by Cryptococcus neoformans is the most com- however, is not specific for primary encephalitis as
mon. The central nervous system is often affected through other CNS disease (e.g. neoplasia) may result in
direct extension of the infection from the nasal pas- a CSF pleocytosis and protein increases.
sages or from disseminated infection from other organs. ● With feline infectious peritonitis (FIP), cere-
brospinal fluid analysis may show a pleocytosis,
Involvement of the intracranial nervous can occur with
parasites such as Cuterebra larvae, toxocara, and aber-
rant heartworm migration.
concentration, often > 1 g /L (0.1 g/dl).
● With toxoplasmosis, cerebrospinal fluid frequently
Clinical signs contains a pleocytosis, usually with mononuclear
cells, and occasionally, eosinophils. Increasing IgG
Depression, inappetence or anorexia and weight loss
or a single positive IgM serum antibody titer is sug-
are common.
gestive of active infection. Animals with neuro-
Clinical signs often reflect multiple levels of neurolog- logic signs and positive IgM titers warrant
ical involvement. Neurological signs may indicate dif- treatment for the disease.
fuse or multifocal disease and often do not localize to
With cryptococcosis, identification of the organism
a single area within the nervous system.
from cytological evaluation of samples such as CSF,
Paresis, gait abnormalities, proprioceptive deficits, cra- nasal discharge and skin lesions supports the diagno-
nial nerve defects, and occasionally stupor or coma sis. A neutrophilic pleocytosis, and occasionally an
may occur. eosinophilic pleocytosis may be found on CSF
analysis. If positive, detection of the cryptococcal
Cerebellar signs such as intention tremor, ataxia, hyper-
capsular antigen in serum is usually diagnostic.
metria, head tilt and nystagmus may occur with
Tissue biopsy and fungal culture of CSF may be
involvement of the cerebellum.
more definitive in the diagnosis as occasionally the
Cervical pain can be present. serum titer is negative.
Fever is an inconsistent finding. With parasites such as Cuterebra larvae, toxocara, and
aberrant heartworm migration, CSF may show inflam-
Fundic examination is important to look for clues of sys-
mation with eosinophils is some instances.
temic inflammatory disease as chorioretinitis, which is
often present with diseases causing systematic infection. Imaging studies (CT and MR) are helpful for defining
structural lesions. Multifocal, contrast-enhancing
Other systemic signs such as vomiting, coughing, and
diarrhea may be seen concurrently.
enhancing lesions are present, especially with toxoplas-
mosis.
Diagnosis
Multifocal signs are more suggestive of encephalitis.
Serum biochemical analysis may show evidence of sys-
temic abnormalities if the disease diffusely affects the Cats with encephalitis may present with signs similar to
body (e.g. vasculitis) such as elevated globulin, CK, other intracranial diseases such as brain tumor, trauma,
liver enzymes or creatinine. hydrocephalus and cerebrovascular disease.
Treatment DISEASES CAUSING FINE TREMOR

Treatment is directed at a specific infectious cause if
found.
TOXINS*
Without a definable cause of the encephalitis, the author
uses trimethoprim-sulfadiazine (30 mg/kg PO q 12 h), Classical signs
clindamycin (25 mg/kg q 12 h), and corticosteroids
● Tremors may be persistent or intermittent.
(prednisone 1–2 mg/kg PO q 12 h) in combination.
● A history of exposure to a toxin is most
While corticosteroids are contraindicated with infec- helpful in diagnosis.
tious diseases, they are often beneficial in the acute ● Diffuse CNS is often present in association
treatment of brain inflammation and edema. These with other systemic signs such as vomiting
associated pathophysiological events often lead to and diarrhea.
more neurologic deterioration than the organism
itself.
If rickettsial diseases are endemic, chloramphenicol Pathogenesis
or doxocycline can be substituted or added to the Toxins may lower the threshold for stimulation or
regime. directly stimulate muscles and nerves to result in
If the animal is receiving phenobarbital, do not use tremor.
chloramphenicol as this drug will decrease the metab- Organophosphate intoxication potentiates the effect
olism of the barbiturate and the animal will become of acetylcholine at the neuromuscular junction and
comatose and possible die. Also, chloramphenicol may other synapses, by binding with and inactivating acetyl-
result in bone-marrow suppression in cats. cholinesterase. This leads to increased acetylcholine
With feline infectious peritonitis (FIP), no specific concentrations at the neuromuscular junction, increased
treatment is effective. Immunosuppressive therapy may receptor stimulation and fatigue.
result in short-term improvement of clinical signs. Hexachlorophene causes vacuolation of white matter
With toxoplasmosis, treatment includes clindamycin that leads to abnormal impulse generation.
and trimethoprim sulfa antibiotics. Ivermectin increases GABA (inhibitory neurotrans-
For cryptococcosis treatments that have had some suc- mitter) concentrations and effects in the CNS.
cess for cyrptococcosis in cats include amphotericin B,
fluconazole, itraconazole and flucytosine. See page 26
(The Cat With Signs of Chronic Nasal Disease) for Clinical signs
treatment details.
Cats with acute organophosphate intoxication may
With CNS parasites, treatment has not been attempted have signs including miosis, salivation, urination,
uniformly and treatment recommendations are anec- defecation, as well as muscle weakness.
dotal.
A more persistent weakness without associated auto-
nomic signs can occur with chronic organophosphate
toxicity. Cats may attempt to walk a few steps, then
Prognosis collapse in sternal recumbency mimicking cato-
plexy/narcolepsy.
Many of the encephalities are poorly responsive to
treatment, and therefore morbidity and mortality is Hexachlorophene toxicity results in tremors as the
> 50%. primary clinical sign.
Some infectious encephalities (e.g. toxoplasmosis) may Ivermectin toxicosis has resulted in generalized ataxia,
be cured with appropriate treatment. tremor, weakness, incoordination and miosis in a kitten.
Diagnosis Classical signs—Cont’d

History of exposure to a toxic product is most helpful ● Sudden startling or running.
in establishing a diagnosis. ● Glazed look with dilated pupils.
For organophosphate toxicity, decreased concentration ● Apparent hallucinations.
of serum cholinesterase activity may lend support to ● Frantic meowing, growling, hissing,
the diagnosis. Depending upon the laboratory, values swishing of the tail.
less than 500 IU/L (normal 900–1200 IU/L) are con- ● Licking or biting of the flank, back or tail.
sidered consistent with organophosphate toxicity. Cats
with polyneuropathy from chronic OP toxicity may
have normal serum cholinesterase activity. Pathogenesis
The cause is unknown.
One theory is that this activity is a manifestation of
Differential diagnosis a focal seizure.
Rule out other diffuse causes of tremor such as meta-
Another theory suggests that it is similar to the obsessive-
bolic disease.
compulsive behavior associated with Tourette’s syn-
Physiological functions such as shivering from cold or drome in humans, which is the result of dopaminergic
apprehension should be considered. hyperinnervation.
Similar clinical signs have been associated with a vacu-
Treatment olar myopathy in cats and toxoplasmosis.
For organophosphate toxicity, treatment includes pro- Others have suggested that this may be behavioral dis-
topam chloride 2-PAM (20 mg/kg q 12 h IV) which order.
reactivates cholinesterase and diphenhydramine (1–2
Some believe that it begins with an inflammatory stim-
mg/kg PO q 8–12 h) which reduces muscle fascicula-
ulus such as flea or food allergy dermatitis.
tions.
● Atropine (0.2–0.4 mg/kg) can be given with acute
toxicity to decrease autonomic signs. Current rec- Clinical signs
ommendations are that it only be used if marked
Cats may become agitated and aggressive and show
bradycardia is present, because it may precipitate
skin rippling and muscle spasms, usually over the
respiratory arrest. Salivation and defecation are
lumbar area with stimulation such as stroking over the
not life threatening and generally do not require
thoracolumbar region.
atropine.
● Diazepam should be avoided in these cats as it Cats may appear as though they were startled, then
may result in generalized muscle tremor, hypersali- exhibit frenzied behavior such as licking or biting at
vation, miotic pupils, and vomiting similar to acute the flanks, back and tail or running.
muscarinic signs of organophosphate toxicosis.
Cats may appear as though they are hallucinating and
No specific antidote exists for the other toxicities have dilated pupils.
described here.
Sudden startling, running, frantic meowing, growling,
hissing, swishing of the tail may also occur.
FELINE HYPERESTHESIA SYNDROME* Episodes may occur multiple times in a day and last 1/2
min to 5 minutes.
Classical signs
● Skin rippling and muscle spasms, usually Diagnosis
over the lumbar area.
Diagnosis is usually made solely on clinical signs.
A complete neurological examination should be per- Prevention

formed to identify pain or deficits suggesting an under-
lying spinal lesion. Flea prevention.
Spinal radiographs should be performed to rule out Decrease stress in the environment.
lumbar and lumbosacral lesions.
Biopsy of the paraspinal muscles should be used to rule HYPOCALCEMIA*
out vacuolar myopathy.
Classical signs
IgM and paired IgG titers 3–4 weeks apart can be used to
help rule out active toxoplasmosis.
● Tremor associated with this disorder is
usually of short duration and episodic.
Differential diagnosis ● Stiffness and muscle spasm may also
occur.
Rule out dermatitis, lumbosacral spinal or nerve ● Twitching of the ears or facial muscles may
root compression and intracranial disease. be present.
Determine if the cat is exhibiting normal behavior dur-
● Weakness, lethargy and anorexia are
ing estrus. typical.
Treatment
Pathogenesis
Initial treatment should be with anti-inflammatory
drugs. Corticosteroid therapy (prednisolone) may help Decreases in calcium decrease the threshold for neu-
if a flea allergy or other inflammatory stimulus is sus- ronal and muscle depolarization.
pected. NSAIDs like piroxicam or meloxicam or mege- Hypocalcemia most often results from iatrogenic
strol can also be tried. injury to the parathyroid gland during surgical
Strict flea control may improve clinical signs. removal of thyroid tumors.
Behavior-modifying drugs such as the tricyclic antide- Primary hypoparathyroidism is reported but is rare.
pressants amitryptyline (2 mg/kg or 5–10 mg/cat PO q Hypocalcemia associated with queening (eclampsia)
24 h), clomipramine (1–5 mg/cat PO q 12–24 h) or the is rarely reported but occurs.
selective seritonin uptake inhibitors fluoxetine (Prozac
0.5–4 mg/cat PO q 24 h) or paroxetine (Paxil, 0.5
mg/kg PO q 24 h) may be helpful in some cats.
Clinical signs
Anticonvulsants (phenobarbital beginning at 3 mg/kg PO
Clinical signs include weakness, tetany and tremors.
q 12 h with dose adjustments to maintain trough serum
levels at 20–35 μg/ml) may help if anti-inflammatory Spontaneous muscle depolarization can manifest as
and behavior-modifying drugs are unsuccessful. muscle fasciculation, cramping, rigidity and twitching.
Feeding food without preservatives has been suggested Queens with preparturient hypocalcemia present with
as helpful. anorexia, lethargy, trembing, muscle twitching and
weakness. They resemble the clinical picture of hypocal-
Carnitine/coenzyme Q12 may help cats with vacuolar
cemia in cows (predominantly weakness), rather than
myopathy. Also antioxidants and omega-3 fatty acids
the violent muscle tremor of eclampsia in dogs.
may be useful.
Cats with primary hypoparathyroidism are more often
Decrease environmental stress.
male and typically range from 6 months to 7 years of
age. Signs include lethargy and anorexia and a sudden
Prognosis
or gradual onset of neuromuscular signs including focal
Consistent results with any treatment have not been (e.g. ears or facial muscles) or generalized muscle
obtained. tremors, seizures, weakness or ataxia.
Diagnosis Prognosis
Diagnosis is confirmed by finding decreased (usually Acute hypocalcemia following bilateral thyroidectomy
less than < 1.5 mmol/l (6 mg/dl) serum calcium on can be fatal if not recognized early and appropriate
serum biochemical analysis. therapy instituted.
Prevention
When performing bilateral thyroidectomy, allow 3–4
Rule out other inflammatory causes of muscle dis-
weeks between removal of each lobe.
ease and acute organophosphate toxicity (history of
exposure, signs and low cholinesterase activity).
ENCEPHALOMYELITIS
Physiological functions such as shivering from cold or
apprehension should be considered.
Classical signs
● Any aged cat may be affected.
Treatment ● A diffuse, whole-body, low-amplitude,
higher-frequency tremor is present
Treatment involves calcium supplementation and vita-
● Animals may twitch periodically.
min D therapy.
● Neurological signs are often diffuse.
If clinical signs are present, rapid institution of treat-
ment is indicated with 0.5–1.5 ml/kg IV of 10% cal-
cium gluconate. Infuse calcium slowly over 10 Pathogenesis
minutes while monitoring heart rate. Stop infusion
This syndrome is associated with histological evidence
if bradycardia occurs.
of inflammation of the CNS. However, a consistent
Short-term maintenance involves either SC calcium infectious etiology has not been identified.
(1–2 ml of 10% calcium gluconate diluted 1:1 in 0.9%
Encephalomyelitis is a much rarer cause of tremor in
saline q 8 hours) or IV calcium (10–20 ml of 10% cal-
cats compared to dogs.
cium gluconate in 500 ml of 0.9% saline) with rate
adjusted to maintain normocalcemia. Monitor calcium
Clinical signs
2–3 times daily initially.
Any age of cat may be affected.
Longer-term maintenance includes oral calcium (25
mg/kg q 8–12 hours) and vitamin D. The active form A diffuse, whole-body, low-amplitude (fine), higher-
of endogenous vitamin D3 (called calcitriol or 1,25 frequency tremor is present.
dihydroxycholecalciferol) is used at 2.5–10 ng/kg q 24
Animals may also twitch periodically.
hours or synthetic vitamin D3 (dihydrotachysterol) at
0.02–0.03 mg/kg q 24 hours for 3 days, then 0.01–0.02 Other neurological signs that may be present in cats
mg/kg q 6–24 hours. with encephalomyelitis include seizures, blindness,
conscious proprioceptive deficits and cranial nerve
Calcium should be monitored carefully, as hyper-
deficits.
calemia is nephrotoxic.
Neurological signs may not localize to a single area
Adjustments to doses should be made every 1–3 days
within the nervous system.
based on calcium concentrations.
Fever and leukocytes may be present but are inconsis-
If hypocalcemia is the result of thyroidectomy, calcium
tent findings.
and vitamin D therapy can be reduced gradually over
2–3 weeks, and stopped if calcium remains in the nor- Evidence of chorioretinitis may be present on fundic
mal range. examination.
Diagnosis HYPOKALEMIA
Cerebrospinal fluid may contain increased numbers
of nucleated cells and/or elevated protein concentra- Classical signs
tions. ● A short duration tremor may be present
Nucleated cell counts can vary from mildly inflamma- episodically and usually when the cat
tory (0.005–0.020 × 109 cells/L [5–20 cells/μl]; normal attempts purposeful movement.
< 0.002–0.005 × 109 cells/L [2–5 cells/μl]) to greatly ● Aged cats or Burmese < 1 year.
inflammatory (> 0.05 × 109 cells/L [50 cells/μl]). ● Ventral neck flexion.
● Stiff, stilted gait.
The nucleated cell type is variable, but most often is ● Reluctance to walk or jump, and physical
a mononuclear cell population. Neutrophils may also inactivity.
be seen. ● +/- Sensitivity to palpation of larger
In cats with FIP, CSF protein concentrations are usually muscle groups.
elevated at greater than 2 g/L (200 mg/dl), and nucle-
ated cell counts are greater than 0.1 × 109 cells/L (100 See main reference on page 893 for details (The Cat
cells/μl). With Neck Ventroflexion) and on page 945 (The
Cat With Generalized Weakness).
In cats with FIP the predominant nucleated cell type
present in the CSF is neutrophils
In cats with encephalitis from other suspected viral eti- Clinical signs
ologies, CSF protein concentrations are usually less Signalment is typically aged cats > 8 years or young
than 1 g/L (100 mg/dl), and nucleated cell counts are Burmese < 1 year (usually 2–6 months).
less than 0.05 × 109 cells/L (50 cells/μl).
Typically there is a history of acute onset of weakness.
Advanced imaging studies (CT or MR) may show However, decreased activity and inappetence are
multifocal lesions. Often these lesions are enhanced often present for weeks to months prior to presenta-
by intravenous contrast administration. tion.
A short-duration tremor may be present episodically
Differential diagnosis and usually when the cat attempts purposeful move-
Rule out other inflammatory, metabolic, and degenera- ment
tive causes of tremor. Clinical signs include ventral neck flexion, stiff,
Physiological functions such as shivering from cold or stilted gait, and a reluctance to walk or jump.
apprehension should be considered. Typically, weak cats do not walk far, but soon sit or lie,
flopping down, instead of carefully sitting as normal
cats do. Sensitivity to palpation of larger muscle groups
Treatment may be noticed.
Treatment with corticosteroids (prednisolone 2 mg/kg Dyspnea occurs when the potassium is very low
q 12 h initially) may improve clinical signs. (2.0–2.5 mmol/L), because of weakness of the respira-
If clinical signs improve, the corticosteroid therapy tory muscles. It may occur after fluid administration
should be slowly tapered (over months) to prevent because volume dilution and increased urinary potas-
recurrence. sium loss induced by diuresis may lead to further wors-
ening of the hypokalemia.
Young Burmese cats are susceptible to this disease,
Prognosis and potassium depletion may have played a role in the
Clinical response to corticosteroid is variable. previously described myopathy of Burmese cats.
Transient episodes of weakness may occur beginning Affected cats often have a stiff, stilted gait and have
between 2–12 months of age. large, bulky muscles on palpation.
Muscle dimpling may occur with direct muscle per-
Diagnosis cussion.
Diagnosis is made by finding decreased serum potas- Tremor, if present, is usually of short duration and
sium concentrations (usually < 3.5 mmol/L) in associ- episodic.
ation with clinical signs. The severity of signs varies
between cats when potassium is 2.5–3.5 mmol/L.
Diagnosis
Below 2.5 mmol/L and especially below 2.0 mmol/L,
signs are life threatening, with death occurring from Electromyography demonstrates the characteristic
respiratory muscle failure. myotonic potentials (sounds like a motorcycle revving
its engines), and muscle biopsies may be supportive of
Serum creatine kinase (CK) may be elevated reflect-
the diagnosis.
ing the mypoathy associated with hypokalemia.
Electrodiagnostic evaluation is rarely performed.
Abnormalities that may be found include increased
insertional activity, fibrillation potentials and positive Rule out other myopathies such as X-linked muscular
sharp waves, and some bizarre high-frequency dis- dystrophy (increased serum creatine kinase, typical
charges. muscle biopsy findings). Myotonia has characteristic
EMG findings.
Muscle biopsies often have minimal change present.
Mild myonecrosis is possible.
Treatment
MYOTONIA No treatment has been described in cats.
Classical signs
● Usually present in young cats as a MYASTHENIA GRAVIS
congenital problem.
● Stiffness and muscle spasm found at gait. Classical signs
● Steps are short and the limbs are stilted.
● Adult cats or Siamese < 1 year of age.
● There is an increase in muscle size.
● Tremor with this disease is usually
episodic and occurs during attempts at
Pathogenesis movement, muscle weakness induced by
movement.
Cats with myotonia have sustained muscle contrac-
● Ventral neck flexion may also be seen.
tion, which is initiated voluntarily or with stimulation,
● Decreased palpebral reflex is a helpful
and sustained involuntarily.
clinical sign.
Myotonia most often occurs as a congenital problem.
Excessive muscle contraction is thought to be due to an
With Generalized Weakness) and page 896 (The Cat
abnormal muscle cell membrane that supports per-
With Neck Ventroflexion).
sistent depolarization.
Clinical signs
Clinical signs
Muscle tremors are usually episodic and occur in mus-
Signs are first evident in young cats < 1–2 years of age. cles that are being used.
This is a rare disease in cats. Generally a disease of Classical signs—Cont’d

adult cats, except for the congenital form in Siamese
which presents at < 6 months of age. ● With the encephalomyelopathy of young
cats reported in the United Kingdom, cats
Exercise intolerance and episodic weakness induced by 3–12 months were affected, however, the
walking or playing are typical signs. The cat may walk disease was seen in cats up to three years
a few steps and flop down. Recovery occurs with rest. of age. Clinical signs usually are
A stiff, stilted gait is often noted prior to collapse. progressive over weeks to months.
● With spongiform encephalopathy of older
Weakness of facial muscle may also be seen, and this cats, muscle tremors may be seen in
is most evident as a decrease in the palpebral reflex association with ataxia and pupillary
and narrowing of the palpebral fissure. This appears to dilation.
be a more consistent finding in cats versus dogs. ● Clinical signs of hypomyelination or
Megaesophagus is uncommon and may lead to aspira- dysmyelination consist of diffuse tremor
tion pneumonia. accompanied by frenzied behavior and
indiscriminate biting. Clinical signs are
One cat has been reported with a jaw-drop and dys- worsened with activity.
phagia as the only clinical signs. ● Motor neuronopathies were in adult cats.
Clinical signs included tremor, progressive
Diagnosis weakness, cervical ventroflexion,
dysphagia and muscle atrophy.
Diagnosis is based upon clinical signs of exercise-
induced weakness that is resolved with edrophonium.
An edrophonium response test may suggest the disease Pathogenesis
if strongly positive. Edrophonium is an anti-
cholinesterase that potentiates acetylcholine (ACH) at A number of degenerative nervous system diseases
the neuromuscular junction. When given IV (0.1 have been reported in various locations around the
mg/kg), this drug can reverse the clinical weakness world. These include encephalomyelopathy, spongi-
seen with myasthenia gravis for a short period of time. form encephalopathy, hypo or dysmyelination and
motor neuronopathies.
Electromyography and nerve conduction studies will
be normal. A decremental response may be seen during Some degenerative diseases occur in younger animals
repeated stimulation of a peripheral nerve in some, but and some in older animals. Some of the degenerative
not all cats. diseases are inherited and signs begin in cats less than
a year of age.
Single-fiber EMG is a relatively new technique that
may aid diagnosis of this disease in the future. An encephalomyelopathy of young cats has been
reported in the United Kingdom. Wallerian degenera-
Documentation of antibodies to the acetylcholine tion was noted primarily involving the spinocerebellar
receptor in serum appears to be the most definitive pathways and the ventral funiculus of the spinal cord.
diagnostic test. In congenital disease, however, these A viral etiology was suggested but not proven.
antibodies will not be present.
A spongiform encephalopathy occurs in older cats in
DEGENERATIVE DISEASES OF THE the United Kingdom and a prion may be the cause.
NERVOUS SYSTEM Hypomyelination or dysmyelination of the CNS has
been reported in two Siamese cats. Pathologically
Classical signs there was a deficiency of myelin primarily in the ven-
● Some degenerative diseases occur in tral and lateral aspects of the spinal cord. Abnormal
younger animals and some in older animals. oligodendrocyte numbers or function is the suggested
pathogenic mechanism.
Motor neuronopathies are diseases that affect the cell Differential diagnosis
bodies of the lower motor neuron leading to degener-
ation of the cell in the ventral horn of the spinal cord Rule out other metabolic, inflammatory, and toxic
and occasionally the cranial nerve nuclei. Histologic causes of tremor.
lesions are most severe in the ventral spinal gray matter Physiological functions such as shivering from cold or
and consist of neuronal cell loss and gliosis. apprehension should be considered.
With the encephalomyelopathy of young cats No treatment is currently helpful or has been attempted
reported in the United Kingdom, cats 3–12 months for affected cats.
were affected, however, the disease was seen in cats up
to 3 years of age. Clinical signs usually are progres- Prognosis
sive over weeks to months.
Clinical signs associated with degenerative diseases
Signs include ataxia, paresis, and “head shaking”. progressively worsen.
Ataxia of the pelvic limbs was the initial clinical sign
noted. Animals are commonly euthanized due to the progres-
sive incapacitation.
Spongiform encephalopathy occurs in older cats, and
clinical signs include muscle tremors, ataxia, dilated Prevention
unresponsive pupils, jaw champing, salivation, and
behavior abnormalities. In one additional cat the tremor Do not breed cats affected that have produced kittens
was most obvious in the pelvic limbs. Signs progressed with a presumed inherited disease.
to severe ataxia and hypermetria.
Clinical signs of hypomyelination or dysmyelination POLIOENCEPHALOMYELITIS
consist of diffuse tremor accompanied by frenzied
behavior and indiscriminate biting. Clinical signs are Classical signs
worsened with activity. Reported cats were young ● Young to middle-aged cats have been
Siamese < 1 year of age. affected.
Motor neuronopathies were reported in adult cats and
● Clinical signs have a slow onset and are
signs included tremor, progressive weakness, cervical chronically progressive.
ventroflexion, dysphagia, and muscle atrophy.
● Signs are variable but include pelvic limb
ataxia, seizures, paresis, hypermetria,
intention tremors, decreased pupillary
Diagnosis light reflexes, and hyperesthesia over the
Antemortem testing for many of these diseases often thoracolumbar area.
results in negative or normal findings.
Pathogenesis
necropsy and histopathological examination of the Lesions primarily occur in the spinal cord and include
nervous tissue. severe degeneration and loss of neurons, perivascular
mononuclear cuffing, lymphocytic meningitis, neuron-
In some instances of motor neuronopathies, mild to phagia and glial nodules.
moderate fibrillation potentials were found in the
appendicular and paraspinal muscles with electromyo- A viral etiology was suggested but not proved.
graphy.
Clinical signs
Cerebrospinal fluid with these degenerative conditions
is normal. Young to middle-aged cats have been affected.
Clinical signs have a slow onset and are chronically

NEOPLASIA
progressive.
Signs are variable but include pelvic limb ataxia, Classical signs
seizures, paresis, hypermetria, intention tremors,
● A cat with multiple meningiomas
decreased pupillary light reflexes, and hyperesthesia
presented with generalized tremors.
over the thoracolumbar area.
Seizures were noted during sleep and were character-
ized by staring, clawing, biting and hissing.
Pathogenesis
Diagnosis A 2-year-old cat with multiple meningiomas presented
with generalized tremors. This cat was receiving
Two affected cats were leukopenic, with one having
chemotherapy for a previously diagnosed lymphoma.
bone marrow hypoplasia.
Diffuse neoplastic involvement was present pathologi-
Cerebrospinal fluid from one cat contained an elevated
cally.
protein content.
One cat had diffuse, hyper-reflective tapetal areas and
Clinical signs
subretinal infiltrative lesions upon fundic evaluation.
Tremor was the initial clinical sign seen.
Definitive diagnosis is often only made at necropsy.
Clinical signs progressed rapidly to ataxia and paresis.
Histological lesions are most severe in the spinal cord
and included severe degeneration and loss of neurons,
perivascular mononuclear cuffing, lymphocytic menin- Diagnosis
gitis, neuronphagia and glial nodules.
Multiple tumors were found at necropsy extending
from the parietal lobes of the brain to the lumbar spinal
cord.
Rule out other inflammatory, metabolic and degenera-
tive causes of tremor.
Treatment Rule out other inflammatory, metabolic and degenera-
tive causes of tremor.
No treatment has been attempted.
Prognosis Treatment
Clinical signs where progressive up until euthanasia. No definitive treatment was attempted.
RECOMMENDED READING
Braund KG. Degenerative and developmental diseases. In: Oliver JE Jr, Hoerlein BF, Mayhew IB (eds) Veterinary
Neurology. Philadelphia, WB Saunders, 1987, p. 186.
deLahunta A. Comparative cerebellar disease in domestic animals. Compend Continu Edu 1980; 2: 8.
Forbes S, Nelson RW, Guptill L. Primary hypoparathyroidism in a cat. J Am Vet Med Assoc 1990; 196: 1285–1287.
Inada S, Mochizuki M, Izumo S, et al. Study of hereditary cerebellar degeneration in cats. AJVR 1996; 57: 296–301.
March PA. Degenerative brain disease. Vet Clinic North Am 1996; 26: 945–971.
Palmer AC, Cavanagh JB. Encephalomyelopathy in young cats. J Small Anim Pract 1995; 36: 57–64.
Peterson ME, James KM, Wallace M, et al. Idiopathic hypoparathyroidism in five cats. J Vet Int Med 1991; 5: 47–51.
Shelton GD, Hopkins AL, Ginn PL, et al. Adult-onset motor neuron disease in three cats. J Am Vet Med Assoc 1998;
212: 1271–1275.
40. The cat with anisocoria or
abnormally dilated or constricted
pupils
Rodney S Bagley
KEY SIGNS
● Inequality of pupil size.
● Inappropriately dilated or constricted pupils.
MECHANISM?
● Anisocoria is a resting inequality in pupil size.
● An abnormally constricted pupil is referred to as a miotic pupil and results from either
excessive parasympathetic tone or decreased sympathetic tone.
● An abnormally dilated pupil is referred to as a mydriatic pupil and results from either
decreased parasympathetic tone or excessive sympathetic tone.
● Mechanical abnormalities of the iris may also result in abnormal pupil size.
WHERE?
● Disease of the eye, the visual pathways, or the pathways innervating the pupil may result in
anisocoria.
WHAT?
● Cats with anisocoria usually have primary ocular disease or abnormalities of iris innervation.
Disease of the iris may also be present such as iris atrophy. Systemic disease that alters auto-
nomic nervous system tone may also cause anisocoria.

Diseases causing anisocoria or abnormally dilated or constricted pupils
MIOTIC (CONSTRICTED) PUPIL(S)
NEOPLASIA
Tumors involving the sympathetic nerves may result in miosis. Other signs consistent with
Horner’s syndrome are usually present. Signs of systemic disease (for example vomiting, diarrhea,
enlarged lymph node size) may be found with diffuse diseases such as lymphoma and leukemia.
Tumors of the middle/inner ear, which affect the sympathetic nerves, may result in pain, swelling
and abnormal discharge from the affected ear.
870
40 – THE CAT WITH ANISOCORIA OR ABNORMALLY DILATED OR CONSTRICTED PUPILS 871
● Anterior uveitis** (p 879)
Infection or inflammation of the anterior chamber of the eye may result in miosis as a reflex
response to pain or due to vascular congestion of the iris. Conjunctivitis, corneal edema and
hypopyon often occur concurrently.
● Spastic pupil syndrome** (p 878)
Cats may have miotic or unresponsive pupils in association with feline leukemia virus (FeLV)
infection. Usually the affected pupils do not dilate with dark adaptation and constrict poorly to
light stimulation. Other signs of FeLV infection may be evident such as anemia, recurrent infec-
tions or neoplasia.
● Middle/inner ear infection** (p 877)
Otitis media/interna infection may affect the sympathetic innervation to the pupil and cause mio-
sis. Other signs of Horner’s syndrome such as prolapse of the third eyelid and enophthalmos are
usually also present. Discharge from the ear or an abnormally appearing tympanic membrane are
usually present.
IDIOPATHIC
● Horner’s syndrome*** (p 875)
Horner’s includes signs of miosis, enophthalmos, prolapse of the third eye, ptosis and vasodilation.
Miosis and prolapse of the third eyelid are most consistent.
TRAUMA
● Brachial plexus avulsion* (p 880)
Characterized by decreased to absent movement, spinal reflexes, and muscle tone in a thoracic
limb following being struck by a car or a fall. Miosis as well as other signs of Horner’s syndrome
can occur in the ipsilateral eye with damage to this area.
● Head trauma** (p 879)
TOXICITY
● Toxins (organophosphate)** (p 880)
Toxins such as organophosphates that interrupt or override sympathetic impulse transmission or
stimulate parasympathetic nerve transmission can result in miosis. Often there are diffuse clinical
signs present including salivation, urination, defecation, vomiting or diarrhea. Historical exposure
to these toxins is important to ascertain.
● Parasympathomimetic drugs (p 882)
Miotic pupils can occur when drugs that stimulate the parasympathetic system centrally or periph-
erally are administered. If the drugs result in systemic parasympathomimetic signs, salivation, uri-
nation, defecation, vomiting, diarrhea or weakness may be present.
continued
continued
MYDRIATIC (DILATED) PUPIL(S)

DEGENERATIVE
● Iris atrophy*** (p 883)
Degeneration of the iris with age may result in a dilated pupil. Irregular pupil margins, tears in the
iris and dyscoria are clues. Animals older than 5 years of age are most often affected.
● Spongiform encephalopathy (p @)
Rare in cats. Other clinical signs in addition to dilated pupils include muscle tremors, ataxia,
jaw clamping, salivation and behavior abnormalities.
● Encephalitis* (p 888)
Signs of diffuse intracranial nervous system dysfunction are often present including alteration in
consciousness, gait abnormalities, paresis and cranial nerve abnormalities. Spinal hyperesthesia
may also be found. If the disease affects diffuse body systems, anterior uveitis or chorioretinitis is
often concurrently present. Fever and leukocytosis are inconsistently found.
NEOPLASIA
Tumors within or compressing cranial nerve III may result in ipsilateral mydriasis. If a space-occu-
pying brain lesion is present, other signs seen may include circling, seizures, paresis and abnor-
malities of vision.
NUTRITIONAL
● Thiamine deficiency** (p 884)
Thiamine deficiency may result in dilated pupils. Anorexia and depression are early signs, ventral
neck flexion and a crouched body position with reluctance to move are typical. Episodes of
seizures – like muscle spasms with neck ventroflexion or opisthotonos may occur. Anorexic cats
or cats on all-fish diets are at the highest risk for development.
IDIOPATHIC
● Dysautonomia** (p 885)
Reported most commonly in Europe, although the frequency has decreased. Sudden onset of
depression and anorexia occur together with signs consistent with a lack of autonomic innervation.
In addition to mydriasis, weakness, dry eye, xerostomia, prolapsed third eyelids, bradycardia, loss
of anal reflex, incontinence and constipation may be seen.
TRAUMA
● Head trauma** (p 883)
hemorrhage may be clues to a previous traumatic incident. Unilateral caudal transtentorial brain
herniation results in similar signs.
TOXICITY
● Toxins* (p 887)
Toxins that interrupt parasympathetic nerve transmission or stimulate sympathetic nervous
impulses can result in mydriasis. Bites from Elapid (cobra type) snakes often result in mydriasis.
Often there are diffuse clinical signs present including weakness, ataxia and prolonged bleeding
from venipuncture sites. Fluoroquirolone toxicity may result in a sudden onset of bilaterally
dilated, non-responsive pupils. Historical information regarding exposure to these toxins is impor-
tant to elucidate.
● Parasympatholytic drugs (p 888)
Dilated pupils are most commonly seen following either systemic or topical administration of
atropine. With systemic administration tachycardia is often also present. Historical administration
of or exposure to these drugs is an important clue.
INTRODUCTION ● The impulse then descends through the brain stem

and cervical spinal cord in the lateral tectotegmen-
tal spinal pathway.
MECHANISM? ● This upper motor neuron (UMN) pathway
Diseases that affect the iris muscle, other ocular struc- synapses on the cell bodies of the preganglionic
tures, the visual pathways, the nervous system innerva- sympathetic nerves located in the intermediolateral
tion to the iris, or systemic autonomic nervous system horns in the T1–3 spinal cord segments.
functions may result in pupillary abnormalities. ● The preganglionic sympathetic nerves exit the
spinal cord and run cranially in the cervical sympa-
Mechanical abnormalities of the iris such as synechia
thetic trunk in the cranial thorax.
and iris atrophy are commonly associated with anisocoria. ● This pathway continues through the cervical
Abnormalities in the parasympathetic or sympa- area with the vagus nerve forming the vagosympa-
thetic input to the eye often are associated with abnor- thetic trunk.
mal pupil size. ● The preganglionic nerves synapse in the cranial
cervical ganglion located just caudal to the ear.
Intraocular causes of aniscoria are covered in The Cat
The postganglionic nerves run through the mid-
With Abnormal Pupil Size, Shape or Response
dle ear, course with cranial nerve (CN) IX (glos-
(page 1287) and The Cat With Abnormal Iris Appearance
sopharyngeal nerve) and then with the carotid
(page 1292).
artery to enter the skull.
● These nerves then course in the cavernous sinus
WHERE? with the carotid artery, and exit the skull through
Disease of the eye, the visual pathways, or the path- the orbital fissure.
ways innervating the pupil may result in anisocoria. ● The postganglionic sympathetic fibers travel with
the ophthalmic branch of CN V (trigeminal nerve)
The visual pathway includes the retina, optic nerve,
to the eye and via the short ciliary nerve synapse on
optic chiasm, optic tract, lateral geniculate body, optic
the dilator muscle of the pupil.
radiations and the occipital cortex. ● Some postganglionic fibers innervate the smooth
Sympathetic innervation to the pupil is responsible muscle fibers in the orbital sheath (musculus
for pupillary dilation and innervation to the vessels of orbitalis).
the iris (Figure 40.1). ● Sympathetic innervation to eye includes the mus-
● Sympathetic control is initiated in the hypothala- cle of the periorbita, eyelids (Muller’s muscle), the
mus of the diencephalon. third eyelid, the dilator muscle of the iris, and the
C
B
Figure 40.1. Schematic of the sympathetic innervation to the pupil. The information is initiated in the
hypothalamus (A), travels caudally bilaterally in the spinal cord to the T1–T3 spinal segments (B), where
the preganglionic fibers exit and travel cranially in the vagosympathetic trunk (C). The postganglionic fibers
originate in the cranial cervical ganglion (D) and travel to the pupil.
vasomotor fibers to the blood vessels and chro- ● In cats, there are only two short ciliary nerves,
matophores of the uveal tract. a nasal (medial) and malar (lateral), compared to
5–8 in dogs.
Parasympathetic innervation to the eye occurs
through cranial nerve (CN) III (oculomotor nerve)
for pupillary constriction (Figure 40.2).
● The afferent pathway for pupillary constriction dur-
WHAT?
ing light stimulation is the same as for vision from
the globe to the lateral geniculate body. Primary disease of the eye such as synechia, iris atro-
● Prior to synapse in this region, the fibers responsi- phy or glaucoma can result in an abnormal pupil.
ble for the pupillary light reflex (PLR) leave the
Primary ocular disease of the eye such as uveitis can
visual pathway and travel to the pretectal nucleus in
result in a constricted pupil.
the midbrain.
● These fibers project to the ipsilateral and contralat- Miotic pupils can result from parasympathetic over-
eral parasympathetic nucleus of CN III (PSN CN stimulation or lack of sympathetic influence.
III).
Miotic pupils can result from an abnormality of
● Contralateral projection is functionally greater than
sympathetic innervation to the eye. This can cause
the ipsilateral projection for this reflex, making the
a miotic pupil alone (Horner’s pupil) or in signs of
direct pupillary light reflex stronger than the
complete sympathetic denervation of the orbit (Horner’s
indirect.
syndrome: miotic pupil, prolapsed third eyelid, ptosis,
● The parasympathetic nucleus of CN III is
enophthalmos, peripheral vasodilation, decreased
excited bilaterally with impulses traveling from
sweating).
one eye. Cranial nerve III exits the skull through the
orbital fissure and projects to the globe. A large, poorly responsive or unresponsive pupil(s)
● The preganglionic portion of CN III synapses on is indicative of parasympathetic denervation of the
the short ciliary nerves, which are the ultimate iris. This can result from disease of cranial nerve III or
effector of pupil constriction. its nucleus.
B
D D
Figure 40.2. Schematic of the parasympathetic innervation to the pupil. The information is initiated by
a light stimulus (A), travels caudally in the optic nerve, chiasm and optic tract (B), to the parasympathetic
nucleus of cranial nerve III (C). The preganglionic and postganglionic fibers travel to the pupil with cranial
nerve III (D).
A larger pupil can be seen ipsilateral to a prechias- Ptosis is drooping of the upper eyelid from paralysis
mic lesion causing decreased vision. Examples include of CNIII or sympathetic innervation.
retinal disease and optic nerve disease (optic neuritis).
A larger pupil can be seen contralateral to an optic
tract lesion. DISEASES CAUSING MIOSIS
Cerebellar disease may occasionally be associated
with anisocoria. HORNER’S SYNDROME***
● With unilateral lesions of the fastigial or interposi-
tal nuclei, pupillary dilation which is slowly Classical signs
responsive to light may be seen.
● Miosis occurs in association with prolapsed
● Occasionally, the third eyelid may protrude and the
third eyelid, enophthalmos and ptosis.
palpebral fissure may be enlarged.
● Any aged cat may be affected.
● The pupillary dilation occurs in the eye ipsilateral
to an interposital nuclear lesion and contralateral to
a fastigial nuclear lesion.
Dyscoria is an abnormality of the form or shape of the Pathogenesis
pupil or an abnormal reaction of the two pupils to light.
Horner’s syndrome occurs because of an abnormality
Enophthamos is a backward displacement of the of, or injury to, the sympathetic innervation to the eye
eyeball in the orbit. and surrounding structures.
Normal sympathetic innervation is responsible for Radiographs of the bulla may show increased opacity
pupillary dilation. or bony abnormalities if middle ear disease is present.
Any disease that interrupts sympathetic transmis- Advanced imaging studies (computed tomography
sion to the eye can result in Horner’s syndrome. (CT) or magnetic resonance (MR) imaging) are used to
● Infiltration of these nerves by lymphoma or look for intracranial, middle ear or spinal disease.
leukemia cells is possible.
Cerebrospinal fluid should be collected and evaluated
● Traumatic damage to the sympathetic system can
for protein content and cellularity.
occur.
If a cervical spinal cord problem is suspected, spinal
Many instances of Horner’s syndrome in cats do not
radiographs, myelography, or advanced imaging (CT,
have a definable cause.
MR) may be needed.

Unilateral or bilateral miosis is the most consistent Primary disease of the eye such as anterior uveitis
clinical sign of sympathetic denervation. should be ruled out by performing a thorough ocular
examination.
The affected pupil will not dilate normally in a dark
environment. A neurologic examination should be performed to rule
out associated intracranial or spinal disease.
Other clinical signs constituting a diagnosis of
Horner’s syndrome include prolapsed third eyelid,
enophthalmus, ptosis, and rarely, vasodilation of uveal
tract vessels. Treatment
If middle or inner ear disease is present, pain and As Horner’s syndrome is a clinical diagnosis and not
swelling around or ventral to the bulla may be present. an etiological diagnosis, any disease of the sympathetic
There may also be pain upon opening the mouth, system should be treated specifically.
swelling in or around the ear, and abnormal discharge No treatment is available for idiopathic Horner’s syn-
in the ear canal may be present. drome.
Diagnosis Prognosis
The clinical diagnosis is based upon the presence of The ultimate prognosis will depend upon the underly-
this constellation of characteristic clinical signs how- ing cause.
ever, these clinical signs are not pathognomonic for any
The prognosis for otitis media is good with appropriate
particular disease.
surgical or antimicrobial treatment.
Pharmacologic testing of the eye to determine the
The prognosis for brain and spinal cord disease
location (pre- or postganglionic) of the disease is rarely
depends upon the nature of these diseases.
helpful.
Cats with idiopathic Horner’s syndrome may improve
An otoscopic examination should be performed to
with time.
examine for signs of middle ear disease.
Idiopathic Horner’s syndrome is not life threatening.
Palpation in the cervical area around the vagosympa-
thetic trunk should be performed to check for masses or While being a cosmetic abnormality, Horner’s syn-
other abnormalities. drome is infrequently irritating to the cat.
Pain on palpation or swelling around or ventral to the

MIDDLE/INNER EAR INFECTION**
bulla may be present.
Classical signs Otits externa may be noted but is not consistently present.
● Miotic pupil and other signs of Horner’s Pain upon opening the mouth and abnormal dis-
syndrome on affected side. charge in the ear canal may be found.
● Pain on palpation or swelling around or
Head tilt, vestibular ataxia with leaning, rolling,
ventral to the bulla may be present.
rolling to the side of the lesion and nystagmus result
● Otits externa may be noted but is not
from inner ear disease. Facial nerve paralysis may
constantly present.
result from middle ear disease, and is evidenced by an
● Pain upon opening the mouth and
inability to close the eyelids and loss of sensory inner-
abnormal discharge in the ear canal may
vation to the inner surface if the pinna.
be present.
● Head tilt, facial nerve paralysis and Abnormal odors may emanate from the ear canal.
nystagmus can result from middle ear
Purulent discharge may be present in the external ear
disease.
canal.
● Abnormal odors may emanate from the ear
canal.
Diagnosis
A discolored and outwardly bulging tympanic mem-
Pathogenesis brane may be noted with otoscopic examination.
Inflammation of the middle ear may result in damage to Increased density or bony changes of the bulla may
the sympathetic nerve for pupillary dilation, as well as be seen with skull radiographs highlighting the bulla.
damage to the VIIth (facial) cranial nerve. Extension to
Advanced imaging studies such as CT or MR provide
the inner ear may damage the VIIIth (vestibular) cranial
the best views of the middle/inner ear.
nerve and receptors resulting in a head tilt, vestibular
ataxia and nystagmus. See page 838 (The Cat With a Definitive diagnosis may be made with myringotomy
Head Tilt, Vestibular Ataxia or Nystagmus). and fluid analysis or with surgical exploration (bulla
osteotomy).
Infection or inflammation of the middle ear can
result via extension of these processes from the exter- Culture and sensitivity of any purulent discharge from
nal ear or eustachian tube. the middle ear cavity should be performed.
Infection can also occur secondary to systemic infec-
tions. Differential diagnosis
Allergic skin conditions, neoplasia, foreign bodies A direct otoscopic evaluation of the ear canal should
and trauma to the ear may be associated with middle reveal foreign bodies.
ear infections.
Tumors can result in associated local middle ear infection.
Organisms present mainly are bacteria and fungi.
Predisposing causes of recurrent otitis externa such as
Grass awn migration into the middle ear is common allergic skin conditions, swimming, immunodeficien-
in some geographic locations. cies or anatomical abnormalities of the external ear
canal may be evident.
Clinical signs
Treatment
On the affected side there is evidence of Horner’s syn-
drome with a constricted pupil that does not dilate nor- Infections from bacterial organisms should be treated
mally in a dark environment. with appropriate topical and systemic antibiotics based
upon culture and sensitivity results. Amoxicillin/clavu- Pathogenesis

lanic acid (14 mg/kg PO q 12 h) in combination is a rea-
sonable antibiotic to begin treatment with prior to Many, if not all, of these cats are positive for the feline
receiving culture and sensitivity results. leukemia virus.
Antifungal drugs may be used locally or systemically A C-type RNA virus has been demonstrated in the
depending upon the offending organism (see section on short ciliary nerves and ganglion of some cats.
antifungal therapy). Additionally, feline immunodeficiency virus may play
Foreign bodies should be removed with forceps or a sim- an associated role.
ilar instrument or during surgery.
Surgical drainage (bulla osteotomy) is often needed
Clinical signs
for curative treatment. The pupils are usually fixed at a midrange size and
do not dilate appropriately with dark adaptation.
Prognosis The pupil diameters may alternate in size between eyes,
and pupil movement is abnormal. There is inability to
The prognosis for treatment of middle ear disease with
fully dilate in the dark and sluggish constriction to light
either appropriate antimicrobials or surgery is usually
stimulation.
good.
Surgery of the bulla may result in complications such
Diagnosis
as a head tilt and facial nerve paralysis which may be
persistent. The diagnosis is suspected in a cat with the appropriate
clinical signs that is also FeLV positive.
Prevention
Early appropriate treatment of otitis externa may be
helpful in preventing extension to the middle ear. Rule out primary iris movement problems such as
synechia.
Correcting anatomical defects of the ear canal
decreases the risk of otitis.
Treatment
Decrease or stop activities that predispose to water or
foreign material collecting in the ear. There is no specific treatment for this disease.
SPASTIC PUPIL SYNDROME** Prognosis

The prognosis for the pupillary abnormality is variable.
Classical signs
The overall prognosis will be determined by other asso-
● Pupils are usually fixed at a midrange size ciated FeLV-related neoplastic conditions that may
and do not dilate appropriately with dark arise.
adaptation.
● Pupil diameters may alternate in size
between eyes. Prevention
● Pupil movement is abnormal (inability to Decrease exposure to other FeLV-positive cats.
fully dilate in the dark; sluggish
constriction to light stimulation). Vaccination of FeLV infection may provide some pre-
vention.
A fine needle aspirate of the anterior chamber may reveal

ANTERIOR UVEITIS**
inflammation. See page 1283 Infectious chorioretinitis or
anterior uveitis in “The Cat With Abnormal Pupil Size,
Classical signs
Shape or Response” for a description of the technique.
● Miosis is often present in association with
Titers for viral diseases (FeLV, FIV) and toxoplasmo-
other signs of ocular inflammation
sis may be helpful.
including aqueous flare, iridal edema,
corneal edema, conjunctivitis, hemorrhage Titers for feline infectious peritonitis are unreliable.
from the iris surface and hypopyon.
● Blepharospasm and photophobia may be Differential diagnosis
seen.
● In some instances, abnormal ocular Rule out other causes of ocular disease such as glau-
discharge is present. coma.
Consider local infections such as herpesvirus,
See main reference, page 1303 “The Cat With Mycoplasma, or Chlamydia, which cause conjunctivitis
Abnormal Iris Appearance” or page 1165 “The Blind and ocular discharge.
Cat or Cat With Retinal Disease”.
Evaluate for systemic organ dysfunction that may
accompany FIP and toxoplasmosis.
Pathogenesis
Treatment
The underlying process is an inflammation within the
anterior chamber of the eye. Treatment depends upon the underlying cause. See
page 1292 “ The Cat With Abnormal Iris Appearance”.
The miosis may result from ocular pain mediated
through a trigeminal (cranial nerve V) constrictor cen-
ter (oculosensory pupillary reflex) or from iridal vas-
cular changes.
HEAD TRAUMA**
Viral disease such as feline infectious peritonitis Classical signs

infection and protozoal diseases such as toxoplasmo-
● Miosis together with superficial
sis are often present.
lacerations, bleeding or bruising may
indicate a traumatic etiology.
● Trauma to the central nervous system
Clinical signs often results in paresis, abnormal
Miosis is often present in association with other signs consciousness or cranial nerve
of ocular inflammation including aqueous flare, iridal abnormalities.
edema, corneal edema, conjunctivitis, hemorrhage ● Trauma to the nerves of the brachial plexus
from the iris surface and hypopyon. may cause lower motor neuron signs
(paresis or paralysis, decreased to absent
Blepharospasm and photophobia may be seen.
spinal reflexes, decreased to absent muscle
In some instances, abnormal ocular discharge is present. tone) in the ipsilateral thoracic limb.
Clinical evaluation of the anterior chamber for signs of External trauma to the body may damage the ocular
inflammation is performed. structures or the nerves to the eye.
Bruising and functional damage (neuropraxia) as well lopathies, platelet abnormalities and vasculitis should
as anatomical disruption (axonotmesis and neu- be performed.
rotmesis) may result.
Brachial plexus avulsion resulting in miosis is most Treatment
often associated with tearing or avulsion of sympathetic
Standard critical care protocols for treatment of trau-
nerves that arise in the T1–T3 spinal cord segments and
matized animals should be implemented as needed.
exit the vertebral canal.
Primary treatment for nervous injury is not possible.
Central nervous system trauma may disrupt the sym-
pathetic pathways in either the brain or cervical spinal If it could be determined that a nerve is compressed or
cord. lacerated, surgical decompression or reconstruction is
theoretically possible but is rarely performed.
Misplaced hypodermic needles in the jugular furrow
during blood collection can rarely damage the sympa-
thetic nerves to the eye. Prognosis
Milder injuries usually result in a favorable prognosis.
Clinical signs Conversely, severe injuries may result in permanent
dysfunction.
Miosis may occur with trauma due to involvement of
the sympathetic system.
Prevention
Superficial lacerations, bleeding or bruising may indi-
cate a traumatic etiology. Keep animals in controlled environments that limit
access to automobiles and other traumatic potentials.
Trauma to the central nervous system often results in
paresis, abnormal consciousness or cranial nerve Use caution during jugular venepuncture.
abnormalities as well as miosis.
Trauma to the nerves of the brachial plexus may
cause lower motor neuron signs (paresis or paralysis, TOXINS (ORGANOPHOSPHATE)**
decreased to absent spinal reflexes, decreased to absent
muscle tone) in the ipsilateral thoracic limb as well as Classical signs
Horner’s syndrome in the ipsilateral eye.
● Acute onset of miosis, salivation, urination,
defecation and muscle weakness.
Diagnosis ● Rarely, lethargy, anorexia and persistent
weakness without associated autonomic
The diagnosis is supported by either a history of known
signs.
trauma or superficial evidence of lacerations or bruising.
Damage to the nerves of the brachial plexus may result
Pathogenesis
in signs of denervation on electromyographic studies.
Abnormal potentials usually begin around 5 days after Organophosphate intoxication potentiates the effect
the trauma. of acetylcholine at the neuromuscular junction and
other synapses, by binding with and inactivating acetyl-
Advanced imaging studies (CT or MR) provide the
cholinesterase. This leads to increased acetylcholine
best views of the central nervous system.
concentrations at the neuromuscular junction, increased
receptor stimulation and fatigue.
A delayed neurotoxicity in cats is reported associated
If active bleeding or bruising is present, an evaluation with the use of chlorpyrifos spray for household appli-
for underlying clotting disorders such as coagu- cation against fleas. There is individual variation in
sensitivity to chorpyrifos, and signs of toxicity have Salivation and defecation are not life threatening and
occurred even when used according to label instruc- generally do not require atropine.
tions. Toxicity has also been reported with the flea col-
Diazepam should be avoided in these cats as it may
lars containing chlorpyrifos.
result in generalized muscle tremor, hypersalivation,
miotic pupils and vomiting similar to acute muscarinic
Clinical signs signs of organophosphate toxicosis.
Cats with organophosphate intoxication may have
acute signs including salivation, urination, defeca- NEOPLASIA*
tion and muscle weakness.
Classical signs
Postural reactions and spinal reflexes may be depressed
in some cats, but may be normal in other cats. ● Miosis with or without signs of Horner’s
syndrome.
The pupils may be bilaterally dilated and poorly
● Accompanying signs depend on the
responsive to light stimulation.
location of the tumor.
Ventroflexion of the neck and muscle tremors may ● Tumors causing miosis can occur in the
be evident. middle ear, ventral cervical area, cervical
spinal chord and brain.
● A mass may be palpated in the ventral
Diagnosis
cervical area with neoplasia of the
History of exposure to an organophosphate. vagosympathetic trunk.
Serum cholinesterase activity may lend support to the
diagnosis, but may be non-diagnostic for chronic
Pathogenesis
organophosphate toxicity. Values less than 500 IU (nor-
mal 900–1200 IU) are considered consistent with Neoplastic disease may infiltrate or compress the
organophosphate toxicity. sympathetic nerves centrally or peripherally.
Electromyographic changes are occasionally present If the middle ear is affected, the most common
and include fibrillation potentials, positive sharp waves tumors are adenocarcinoma and squamous cell car-
and bizarre high-frequency discharges. A decremental cinoma.
response to repetitive nerve stimulation may be present.
Diffuse neoplastic diseases such as lymphoma and
Beware that edrophonium (used to test for myasthe- leukemias may infiltrate the sympathetic nerves.
nia gravis) will produce an acute worsening of signs, ● Lymphoma can be associated with feline leukemia
which should be treated with atropine (0.05 mg/kg IV). virus infection.

Rule out other diffuse causes of weakness. Miosis may be the primary sign or it may occur with
other signs of Horner’s syndrome. Other neurological
signs depend on the location of the tumor.
Treatment
Neoplasia involving the middle ear can result in pain
Treatment includes 2-PAM (20 mg/kg q 12 h IV) and
upon opening the mouth or during palpation around the
diphehydramine (1–2 mg/kg q 8–12 h).
ear, abnormal otic discharge and swelling around the
Atropine (0.2–0.4 mg/kg) can be given with acute tox- ear.
icity to decrease autonomic signs. Current recommen- ● Head tilt, facial paralysis and nystagmus can also be
dations suggest its use only if marked bradycardia is present when both the middle and inner ear are
present as this drug may precipitate respiratory arrest. involved.
Neoplasia of the intracranial nervous system can be Treatment

associated with circling, seizures, behavioral abnormal-
ities, paresis or cranial nerve abnormalities. Chemotherapies are used as definitive treatment of
diffuse neoplastic diseases such as lymphoma and
Neoplasia of the cervical spinal cord can result in leukemia.
tetraparesis or hemiparesis and cervical pain. If the
neoplasia involves the cervical intumescence or the Focal masses may be amenable to surgical resection.
brachical plexus, lameness, decreased reflexes, muscle Radiation therapy may help some neoplastic lesions.
atrophy and decreased muscle tone may be present in
the ipsilateral thoracic limb.
Prognosis
A mass may be palpated in the ventral cervical area
with neoplasia of the vagosympathetic trunk. Long-term prognosis with neoplastic conditions such
as adenocarcinoma and squamous cell carcinoma
Lymph node enlargement may be found diffusely if involving the ear is poor.
a systemic neoplastic disease is present or locally in the
submandibular nodes if middle ear disease is present. Remission may be achieved with lymphoma following
Diagnosis PARASYMPATHOMIMETIC DRUGS

Palpation of the mass lesion in or around the location Classical signs
of the sympathetic nerves is helpful for diagnosis.
● Local instillation of parasympathomimetic
FeLV-positive status may suggest the presence of asso- drugs into the eye can cause miosis.
ciated lymphoma. ● Systemically administered drugs such as
Fine-needle aspiration of a mass may reveal neoplas- bethanecol result in systemic
tic cells. parasympathomimetic signs, salivation,
urination, defecation, vomiting, diarrhea or
CBC may reveal circulating neoplastic cells or high weakness.
WBC counts.
Bone marrow analysis may show the presence of lym- Pathogenesis
phoma or leukemia.
Drugs or toxins can stimulate parasympathetic
Advanced imaging studies (CT or MR) provide the receptors of the iris locally or of the parasympathetic
best views of the nervous system. system centrally.
CSF analysis may rarely show neoplastic cells.
Increased density or bony changes of the bulla may be Clinical signs
seen with radiographs, however, advanced imaging If there is only local instillation of parasympath-
studies (CT or MR) provide the best views of the mid- omimetic drugs into the eye (e.g. pilocarpine, deme-
dle/inner ear. carium), miosis is likely to be the only clinical sign.
Definitive diagnosis is made with surgical biopsy of If systemic drug administration occurs causing dif-
a mass. fuse parasympathetic stimulation (e.g. bethanecol)
other clinical signs could include salivation, urination,
defecation, vomiting, diarrhea and weakness.
If a mass lesion is found, other causes of proliferative
Diagnosis
tissue such as inflammation, infection, hemorrhage and A history of instillation or administration of these
fluid should be ruled out. drugs in most helpful.
If the drug works by inhibiting acetylcholinesterase See main reference page 1299 “The Cat With
(e.g. organophosphate or carbamate), cholinesterase Abnormal Iris Appearance”.
activity measured in blood may be helpful. Values
less than 500 IU (normal 900–1200 IU) are considered
Pathogenesis
consistent with toxicity.
Iris atrophy is an age-related degeneration of the iris.
Blood cholinesterase activity, however, may not be
reflective of drug exposure in all instances, especially
in chronic toxicity. Clinical signs
Degeneration of the iris is a common cause of poor
Differential diagnosis pupillary constriction in older animals.
Rule out other causes of miosis. Pupils are usually inappropriately dilated.
Often the margins of the iris are irregular or have tears
Treatment
within.
If the drug was administered locally in the eye, stop-
The pupils constrict poorly with light stimulation.
ping additional administrations and allowing time for
the drug to be metabolized is most sensible, as this is Dyscoria may also be present.
rarely life threatening for the animal.
In some instances, local administration of a parasym- Diagnosis
patholytic drug or sympathomimetic drug may coun-
Diagnosis is based upon the characteristic clinical
terbalance the effects of the parasympathomimetic.
signs consistent with iris degeneration in an aged cat.
Prognosis
The prognosis is good if the drug was only administered
Rule out other causes of mydriasis.
locally in the eye as stopping additional administrations
and allowing time for the drug to be metabolized will
often bring about resolution of clinical signs. Treatment
No treatment is necessary.
Prevention
Prognosis
Avoid excessive or inappropriate use of these drugs.
Iris atrophy is a non-life-threatening problem that does
not result in morbidity.
DISEASES CAUSING MYDRIASIS
HEAD TRAUMA**
IRIS ATROPHY***
Classical signs
Classical signs ● Mydriasis may occur secondary to caudal
● Older cats, usually > 5 years of age. transtentorial brain herniation after brain
● Pupils are inappropriately dilated. trauma.
● Often the margins of the iris are irregular ● Facial lacerations, bleeding from the nose
or have tears within. and mouth, bruising, or hemorrhage in the
● The pupils constrict poorly with light external ear canals.
stimulation.
● Dyscoria may also be present. See main reference on page 823 (The Cat With Stupor
or Coma).
Clinical signs Thiamine deficiency results in polioencephalomala-

cia of the oculomotor and vestibular nuclei, the caudal
Signs usually begin acutely after trauma. colliculus and the lateral geniculate body.
Intracranial signs most commonly seen include stu- Early, non-specific signs are typically lethargy and
por and coma, paresis and gait abnormalities, and cra- inappetence.
nial nerve deficits.
With caudal transtentorial herniation, cranial nerve ataxia, which appears as an abnormal broad-based
III is compressed and becomes dysfunctional. stance, loss of balance and vertigo.
This results in an ipsilateral dilated pupil which is There is weakness and an inability or reluctance to
poorly responsive to light stimulation. walk. The cat sits crouched with ventral flexion of the
Evidence of external trauma to the head and face such neck.
as facial lacerations, bleeding from the nose and mouth, Pupils are dilated and non-responsive or poorly
bruising or hemorrhage in the external ear canals may responsive to light reflexes.
be clues to the traumatic etiology.
Diagnosis vocalization, opisthotonos and death.
The diagnosis of trauma is usually straightforward Episodes of spastic opisthotonos or ventroflexion of

when the trauma is witnessed. the neck and muscle spasm may occur especially when
the cat is lifted or stressed. They may be interpreted as
In some instances, animals are presented with an acute seizures, but true seizure activity rarely occurs.
onset of neurological signs and an unknown history,
examining for external signs of trauma such as lac-
erations or skull fractures is important. Diagnosis
Evaluating the retinas and external ear canals for No antemortem diagnostic test is available.
acute hemorrhage may also provide clues to the diag-
nosis. Diagnosis is based on clinical signs and rapid response
to thiamine.
Advanced imaging studies such as CT or MR imag-
ing are useful, primarily for determining structural
damage to the brain. Differential diagnosis
Other encephalopathies and encephalitis are differ-
THIAMINE DEFICIENCY** entiated on history, CSF findings and lack of response
to thiamine.
Classical signs Head trauma may appear similar to late signs of thi-
● Initially, lethargy, inappetence and ataxia. amine deficiency, but can usually be differentiated on
● Later, weakness, ventral flexion of the history and evidence of trauma. Thiamine-deficient
neck, dilated pupils, stupor and coma. cats are lethargic and inappetent days and weeks before
signs are severe.
See main reference on pages 848, 899 for details, “The Hydrocephalus can present with central blindness and
Cat With a Head Tilt, Vestibular Ataxia or Nystagmus” ataxia, but there is no response to thiamine.
and “The Cat With Neck Ventroflexion”.
Dysautonomia is a consideration in countries where it
Clinical signs troflexion of the neck may appear similar to thiamine
Occurs in anorexic cats, or cats that are fed all-fish deficiency, but there is no response to thiamine.
diets containing thiaminase, or cats fed meat con- Hypokalemic myopathy, myasthenia gravis, polymyosi-
taining the preserver sulfur dioxide. tis and organophosphate toxicity can all cause ventral
flexion of the neck, but do not cause dilated pupils acting parasympathomimetic, physostigmine (0.02
unresponsive to light. mg/kg IV) produces no ocular response, but direct-
acting pilocarpine (topically) results in immediate miosis,
demonstrating post-glanglionic denervation hypersensitiv-
DYSAUTONOMIA**
ity. Normal cats do not demonstrate these responses.
Classical signs
● Younger cats (< 3 years).
● Acute onset of depression and anorexia. Differential diagnoses are many, depending on the
● Dilated pupils, xerostomia, predominant signs. Cats may present with a history of
keratoconjunctivitis sicca, prolapsed third constipation or inability to urinate or dilated pupils,
eyelids. suggesting disease of the colon, lower urinary tract or
● Bradycardia. eyes. Typical cases which exhibit most signs are classi-
● Megacolon, constipation, loss of anal cal for dysautonomia.
reflex.
● Incontinence, dysuria or distended bladder.
● Weakness.
Treatment
No specific treatment is available, but supportive
See main reference on page 792, “The Constipated or care is important, such as syringe or tube feeding
Straining Cat”. and maintenance of fluid and electrolyte balance.
The urinary bladder should be emptied regularly to pre-
Clinical signs vent distention and urinary tract infection.
Disease is confined to Europe or occurs in imported Parasympathomimetic agents may improve some clini-
cats. The prevalence has decreased markedly and it is cal signs.
now uncommon. ● Pilocarpine ophthalmic drops (state frequency)
may result in pupillary contraction and increase
Younger cats (< 3 years) are more often affected.
salivation.
Clinical signs are often acute in onset over 48 hours ● Bethanechol (1.25–5 mg PO q 8–12 h) may bene-
with all cats showing depression and anorexia. fit constipation and urinary retention.
● Metoclopromide (0.2–0.5 mg/kg PO, SC, q 8 h)
Other signs reflect autonomic system dysfunction
may improve gastric motility.
and include ocular, gastrointestinal and urinary tract
signs. Up to a 70% mortality rate has been reported and sur-
viving cats may have residual dysfunction such as uri-
Ocular signs include fixed, dilated pupils without
nary or fecal incontinence and pupillary abnormalities.
blindness, prolapsed third eyelids and dry eyes (kerato-
conjunctivitis sicca develops).
Gastrointestinal signs include regurgitation, megae- NEOPLASIA*
sophagus, constipation and megocolon, loss of the anal
reflexes, dry mouth (xerostomia). Classical signs
Bradycardia (90–120 beats/min). ● ± Mydriasis.
● Circling, seizures, behavior abnormalities,
Dysuria and/or distended bladder or incontinence.
paresis or cranial nerve abnormalities.
Generalized weakness. ● ± Discharge from the ear.
Diagnosis is based primarily on clinical signs and Neoplastic disease may infiltrate or compress the
evidence of autonomic dysfunction. The indirect- cranial nerve III centrally or peripherally.
Diffuse neoplastic diseases such as lymphoma and Treatment

leukemias may infiltrate the nerves.
Chemotherapies are used as definitive treatment of
Lymphoma can be associated with feline leukemia diffuse neoplastic diseases such as lymphoma and
virus infection. leukemia, see page 742 “The Cat With Signs of
The most common intracranial neoplasia in cats is Chronic Small Bowel Diarrhea”.
meningioma. Focal masses such as meningioma may be amenable to
Peripheral involvement of cranial nerve III, most com- surgical resection.
monly occurs in the middle ear associated with squa- Radiation therapy may help some neoplastic diseases.
mous cell carcinoma or adenocarcinoma.
Prognosis
Clinical signs Long-term prognosis for cats with meningiomas is
good (~24 month median survival).
Mydriasis may occur with involvement of the
parasympathetic system within cranial nerve III. Remission may be achieved with lymphoma following
Neoplasia of the intracranial nervous system can be
associated with circling, seizures, behavior abnormali-
ties, paresis or cranial nerve abnormalities.
ENCEPHALITIS*
Lymph node enlargement may be found diffusely if
a systemic neoplastic disease is present or locally in the Classical signs
submandibular nodes if middle ear disease or other
● Mydriasis can occur due to involvement of
head neoplasms are present.
the oculomotor nerve.
● Neurological signs are often diffuse or
multifocal, but may localize to a single
Diagnosis
area.
FeLV-positive status may suggest the presence of asso- ● Cervical pain can be present.
ciated lymphoma. ● Fever is an inconsistent finding.
● Chorioretinitis is often present.
CBC rarely may reveal circulating neoplastic cells or
high WBC counts.
See main reference on page 859 for details “The Cat
Bone marrow analysis may show the presence of lym- With Tremor or Twitching”.
phoma or leukemia.
Clinical signs
Advanced imaging studies (CT or MR) provide the
best views of the nervous system. Infectious agents causing brain disease include viral
(feline infectious peritonitis), fungal (cryptococcosis,
CSF analysis rarely may show neoplastic cells. The
blastomycosis, histoplasmosis, coccidioidomycosis,
most common change is a mild increase in CSF protein
aspergillosis), protozoal (toxoplasmosis), bacterial,
and normal or slightly increased cell counts.
rickettsial, and unclassified organisms (prototheco-
Definitive diagnosis of neoplasia is made with surgical sis). Signs depend on the area of the brain affected.
biopsy of a mass.
Mydriasis occurs secondary to involvement of the
oculomotor nerve via direct inflammation of the nerve
Differential diagnosis or damage due to nerve compression (i.e. from cerebral
swelling).
If a mass lesion is found, other causes of proliferative
tissue such as inflammation, infection, hemorrhage and Neurological signs are often diffuse or multifocal but
fluid should be ruled out. may localize to a single area.
Cervical pain can be present. Imaging studies (CT and MR) are helpful for defin-
ing structural lesions. Multifocal, contrast-enhancing
Fever is an inconsistent finding.
Fundic examination is important to look for clues of enhancing lesions are present, especially with toxoplas-
systemic inflammatory diseases, as chorioretinitis is mosis.
often present.
TOXINS*
Diagnosis
Complete blood cell count may show evidence of sys- Classical signs
● Cats with organophosphate intoxication
Serum biochemical analysis may show evidence of may have acute signs including miosis,
systemic abnormalities if the disease diffusely affects salivation, urination, defecation and muscle
the body (e.g. hyperglobulinemia). weakness.
● Envenomation from snakes may also cause
Cerebrospinal fluid (CSF) analysis will usually show
dilated pupils. Weakness, ataxia and
coagulopathy may occur.
● Sudden onset of unresponsive, bilaterally
● Evidence of inflammation on CSF evaluation alone,
dilated pupils occasionally occurs with
however, is not specific for primary encephalitis as
fluoroquinolone.
other CNS disease (e.g. neoplasia) may result in
CSF pleocytosis and protein increases.
See main reference on page 949 “The Cat With
Evaluation of titers for specific infectious diseases, is Generalized Weakness” and page 861 “The Cat With
often necessary to make a diagnosis. Tremor or Twitching”.
With feline infectious peritonitis (FIP), cerebrospinal
fluid analysis may show a pleocytosis, with either Clinical signs
mononuclear cells or neutrophils as the predominant
Cats with organophosphate intoxication may have
cell type.
acute signs including miosis, salivation, urination, defe-
With toxoplasmosis, cerebrospinal fluid frequently cation and muscle weakness or tremor.
contains a pleocytosis, usually with mononuclear cells, ● Occasionally the pupils have been reported to be
and occasionally, eosinophils. An increasing IgG titer or bilaterally dilated and poorly responsive to light
a single positive IgM serum antibody titer is suggestive stimulation.
of active infection. Animals with neurologic signs and
Snake envenomation may be associated with dilated
positive IgM titers warrant treatment for the disease.
pupils as well as ataxia, weakness or paralysis.
With cryptococcosis, identification of the organism
Sudden onset of bilaterally dilated pupils that are unre-
from cytological evaluation of samples such as CSF,
sponsive to light occasionally occurs following fluoro-
nasal discharge and skin lesions support the diagnosis.
quinolone use, especially when used at higher than
A neutrophilic pleocytosis and occasionally an
recommended doses. Retinas appear normal on fun-
eosinophilic pleocytosis may be found on CSF analy-
doscopy. Prognosis for return of vision is guarded
sis. Detection of the cryptococcal capsular antigen is
unless the toxicity is recognized early and the drug
possible in serum, or CSF. Tissue biopsy and fungal
stopped.
culture, or culture of CSF may be more definitive in the
diagnosis.
Diagnosis
With parasites such as Cuterebra larvae, toxocara,
and aberrant heartworm migration, CSF may show Serum cholinesterase activity may lend support to the
inflammation with eosinophils is some instances. diagnosis of organophosphate toxicity, but may be
non-diagnostic for chronic organophosphate toxicity. Treatment

Values less than 500 IU/L (normal 900–1200 IU/L) are
considered consistent with organophosphate toxicity. If the drug was administered locally in the eye, stop-
ping additional administrations and allowing time for
Diagnosis of snake bite depends on the type of snake. the drug to be metabolized in most sensible as this is
Weak cats with mydriasis and evidence of rhabdomyol- rarely life threatening for the animal. It may take 1–2
ysis (markedly elevated creatine kinase) or coagulopa- weeks for normal pupil responses to return.
thy (bleeding from venepuncture sites or increased
activated clotting time) should be suspected if the snake
bite is from an Elapid (cobra type) snake if in the right SPONGIFORM ENCEPHALOPATHY
geographical location and season.
Classical signs
History of recent fluoroquinolone use, especially of
doses higher than the recommended dose of 5 mg/kg q
● Dilated pupils in association with other
24 h. clinical signs including muscle tremors,
ataxia, jaw clamping, salivation and
behavior abnormalities.
PARASYMPATHOLYTIC DRUGS
Classical signs Pathogenesis
● Mydriasis with or without dry mouth, There is vacuolation within areas of the central nerv-
tachycardia, and ileus or constipation may ous system.
be seen. No causative agent has been identified.
Speculation of an infectious agent (prion) as in other
spongiform encephalopathies as a cause has been sug-
Pathogenesis gested.
Some drugs or toxins prevent or reverse stimulation of
the parasympathetic receptors. Atropine would be Clinical signs
a commonly used example. Dilated pupils.
Other signs include muscle tremors, ataxia, jaw
Clinical signs clamping, salivation and behavior abnormalities.
If there is only local stimulation of the eye, mydriasis is Signs may progress to severe ataxia and hypermetria.
likely to be the only clinical sign.
If systemic parasympathetic stimulation occurs, Diagnosis
other clinical signs could include dry mouth, tachycar- Definitive diagnosis is made only at necropsy and
dia, ileus or constipation. histologic examination of the nervous system.
Diagnosis
Rule out other causes of mydriasis.
Determining a history of instillation or administra-
tion of these drugs is the only practical way of diag-
Treatment
nosing this problem.
No treatment has been used.

Rule out other causes of mydriasis. Affected cats have died or been euthanized.
RECOMMENDED READING
Collins BK. Disorders of the pupil. In: August JR (ed) Consultations in Feline Internal Medicine, 2nd ed.
Philadelphia, WB Saunders, 1994, pp. 421–428.
Holland CT. Horner’s syndrome and ipsilateral hemipelgia in three cats. J Small Anim Pract 1996, 37: 442–446.
Kern TJ, Aromando MC, Erb HN. Horner’s syndrome in dogs and cats: 100 cases (1975–1985). J Am Vet Med Assoc
1989; 195: 369.
Morgan RV, Zanotti SW. Horner’s syndrome in dogs and cats: 49 cases (1980–1986). J Am Vet Med Assoc 1989;
194: 1096.
Neer TM. Horner’s syndrome: Anatomy, diagnosis and causes. Comp Contin Ed Pract Vet 1984; 6: 740–746.
Neer TM, Carter JD. Anisocoia in dogs and cats: Ocular and neurologic causes. Comp Contin Ed Pract Vet 1987; 9:
817–823.
Scagliotti RH. Neuro-ophthalmology. Prog Vet Neurol 1990; 1: 157.
41. The cat with neck ventroflexion
Danièlle Gunn-Moore
KEY SIGNS
● Ventral flexion of neck and lowered head.
● ± Stiff stilted gait.
● ± Muscle weakness.
● ± Muscle pain.
MECHANISM?
● Neck ventroflexion is typically seen as part of generalized muscle weakness.
WHERE?
● The muscles, neuromuscular junction or nervous system.
WHAT?
● The most common cause of neck ventroflexion is hypokalemic myopathy resulting from
chronic renal failure; less common causes include hyperthyroidism, hypokalemic myopathy
of Burmese, myasthenia gravis, polymyositis and thiamine deficiency.

Diseases causing neck ventroflexion
ANOMALY
● Hypokalemic myopathy (of Burmese kittens)* (p 893)
Burmese cats from 2–6 months of age. Generalized weakness, stiff stilted gait, muscle pain and, in
severe cases, respiratory paralysis.
● Devon Rex myopathy (p 900)
Devon Rex cats from 8 weeks of age. Generalized weakness, marked neck ventroflexion and dor-
sal protrusion of scapulae. Exacerbated by exercise or stress.
● Congenital myasthenia gravis (p 896)
Seen in cats of less than a year old. Exercise-induced muscular weakness, progressive stiffness,
and muscle tremors. Rarely, regurgitation or dyspnea.
890
41 – THE CAT WITH NECK VENTROFLEXION 891
METABOLIC
● Chronic renal failure (hypokalemic myopathy)*** (p 893)
Most commonly seen in older cats. Polyuria, polydipsia, weight loss, generalized weakness, stiff
stilted gait, muscle pain and, in severe cases, respiratory paralysis.
● Hypokalemic myopathy*** (p 893)
Occurs in any age or breed of cat, but most commonly in older cats associated with chronic renal
failure or hyperthyroidism. Also occurs in Burmese cats from 2–6 months of age. Generalized
weakness, stiff stilted gait, muscle pain and, in severe cases, respiratory paralysis.
● Hyperthyroidism (hypokalemic myopathy and/or thiamine deficiency)** (p 893, 899)
Usually seen in older cats. Polyphagia, agitation, weight loss, generalized weakness, stiff stilted
gait, muscle pain and, rarely, respiratory paralysis.
● Iatrogenic** (p 893)
Administration of inappropriate IV fluids or excessive furosemide. Generalized weakness and,
rarely, respiratory paralysis.
● Hypernatremic myopathy (p 903)
Very rare cause of inappetence, muscle weakness, depression and myoglobinuria.
NEOPLASTIC
● Hyperaldosteronism (hypokalemic myopathy) (p 893)
Disease of older cats. Generalized weakness, stiff gait, muscle pain, polyuria, polydipsia and
weight loss, and/or signs of systemic hypertension.
NUTRITIONAL
Often with a history of fish-only diet. Anorexia and depression, followed by ataxia and vestibular
signs. May progress to seizure-like episodes, stupor and death.
● Inappropriate diet (hypokalemic myopathy) (p 893)
Seen occasionally, due to inadequate potassium or over-acidification. Generalized weakness, stilted
gait and muscle pain. May progress to renal failure.
INFECTIOUS
● Toxoplasmosis polymyositis (p 897)
Generalized weakness, muscle pain and reluctance to move. Often part of systemic illness.
May have dysphagia, megaesophagus or pneumonia.
IMMUNE
● Acquired myasthenia gravis* (p 896)
Exercise-induced muscular weakness, progressive stiffness, muscle tremors, and occasionally,
regurgitation and/or respiratory distress.
● Immune-mediated polymyositis (p 897)
Generalized weakness and pain. Occasionally with dysphagia or megaesophagus.
continued
continued
IDIOPATHIC
● Adult-onset motor neuron disease (p 903)
Chronic progressive generalized weakness with muscle tremors and fasciculations.
TOXIC
● Subacute organophosphate toxicity (p 901)
Generalized weakness, stiff stilted gait, muscle fasciculations or tremors. Muscarinic signs
(miosis and salivation) may be absent.
acetylcholine receptor antibodies, determination of

INTRODUCTION serum cholinesterase levels, serology for toxoplasmo-
sis, FIV and FeLV, muscle and/or nerve biopsies, or
MECHANISM? a combination of these tests may be required to confirm
a definitive diagnosis.
Neck ventroflexion is typically seen as part of more
generalized muscle weakness. Since cats lack a nuchal
WHAT?
ligament, muscle weakness in this species is often seen
first as ventroflexion of the neck. The most common cause of neck ventroflexion is
hypokalemic myopathy resulting from chronic renal
Affected cats often have a stilted gait and limb weak-
failure.
ness, which may worsen on exercise. ● Other causes of hypokalemic myopathy are seen
They may also show muscle pain, dyspnea, dysphagia, less frequently. They include a hereditary defect in
or megaesophagus. Burmese kittens, administration of inappropriate
IV fluids or excessive furosemide, feeding inap-
Cats with hypokalemic myopathy, polymyositis or
propriate diets and, occasionally, hyperthy-
adult-onset motor neuron disease may show evidence
roidism or hyperaldosteronism.
of muscle pain.
Other causes of neck ventroflexion include primary
myopathies (immune-mediated or toxoplasmosis
WHERE? polymyositis, Devon Rex myopathy), neuromuscular
junction diseases (myasthenia gravis, organophos-
Neck ventroflexion can result from disease affecting
phate toxicity, spider bite), polyneuropathies (adult-
the muscles, the neuromuscular junction or the
onset motor neuron disease) and, very rarely,
nervous system.
hypernatremia.
Physical examination should look for evidence of car-
Although thiamine deficiency can cause neck ven-
diovascular disease or systemic illness. In many neuro-
troflexion, it usually causes an active rather than pas-
muscular diseases generalized muscle weakness may
sive ventroflexion, together with excessive muscle
be the only abnormality.
tone, torticollis and seizure-like episodes of paddling or
A complete blood count may rule out anemia or sys- limb spasticity and opisthotonos.
temic infections. Serum biochemistry may indicate
This chapter deals with disorders that are likely to
hypokalemia, hypernatremia, raised creatinine kinase
present with neck ventroflexion. While this is
level, renal insufficiency or hyperthyroidism.
mostly seen as part of generalized muscle weak-
Electromyographic studies, an intravenous edropho- ness, not all cases of generalized muscle weakness
nium test (Tensilon test), assessment of serum anti- present with neck ventroflexion. Disorders that pri-
marily cause generalized weakness, of which neck ● This results from excessive urinary losses, and can
ventroflexion may merely be a factor, include be exacerbated by feeding a diet with insufficient
polyneuropathies (long-standing diabetes mellitus, potassium (see below).
idiopathic polyradiculoneuropathy), ethylene glycol
toxicosis (or primary hyperoxaluria), various elec- Diets that contain insufficient potassium, particularly
trolyte abnormalities (hypophosphatemia), and when high in protein, or that are acidified, have the
severe anemia. For discussion of these conditions potential to induce hypokalemia, particularly when fed
please refer to the chapter on The Cat With General- to a cat with existing renal failure.
ized Weakness. ● Long-term feeding of these diets can result in renal
damage.
DISEASES CAUSING NECK The administration of IV fluids with insufficient
VENTROFLEXION amounts of potassium** can result in clinically signif-
icant hypokalemia. This is most likely to occur in cats
that have renal failure, have post-obstructional diuresis,
HYPOKALEMIC MYOPATHY*** have not eaten recently, or have been experiencing vom-
(INCLUDING HYPOKALEMIC MYOPATHY iting and/or diarrhea. The administration of excessive
OF BURMESE KITTENS) amounts of furosemide, particularly to animals that have
not eaten recently, can have a similar effect.
Classical signs
Congenital hypokalemic myopathy may be seen in
● General muscle weakness, neck Burmese kittens*.
ventroflexion, a stiff, stilted gait and ● It is similar to periodic hypokalemic paralysis in
muscle pain. man.
● In severe cases, respiratory paralysis. ● It is believed to result from a sudden shift of potas-
● Other signs relate to the underlying sium from the extracellular to the intracellular com-
disease, e.g. polyuria and polydipsia in partment.
● May be seen with no other signs in Hyperthyroidism** may occasionally present with
Burmese kittens. hypokalemia and/or thiamine deficiency and therefore
result in generalized muscle weakness.
● It has been suggested that the hyperadrenergic state
Pathogenesis of hyperthyroidism enhances insulin release, which
may lead to a shift in potassium into the intracellu-
Hypokalemia may result from:
lar compartment.
● Decreased potassium intake (incorrect diets).
● Hypokalemia most typically occurs immediately
● Excessive losses (chronic renal failure, renal
after thyroidectomy, or may be associated with the
tubular acidosis, inappropriate IV fluid adminis-
stress of handling.
tration, excessive frusemide administration, ● Hypokalemia and hypocalcemia may occur concur-
hyperaldosteronism, vomiting and diarrhea).
rently.
● Increased potassium entry to cells (Burmese kit-
● Correction of the hypokalemia may precipitate clin-
tens, hyperthyroidism, insulin over-dose).
ical signs of hypocalcemia.
● Varying combinations of all three.
● Hyperthyroidism may also cause weakness by
Hypokalemia induces muscle weakness by causing affecting other mechanisms of muscle or nerve
a state of persistent depolarization and loss of excitability. function.
● Severe hypokalemia can result in rhabdomyolysis,
Hyperaldosteronism (Conn’s syndrome) is being
however, the mechanism of action is unclear.
reported more frequently.
Hypokalemic myopathy is most commonly associated ● It is caused by a functional adrenal tumor, or ade-
with chronic renal failure***. nomatous hyperplasia of the adrenal glands.
● The production of aldosterone results in excessive ● Head tremors, peculiar knuckling of the carpus, a
urinary potassium losses. tendency to sink on their hocks, and to sit with their
stifles abducted.
Clinical signs
Hypokalemia can affect any age, sex or breed of cat. Diagnosis
● It is seen most frequently in older cats; associated
Signs of myopathy usually occurs when the serum
with chronic renal failure, hyperthyroidism and,
potassium level falls below 3.5 mmol (Eq)/L (normal
occasionally, hyperaldosteronism.
4–5 mmol(Eq)/L).
● Hypokalemia in Burmese kittens is usually seen in
kittens, of either sex, from 2–6 months of age. Serum creatinine kinase (CK) levels are usually
elevated (500–10 000 IU/L; normal 50–150 IU/L). In
Clinical signs of hypokalemia often take one of two
hypokalemic Burmese kittens CK can be very ele-
forms; mild and chronic, or severe and acute.
vated (> 50 000 IU/L).
● The mild and chronic form produces vague signs
of inappetence, gradual weight loss and reduced Once hypokalemic myopathy has been diagnosed it
activity (reluctance to walk or jump). In older cats is necessary to differentiate between the various
these signs are often attributed to aging. causes.
● The severe form presents acutely with general ● Assessment of serum urea and creatinine levels, and
muscle weakness, often with neck ventroflexion, a urine specific gravity, will determine whether there
stiff, stilted gait, reluctance to walk, and muscle pain. is underlying renal disease.
● Signs of mild hypokalemia have often been present ● Serum thyroxine levels will be elevated in cases of
for weeks to months before the acute crisis. hyperthyroidism.
● Some cats are anorexic or dysphagic. ● Cats with hyperaldosteronism become dehy-
● Some cats develop ataxia or collapse. drated, and eventually develop raised urea and cre-
● Severely affected cats may die of respiratory atinine levels.
paralysis. – This should not be misinterpreted as renal failure.
● Clinical signs may be transient, episodic or persistent. – The adrenal tumor can usually be visualized by
● Postural reactions and spinal reflexes are normal. ultrasonography.
– Plasma aldosterone levels will be moderately to
Cats with underlying chronic renal failure may also
markedly raised. In the case of hyperplastic
show:
change, the plasma aldosterone level may only
● Polyuria, polydipsia, progressive weight loss and an
be at the top end of the reference range, but the
ill-kept coat.
plasma renin activity will be mildly to moder-
Cats with underlying hyperthyroidism may also show: ately reduced.
● Polyphagia, hyperactivity, irritability and weight ● Calculating the fractional excretion of potassium
loss. (FEK+) can make an assessment of urinary potas-
● Some cats may be episodically or consistently sium loss.
“apathetic”. – Collect urine and serum at the same time.
● This may result from concurrent cardiac disease or
hypokalemia. Urine potassium × Serum creatinine × 100
FEK+ % =
Serum potassium Urine creatinine
Cats with underlying hyperaldosteronism may also
show:
– The potassium and creatinine units must be the
● Insidious weight loss, and signs of systemic hyper-
same.
tension.
– FEK+ should be < 5% in potassium-depleted cats
Burmese cats with hypokalemic myopathy may also with normal renal function (e.g. Burmese).
show: – FEK+ > 10–15% indicates significant renal
● Clinical signs induced by exercise or stress. loss.
– Losses can be determined more accurately – Where possible, give oral potassium prior to
measuring 24-hour urinary potassium loss. IV fluids.
– Oral administration of potassium is more
Electrodiagnostic testing may be normal, or may show
effective in normalizing potassium than IV
positive sharp waves and fibrillation potentials. Nerve
administration.
conduction velocities are normal.
– Only use fluids to administer potassium in the
Muscle biopsies may reveal normal muscle, or mild most severely affected cats.
myofiber necrosis, with little or no evidence of inflam- – When using fluids give a low volume with a high
mation. potassium concentration e.g. 160 mmol (Eq)/L
at 2.0 ml/kg/h. Ideally, do not exceed 0.5 mmol
(Eq)/kg/h or cardiac arrest may occur.
Oral supplementation is necessary in all cases.
Myasthenia gravis, polymyositis and organophos- ● It should be started immediately, as IV administra-
phate toxicity can all cause similar clinical signs. tion is often not adequate to normalize potassium.
● Potassium gluconate solution (Kaon Elixir), tablets
Since hypokalemia is so readily detected by assessment
or powder (Tumil K) can be added to food (4–10
of serum biochemistry, more sophisticated diagnostics
mmol (Eq)/PO q 24 h, in divided doses).
are not usually required.
● Feeding a diet that is high in potassium can also
● If it becomes necessary to rule out specific differ-
help.
entials, electromyographic studies, IV edropho-
● The level of supplementation should be adjusted
nium (Tensilon test), assessment of serum
according to serum potassium levels.
anti-acetylcholine receptor antibodies and serum
● The duration of supplementation will depend on the
cholinesterase levels, toxoplasmosis serology
underlying cause.
and/or muscle biopsy may be required.
– Cats that had been fed an unsuitable diet, given
inappropriate IV fluids or excessive amounts of
frusemide will cease to require additional potas-
Treatment
sium once the precipitating cause has been cor-
Severely affected cases may require immediate IV rected.
potassium infusion. – Cats with chronic renal failure will require long-
● This requires the use of an infusion pump, constant term supplementation. Maintenance doses are
cardiac monitoring, and repeated evaluation of typically 2–5 mmol (Eq)/cat q 12–24 h.
serum potassium levels (every 2–4 hours until the – Some Burmese cease to need supplementation
serum level has risen to 3.5 mmol (Eq)/L). after they are about a year old, others need life-
● In severe cases, despite potassium supplementation, long supplementation, with an increasing need
IV fluid administration may result in hemodilution, during periods of stress.
diuresis with exacerbation of urinary potassium
Where possible, treat the underlying disease or cor-
loss, progressive hypokalemia, and worsening clin-
rect the dietary or fluid imbalance.
ical signs resulting in respiratory muscle paralysis
and respiratory arrest. Cats with hyperaldosteronism may benefit from
– Inappropriate fluid administration is the most spironolactone (an aldosterone antagonist; up to 50
common cause of death in hypokalemic cats. mg/kg PO q 24 h), in addition to potassium supple-
– It is therefore essential to monitor these patients mentation.
closely.
– Respiratory muscle paralysis typically occurs
when serum potassium levels fall below 2
Prognosis
mmol/L.
– Ventilatory support is required to save the cat Severely affected cats, particularly those with respira-
and may need to be continued for 24–48 hours. tory distress, carry a guarded short-term prognosis.
The long-term prognosis is dependent on the nature of Clinical signs

the underlying disorder.
● Complete recovery of muscle strength can take sev-
Compared to dogs, myasthenia gravis is relatively
eral weeks. rare in cats.
● The congenital form is seen in young cats, usually
● In many cases, ongoing renal disease, hyperthy-
roidism or hyperaldosteronism will ultimately kittens of less than 6 months of age.
● The acquired form occurs in adults, and
result in the cat’s death.
Abyssinian and Somali cats may be predisposed.
Hypokalemic Burmese generally have a good progno-
sis, although some need life-long supplementation. The clinical signs are the same in both forms of the
disease.
Prevention Affected cats tend to sleep excessively and are reluc-

tant to exercise.
Feed diets with sufficient potassium. ● When they do exercise they develop muscular
Measure serum potassium in ‘at-risk’ cats and sup- weakness, which may be seen as progressive stiff-
plement when levels are found to be low. ‘At-risk’ cats ness, a crouching gait, neck ventroflexion and
include: superimposed muscle tremors.
● They eventually collapse in sternal recumbency,
● Cats with chronic renal failure.
● Hospitalized anorexic cats.
often with their head to one side of their front paws.
● Weakness may involve all four limbs simultane-
● Those receiving intravenous fluid therapy, high
doses of frusemide or insulin therapy. ously, or affect the fore- or hindlimbs more
● Those with severe vomiting and diarrhea.
severely.
In Burmese cats, pedigree analysis and a selective Weakness of the facial muscles may result in paresis
breeding program may help to remove the condition. of eyelids causing narrowing of the palpebral fissure,
absence of a palpebral reflex, protrusion of the third
eyelids, inability to close the mouth and apparent
MYASTHENIA GRAVIS (CONGENITAL AND hypersalivation.
ACQUIRED)*
Dysphonia may be noticed, with a low or barely audi-
Classical signs ble miaow.
● Exercise-induced muscular weakness, Megaesophagus may occur occasionally, and lead to

progressive stiffness, neck ventroflexion aspiration pneumonia.
and muscle tremors. Severe weakness of the respiratory muscles can also
● Facial weakness, narrowing of the lead to respiratory distress.
palpebral fissure and protrusion of the
third eyelids. Some cases of acquired myasthenia gravis have been
● Occasionally, regurgitation and/or associated with thymic abnormalities (thymoma, cystic
respiratory distress. thymus, thymic hyperplasia), and/or immune-mediated
polymyositis (see below).
● Cats with thymoma may show signs of regurgita-
Pathogenesis tion, and/or dyspnea.
● The latter may result from the mass within the
Two forms of myasthenia gravis have been reported in
cats, a congenital and an acquired* form. chest, or pleural effusion.
The congenital form may be caused by a lack of acetyl-

choline receptors. Diagnosis
The acquired form occurs when auto-antibodies are Cats with myasthenia gravis are usually of good body
directed against acetylcholine receptors. condition, with normal complete blood counts and
serum biochemistry. Some may show slightly elevated needs to be adjusted for each individual cat, starting
creatinine kinase levels. from a low dose.
Thoracic radiography may occasionally show megae- Neostigmine (Prostigmine; 0.01–0.1 mg/kg IV, IM,
sophagus, thymic enlargement and/or aspiration pneu- SC) can be used to treat a myasthenic crisis. For longer-
monia. term use it can be given orally (0.1–0.25 mg/kg), but its
short half-life requires it to be given q 4–6 h.
Tensilon test: Affected cats will usually show a brief
positive response to the ultra-short-acting cholinesterase Some acquired cases require the addition of prednisolone
inhibitor edrophonium chloride (Tensilon: 0.2–0.5 (1–2 mg/kg PO q 12 h). The dose of corticosteroid can
mg/kg IV). usually be reduced after a few days to weeks, and discon-
● Response is usually brief and may only be slight, tinued after a few weeks of alternate day dosing.
e.g. widening of the palpebral fissure.
Some cats may go into remission. It can therefore be
● Unfortunately, this test is not specific for myasthe-
useful to monitor the serum anti-acetylcholine receptor
nia gravis.
antibody titer. Once it has fallen back to zero medica-
● When using lower doses it is rare to produce a
tion may be discontinued.
cholinergic crisis (bradycardia, hypersalivation,
dyspnea and cyanosis). If this does occur it can be Where a thymoma is present, its removal may be bene-
treated with atropine (0.05 mg/kg IV). ficial.
Electrodiagnostic testing will show a decremental
response to repetitive nerve stimulation. Prognosis
In the acquired form, anti-acetylcholine receptor Prognosis is very variable. Severe cases may die from
antibodies can be detected in the serum and anti-recep- aspiration pneumonia.
tor antibodies can be seen in muscle biopsies at the neu-
Some congenital and acquired cases will maintain
romuscular junction.
improvement after withdrawal of medication.
It is not uncommon for acquired cases to go into remis-
Differential diagnosis sion, and recurrences may occur.
Hypokalemic myopathy, polymyositis and organo-
phosphate toxicity can all cause similar clinical signs. POLYMYOSITIS (IMMUNE-MEDIATED AND
TOXOPLASMOSIS)
The lack of changes in serum biochemistry, adequate
serum cholinesterase levels, and the specific elec-
Classical signs
tromyographic findings will help to rule out these dif-
ferentials. While cats with either myasthenia gravis or ● Generalized muscle weakness, neck
organophosphate toxicity may show a decremental ventroflexion and/or dysphagia.
response to repetitive nerve stimulation, the clinical ● Megaesophagus, regurgitation and/or
signs will worsen if a cat with organophosphate toxicity aspiration pneumonia.
is given IV edrophonium. ● Muscle pain, depression and reluctance to
move.
Definitive diagnosis of myasthenia gravis requires pos-
● Often part of systemic illness.
itive electromyographic studies and response to edro-
phonium and, in the acquired form, the presence of
serum anti-acetylcholine receptor antibodies. Pathogenesis
Polymyositis may be idiopathic, immune-mediated, or
Treatment result from Toxoplasma gondii or retroviral infection.
Treatment usually consists of pyridostigmine bromide Polymyositis may affect both skeletal and smooth muscle,
(Mestinon: 0.5–3.0 mg/kg PO q 8–12 h). The dose resulting in generalized weakness and megaesophagus.
Immune-mediated polymyositis may be associated Serum antinuclear antibody tests may be positive in
with thymoma. When this occurs myasthenia gravis immune-mediated polymyositis.
may be seen concurrently (see above).
Serum toxoplasmosis IgM (and sometimes IgG) levels
In cats, most T. gondii infections are asymptomatic. are likely to be elevated in cases of toxoplasmosis
When clinical signs are seen they most frequently relate polymyositis. Where only IgG levels can be assessed,
to the lungs, liver, gastrointestinal tract, eyes or brain. paired serum samples usually show a fourfold increase
Signs relating to muscle involvement are rare. in titer over a 2–4-week period.
● Toxoplasmosis polymyositis is seen most fre-
All cases of polymyositis should be assessed for FIV
quently as part of more generalized disease.
and FeLV infection.
● It occurs most commonly in peri-natally infected
kittens or immunosuppressed adults. Electromyographic abnormalities may include sponta-
neous positive waves and fibrillation potentials.
While Neospora caninum has been shown to cause
polymyositis experimentally, natural feline neosporosis Muscle biopsies may show multifocal infiltration of
has not been detected. muscle fascicles with lymphocytes, macrophages and,
occasionally, neutrophils. In the cases of toxoplasmosis
FIV infection may be able to cause an inflammatory
polymyositis the organisms may be detected. However,
polymyositis.
failure to detect T. gondii cysts does not rule out this
etiology.
Clinical signs
Polymyositis may cause generalized muscle weak-
ness, including neck ventroflexion and/or dysphagia.
While myasthenia gravis and organophosphate toxi-
Muscle pain may be present, the cats are often
city can cause similar clinical signs, the most impor-
depressed and reluctant to move.
tant differential is hypokalemic myopathy.
Signs of megaesophagus may include regurgitation ● Polymyositis and hypokalemic myopathy can be
and/or aspiration pneumonia. clinically identical, and both can have moderate to
markedly elevated serum creatinine kinase levels.
Cats with concurrent thymoma may show regurgitation
● The lack of other changes in serum biochemistry,
and/or dyspnea. The latter may result from the mass
adequate serum cholinesterase levels, lack of serum
within the chest or pleural effusion.
anti-acetylcholine receptor antibodies, and elec-
Toxoplasmosis polymyositis is typically seen as part of tromyographic studies, will help to rule out these
more generalized disease. Affected cats are usually sys- differentials.
temically ill, often with signs of pneumonia.
Definitive diagnosis of polymyositis requires muscle
biopsy and serological testing.
Diagnosis
Thoracic compression may be reduced when a thy- Treatment
moma is present. The presence of a thymoma can usu-
Immune-mediated myositis may respond to pred-
ally be confirmed by assessment of pleural fluid, a fine
nisolone (1.5–2 mg/kg PO q 12 h).
needle aspirate of the mass, or a Tru-cut needle biopsy.
● The dose of steroids can usually be reduced after a
Thoracic radiography may reveal megaesophagus, few weeks as the clinical signs resolve.
pneumonia or thymoma (and possibly pleural fluid). ● Some cases need long-term, alternate-day, medica-
tion.
In all except very chronic cases, serum creatinine
● Assessment of serum creatinine kinase levels may
kinase levels (and other muscle-associated enzymes)
be helpful in monitoring these cases.
are elevated. In most cases the levels are moderate to
markedly increased. If a thymoma is present it should be surgically removed.
First-line treatment for toxoplasmosis (or neosporosis) Since the central nervous system depends almost
consists of clindamycin (12–25 mg/kg q 12 h, PO or IM). entirely on carbohydrate metabolism for its energy, it is
If necessary, this can be given for a number of weeks. particularly susceptible to the effects of thiamine defi-
● Alternatively, trimethoprim/sulfadiazine (30 mg/kg ciency.
PO q 12 h) may be given either alone or in combi-
Thiamine deficiency results in a progressive polioen-
nation with pyrimethamine (0.5 mg/kg PO q 24 h).
cephalomalacia (hemorrhage and necrosis). It predom-
– Unfortunately, both of these drugs are unpalat-
inantly affects the subcortical gray matter of the brain
able.
stem nuclei, particularly the vestibular, lateral genicu-
– Since cats are particularly susceptible to the
late and oculomotor (pupillary constriction) nuclei.
toxic effects of pyrimethamine it should be given
for a maximum of 2 weeks. Thiamine deficiency can effect any age, breed or sex
– Supplementation with folate (folic acid) is rec- of cat.
ommended (1 mg/kg PO q 24 h).
It occurs most frequently in cats that are fed a diet of
● Other, more modern, drugs may also be useful.
mainly fish (usually uncooked) that contain thiaminase
These include azithromycin (7–15 mg/kg q 24 h,
(e.g. cod, catfish).
PO) or clarithromycin (7.5 mg/kg q 12 h PO, com-
bined with pyrimethamine). Prolonged treatment It may also result from prolonged anorexia or malab-
may be necessary. sorption, or the destruction of thiamine during food
preparation (over-cooking) or prolonged storage. The
meat preserver, sulfur dioxide, destroys thiamine and
Prognosis
may produce thiamine deficiency in cats fed pet mince
Prognosis for immune-mediated myositis is fair. preserved with this compound. This can occur even
when the mince is mixed with other food or supple-
Despite aggressive therapy, prognosis for toxoplasmo-
mented with vitamins or brewer’s yeast.
sis myositis is generally poor.
Prevention Clinical signs

It is not possible to prevent immune-mediated myositis. Early signs include anorexia, intermittent vomiting,
Cats may be prevented from becoming infected with depression, ataxia and pupillary dilation.
toxoplasmosis by keeping them indoors, preventing
Progression may result in central vestibular signs
them from hunting, and by feeding well-cooked food.
(including curling up when lifted, and/or a head tilt),
neck ventroflexion, torticollis, behavioural changes,
THIAMINE DEFICIENCY* mydriasis, seizure-like muscle spasms or stupor.
True seizures are rare but episodes of opisthotonic pos-
Classical signs turing with paddling, spastic neck ventroflexion, and
● Anorexia and depression, followed by body contortions may occur, especially if the cat is
ataxia, neck ventroflexion, torticollis and lifted. These can have a seizure-like appearance.
vestibular signs. Further progression may lead to coma and death.
● May progress to seizure-like muscle
spasms, stupor and death.
● History of fish-only diet.
Diagnosis
Measurement of blood thiamine level is not readily
Pathogenesis available.
Thiamine (vitamin B1) is essential for normal carbohy- Diagnosis is supported by improvement within 24
drate metabolism and gluconeogenesis. hours of thiamine supplementation.
Differential diagnosis DEVON REX MYOPATHY

Hypokalemic myopathy, myasthenia gravis,
polymyositis and organophosphate toxicity can all Classical signs
cause neck ventroflexion. ● Young Devon Rex cats.
However, thiamine deficiency usually causes an ● Generalized muscle weakness, with
active rather than passive ventroflexion, together marked ventroflexion of the head and neck,
with excessive muscle tone, torticollis, and more and dorsal protrusion of the scapulae.
obvious central signs, such as a head tilt, behavioral ● Signs may become accentuated during
changes, or seizure-like paddling or spasticity with locomotion, micturition, defecation, stress
opisthotonos. or excitement.
Other differentials can usually be excluded by perform-

ing a thorough physical and neurological examination,
assessing serum biochemistry (including renal Pathogenesis
enzymes, creatinine kinase and electrolytes), and a rest- The disease is inherited in an autosomal recessive
ing thyroxine level. Occasionally it may be necessary to manner.
assess serum cholinesterase levels or look for serum
anti-acetylcholine receptor antibodies. The pathology is suggestive of a muscular dystrophy.
Skeletal and smooth muscles are affected (neck ven-
troflexion, megaesophagus).
Treatment
10–20 mg/cat of thiamine IM, q 8–12 h. For longer- Clinical signs
term supplementation; 5–30 mg/cat PO q 24 h.
The disease is sometimes termed “spasticity” by breed-
If clinical signs are severe, oxygen may be beneficial. ers. However, there are no signs of central nervous sys-
The underlying cause should be corrected, e.g. feed a tem involvement.
suitable diet. Oral thiamine supplementation is usu- Disease is seen in Devon Rex cats of either sex, with
ally needed for a week after the diet has been cor- signs becoming apparent from 3 weeks to 6 months
rected. of age.
The severity of the disease varies between cats, and
may be static or slowly progressive.
Prognosis
Affected cats show generalized muscle weakness,
The prognosis is good if the condition is recognized often with very marked ventroflexion of the head and
and treated early. neck, and dorsal protrusion of the scapulae.
Once a cat has become semiconscious, prognosis is ● They typically have a high-stepping forelimb gait,
poor. and tire easily, with head bobbing, progressive pro-

trusion of the scapulae, shortening of the stride, and
Some chronic cases respond to treatment, but may be superimposed muscle tremors.
left with neurological deficits. ● They eventually collapse in sternal recumbency,
usually with their head to one side of their
forepaws.
Prevention Clinical signs may be exacerbated by micturition, defe-
Feed suitable diets and supplement anorexic cats with cation, stress, concurrent illness, cold ambient temper-
B vitamins. ature or excitement.
At rest they often adopt a characteristic “dog-begging” Differential diagnosis

position, with their forepaws resting on a convenient
raised object. Hypokalemic myopathy, myasthenia gravis,
polymyositis and organophosphate toxicity can all
Signs of megaesophagus may include regurgitation cause similar clinical signs. The most important differ-
and/or aspiration pneumonia. entials are probably hypokalemia and congenital myas-
Difficulty in maintaining a normal head position may thenia gravis.
result in frequent episodes of laryngospasm after Devon Rex myopathy is the most likely diagnosis in
obstruction of the pharynx with food. This is the a young Devon Rex cat which is showing typical clini-
most usual cause of death in these cats. cal signs, its serum biochemistry is normal, it lacks
Mild muscle atrophy may occasionally be evident. a decremental response to repetitive nerve stimulation,
has adequate serum cholinesterase levels, and its clini-
cal signs worsen when it is given IV edrophonium
(Tensilon test). Confirmation of the diagnosis requires
Diagnosis pedigree analysis and muscle biopsy.
Complete blood count and serum biochemistry, includ-
ing creatinine kinase and aspartate aminotransferase Treatment
(AST), are usually normal. There is no treatment for this condition. Aspiration
Thoracic radiography will usually reveal a megaesopha- pneumonia will require antibiotics.
gus and/or aspiration pneumonia.
Neurological examination, muscle tone and withdrawal Prognosis
reflexes are normal. Clinical signs may deteriorate up to 6–9 months of age,
Electrodiagnostic studies may show sparse fibrillation after which time the disease is usually stable or only
potentials, and positive sharp waves. Nerve conduction slowly progressive.
velocities are normal and there is no decremental The course of the disease will depend on the severity of
response to repetitive nerve stimulation. the myopathy, particularly the degree of pharyngeal
Gross post-mortem examination may reveal megae- involvement. Laryngospasm is the usual cause of death.
sophagus, reflux oesophagitis, aspiration pneumonia
and/or gastroparesis. Prevention
Skeletal muscle appears grossly normal. Since the disease is inherited, pedigree analysis and a
Histopathological changes vary between cats, and also selective breeding program are being used to remove
within different muscles of the same cat. the condition from the breed.
● Findings range from normal, to those indicative
of myopathy, possibly muscular dystrophy. They
include increased variability in myofiber size, SUBACUTE ORGANOPHOSPHATE
individual myofiber necrosis, regeneration and TOXICITY
fibrosis.
● The degree of change depends on the severity of
Classical signs
disease, and the advancing age of the cat.
● The dorsal cervical and proximal forelimb muscles, ● Muscarinic signs (miosis and salivation)
especially the m. triceps brachii, are usually most may be absent.
severely affected, and are therefore recommended ● Generalized muscle weakness may be
for biopsy. seen as neck ventroflexion, and/or a stiff
stilted gait.
Nerves are not affected.
continued
Classical signs—Cont’d Electrodiagnostic testing will show a decremental

response to repetitive nerve stimulation.
● Muscle fasciculations or tremors may be
present. Tensilon test: IV edrophonium (Tensilon: 0.2–0.5
mg/kg) will usually induce a cholinergic crisis (brady-
cardia, hypersalivation, dyspnea and cyanosis), without
Pathogenesis a positive improvement in muscle strength. If this
occurs it can be treated with IV atropine (0.05 mg/kg).
Organophosphate toxicity can affect any age, breed or
sex of cat.
Organophosphate compounds irreversibly bind to Differential diagnosis
acetylcholinesterases at cholinergic synapses, resulting Hypokalemic myopathy, myasthenia gravis and
in continuous stimulation. polymyositis can all cause similar clinical signs.
In cats, chronic exposure can result in peripheral Lack of changes in serum biochemistry, lack of serum
neuropathies. anti-acetylcholine receptor antibodies, and a negative
Unlike other organophosphates fenthion toxicity response to IV edrophonium in the face of a decremen-
produces predominantly nicotinic signs (muscle tal response to repetitive nerve stimulation, will help to
weakness), with few muscarinic signs (autonomic rule out the differential diagnoses.
effects). Diagnosis is usually confirmed on finding reduced
serum cholinesterase levels, typically with a history of
exposure to organophosphate.
Clinical signs
The variety of clinical signs will depend on the degree
of concurrent muscarinic involvement. In subacute or Treatment
chronic cases these signs (miosis, salivation, vomiting, Supportive therapy may include use of IV fluids, nutri-
bradycardia) may be absent. tional support, control of body temperature and good
In chronic cases, or in fenthion toxicity, the only sign nursing care.
may be generalized muscle weakness, often seen as Atropine (0.1–0.2 mg/kg SC, as required) may be used
neck ventroflexion and/or a stiff stilted gait. Severe to chemically compete with acetylcholine binding to
muscle weakness may cause respiratory paralysis. acetylcholine receptors.
Muscle fasciculations or tremors may be present. Oximes (pralidoxime chloride; 20 mg/kg IM q 8 h)
There is no muscle pain. may help by releasing the inhibited cholinesterase.
However, oximes are of most benefit if given within the
first 24 hours of exposure.
Diagnosis Diphenhydramine has been used to reverse nicotinic
There is usually a history of exposure to an signs in dogs with fenthion toxicity.
organophosphate, typically in the form of insecticide.
Complete blood count and serum biochemistry (includ- Prognosis
ing creatinine kinase) are usually normal. It is often not possible to save severely affected cats.
A low serum cholinesterase level will support this Less severely affected cats may recover, often follow-
diagnosis. In affected cats the levels are usually less than ing weeks of nursing.
500 IU (normal 900–1200 IU). However, in cases where
chronic exposure has caused polyneuropathy the serum Chronically affected cats may be left with permanent
cholinesterase levels may be normal. nerve damage.
Prevention Differential diagnosis

Prevent access to organophosphate compounds. Hypokalemic myopathy, myasthenia gravis,
polymyositis and organophosphate toxicity can all
cause similar clinical signs.
ADULT-ONSET MOTOR NEURON DISEASE
Lack of changes in serum biochemistry, lack of serum
Classical signs anti-acetylcholine receptor antibodies, adequate serum
cholinesterase levels, electromyographic studies, and
● Adult-onset, chronic, progressive disease.
slowly progressive disease all help to rule out the dif-
● Generalized weakness, neck ventroflexion,
ferential diagnoses.
and dysphagia.
● Muscle tremors/fasciculations (particularly Histopathology of the spinal cord is required to make a
of the head and tongue). definite diagnosis.
● Muscle atrophy.
Treatment
Pathogenesis
There is no known treatment.
The cause of this rare disease is unknown.
Clinical signs result from chronic degeneration and loss
of motor neurons. Prognosis
Disease may take months to years to progress to the
Clinical signs
point where the cat requires euthanasia on humane
Disease is seen in adult cats. grounds.
Chronically progressive signs include generalized weak-
ness, neck ventroflexion, dysphagia and muscle atrophy.
HYPERNATREMIC MYOPATHY
Muscle tremors particularly affect the head.
Muscle fasciculations may be localized to the tongue. Classical signs
Muscle palpation may cause pain. ● Inappetence, progressive muscle
weakness, and depression.
Diagnosis ● Brown-stained urine (myoglobinuria).
Complete blood count and serum biochemistry (includ-
ing creatinine kinase) are usually normal.
Pathogenesis
Neurological examination reveals normal mentation,
This very rare cause of myopathy has only been doc-
cranial nerve function and conscious proprioception.
umented in a single, 7-month-old, cat.
Spinal reflexes are present initially, but are lost as dis-
Hypernatremia resulted from “neurogenic” hypodipsia,
ease progresses.
related to hydrocephalus.
Electromyographic studies may reveal fibrillation
Severe hypernatremia may induce myopathy by accel-
potentials. Nerve conduction velocities may be normal
erating sodium–potassium exchange in myocytes. This
or slightly reduced.
can cause an increase in intracellular sodium and a
Muscle biopsies reveal evidence of denervation. reduction in intracellular potassium. The clinical signs
are therefore similar to those of hypokalemia.
Histopathology of the spinal cord reveals neuron loss
and gliosis in the ventral horns, and consequent atrophy Severe myocyte dysfunction can lead to membrane
of the ventral nerve rootlets. damage, myoglobinemia and myoglobinuria.

The cat showed inappetence, depression and progres- Hypokalemic myopathy, polymyositis, myasthenia
sive muscle weakness, including neck ventroflexion. gravis and organophosphate toxicity can all cause sim-
ilar signs.
Myoglobinuria caused the urine to be brown.
The presence of severe hypernatremia should alert the
Clinical signs were transient. They resolved on correc-
clinician to the possibility of hypernatremic myopathy.
tion of the hypernatremia.
Lack of hypokalemia and resolution of clinical signs on
the correction of the fluid balance, would support the
Diagnosis diagnosis.
Serum biochemistry revealed marked hypernatremia

(> 200 mmol (Eq)/L; normal 148–165 mmol (Eq)/L), Treatment
and increased serum osmolality (431 mmol/kg
(mOsm/L); normal 295–300 mmol/kg (mOsm/L). The To increase the cat’s water consumption it was fed a
serum creatinine kinase level was moderately raised. low-salt diet (PVD CV or NF, Nestlé Purina; Feline
H/D, Hill’s Pet Foods), to which water was added in
Electromyographic abnormalities included prolonged excess of maintenance needs.
insertional activity, fibrillation potentials, positive
sharp waves and bizarre high-frequency discharges. Correction of fluid balance resulted in resolution of
Nerve conduction velocities were normal. clinical signs, and restoration of the hypothalamic-pitu-
itary-adrenal axis.
Muscle biopsies were normal.
Contrast-enhanced computer tomography revealed
marked hydrocephalus. Prognosis
Endocrine studies revealed hypopituitarism, with While correcting the serum osmolality resulted in reso-
hypoadrenocorticism, hypothyroidism and a lack of lution of clinical signs in this case, this may not work
luteinizing hormone. The cat was small for its age, and in future cases, since response will depend on the
never showed signs of estrus. nature of the underlying disorder.
RECOMMENDED READING
Ash RA, Harvey AM, Tasker S. Primary hyperaldosteronism in the cat: a series of 13 cases. J Feline Med Surg 2005;
7: 173–182.
Ducote JM, Dewey CW, Coates JR. Clinical forms of aquired myasthenia gravis in cats. Compend Contin Educ Pract
Vet 1999; 21(2): 440–448.
Javadi S, Djajadiningrat-Laanen SC, Kooistra HS, et al. Primary hyperaldosteronism, a mediator of progressive renal
disease in cats. Domest Anim Endocrinol 2005; 28: 85–104.
Jones BR. Hypokalemic myopathy in cats. In: Bonagura JD (ed) Kirk’s Current Veterinary Therapy XIII.
Philadelphia, PA, W B Saunders, 2000, pp. 985–987.
Malik R, Mepstead K, Yang F, Harper C. Hereditary myopathy of Devon Rex cats. J Small Anim Prac 1993; 34:
539–546.
Nemzek JA, Kruger JM, Walshaw R, Hauptman JG. Acute onset of hypokalemia and muscular weakness in four
hyperthyroid cats. J Am Vet Med Assoc 1994; 205: 65–68.
Podell M. Neurological manifestations of systemic disease, Chapter 103. In: Ettinger SJ, Feldman EC (eds) Textbook
of Veterinary Internal Medicine, 5th edn., Vol 1. Philadelphia, PA, WB Saunders, 1999, pp. 548–552.
Shelton GD. Diseases of the muscle and the neuromuscular junction, Chapter 46. In: Sherding RG (ed) The Cat:
Diseases and Clinical Management, 2nd edn., Vol 2. New York, Churchill Livingston, 1994, pp. 1569–1576.
Shelton GD, Hopkins AL, Ginn PE, et al. Adult-onset motor neuron disease in three cats. J Am Vet Med Assoc 1998;
212: 1271–1275.
PART 11
Cat with an abnormal gait
42. The weak and ataxic or paralyzed cat

Paul A Cuddon
KEY SIGNS
● Incoordination and decreased proprioception (misplacement or knuckling of the
foot).
● Weakness of one or more limbs (feet cross or are placed too far apart).
● Complete loss of any voluntary movement (paralyzed).
MECHANISM?
● Ataxia and paresis occurs when there is physical or functional disruption to both the
motor and sensory pathways of the nervous system.
● This can occur at any point along the neuraxis from the cerebrum to the peripheral nervous
system.
WHERE?
● Cats solely presenting with ataxia and paresis/paralysis most commonly have spinal cord
disease.
WHAT?
● The most common causes of spinal cord ataxia and paresis in cats are
infection/inflammation and trauma.
906
42 – THE WEAK AND ATAXIC OR PARALYZED CAT 907

Diseases causing a weak and ataxic or paralyzed cat
ANOMALY
● Congenital abnormalities of the vertebral body* (p 918)
Tetraparesis or paraparesis and ataxia (UMN or LMN) usually in cats less than one year of age due
to static or dynamic cord compression.
● Congenital abnormalities of the spinal cord (spina bifida, etc.)* (p 918)
LMN urinary/fecal incontinence, an easily expressible atonic bladder, megacolon and a hopping
gait in young kittens at or soon after birth.
NEOPLASIA
● Spinal lymphosarcoma*** (p 909)
Chronic progressive ataxia, asymmetrical paraparesis and focal spinal pain in young adult cats
often associated with FeLV infection.
● Spinal meningioma** (p 914)
Spinal pain and chronic progressive UMN or LMN tetraparesis or paraparesis in cats greater than
9 years of age.
NUTRITIONAL
● Hypervitaminosis A* (p 921)
Cervical pain and rigidity, thoracic limb lameness, and tetraparesis/tetraplegia in cats usually
between 2–9 years of age.
● Feline infectious peritonitis*** (p 911)
Chronic progressive tetraparesis or paraparesis in young cats less than 3 years of age, commonly
accompanied by decreased mentation, seizures, intention tremor and/or central vestibular signs.
INFLAMMATION (IDIOPATHIC)
● Feline polioencephalomyelitis* (p 917)
A stiff, staggering gait with paraparesis and thoracolumbar spinal pain in cats of any age, often
with decreased mentation and seizures.
ISCHEMIA
● Aortic thromboembolism** (p 915)
Acute femoral and sciatic nerve hyporeflexia, cold cyanotic pelvic limbs and painful firm gastroc-
nemius muscles in any aged cat.
● Fibrocartilaginous embolism* (p 922)
Acute, non-painful LMN paraparesis/paraplegia and urinary and fecal incontinence in any aged cat.
TRAUMA
● Spinal cord trauma – fractures and luxations*** (p 912)
An acute transverse myelopathy with varying degrees of UMN or LMN paresis to paralysis with
spinal pain. Other signs include split nails and skin abrasions and bruising.
908 PART 11 CAT WITH AN ABNORMAL GAIT
● Cats with brainstem disease will demonstrate cra-

INTRODUCTION nial nerve abnormalities as well as an ipsilateral
hemiparesis or tetraparesis.
MECHANISM? Most polyneuropathies manifest as generalized weak-
Ataxia and paresis occur when there is physical or ness without ataxia. In many cases of peripheral nerve
functional disruption to both the motor and sensory disease, sensory tests such as proprioception and tactile
pathways of the nervous system. placing will be normal despite obvious muscle weak-
ness.
Paresis is a deficit of voluntary movement, leading to
weakness in one limb (monoparesis), both pelvic limbs Localization of myelopathies is dependent on deter-
(paraparesis), the limbs on one side of the body (hemi- mining whether the thoracic and pelvic limbs have
paresis), or all four limbs (tetraparesis). It is caused by upper (UMN) or lower motor neuron (LMN) signs.
disruption of the voluntary motor pathways anywhere Cats with UMN paresis will demonstrate normal to
from the cerebral cortex through the brainstem and increased segmental spinal reflexes (myotatic or tendon
spinal cord to the spinal cord segments and the peri- reflexes, muscle tone and withdrawal reflexes) whereas
pheral nerves supplying muscles. Neurological testing cats with LMN paresis will show decreased to absent
to determine whether a cat is paretic includes gait segmental spinal reflexes. An UMN bladder, likewise,
analysis and postural reaction testing, which includes will have increased tone and be difficult to express due
hopping, wheel-barrowing, hemi-standing/hemi-walking, to external (+/− internal) urethral sphincter hypertonia,
and the extensor postural thrust. The term paralysis is whereas a LMN bladder will be flaccid (or atonic) and
reserved for the patient who has a complete loss of any easily expressed due to external urethral sphincter
voluntary movements. hypo- to atonia.
Ataxia is a lack of coordination of the limbs or trunk The classic spinal cord divisions when localizing a
produced by disruption of the sensory proprioceptive myelopathy are as follows:
pathways of the spinal cord and brainstem. Lesions of ● Cervical spinal cord (C1–C5) – UMN tetraparesis
the cerebellum and the vestibular system also can pro- to tetraplegia.
duce ataxia. Sensory ataxia, the disruption of sensory ● Cervical intumescence (C6–T2) – LMN signs to
proprioceptive pathways, can be assessed via such tests thoracic limbs and UMN signs to pelvic limbs.
as proprioception and tactile placing. ● Thoracolumbar spinal cord (T3–L3) – UMN para-
paresis to paraplegia. UMN bladder dysfunction.
Most cats with spinal cord disease have a combination ● Lumbar spinal cord (L4–L6) – mixed UMN and
of both ataxia and paresis, since most myelopathies
LMN paraparesis to paraplegia (LMN to the
cause disruption of both the motor and sensory sys-
femoral nerve and UMN to the sciatic nerve). UMN
tems. In many circumstances, therefore, separation of
bladder and perineal reflexes.
ataxia and paresis becomes almost impossible on rou- ● Lumbosacral spinal cord (L6–S2) or cauda
tine neurological examination.
equina injury – LMN paraparesis to paraplegia
associated with the sciatic nerve and LMN bladder.
WHERE?
Cats presenting solely with ataxia and paresis/paralysis
WHAT?
most commonly have spinal cord disease.
The most common causes of spinal cord ataxia and
Weakness and ataxia can also occur with cerebral and
paresis in cats are infectious (including feline infec-
brainstem disease.
tious peritonitis virus (coronavirus)), neoplasia (lym-
● However, cats with cerebral disease will usually
phosarcoma) and trauma.
show seizures, behavior change, aimless wander-
ing, and pacing along with the ataxia and contralat- Primary spinal neoplasia (meningioma), inflamma-
eral hemiparesis or tetraparesis. tion (feline polioencephalomyelitis), and ischemia
(aortic thromboembolism and fibrocartilaginous Tumors occur predominantly between T3–L4.

embolism) are less common.
Involvement of the brachial intumescence and plexus
Intervertebral disc disease is very rare. also can occur.
Cervical spinal cord involvement is rare.
DISEASES CAUSING A WEAK AND
ATAXIC OR PARALYZED CAT The most common clinical signs include progressive
ataxia, asymmetric paraparesis and focal spinal
pain.
SPINAL LYMPHOSARCOMA***
If there is involvement of the brachial or lumbosacral
Classical signs intumescences, LMN signs will occur.
● Chronic progressive ataxia. Nerve root involvement may result in lameness and
● Asymmetric paraparesis. limb pain.
● Focal areas of spinal pain. Acute exacerbation of signs is commonly associated
with hemorrhage.
Pathogenesis Weight loss is the most common extraneural sign.
Lymphosarcoma is the most common feline The most common extraneural tumor site associated
neoplasia. with spinal lymphosarcoma is the kidney.
5–15% of cats with lymphoreticular malignancies

develop neurologic involvement. Diagnosis
88% of cats with CNS involvement show thoracic and Complete blood count, biochemistry parameters and
lumbar myelopathy, although the brain may also be urinalysis are often normal, although non-regenerative
affected. anemia or leukemia may occasionally be seen.
Spinal lymphosarcoma is often FeLV related. Many cats are seropositive for FeLV or positive on
indirect fluorescent antibody testing of bone marrow.
Epidural lymph channels and extramedullary hemato-
poietic tissue are possible sites for development of pri- Cerebrospinal fluid (CSF) analysis usually shows
mary spinal lymphosarcoma. a mixed pleocytosis (mean of 161 cells/mm3 [161 cells/μl]
with a range of 0–1625 cells/mm3 [0–1625 cells/μl]) and
Tumor growth commonly occurs longitudinally along a protein increase (mean of 1.34 g/L [134 mg/dl] with
the spinal canal (the epidural space is a low-resistance a range of 0.12–4.05 g/L [12–405 mg/dl]).
channel).
A monomorphous population of neoplastic lympho-
79% of cats with spinal lymphosarcoma have solitary cytes will be seen in some cases.
epidural lesions.
Survey spinal radiographs are usually normal.
Multifocal lesions are also possible, as is tumor
involvement of multiple nerve roots. MRI scan or myelography shows single or multiple
asymmetric extradural spinal cord compression(s).
Clinical signs
Spinal lymphosarcoma is most commonly seen in
young cats (≤ 3 years). Infectious diseases, such as feline infectious peritonitis,
toxoplasmosis and cryptococcosis also may produce
Males are more commonly affected. signs of progressive spinal cord dysfunction.
Most cats present with an initial insidious course of neu- However, unlike spinal lymphosarcoma, most infectious
rologic dysfunction followed by acute deterioration. conditions usually result in multifocal neurologic
dysfunction, with involvement of the cerebrum, brain- Treatment

stem and/or cerebellum.
● Ocular manifestations secondary to uveitis, chori-
Spinal lymphosarcoma is radiosensitive.
● Rapid reduction in tumor volume can occur within
oretinitis and optic neuritis are also often present
with CNS infections. hours of delivering a single large palliative dose of
radiation (3–4 Gy).
CSF analysis often helps differentiate between infec-
tious diseases and spinal lymphosarcoma. Chemotherapy is important for systemic control
● Feline infectious peritonitis usually produces
of lymphosarcoma although most chemotherapeutic
a marked increase in protein (usually greater than agents do not cross the blood–brain barrier.
1 g/L [100 mg/dl] and often greater than 2 g/L Cytosine arabinoside may also help control spinal
[200 mg/dl]) and white blood cells (mean of lymphosarcoma.
734 cells/mm3 [734 cells/μl] with a range of ● This anti-metabolite drug crosses the blood–brain
69–2000 cells/mm3 [69–2000 cells/μl]), with a barrier and reaches appropriate CSF levels.
predominance of non-degenerate neutrophils ● The recommended dosage is 100 mg/m2/day as a
(50–90%). constant rate infusion intravenously for 4 days.
● CSF commonly reveals the organism in cats with ● An alternative regimen is 300 mg/m2 subcuta-
cryptococcosis. neously twice daily for 2 days.
● Toxoplasma gondii usually produces a mild to ● Potential toxicity includes myelosuppression (at
moderate increase in protein (0.6–1 g/L [60–100 5–7 days); vomiting; and anorexia.
mg/dl]) and cell counts (30–100 cells/mm3 [30–100 ● Tumor cells rapidly become resistant to this drug’s
cells/μl]), with the cell distribution being a mixed action.
mononuclear and polymorphonuclear pleocytosis
+/− eosinophils). Surgical decompression of the spinal cord and/or
nerve roots, and tumor resection or debulking is a
Serologic antibody or capsular antigen assays will also potential treatment option, especially if the tumor is
help differentiate the infectious diseases. localized.
Feline polioencephalomyelitis can produce a primary Follow-up radiation and chemotherapy is recom-
thoracolumbar myelopathy. mended.
● Since CSF in this disease also commonly shows
a mild to moderate protein elevation (mean of
0.48 g/L [48 mg/dl] with a range of 0.1–0.7 g/L Prognosis
[10–70 mg/dl]) and a mild mononuclear pleocytosis Prognosis is poor for long-term survival, especially
(mean of 19 cells/mm3 [19 cells/μl] with a range of when most cats are infected with the FeLV virus.
0–46 cells/mm3 [0–46 cells/μl]), differentiation
from lymphosarcoma may be difficult.
● Cats with polioencephalomyelitis, however, usually
Prevention
are FeLV negative. The only effective means of prevention is test and
removal programs directed at controlling the spread
Spinal neoplasia (especially meningioma) can mimic
of FeLV.
focal spinal lymphosarcoma.
● CSF analysis with meningioma usually only Routine vaccination with FeLV vaccines is recom-
demonstrates a protein increase. mended. However, there is the risk of development of
● Cats with neoplasia are usually much older vaccine-induced sarcomas with adjuvant killed FeLV
(> 9 years of age) than cats with lymphosarcoma vaccines. A new recombinant FeLV vaccine is now
(≤ 3 years). available.
Myelopathy is seen either as the sole abnormality or as

FELINE INFECTIOUS PERITONITIS***
part of a multifocal distribution in 25% of cases.
Classical signs The onset of FIP can be acute, although most cats have
a chronic progressive course over 1 week to 3 months.
● Decreased mentation and menace.
● Central vestibular disease and facial Extraneural signs may include fever, cachexia, poor
paralysis. body condition, dehydration, lethargy, muscle atrophy,
● Chronic progressive tetraparesis to chorioretinitis, dyspnea and gastrointestinal/hepatic
tetraplegia or paraparesis. signs.
● Seizures and behavior change.
Many cats present with the neurological form of FIP
● Intention tremor.
without extraneural signs.
● Systemic signs such as fever, inappetance,
weight loss, dyspnea and gastrointestinal
signs. Diagnosis
The diagnosis is best established via CSF analysis –
marked elevation in protein (usually greater than 1 g/L
[100 mg/dl] and often greater than 2 g/L [200 mg/dl])
Clinical signs
and white blood cells (mean of 734 cells/mm3
Feline infectious peritonitis (FIP) may produce a non- [734 cells/μl] with a range of 69–2000 cells/mm3
suppurative meningoencephalitis in 29% of infected [69–2000 cells/μl]), with a predominance of non-
cats. degenerate neutrophils (50–90%).
The CNS signs are usually associated with the non- The CSF FIP viral titer is usually positive if CNS
effusive (“dry”) form of FIP (cell-mediated immunity signs are present. It is probable that CSF anti-FIP viral
is defective but not absent) immunoglobulin G is produced within the CNS.
The neurological form of FIP has no breed or sex Serum biochemical changes often consist of an eleva-
predilection, although most cases are < 3–4 years of tion in total protein and hypergammaglobulinemia.
age.
Serum FIP antibody titers are not reliable, and are
In most cases, the neurological signs are multifocal elevated in only 58% of cats with the neurological form
with a predominance of caudal fossa signs (brain- of FIP and are even negative in some cats.
stem, vestibular nuclei and cerebellum).
● Signs can include nystagmus (positional, non-
constant, rotatory, horizontal or vertical in nature),
head tilt, body lean or rolling, facial paralysis, an Numerous other infectious and immunological diseases
ipsilateral hemiparesis or tetraparesis, intention can produce meningitis and encephalomyelitis in cats.
tremor, and hypermetria or dysmetria.
FeLV-associated CNS lymphosarcoma can usually be
The spinal cord and the cerebrum also can be involved. differentiated by CSF analysis, and a positive FeLV
● Signs of cerebral disease can include seizures, serum titer.
behavior change, decreased mentation, decreased
Cryptococcal organisms are usually visible in CSF
menace response, compulsive walking, ipsiversive
with confirmation made by a latex agglutination assay
wide circling and head pressing.
or culture.
● Spinal cord involvement will manifest as UMN
and/or LMN tetraparesis or paraparesis with ataxia. CNS toxoplasmosis is rare in the cat, usually producing
Tetraplegia or paraplegia are the most severe conse- signs of intracranial disease rather than myelopathy.
quences of spinal cord involvement. Recent or active infection is diagnosed by demonstrating
a positive IgM titer, a four-fold increase or decrease in Most spinal fractures occur at the junction of mobile
IgG serum titer, a CSF IgM antibody titer or a CSF IgG and immobile segments of the spine, such as the tho-
titer present at a higher CSF:serum ratio than another racolumbar, lumbosacral and sacrocaudal junctions.
antibody present in serum that is not produced in CSF,
Traction on the cauda equina in sacrocaudal luxations
e.g. calicivirus.
can also damage the nerve cell bodies in the caudal
Feline polioencephalomyelitis usually produces only a lumbar and sacral spinal cord due to cranial transmis-
mild to moderate increase in protein (mean of 0.48 g/L sion of the forces through the dura mater and filum ter-
[48 mg/dl] with a range of 0.1–0.7 g/L [10–70 mg/dl]) minale of the cord.
and a mild mononuclear pleocytosis (mean of
The degree of spinal cord compression; the length of time
19 cells/mm3 [19 cells/μl] with a range of 0–46
of compression; and the velocity of the initial impact
cells/mm3 [0–46 cells/μl]) on CSF. This is not typical
injury are important contributors to the resultant spinal
of FIP.
cord injury.
Treatment There are two forms of spinal cord injury – mechanical
(primary) injury, consisting of physical disruption of
No effective therapy is known against FIP.
vessels and axons and ischemic (secondary) injury.
Immunosuppressive corticosteroid therapy may slow
The latter leads to energy compromise within the spinal
the disease course (1–2 mg/kg prednisone or pred-
cord, cellular accumulation of calcium and resultant
nisolone orally twice daily).
intracellular stimulation of enzymes.
All cats with the neurological form of FIP will eventu-
This leads to protein and lipid breakdown (phospho-
ally die from their disease.
lipid hydrolysis), release of arachidonic acid, free radi-
cal and eicosanoid formation, and cell death.
SPINAL CORD TRAUMA – FRACTURES AND
Gray matter hemorrhages and white matter edema
LUXATIONS***
occur within minutes following acute spinal cord
injury, progressing rapidly over the 4–6-hour post-
Classical signs
traumatic period.
● Acute variably located spinal cord
dysfunction (UMN or LMN signs).
Clinical signs
● Focal spinal hyperesthesia.
● Spinal crepitus. Signs depend on the injury level and the degree of
● External abrasions and bruising. physical or functional disruption of the cord.
Signs in cats with sacrocaudal injuries range from
hyperesthesia over the tail base to flaccid analgesic
Pathogenesis
tails with varying degrees of urinary reflex dyssynergia
External spinal trauma can result from automobile or LMN urinary/fecal incontinence.
accidents, gunshot injuries, falls from heights and ● Reflex dyssynergia involves a failure of urethral
blunt trauma. relaxation when the cat attempts to urinate and the
bladder undergoes contraction. This leads to the
Sacrocaudal fractures most often occur when the cat’s
production of only very small quantities of urine.
tail is forcefully pulled away from the body.
The bladder will still be large and the cat will often
● This most commonly occurs when the cat’s tail
dribble urine in between attempts to urinate.
is trapped under the tire of an automobile. The
rotating tire luxates the tail at the sacrococcygeal Many cats with sacrococcygeal trauma also show signs
junction or between two coccygeal vertebrae, result- of LMN paraparesis (sciatic nerve injury), consisting
ing in damage to the coccygeal, sacral and lumbar of dragging of the hind paws on their dorsum and a fail-
nerve roots (cauda equina). ure to flex the pelvic limb(s) when walking or when
the withdrawal reflex is performed. There will also be a intumescence as is the case with sacrococcygeal
hypo- to areflexia of the cranial tibial and gastro- trauma.
cnemius reflexes. ● A differentiating feature of ischemic myelopathy is
the absence of spinal pain.
Palpation of the sacrocaudal area of the spine will
result in crepitus and pain. The tail will often be
malaligned with the sacrum and the rest of the vertebral Treatment
column.
Initial medical emergency treatment should include
Cats with spinal trauma commonly have concurrent tho- intravenous methylprednisolone sodium succinate
racic, abdominal or pelvic trauma. (30 mg/kg), administered within 8 hours (and prefer-
ably within 3 hours) of the spinal trauma.
Diagnosis Continued treatment consists of a constant rate intra-
venous infusion of methylprednisolone at 5.4 mg/kg/hour
Neurological and physical examination determine the
or, if not possible, a second bolus intravenous injection
localization and severity of the cord injury.
(15 mg/kg) at 2 hours after the initial treatment, fol-
Non-contrast spinal radiographs (lateral and across lowed by 15 mg/kg at 6 hours and then 4 times daily for
the table ventrodorsal views of the entire spine) estab- 24–48 hours.
lish the type of vertebral disruption (fracture vs. sub-
Most cases of spinal trauma will require emergency
luxation) and the location(s) of the vertebral trauma.
surgical intervention (spinal cord decompression
Myelography, MRI or CT scans will determine the [laminectomy and/or hemilaminectomy] and spinal
degree of spinal cord compression. fixation).
The type of decompression and stabilization technique
Differential diagnosis is determined by non-contrast and contrast spinal radi-
ographs or CT/MRI scans.
Any other cause of acute myelopathy must be considered
as a differential diagnosis in cats with spinal trauma. Surgical spinal stabilization is rarely necessary in
sacrocaudal fractures/luxations and, due to the often-
Most other causes can be eliminated based on history and
marked separation of the involved vertebrae, is difficult
physical examination – external abrasions, bruising,
to achieve.
splintering of claws and spinal pain are seen with trauma.
Surgical decompression of the cauda equina in sacro-
Sacrocaudal fractures must be differentiated from aortic
caudal trauma is also unnecessary since it is a traction,
thromboembolism, which also can produce an acute
not compressive, injury.
onset of LMN paraparesis to paraplegia, with pain.
● However, cats with this disease do not have dys- If the cat is incontinent, attention should be paid to
function associated with the perineum, bladder, rec- cleanliness, bladder and bowel management, and pre-
tum and tail. vention of decubital ulcers, urine scalding, and cystitis.
● The lack of femoral pulses and the presence of
If there is UMN or LMN urinary incontinence, manual
cold, cyanotic pelvic limbs would strongly support
expression or indwelling catheterization of the blad-
aortic thromboembolism.
der is required.
Pathologic vertebral fracture secondary to neo-
Pharmacological management of UMN urinary
plasia will present as an acute, painful myelopathy, and
incontinence or reflex dyssynergia, related to
may appear superficially similar to a traumatic fracture
sacrocaudal trauma, consists of phenoxybenza-
on non-contrast spinal radiographs. However, closer
mine, an alpha-adrenergic receptor antagonist, to
examination should reveal areas of lysis within the
relax the internal sphincter (5 mg orally three times
involved vertebral body.
daily) together with diazepam (1.25–2 mg/cat
Ischemic myelopathy secondary to fibrocartilaginous orally two to three times daily) to relax the external
embolism most commonly involves the lumbosacral sphincter.
Bladder detrusor dysfunction can then be treated Pathogenesis

with bethanechol, a parasympathomimetic agent
(5–10 mg orally two to three times daily). Although most meningiomas are found intracranially,
they may also develop along the spinal cord with an
Bethanechol may help LMN urinary incontinence intradural, extramedullary predilection site.
(encourages detrusor muscle contraction).
Meningiomas arise from any cell of the meninges –
Fecal retention can be treated by increasing the bulk blood vessels, fibroblasts or arachnoid cells.
of the feces with bran, psyllium or canned mashed
pumpkin. Spinal meningiomas are usually solitary.
In cats with sacrocaudal injury with only tail paresis, Meningiomas produce signs by compressing the adja-
conservative medical management will often result in cent spinal cord causing vasogenic edema
return of tail function. Occasionally, other tumors such as an astrocytoma
● If this does not occur after 4–6 months, amputation occur.
of the tail is recommended.
Clinical signs
Prognosis
Most cats are > 9 years of age.
Prognosis is based on the severity of the spinal cord
injury. The milder the neurological deficits, the bet- The nature of the ataxia and paresis (UMN versus LMN
ter the prognosis for recovery. signs) depends on the tumor’s location.
Cats with severe myelopathy or cauda equina injury A focal area of spinal pain or more diffuse spinal
with analgesia have a very poor to hopeless prognosis discomfort may occur weeks prior to the development
since they commonly have physical or functional spinal of neurological dysfunction.
cord or cauda equina transection. Signs are slowly progressive.
● Only 25% or less of cats with flaccid tail, perineal
analgesia and LMN urinary and fecal incontinence
from a sacrocaudal injury will regain neurologic Diagnosis
function. Non-contrast spinal radiographs may reveal thinning or
● 75% of cats with only tail flaccidity can regain tail
deformation of the vertebral lamina secondary to pres-
function. sure necrosis from the expanding tumor.
Prognosis should NEVER be determined based on Lumbar CSF most commonly reveals increased pro-
the degree of radiographic displacement of the tein (> 0.25 g/L [25 mg/dl]) without an accompanying
involved vertebra(e). pleocytosis. Tumor cells are rarely seen.
MRI scan or myelography reveals an intradural,
Prevention
extramedullary mass.
The only preventative measure is for cats to avoid situ-
ations where trauma is a distinct possibility. Differential diagnosis
Any cause of chronic, progressive myelopathy should
SPINAL MENINGIOMA** be considered.
Classical signs The focal nature of the myelopathy with meningioma

eliminates most infectious and inflammatory myelo-
● Chronic, progressive UMN or LMN pathies, with the exception of FeLV-associated spinal
tetraparesis or paraparesis dependent on lymphosarcoma.
tumor location.
● Focal areas of spinal pain. Ischemia and trauma produce an acute myelopathy and
can usually be eliminated.
Age of disease onset for meningiomas would eliminate In cats it is most commonly associated with hyper-
congenital and inherited myelopathies. trophic, dilated and restrictive cardiomyopathy,
with thrombus formation in the left atrium. It also
Differentiation from lymphosarcoma often is based on
occurs with thyrotoxic cardiac disease.
CSF analysis (malignant lymphocytes).
Thrombus formation requires either damage to the
Differentiation from nerve root tumors often re-
endocardium as occurs in cardiomyopathy, especially
quires histopathology following surgical removal.
the dilated left atrium; blood stasis which also occurs in
the dilated left atrium; or altered blood coagulability.
Treatment Disseminated intravascular coagulation (DIC) was
Surgical removal of the tumor is the only definitive found in 75% of cats with cardiomyopathy and was
treatment. associated with consumptive or liver-mediated coagu-
lopathy or thromboembolism.
Post-operative radiation therapy is recommended.
Embolism occurs when the thrombus lodges in a blood
Corticosteroids only transiently improve neurological vessel.
function.
The thrombus most often lodges in the distal aorta
at the trifurcation, leading to a saddle thrombus and
Prognosis occlusion of blood supply to the hindlimbs. Ischemic
The long-term prognosis is guarded to fair if surgical neuromyopathy occurs and is most severe distal to the
removal of the tumor appears complete. Follow-up stifle. Signs are usually asymmetrical. Occasionally the
radiation probably further improves this prognosis. right brachial artery is occluded, resulting in lameness
or paresis of the right forelimb.
Without surgery, the long-term prognosis is poor.
Occasionally cats with thromboembolic disease do not
have underlying heart disease. Thrombosis may also
Prevention
occur with infectious or neoplastic disease.
There is no known prevention of spinal meningiomas in
cats.
Clinical signs
There is no breed or age predilection (average 9 years,
AORTIC THROMBOEMBOLISM**
range 2–16 years) although males are twice as likely to
be affected.
Classical signs
Aortic thromboembolism usually produces an acute
● Acute LMN paraplegia.
onset of LMN paraplegia and severe pain.
● Severe pain associated with the pelvic limb
musculature. The hindlimbs drag behind the cat, as the hocks cannot
● Vocalization and anxiety. be flexed. Hip extension and flexion is present.
● Weak or absent femoral pulses.
Less severe ischemia leads to mild to moderate para-
● Cyanotic and cold nail beds and foot pads.
paresis or pelvic limb lameness.
The gastrocnemius muscles usually are firm, but
soften 1–3 days after embolization.
Pathogenesis
Femoral pulses are weak or absent and the nail beds
Aortic thromboembolism results from a thrombus
and footpads are cyanotic and cold. The distal limbs
that is dislodged from within the left heart or
are often swollen.
aorta, leading to obstruction of the aortic trifurca-
tion and severe ischemia to pelvic limb muscles and Extraneural signs include vocalization, tachypnea/
nerves. dyspnea, a cardiac murmur and arrhythmias. Heart
failure is present in about 50% of cats with aortic ● Physical removal is via surgery or balloon embo-
thromboembolism. lectomy.
● Thrombolytic agents include tissue plasminogen acti-
Dehydration and hypothermia are often present.
vator, urokinase and streptokinase.
Tail movement, perineal reflexes and urinary function – Current information should be consulted on
remain intact. administration and monitoring of thrombolytic
and intensive anti-thrombotic therapies if they
are to be used.
Diagnosis
● Reperfusion effects are a major problem with
Increases in serum creatine kinase (often 1000–10 aggressive thrombolytic therapies and physical
000 IU/L [normal: 60–300 IU/L]) occur secondary to removal. Rapid onset of severe hyperkalemia
severe muscle damage. associated with reperfusion is common and often
fatal. Renal hemorrhage may also occur during
Creatinine and BUN are increased in more than 50% of
thrombolysis, adversely affecting survival. Clinical
cats and may be prerenal or renal. In some cats, con-
hemorrhage may require a blood transfusion to
current embolization of the renal artery occurs.
control.
Thoracic radiography reveals cardiomegaly (85–90%
Pallative therapy consists of relieving pain, heparin
of cats) and pulmonary edema and/or pleural effu-
to help prevent another clot forming in the left atrium,
sion (66%).
fluid, electrolyte and nutritional support, warmth,
Echocardiography most often reveals hypertrophic physiotherapy (passive massage and flexing/extending
cardiomyopathy (± a left atrial thrombus). legs) and treatment of underlying heart disease.
Potassium concentrations should be monitored care-
Electrocardiography most commonly reveals sinus
fully.
tachycardia. Atrial fibrillation, and supra-/ventricular
arrhythmias can also be seen. Pain control is an important part of management.
Injectable analgesics and a fentenyl patch should be
Doppler (color flow) will often demonstrate the
used to provide adequate levels of pain relief.
decrease in blood flow through the site of thrombo-
embolism. Excessive licking or chewing of the affected limb
may occur resulting in self-mutilation. Loose bandag-
MRI angiography will reveal a complete or partial
ing of the limb or an Elizabethan collar are usually
blood flow obstruction at the aortic trifurcation.
effective.
Dehydration and electrolyte imbalances, especially
hyper- and hypokalaemia, need correcting. Nutritional
A major feature that differentiates aortic thrombo- needs should be met in anorexic cats by the placement
embolism from traumatic, infectious, neoplastic and of a nasoesophageal tube for feeding.
ischemic myelopathies is the presence of paraparesis to
Treatment of the underlying cardiac disease is
paraplegia without involvement of the perineum, tail
essential (see Chapter 25).
and bladder.
Acutely, heparin (400 U/kg subcutaneously followed
Cold, cyanotic pelvic limbs without femoral pulses and
by 200 U/kg subcutaneously three times daily) can be
firm gastrocnemius muscles also are unique.
given to prevent further activation of the coagulation
cascade, although it will not have any effect on the
Treatment formed thrombus.
With current treatment modalities, the results of palla- Continue palliative therapy for 5–6 days and look for
tive therapy are as good as aggressive thrombolytic rewarming of the toes and returning pulses as an initial
therapies or physical removal of the thrombus, and sign of improvement. Doppler is useful for detecting
considerably less expensive. blood flow. If there is no sign of reperfusion after
6 days, the prognosis is hopeless and the cat should be thrombus in the left atrium also decreases the long-term
euthanized. prognosis.
Various other treatments have been advocated but
there are no studies showing increased survival. These Prevention
include aspirin, periactin, acepromazine and vasodilator
Little can be done to prevent aortic thromboembolism
agents.
if the underlying cardiac disease has not been previ-
Aspirin may be beneficial during and after an episode ously recognized.
of thromboembolism due to its antiplatelet effects and
If cardiac disease is diagnosed, the risk of thromboem-
decreased production of the vasoconstrictor thromb-
bolism may be reduced by appropriate treatment of
oxane A2, as well as analgesic effects. The dosage is
the cardiomyopathy (see Chapter 6). Efficacy of long-
1/4 × 325 mg adult aspirin (81 mg) every second to
term aspirin (low dose 1–5 mg/cat q 24 h or a regular
third day. Blockade of prostacyclin production by the
dose 81 mg/cat, q 48–72 h PO) or warfarin therapy in
endothelium with aspirin is of concern, and some advo-
preventing thromboembolism has not been demon-
cate lower doses of aspirin more frequently (1–5 mg/cat
strated, and most cats rethrombose.
q 24 h). Prostacyclin inhibits platelet aggregation and
vasoconstriction.
FELINE POLIOENCEPHALOMYELITIS*
Acepromazine (0.1–0.5 mg subcutaneously three
times daily) can be used for sedation and vasodilation.
Classical signs
Vasodilation with alpha-blockers is advocated by some
● Stiff staggering gait.
but unproven.
● Inability to jump.
Long-term warfarin therapy may decrease the fre- ● Chronic pelvic limb ataxia and paraparesis.
quency of rethrombosis, but needs careful monitoring ● Inability to retract their claws.
using the International Normalization Ratio (INR) for ● Thoracolumbar hyperesthesia.
PT to achieve a INR between 2 and 3. Doses of ● Thoracic limb paresis and ataxia.
0.06–0.20 mg/kg PO q 24 h have been advocated. ● Decreased mentation and seizures.
A lower dose of 0.5 mg/cat PO q 48 h has also been ● Fever (in 50% of cases).
used.
Pathogenesis
Prognosis Feline polioencephalomyelitis is a chronic, progres-
sive disease affecting the spinal cord and brain of
Only 30–50% of cats survive the initial episodes and go
cats.
home.
The cause is unknown, although neuropathology is
Most will re-embolize – long-term prognosis is poor
suggestive of a neurotrophic virus.
(average survival is 6–11 months with therapy) with
less than 50% surviving 1 year. Recently, specific antibodies to the Borna disease
● 50% of cats have rethrombosis even when treated virus have been found in 44% of cats with feline
with warfarin. polioencephalomyelitis in Sweden.
Most cats that survive an initial episode will show vary- Feline polioencephalomyelitis is a sporadic worldwide
ing degrees of neurological recovery to their pelvic disease.
limbs, although this often takes weeks to months.
Rarely does the neuromuscular function fully recover.
Clinical signs
Hypothermia and azotemia prior to therapy and hyper-
Affected cats range from 4 months to 12 years of age.
kalemia during thrombolysis are negatively associated
with survival. Echocardiographic evidence of another Both male and female cats are affected.
All domestic cat breeds as well as large non-domesti- CSF analysis may help differentiate between the infec-
cated cat species can contract the disease. tious diseases, lymphosarcoma and feline polioen-
cephalomyelitis (see sections on lymphosarcoma and
Neurologic signs usually develop over 2–3 months
FIP), although the range of values overlap between the
with a subacute to chronic progressive course.
diseases.
The most striking neurologic signs include a stiff stag-
gering gait, inability to jump, pelvic limb ataxia and Treatment
paraparesis.
Immunosuppressive steroid therapy (prednisone
● Some cats have decreased spinal reflexes and some
1–2 mg/kg BID) is the recommended treatment against
are unable to retract their claws.
this disease, although data are lacking.
Other signs may include thoracic limb ataxia and
This may be combined with other immunosuppressive
paresis, hyperesthesia over the thoracolumbar and
agents such as cytosine arabinoside.
lumbosacral regions, decreased mentation, behavior
change, decreased pupillary light reflexes, hypersen- Aggressive and persistent therapy may result in remis-
sitivity to external stimuli, impaired vision, seizures, sion and possible cure after several months.
increased salivation, intention tremors and pruritis.
Prognosis
With disease progression, paraplegia eventually
occurs. Prognosis is guarded. The disease tends to be pro-
gressive if untreated.
A fever is present in approximately 50% of cats.
CSF analysis usually reveals a non-specific mild Since this disease is of unknown etiology and very spo-
to moderate elevation in protein (mean of 0.48 g/L radic, there are no recommendations for prevention.
[48 mg/dl] with a range of 0.1–0.7 g/L [10–70 mg/dl])
and a mild mononuclear pleocytosis (mean of
CONGENITAL ABNORMALITIES OF THE
19 cells/mm3 [19 cells/μl] with a range of 0–46 cells/
SPINAL CORD AND VERTEBRAE*
mm3 [0–46 cells/μl]).
Serologic testing for FIV and FeLV antibodies is negative. Classical signs
Definitive diagnosis can only be made on necropsy. ● UMN or LMN paraparesis or tetraparesis
dependent on the anomaly and its location.
Histopathology reveals a disseminated meningoen-
● Scoliosis (lateral curvature of the spine),
cephalomyelitis with lymphocytic perivascular cuffs
lordosis (downward arching spine), or
that is most severe in the spinal cord (gray matter) and
kyphosis (upward arching spine) resulting
brainstem.
from a hemivertebra.
● Cervical pain and UMN tetraparesis to
paralysis (atlantoaxial subluxation).
Infectious diseases (FIP and toxoplasmosis) also may ● LMN paraparesis to paraplegia (spina
produce signs of progressive spinal cord dysfunction, bifida and sacrococcygeal dysgenesis).
making differentiation based on neurological signs ● LMN urinary and fecal incontinence (spina
difficult. Uveitis, chorioretinitis and optic neuritis bifida and sacrococcygeal dysgenesis).
are often present with CNS infections, but not with ● Dorsal midline spinal defects or cystic
polioencephalomyelitis. structures – may drain CSF (spina bifida).
● Abnormal hair growth direction, a dimple
Cats with spinal CNS lymphosarcoma commonly are
on the skin surface or an open tract (spina
FeLV positive and may have other systemic signs of
bifida).
tumor involvement.
Pathogenesis abnormal formation and/or protrusion of the

meninges and/or spinal cord.
Spinal cord and vertebral anomalies are classified into – Pathogenesis may involve initial failure of clo-
abnormalities originating in the tissues of mesodermal sure or the reopening of a previously closed neu-
origin (vertebral body and intervertebral disc) and ral tube.
those arising from tissues of ectodermal origin (spinal – Spina bifida occulta represents an incomplete
cord and meninges). closure of one or more vertebral arches without
Malformations of mesodermal origin. protrusion of meninges or spinal cord.
● Block vertebrae. – Spina bifida manifesta includes meningocele
– Caused by improper segmentation of somites, (meningeal herniation through the vertebral arch
resulting in stable vertebral fusion. defect) and meningomyelocele (herniation of
● Butterfly vertebrae. the spinal cord and meninges).
– Abnormal persistence of the notochord (the – The meningeal and/or spinal cord herniation may
embryological precursor of intervertebral discs), or may not communicate with the environment.
producing a midline cranial to caudal cleft in the ● Sacrococcygeal dysgenesis of Manx cats.
vertebral body (when viewing the vertebra from – An autosomal semi-lethal dominant trait,
the dorsoventral direction). providing the genetic basis for the absent tail
● Hemivertebrae. as well as numerous vertebral and spinal cord
– Produced by fusion of one lateral somite to one abnormalities.
on the contralateral side that is not directly – Homozygotes usually do not survive.
opposed or by a lack of vascularization, lead- – There are four phenotypic subgroups – a com-
ing to a failure of ossification in part of the ver- plete absence of coccygeal, sacral +/− caudal
tebral body. This produces a wedge-shaped lumbar vertebrae (the most severe); fused caudal
vertebra, and scoliosis, lordosis or kyphosis. vertebrae; mobile but kinked caudal vertebrae;
● Transitional vertebrae. and a normal tail.
– Sacralization of the last lumbar vertebra is the
most common in cats. In this condition, the last Clinical signs
lumbar vertebra has characteristics of both lum-
bar vertebrae and the sacrum. Clinical signs are dependent on the type of congenital
● Atlantoaxial subluxation. malformation and its location.
– Results from hypoplasia or aplasia of the dens Block vertebrae are usually stable.
with secondary atlantoaxial instability. ● Occasionally they can be stenotic or angulated,
– It is either caused by a developmental failure causing extradural spinal cord compression.
of dens ossification or an ischemic necrosis ● Disc extrusion can occur at disc spaces immediately
and partial resorption of the dens as a result of cranial and caudal to the block vertebrae.
trauma.
– The cranial portion of the axis is displaced into Butterfly vertebrae are generally incidental findings.
the spinal canal producing cord compression. Hemivertebrae commonly lead to scoliosis, lordosis
Malformations of ectodermal origin. or kyphosis.
● Abnormalities of the vertebral arch and spinal cord ● Signs are due to spinal cord compression or
are primarily influenced by neural tube devel- repeated trauma associated with vertebral instabil-
opment. ity. Instability produces osseous changes that sec-
● The most common anomaly is spina bifida. ondarily compress the spinal cord.
● Spina bifida. ● Signs may be acute, chronic, progressive or inter-
– The defects of spina bifida vary from incom- mittent, but are usually first noted within the first
plete fusion of the vertebral arch to incom- 1–2 years of life.
plete fusion of the neural tube, resulting in ● Conformation may be visibly or palpably abnormal.
Sacralization of the caudal lumbar vertebrae can result ● Hemivertebra – abnormal vertebral wedging and
in pain and LMN paraparesis secondary to cauda shortening.
equina compression. ● Atlantoaxial subluxation – abnormally shaped or
absent dens.
Atlantoaxial malformation can produce episodic
● Spina bifida – vertebral arch defect.
cervical pain or acute/chronic UMN tetraparesis to
tetraplegia, usually in cats less than 1 year of age. Myelography demonstrates cord compression or a
● If spinal cord injury is severe, the cat can develop meningocele/meningomyelocele.
respiratory paralysis and caudal brainstem dys-
MRI scan or CT myelography reveals soft tissue abnor-
function.
malities associated with a spinal cord that is tethered
● Episodic opisthotonos and rigidity occasionally
(fixed) by either meningocutaneous attachments (spina
occur which can be misinterpreted as seizures.
bifida) or by a failure of the terminal cord-like attach-
Spina bifida occulta is an incidental finding. ment from the spinal cord to the dura to stretch with
growth. They will also reveal cord compression.
Spina bifida manifesta produces myelopathy depend-
ent on the degree of incorporation of the spinal cord
and/or cauda equina into the herniated meningeal sac. Differential diagnosis
● Most commonly the caudal lumbar and sacral
Major differentials for hemivertebra include trau-
spine is affected, resulting in LMN paraparesis/
matic or pathologic fracture with secondary collapse
plegia and urinary/fecal incontinence in newborn
of the vertebral body.
kittens.
● Hemivertebrae, however, have smooth end plates
● Spina bifida can be observed at birth as dorsal mid-
and well-formed adjacent disc spaces.
line, open regions of the spinal canal or cystic
● Difficulty in differentiation arises when vertebral
structures that may drain CSF.
osteophytes are present.
● Abnormal hair growth, a skin dimple or an open
tract are less severe manifestations. Differential diagnoses for block vertebrae include ver-
tebral fusion secondary to discospondylitis, vertebral
Sacrococcygeal dysgenesis produces a hopping gait.
fracture/luxation, collapsed disc space secondary to disc
● More severe signs at or soon after birth include
extrusion, or previous disc surgery. However, all have
LMN urinary/fecal incontinence, megacolon,
associated reactive bone, which is not present with block
and LMN paraparesis/paraplegia.
vertebrae.
● Some are normal at birth but develop progressive
signs over several weeks to months as the cat Atlanto-axial subluxation and spina bifida have few
matures. Damage to the spinal cord with growth rule-outs, except trauma.
occurs as a result of spinal cord tethering (fixation).
Treatment
Diagnosis Spinal cord compression from a hemivertebra can be
treated via surgical decompression and stabilization
Breed association (Manx cat).
(if necessary).
Signs are most commonly observed in immature ani-
Treatment for atlantoaxial subluxation involves stabi-
mals (< 6 months of age).
lization of the atlantoaxial joint via ventral cross-
The cat’s conformation may be visibly or palpably pinning or screws (preferred) or dorsal wiring.
abnormal (scoliosis, skin dimple, etc.).
Specific treatment for spina bifida and sacrococcygeal
Non-contrast spinal radiography demonstrates the dysgenesis is rarely attempted.
anomaly. ● If signs are associated with spinal cord tethering or
● Block vertebra – joining of two adjacent vertebral there is a meningocutaneous fistula without primary
bodies. spinal cord anomalies, reconstructive surgery may
● Butterfly vertebra – sagittal vertebral body cleft. be possible.
Prognosis Signs include cervical and thoracic limb hyperesthe-

sia and rigidity due to extensive confluent exostosis in
Prognosis depends on the type of congenital anomaly the cervical and thoracic spine, thoracic limb lame-
and the degree of dysfunction. ness, ataxia, reluctance to move, and tetraparesis to
Cats with mild signs due to a surgically treatable paralysis.
hemivertebra or block vertebra, have a guarded to good Other signs include lethargy, anorexia, constipation,
prognosis for improvement. weight loss and an unkempt haircoat due to an inability
Morbidity and mortality is high with surgical stabi- to groom.
lization of atlantoaxial subluxation. Exostoses develop insidiously with the above signs
● With successful stabilization, however, cats with
occurring only after the disease is advanced.
initially mild to moderate neurological dysfunction
have a fair to good prognosis.
Diagnosis
Prognosis for cats with spina bifida or sacrococcygeal
dysgenesis with anomalies associated with the spinal Non-contrast spinal radiographs show new bone for-
cord or cauda equina, is grave. These cats should be mation involving the cervical vertebrae.
euthanized if the neurological dysfunction is incompat- ● The sternum, costal cartilages, and long bone meta-
ible with a good quality of life. physes also show new bone formation.
● Joints may show arthrodesis.
Cats with spinal cord tethering (spina bifida) have a
potentially fair to good prognosis with surgery.
Prevention Based on the clinical and neurological examinations,
other differentials include infectious meningitis and
Prevention of further congenital malformations is best myelitis, vertebral neoplasia, mucopolysaccharidosis
achieved by a spay/neuter program. and discospondylitis (rare).
Non-contrast spinal radiographs eliminate all differen-
HYPERVITAMINOSIS A* tials with the possible exception of mucopolysacchari-
dosis VI, a rare autosomal recessive storage disease
Classical signs produced by deficiency of the lysosomal enzyme, aryl-
● Cervical and thoracic limb hyperesthesia sulfatase B.
and rigidity. ● Mucopolysaccharidosis VI occurs in 4–7-month-
● Thoracic limb lameness. old Siamese cats, producing spinal cord com-
● Chronic progressive ataxia. pression secondary to fusion of the cervical
● Reluctance to move. and thoracolumbar vertebrae with bony proli-
● Chronic tetraparesis to paralysis. feration.
● These cats also have a flat, broad face, widely
spaced eyes, corneal clouding and enlarged feet.
Pathogenesis
Hypervitaminosis A is a skeletal disease, secondary to Treatment
excessive intake of vitamin A (liver or vitamin A sup- Remove excess vitamin A from the diet to prevent
plementation (cod liver oil) (> 1000 IU/ml). further development of exostoses.
Use a balanced commercial cat diet.
Clinical signs
Skeletal improvement is monitored by radiography and
Affected cats are usually 2–9 years of age. neurological examinations.
Analgesics may symptomatically treat the clinical Diagnosis

signs.
● Aspirin – 10 mg/kg PO q 48 h.
Diagnosis is based on exclusion of other etiologies.
● Narcotic analgesics such as morphine (4 mg/ml) –
History and neurological exam are important.
0.5 mg/kg PO three times to four times daily. Survey radiographs are normal.
● Non-steroidal anti-inflammatory drugs.
● Fentanyl patch.
CSF analysis is variable, ranging from normal, hemor-
rhagic, or showing a mild mixed pleocytosis (6–25
cells/mm3 [6–25 cells/μl]).
FIBROCARTILAGINOUS EMBOLISM Myelography will either be normal or occasionally

show cord edema.
Classical signs MRI diffusion studies may reveal the ischemic area of
● Acute, non-progressive, non-painful, spinal cord, if the affected area is large enough.
asymmetrical LMN paraparesis to Definitive diagnosis can only be made at necropsy.
paraplegia.
● LMN urinary and fecal incontinence.
Differential diagnosis includes any cause of acute para-
Pathogenesis paresis to paraplegia.
Spinal cord infarction secondary to fibrocartilagi- The unique clinical signs and usual absence of abnor-
nous embolism is uncommon. malities on work-up separate fibrocartilaginous embol-
The embolus is histochemically identical to the fibro- ism from other acute myelopathies.
cartilage of the nucleus pulposus.
It is unknown how the embolus reaches the spinal vas- Treatment
culature from its origin. Immediate treatment consists of methylprednisolone
Embolization of arteries, veins or a combination of the sodium succinate (see spinal trauma).
two may occur. Embolic myelopathy is non-surgical.
Sudden increases in intra-abdominal pressure (hard Long-term corticosteroid therapy is not recommended.
exercise) may facilitate retrograde passage of disc
material through the venous sinuses and spinal veins.
Prognosis
Embolism results in segmental hemorrhagic necrosis
and malacia of the spinal cord. Prognosis depends on density of neurological dysfunc-
tion and degree of irreversible cord damage.
Clinical signs Cats with severe LMN paraplegia, absent pain sensa-
tion and LMN urinary incontinence associated with
Clinical signs reflect the location of the lesion along the
involvement of the lumbosacral intumescence have a
spinal cord.
poor to hopeless prognosis.
In cats, the lumbosacral intumescence is the most
Cats with less severe signs have a guarded to favor-
common site of myelopathy, resulting in an acute
able prognosis for partial to full recovery.
LMN paraparesis to paraplegia, and LMN urinary
and fecal incontinence.
Other findings include a lack of spinal pain, lack of
Prevention
disease progression and marked asymmetry of neuro- There are no preventive measures that can be under-
logical dysfunction. taken.
RECOMMENDED READING
Baroni M, Heinold Y. A review of the clinical diagnosis of feline infectious peritonitis viral meningo-
encephalomyelitis. Prog Vet Neurol 1995; 6(3): 88–94.
Fenner WR. Inflammations of the nervous system, Chapter 66. In: August JR (ed) Consultations in Feline Internal
Medicine 1. W.B. Saunders Company, Philadelphia, 1991, pp. 507–517.
Fox PR. Feline cardiomyopathies, Chapter 117. In: Ettinger S, Feldman E (ed) Textbook of Veterinary Internal
Medicine. W.B. Saunders Company, Philadelphia, 2000, pp. 896–923.
Kroll RA, Constantinescu GM. Congenital abnormalities of the spinal cord and vertebrae, Chapter 52. In: August JR
(ed) Consultations in Feline Internal Medicine 2. W.B. Saunders Company, Philadelphia, 1994, pp. 413–420.
Lane SB, Kornegay JN. Spinal lymphosarcoma, Chapter 61. In: August JR (ed) Consultations in Feline Internal
Medicine 1. W.B. Saunders Company, Philadelphia, 1991, pp. 487–490.
Lundgren A-L. Feline non-suppurative meningoencephalomyelitis. A clinical and pathological study. J Comp Pathol
1992; 107: 411–425.
Munana KR. Inflammatory disorders of the central nervous system, Chapter 54. In: August JR (ed) Consultations in
Feline Internal Medicine 4. WB Saunders Company, Philadelphia, 2001, pp. 425–433.
Munana KR. Encephalitis and meningitis. In: Bagley R (ed) Veterinary Clinics of North America Small Animal
Practice – Intracranial Disease. WB Saunders Company, Philadelphia, 1996, pp. 857–874.
Pion P. Feline Thrombotic Disease Veterinary Information Network. http:www.vin.com/Members/SearchDB /rounds/
lc990711/lc990711.htm
Thomas WB. Vascular disorders, Chapter 52. In: August JR (ed) Consultations in Feline Internal Medicine 4. WB
Saunders Company, Philadelphia, 2001, pp. 405–412.
43. The cat with ataxia without weakness
Rodney S Bagley
KEY SIGNS
● Falling.
● Incoordination.
● Swaying from side to side.
● Goose stepping gait.
MECHANISM?
● Ataxia results from sensory proprioception dysfunction and causes falling and incoordination.
WHERE?
● Cerebellum, cerebral cortex (central controlling centers for movement), vestibular system
(peripheral or central) or spinal cord (sensory spinocerebellar pathways).
WHAT?
● Diseases causing ataxia without weakness most commonly involve the cerebellum and
include cerebellar hypoplasia (panleukopenia virus infection), hydrocephalus, storage
disease, tumors and encephalitis.
● Diseases of the vestibular system most commonly involve the peripheral apparatus and
include otitis media/interna, idiopathic vestibular disease and tumors.
● Diseases of the spinal cord rarely cause ataxia without weakness.
● Intracranial, cerebellar and vestibular causes of ataxia without weakness.

Diseases causing ataxia without weakness
DEGENERATIVE
● Inherited cerebellar diseases** (p 934)
Hereditary cerebellar degeneration occurs in Japans. Clinical signs begin around 7–8 weeks
of age and include ataxia, dysmetria, head tremor and intention tremor. Inherited spongiform
encephalopathy occurs in Egyptian Mau cats in the USA resulting in ataxia and hypermetria
beginning at 7 weeks of age. A different spongiform encephalopathy has been reported in older
Egyptian Mau cats in the United Kingdom. Clinical signs include muscle tremors, ataxia, dilated
unresponsive pupils, jaw champing, salivation and behavior abnormalities. Signs may progress to
924
43 – THE CAT WITH ATAXIA WITHOUT WEAKNESS 925
severe ataxia and hypermetria. Neuroaxonal dystrophy in domestic tri-colored cats results in
a head tremor beginning at 5–6 weeks of age with signs progressing to ataxia and hypermetria.
Affected kittens have a lilac color, which darkens with age. A similar but separate neuroaxonal
dystrophy has been described in cats of various colors. Clinical signs begin at 7–9 months of age
and include ataxia with paraparesis.
● Storage diseases** (p 935)
Sphingomyelinosis (Niemann–Pick type C disease) results in ataxia and tremors beginning at
less than 6 months of age. Clinical signs progress to hypermetria, absent menace responses, and
occasionally positional nystagmus. Death usually occurs by 8–10 months of age. Niemann–Pick
type A disease occurs in Siamese and Balinese cats. Head tremor, head bobbing and dysmetria
begin at 3–4 months of age. Clinical signs progress to ataxia and paresis, worse in the pelvic limbs.
ANOMALY
● Cerebellar hypoplasia*** (p 927)
Cerebellar degeneration usually occurs in neonatal to younger animals due to congential deformi-
ties or infectious causes (panleukopenia virus infection). Cerebellar hypoplasia results from in
utero or immediately postnatal infection with the panleukopenia virus. Clinical signs are most
apparent when the animal begins purposeful movement and attempts to walk. Ataxia, dysmetria,
intention tremor and absent menaces responses with normal vision are common clinical signs.
Clinical signs usually remain static or improve with growth. No treatment is helpful.
● Hydrocephalus** (p 932)
If hydrocephalus is congenital, cats may have an enlarged, “dome-shaped” skull. A fontanelle that
persists during maturation may be palpable. Acquired hydrocephalus in adults will show no out-
ward anatomical signs. Clinical signs include seizures, poor learning ability, behavior changes,
paresis, cranial nerve deficits and changes in consciousness.
● Congenital vestibular disease** (p 933)
Congenital peripheral vestibular disease is seen in Siamese and Burmese cats. Clinical signs
include head tilt, vestibular ataxia (cat leans, drifts, falls, or rolls to side of head tilt) and, in some,
deafness. Signs may remain persistent throughout life or may improve spontaneously.
METABOLIC
● Vascular diseases* (p 937)
Rarely, thromboembolic disease or hemorrhage involves the cerebellum. An acute onset of cerebel-
lar signs (incoordination, swaying from side to side, goose-stepping gait, intention tremor and
reduced menace) in an older animal is most common with these types of diseases. A cat with poly-
cythemia was presented for ataxia, possibly due to increases in serum viscosity.
NEOPLASTIC
● Cerebellar and vestibular tumor*** (p 928)
Primary or secondary neoplasia involving the cerebellum is uncommon. Intracranial tumors such
as meningioma and choroid plexus tumors can affect both the cerebellum or vestibular system and
result in ataxia. Other signs such as an intention tremor, goose-stepping gait, menace deficits, nys-
tagmus and head tilt may be present. Occasionally tumors of the ear cause peripheral vestibular
ataxia (cat leans, drifts, falls or rolls towards the side with a head tilt). Neoplastic disease occurs
more often in older cats.
continued
continued
NUTRITIONAL
tic ventroflexion of the neck or opisthotonos, dilated pupils, stupor and coma.
INFLAMMATORY/INFECTIOUS
● Encephalitis*** (p 930)
Neurological signs are often diffuse and may not localize to a single area within the nervous system.
Fever and leukocytosis are inconsistent findings. Systemic signs of disease such as fever, coughing,
vomiting and diarrhea may accompany the neurologic signs. Feline infectious peritonitis, toxoplas-
mosis and Cryptococcus are more common causes of encephalitis. Non-infectious causes are less
common but include feline non-suppurative meningoencephalomyelitis (“staggering disease”).
● Idiopathic encephalopathy* (p 939)
An encephalomyelopathy of young cats reported in the United Kingdom had clinical signs of
ataxia, paresis and “head shaking”. Cats 3–12 months old were affected, however, the disease was
seen in cats up to 3 years of age. Ataxia of the pelvic limbs was the initial clinical sign noted.
● Otitis media/interna** (p 936)
Clinical signs may reflect either primary ear, vestibular, or auditory dysfunction. Head tilt is most
common, but nystagmus and vestibular ataxia (leaning or falling to one side) may also be present.
A painful external ear and or pain on opening the mouth is often present. The facial nerve may be
involved. On otoscopic examination, the tympanic membrane is often discolored (hyperemic),
opaque and bulging outward with middle ear disease.
Idiopathic:
● Idiopathic peripheral vestibular disease*** (p 931)
Acute onset of peripheral vestibular signs with nystagmus (horizontal or rotary), head tilt (toward
the side of the lesion), rolling and falling. No other neurological signs are seen. Clinical signs, while
initially severe, are restricted to the vestibular system. Otoscopic examination, bulla radiographs and
other advanced imaging studies (computed tomography (CT), magnetic resonance (MR) imaging)
are normal. Signs usually improve dramatically in 1–2 weeks regardless of treatment.
Trauma:
● Head trauma*** (p 932)
Toxicity:
● Toxins* (p 938)
Metronidazole at high doses has been reported to result in ataxia as the initial clinical sign.
Paresis is usually present, and seizures and cortical blindness may also be noted. Bromethalin
toxicosis may also result in ataxia in the early stages. Signs progress to paresis, depression,
tremors, seizures and decerebrate posture. Ivermectin toxicosis has resulted in generalized ataxia,
tremor, weakness, incoordination and miosis in a kitten. Griseofulvin therapy resulted in ataxia in
a 12-week-old kitten. Aminoglycosides, administered either systemically or topically, may cause
vestibular signs. Streptomycin and gentamicin have the most pronounced effects on the vestibular
receptors, while neomycin, kanamycin and amikacin preferentially damage auditory receptors.
Chlorhexidine solution used to clean the external ear may result in vestibular signs.
Diseases of the vestibular system include those affect-

INTRODUCTION ing the central vestibular areas (developmental diseases,
hydrocephalus, storage disease, tumors, encephalitis
MECHANISM? and vascular-based diseases) and peripheral vestibular
areas (congenital vestibular disease, trauma, otitis
Ataxia is an abnormality of movement wherein the ani-
media/interna, idiopathic vestibular disease and
mal does not move in a straight line when walking but
tumors).
rather sways or falls, usually from side to side.
Diseases of the spinal cord include compressive, degen-
Ataxia indicates a problem with unconscious, sensory
erative, inflammatory, vascular, neoplastic, and congen-
proprioception.
ital diseases (see “The Cat With Limb Weakness”).
Lack of unconscious, sensory proprioceptive informa-
tion can also result in dysmetria, including hyperme- DISEASES CAUSING ATAXIA
tria (“goose-stepping”; overflexing of the limbs when WITHOUT WEAKNESS
walking) and hypometria (failure to flex and extend
the limb properly) resulting in a “stiff” appearance of
limb movement, and tremor. CEREBELLAR HYPOPLASIA***
Classical signs
WHERE?
● Signs are present from the early prenatal
Disease of the cerebellum, central controlling cen- period.
ters for movement, or sensory pathways traveling ● Clinical signs usually remain unchanged or
from the spinal cord to the cerebellum are often may improve during life.
affected. ● Coarse tremor that worsens when the cat
Disease of the vestibular system may also result in moves in a goal-oriented fashion (intention
ataxia and incoordination. tremor).
● Other signs include ataxia, hypermetria,
Diseases of the spinal cord can result in ataxia due to menace deficits, head tilt and nystagmus.
involvement of the spinocerebellar pathways.
Pathogenesis
WHAT?
Cerebellar hypoplasia results from in utero or imme-
Diseases of the intracranial nervous system resulting in diately postnatal infection with the panleukopenia
ataxia often involve the cerebellum. virus (parvovirus).
These include cerebellar hypoplasia (panleukopenia Infection of the fetus may occur when a pregnant queen
virus infection), hydrocephalus, storage disease, is vaccinated with a modified-live panleukopenia
tumors, encephalitis and vascular-based diseases. virus vaccination.
This virus destroys the external germinal layer of the Differential diagnosis
cerebellum and prevents the formation of the granular
layer. In this age of cat, other inflammatory central nervous
system abnormalities such as toxoplasmosis infection
Some affected cats have a concurrent hydrocephalus are possible.
and hydranencephaly.
Congenital anatomical defects of the cerebellum may
cause similar signs.
Clinical signs Trauma occurring at a young age may permanently
Clinical signs are present from the early prenatal period damage the cerebellum producing similar signs.
but are most apparent when the animal begins purpose-
ful movement and attempts to walk. Treatment
Tremor accompanying the disease usually has a slow No treatment is currently helpful for cats affected with
frequency (2–6 times/second) and large amplitude this disease.
(course tremor). The tremor worsens (increases in fre-
quency or amplitude), when the cat moves in a goal-
oriented way (e.g. bends down to eat), which is termed Prognosis
an intention tremor. Clinical signs associated with previous panleukopenia
Other signs include ataxia (incoordination; swaying virus infection of the developing cerebellum usually
from side to side), hypermetria (“goose-stepping”; remain static or improve with growth, causing the
overflexing of the limbs when walking), menace tremor to become less apparent.
deficits (with normal vision and pupillary light
reflexes), head tilt and nystagmus (combination quick Prevention
followed by slow movement of the eyes).
Do not vaccinate queens with modified live pan-
Clinical signs usually remain static or improve with leukopenia virus vaccine.
growth as the cat compensates, causing the tremor to
become less apparent.
CEREBELLAR OR VESTIBULAR TUMOR***
Diagnosis Classical signs

Antemortem testing for panleukopenia often results in ● Signs usually begin in cats 5 years of age
negative findings. or older.
Routine laboratory investigations are normal.
● Signs usually are progressive over weeks
to months.
Definitive diagnosis is usually only obtained at ● Occasionally, clinical signs begin acutely.
necropsy and histopathological examination of the ● Intention tremor is often associated with
nervous tissue. other signs of cerebellar disease including
In some instances of cerebellar atrophy, a smaller than ataxia, dysmetria, menace deficits, head tilt
normal cerebellum may be seen on magnetic reso- and nystagmus.
is most readily seen on the sagittal view. See main reference on page 821 for details (The Cat
With Stupor or Coma).
Occasionally, inflammatory cells may be present in cere-
brospinal fluid examination in cats with active pan-
Clinical signs
leukopenia viral infection. Cerebrospinal fluid with the
other degenerative cerebellar conditions and with previ- Clinical signs usually begin in cats 5 years of age or
ous panleukopenia infection is usually normal. older.
Signs are usually progressive over weeks to months. mass on CT or MR imaging is found in most
instances of meningioma.
Occasionally, clinical signs begin acutely.
● The CT and MR appearance of gliomas is varied
Intention tremor is often associated with other signs and enhancement after contrast administration may
of cerebellar disease including ataxia (incoordination; not be present. As these tumors arise from brain
swaying from side to side), dysmetria (“goose-step- parenchymal cells, they are found within the neu-
ping”; overflexing of the limbs when walking), menace roaxis (intra-axial).
deficits (with normal vision and pupillary light ● Choroid plexus tumors often enhance markedly
reflexes), head tilt, and nystagmus (combination quick after contrast administration because of the
followed by slow movement of the eyes). increased concentration of blood vessels within
the tumor. Because of their association with the
Signs reflect either primary nervous parenchymal
ventricular system, associated hydrocephalus is
damage from the tumor or secondary pathophysiolog-
common.
ical sequelae such as hemorrhage and edema.
Cerebrospinal fluid often has increased protein con-
Meningiomas are the most common brain tumor in
centration but this finding is not pathognomonic for
cats and are usually histologically benign.
neoplasia.
● Less-frequent tumors arise from astrocytes, oligo-
dendrogliocytes, ependymal cells and choroid Cerebrospinal fluid may have evidence of inflamma-
plexus cells. tion (increased nucelated cells and protein content). If
● Medulloblastoma is a rare primary brain tumor that CSF is the only assessment made, encephalitis may be
involves the cerebellum. erroneously diagnosed.
● Neoplasia may also secondarily involve the brain
Skull radiographs or advanced imaging are necessary
via metastasis or via direct extension from extra-
to assess the middle and inner ear. Abnormalities seen
neural sites.
with these studies, however, are not always definitive for
Tumors involving the inner ear may damage the neoplasia, and tissue diagnosis at surgery is often nec-
peripheral vestibular system, resulting in vestibular essary to accurate assessment. Destruction (lysis) of the
ataxia, in which the cat leans, drifts, falls or rolls bone of the bulla is more often associated with neopla-
toward the side of the lesion and has a head tilt. sia as compared to inflammation.
Nystagmus may also be present. Occasionally tumors
extend through the tympanic membrane and are evident
during otoscopic examination, but this is rare. See page
845 “The Cat With a Head Tilt, Vestibular Ataxia or Congential and inherited cerebellar diseases occur in
Nystagmus”. younger animals.
Squamous cell carcinoma and adenocarcinoma are the Cerebrovascular, traumatic and inflammatory condi-
most common tumors affecting the peripheral vestibu- tions can mimic the signs of a brain tumor.
lar system.
Treatment
Diagnosis Corticosteroids (prednisolone 1–2 mg/kg q 12 h) may
reduce peritumoral edema and improve clinical signs.
Routine laboratory data (e.g. hematology, biochem-
istry, urinalysis) are normal. Surgical removal of primary brain tumors may be
accomplished, especially with meningioma.
Diagnosis of a structural intracranial abnormality in the
brain is most readily accomplished with magnetic res- A well-encapsulated, firm whitish mass is most often
onance (MR) imaging or computed tomography encountered at surgery in cats. Cortical parenchyma is
(CT) of the brain. usually not infiltrated but rather compressed in cats,
● A broad-based, extra-axial (arising outside and leaving indentations in the nervous tissue parenchyma
pushing into the parenchyma) contrast-enhancing after resection.
Radiation therapy (45–48 Gy) may control tumor Other systemic signs such as vomiting, coughing and
growth of some brain tumors. diarrhea may be seen concurrently.
Treatment options of tumors of the ear include surgical
resection/debulking, radiation and chemotherapies. Diagnosis
ENCEPHALITIS*** temic inflammation (e.g. leukocytosis).
Classical signs Serum biochemical analysis may show evidence of

systemic abnormalities if the disease diffusely affects
● Diffuse or multifocal neurological signs. the body (e.g. vasculitis) such as elevated globulin, CK,
● Cerebellar signs such as intention tremor, liver enzymes or creatinine.
ataxia, hypermetria, head tilt and nystagmus.
● Cervical pain can be present. Evaluation of titers for the infectious diseases often helps
● Fever is an inconsistent finding. to rule in or rule out the diseases.
● Infectious agents causing brain disease include
● Clues of systemic inflammatory disease
such as chorioretinitis are often present. viral (feline infectious peritonitis), fungal (crypto-
● Other signs of polysystemic disease such coccosis, blastomycosis, histoplasmosis, coccidioido-
as coughing, vomiting or diarrhea may be mycosis, aspergillosis), protozoal (toxoplasmosis,
present. neosporosis), bacterial, rickettsial, and unclassified
organisms (protothecosis).
● Involvement of the intracranial nervous system can
With Tremor or Twitching). occur with parasites such as Cuterebra larvae, tox-
ocara and aberrant heartworm migration.
Clinical signs Cerebrospinal fluid analysis (CSF) will usually show

Depression, inappetence or anorexia and weight loss
are common. ● Evidence of inflammation on CSF evaluation alone,
Clinical signs often reflect multiple levels of neurolog- however, is not specific for primary encephalitis as
ical involvement. Neurological signs may indicate dif- other CNS disease (e.g. neoplasia) may result in a
fuse or multifocal disease and often do not localize to CSF pleocytosis and protein increases.
a single area within the nervous system. ● With feline infectious peritonitis (FIP), cere-
brospinal fluid analysis may show a pleocytosis,
Paresis, gait abnormalities, proprioceptive deficits,
cranial nerve defects, depression and occasionally
stupor or coma may occur depending on the areas of
concentration, often > 1 g/L (0.1 g/dl). High serum
brain involved.
coronavirus titers are not diagnostic.
Signs such as intention tremor, cerebellar ataxia (incoor- ● With toxoplasmosis, cerebrospinal fluid frequently
dination and swaying from side to side), hypermetria, contains a pleocytosis, usually with mononuclear
head tilt and nystagmus may occur with involvement of cells, and occasionally, eosinophils. Increasing IgG
the cerebellum. or a single positive IgM serum antibody titer is
suggestive of active infection. Animals with neuro-
Cervical pain can be present.
logic signs and positive IgM titers warrant treat-
Fever is an inconsistent finding. ment for the disease.
Fundic examination is important to look for clues of sys- With cryptococcosis, identification of the organism
temic inflammatory disease as chorioretinitis, which is from cytological evaluation of samples such as CSF,
often present with diseases causing systematic infection. nasal discharge and skin lesions supports the diagnosis.
A neutrophilic pleocytosis, and occasionally an Disease occurrence may have a seasonal bias. Cats in
eosinophilic pleocytosis, may be found on CSF analy- the northeast United States are commonly affected in
sis. If positive, detection of the cryptococcal capsular late summer and early fall.
antigen in serum is usually diagnostic. Tissue biopsy
and fungal culture or fungal culture of CSF may be
more definitive in the diagnosis, as occasionally the Diagnosis
serum titer is negative. Otoscopic examination, bulla radiographs, and other
With parasites such as Cuterebra larvae, toxocara and advanced imaging studies (computed tomography
aberrant heartworm migration, CSF may show inflam- (CT), magnetic resonance (MR) imaging) are normal.
mation with eosinophils in some instances. Diagnosis is based on clinical signs and lack of evi-
Imaging studies (CT and MR) are helpful for defining dence of other causes of peripheral vestibular disease
structural lesions. Multifocal, contrast-enhancing on imaging.
enhancing lesions are present, especially with toxo-
plasmosis. Differential diagnosis
Differential diagnosis of peripheral vestibular disease
includes otitis interna, middle ear polyps in cats, and
IDIOPATHIC PERIPHERAL VESTIBULAR neoplasia (squamous cell carcinoma of the middle ear).
DISEASE*** These diseases can be differentiated from idiopathic
peripheral vestibular disease because lesions are evi-
Classical signs dent via otoscopic examination of the ear canal and
● Signs can occur in any age but are tympanic bulla and/or with imaging studies (radi-
commonly young to middle-aged animals. ographs, CT, MRI).
● Acute-onset severe head tilts and
nystagmus are most common.
● Cats often cannot stand initially and will
Treatment
continually roll. No specific treatment has been shown effective.
Antihistamines (diphenhydramine at 0.5–1 mg/kg q 8 h)
may help some animals.
With a Head Tilt, Vestibular Ataxia or Nystagmus).

Clinical signs are of an acute peripheral vestibular dis- Clinical signs of idiopathic vestibular disease usually
order with nystagmus (horizontal or rotary), head tilt improve dramatically in 1–2 weeks regardless of
(toward the side of the lesion), rolling and falling. treatment.
No other neurological signs are seen. The nystagmus usually resolves quickly (within the
first few days).
Often these animals are initially so incapacitated that
they are misdiagnosed with cerebrovascular accidents. Improvements in posture and walking occur within 5–7
days, whereas a mild head tilt may remain persistent.
Clinical signs, while initially severe, will usually
improve in 3–5 days. The nystagmus is the first sign to While most animals compensate well, some may have
abate. episodic ataxia when performing tasks such as jumping
up on furniture.
If Horner’s syndrome or facial nerve paresis are also
present, other differentials should be considered. Recurrence is possible.
● Evaluating the retinas and external ear canals for acute

HEAD TRAUMA***
hemorrhage may also provide clues to the diagnosis.
Classical signs Advanced imaging studies such as CT or MR imaging
are useful, primarily for determining structural damage
● Acute onset of signs following a traumatic
to the brain.
event.
and face such as facial lacerations, HYDROCEPHALUS**
bruising, retinal hemorrhage, or Classical signs
hemorrhage in the external ear canals.
● Cerebellar involvement may result in ● Dome-shaped or bossed appearance to the
intention tremor, decerebellate rigidity, head or persistent fontanelles in a young cat.
ataxia, hypermetria, head tilt and nystamus. ● Seizures, poor learning ability, behavior
changes, paresis, cranial nerve deficits and
See main reference on page 823 for details (The Cat changes in consciousness.
Clinical signs
Exogenous injury to the brain occurs most commonly
Clinical signs
from automobile trauma, although gunshot wounds and
falls may also occur. In young cats prior to ossification of the cranial
sutures, hydrocephalus may contribute to abnormalities
Cerebellar involvement may result in intention tremor,
of skull development such as a thinning of the bone
decerebellate rigidity (extension of all four limbs and the
structure, a dome-shaped or bossed appearance to the
trunk), ataxia, hypermetria, head tilt and nystagmus.
head or persistent fontanelles.
Signs usually begin acutely after trauma.
Clinical signs of hydrocephalus reflect the anatomical
Intracranial signs most commonly seen include stupor level of disease involvement.
and coma, paresis and gait abnormalities and cranial
Supratentorial, vestibular and cerebellar signs are
nerve deficits.
most common.
Evidence of external trauma to the head and face
As the supratentorial structures are often involved with
such as facial lacerations, bleeding from the nose and
hydrocephalus, alterations in awareness and cogni-
mouth, bruising or hemorrhage in the external ear
tion are common.
canals may provide clues to the traumatic etiology.
● Occasionally, some animals that are incoordinated Many animals affected congenitally may appear to be
may fall and injure themselves secondarily, but this less intelligent than normal.
can usually be differentiated with good history taking.
Behavioral changes, paresis, cranial nerve deficits and
changes in consciousness may occur.
Diagnosis
Circling, paresis and seizure may also be seen.
The diagnosis of trauma is usually straightforward
Severity of clinical signs is not dependent upon the
when the trauma is witnessed.
degree of ventricular dilation, but rather on a host of
In some instances, when animals are presented with an concurrent abnormalities including the underlying dis-
acute onset of neurological signs and an unknown his- ease process, associated intracranial pressure changes,
tory, examining for external signs of trauma such as intraventricular hemorrhage, and the acuity of ventric-
lacerations or skull fractures is important. ular obstruction.
There are no pathognomonic clinical signs for vides for better parenchyma resolution than CT, and is
acquired hydrocephalus in adult animals. especially useful for evaluation of the infratentorial
structures.
Correlation of degree of ventricular enlargement
and clinical signs is poor. Diffuse ventricular enlargement suggests congenital
ventricular dilation or obstruction at the level of the lat-
Diagnosis eral apertures or foramen magnum. Focal ventricular
enlargement suggests focal obstruction or parenchy-
Routine laboratory data (e.g. hematology, biochem- mal cell loss.
istry, urinalysis) are normal.
Animals with an asymmetric appearance of the ven-
Historical, invasive techniques for diagnosis of hydro- tricles should be critically evaluated for focal obstruc-
cephalus such as pneumo- or contrast ventriculography tion of the ventricular system due to mass effect.
have been replaced by non-invasive diagnostic modalities.
Survey radiographs may suggest the presence of hydro-
CONGENITAL VESTIBULAR DISEASE**
cephalus, however they are usually not helpful for defin-
itive diagnosis. Findings associated with congenital
Classical signs
hydrocephalus include loss of gyral striations, sepa-
ration of cranial sutures (diastasis) and persistent ● Signs are usually present from the time
fontanelles. If hydrocephalus is acquired after the skull the animal begins to walk.
has formed, abnormalities are rarely encountered. ● Head tilt and cat leans, drifts, falls or rolls
to side of head tilt.
Electroencephalography has been used to diagnose
● ± Deafness.
hydrocephalus, primarily prior to advanced imaging.
Classically, slow-frequency, high-voltage (amplitude)
activity is noted. This pattern, however, can be seen
with other encephalopathies that destroy cortical Pathogenesis
parenchyma. Because of this, EEG is rarely used as the
Congential abnormality of the vestibular system usu-
sole means of diagnosing hydrocephalus.
ally involves the peripheral vestibular system.
Ultrasound can be used to diagnosis hydrocephalus.
Histologic lesions are often not found.
● This is most readily accomplished when a font-
anelle is present providing an “acoustic window”
as ultrasound waves do not usually penetrate the Clinical signs
skull well enough.
● If the bone is intact, a craniotomy defect can be
Siamese and Burmese cats are often affected.
created. Clinical signs are usually present from the time the ani-
● For imaging of the lateral and third ventricles, the mal begins to walk or begin early in life.
bregmatic fontanelle may be used.
● Often, ultrasound can be performed in awake cats
Signs are usually referable to unilateral vestibular
disease; bilateral disease is less common.
as a screening test to determine ventriculomegaly.
● Depending upon the size of the fontanelle, the lat- The most common clinical signs are head tilt and
eral and third ventricles as well as the mesen- vestibular ataxia (cat leans, drifts, falls or rolls to side
cephalic aqueduct are usually easily identified. of head tilt).
Computed tomography (CT), as a non-invasive In some cases deafness is also present.
intracranial imaging modality, is often useful in defin-
With bilateral disease, there is no head tilt but the
ing ventricular size.
head moves from side to side in exaggerated motions.
Magnetic resonance (MR) imaging also affords eval- Normal physiological nystagmus (movement of eyes
uation of the ventricular system. This modality pro- side to side with movement of head) is absent.
Clinical signs are non-progressive and usually Cerebellar degeneration with neuroaxonal dystro-
decrease in severity with time, but remain life-long. phy has been reported in domestic tri-colored cats. This
is inherited as an autosomal-recessive trait.
Diagnosis
Diagnosis is based primarily upon clinical signs. Clinical signs
Skull radiographs, advanced imaging studies (MR or CT), Clinical signs usually begin between 3–12 months of
CSF analysis and otoscopic examinations are normal. age.
Brain stem auditory-evoked potential testing may be Cerebellar disease usually results in a coarse tremor
abnormal if there are associated problems with hearing. that worsens (increases in frequency or amplitude)
(intention tremor).
Other signs of cerebellar disease that accompany
Otitis interna should be evaluated for. cerebellar tremor include ataxia (incoordination;
Other inflammatory processes involving the vestibu- swaying from side to side), dysmetria (“goose-step-
lar receptors may produce similar signs. ping”; overflexing of the limbs when walking), men-
ace deficits (with normal vision and pupillary light
Trauma to the vestibular receptors is possible. reflexes), head tilt, and nystagmus (combination
quick followed by slow movement of the eyes).
Treatment
An hereditary cerebellar degeneration is described
No treatment is helpful. in Japan in cats with signs beginning around 7–8 weeks
of age.
● Signs include head tremor along with ataxia, dys-
Prognosis
metria and intention tremor. An autosomal reces-
Clinical signs may remain persistent or improve sive mode of inheritance was presumed.
throughout life.
Cerebellar degeneration with neuroaxonal dystro-
phy in domestic tricolored cats results in head
INHERITED CEREBELLAR DISEASES** tremors and shaking. Clinical signs begin at 5–6
weeks of age and progress to ataxia and hyperme-
Classical signs tria. Affected kittens have a lilac color that darkens
● Signs usually begin or are present in cats with age.
● A similar but separate neuroaxonal dystrophy has
less than 1 year of age.
● Signs usually are slowly progressive or been described in cats of various colors. Clinical
remain unchanged. signs begin at 7–9 months of age and include ataxia
● Signs include coarse tremor, hypermetria, with paraparesis.
ataxia, intention tremor and menace deficits. Spongiform encephalopathy in Egyptian Mau cats
results in ataxia and hypermetria, and it is presumed
inherited. Clinical signs begin at 7 weeks of age.
Pathogenesis ● Another spongiform encephalopathy has been
reported in older Egyptian Mau cats in the United
Cerebellar degeneration is usually an inherited disease.
Kingdom. Clinical signs include muscle tremors,
A hereditary cerebellar degeneration has been ataxia, dilated unresponsive pupils, jaw champing,
described in Japan in cats. An autosomal recessive salivation and behavior abnormalities. Signs may
mode of inheritance was presumed. progress to severe ataxia and hypermetria.
Antemortem testing for these diseases often results in Do not breed cats affected that have produced kittens
negative or normal findings. with a presumed genetic or congenital cerebellar
disease.
Routine laboratory investigations (CBC, serum bio-
chemical analysis, urinalysis) are normal.
STORAGE DISEASES**
Classical signs
nervous tissue.
● Signs usually begin or are present in cats
In some instances of cerebellar atrophy, a smaller than
less than 1 year of age.
normal cerebellum may be seen on magnetic reso-
● Signs usually are slowly progressive or
remain unchanged.
is most readily seen on the sagittal view.
● Signs include coarse tremor, hypermetria,
Cerebrospinal fluid with these degenerative cerebellar ataxia, intention tremor and menace
conditions is normal. deficits.
With hereditary cerebellar degeneration described in
Japan there is marked loss of Purkinje cells on histo- Pathogenesis
logical evaluation of the cerebellum.
Storage diseases result from inherited (or less com-
Neuroaxonal dystrophy is associated with pathologic monly, acquired) intracellular metabolic derangements
changes in the brain, brain stem, cerebellum and spinal that result in abnormal metabolism of cellular products.
cord.
Cellular products accumulate and afferent neuronal
cells physiologically or mechanically, resulting in cel-
Differential diagnosis lular dysfunction, and hence, clinical signs.
In this age cat, other inflammatory central nervous Although signs of storage diseases are predominately
system abnormalities, such as toxoplasmosis infection referable to the brain and especially the cerebellum,
should be considered. CSF analysis and serologic test- some of the storage diseases also affect the peripheral
ing help to differentiate it from inherited cerebellar nervous system.
degeneration.
Examples include gangliosidosis, sphingomyelinosis,
Congenital anatomical defects of the cerebellum may globoid cell leukodystrophy, and mannosidosis.
be present with similar signs.
Trauma occurring at a young age may permanently Clinical signs
damage the cerebellum and result in similar signs.
Clinical signs usually begin between 3–12 months of
age.
Treatment
Cerebellar disease usually results in a coarse tremor
No treatment is currently helpful for affected cats. that worsens (increases in frequency or amplitude)
(intention tremor).
Prognosis
Other signs of cerebellar disease that accompany cere-
Clinical signs associated with degenerative cerebellar
bellar tremor include ataxia (incoordination; swaying
diseases progressively worsen.
from side to side), dysmetria (“goose-stepping”; over-
Animals are commonly euthanized due to the progres- flexing of the limbs when walking), menace deficits
sive incapacitation. (with normal vision and pupillary light reflexes), head
tilt, and nystagmus (combination quick followed by Congenital anatomical defects of the cerebellum may
slow movement of the eyes). be present with similar signs.
In cats with sphingomyelinosis (Niemann–Pick type C Trauma occurring at a young age may permanently
disease) clinical signs begin early in life (< 6 months) damage the cerebellum and result in similar signs.
and progress to ataxia and hypermetria, absent menace
responses, and occasionally positional nystagmus.
Treatment
Death usually occurs by 8–10 months of age.
● Similar clinical signs have been reported in a case No treatment is currently helpful for affected cats.
of type IV glycogen storage disease in a
Norwegian Forest cat.
Prognosis
Niemann–Pick type A disease occurs in Siamese and
Clinical signs associated with storage diseases usually
Balinese cats. Head tremor, head bobbing, and dysme-
progressively worsen.
tria begin at 3–4 months of age. Clinical signs progress to
ataxia and paresis, worse in the pelvic limbs. Animals are commonly euthanized due to the progres-
● An associated demyelinating polyneuropathy was sive incapacitation.
found in one family of affected cats.
Prevention
Diagnosis
Do not breed cats affected that have produced kittens
Antemortem testing for these diseases often results in
with a presumed genetic or congenital cerebellar
negative or normal findings.
disease.
Routine laboratory investigations (CBC, serum bio-
chemical analysis, urinalysis) are normal.
OTITIS MEDIA/INTERNA**
Definitive diagnosis is often only obtained at
necropsy and histopathological examination of the Classical signs
nervous tissue.
● Signs can occur in any age.
In some instances of cerebellar atrophy, a smaller than ● Head tilt and nystagmus are most
normal cerebellum may be seen on magnetic reso- common.
nance imaging of the intracranial nervous system. This ● Discharge from the ear, abnormal odors
is most readily seen on the sagittal view. and ear pain may be present.
● Polyploid masses may be seen in the
Cerebrospinal fluid with these degenerative cerebellar
oropharynx or ear canal.
conditions is normal.
In cats with sphingomyelinosis (Niemann–Pick type C See main reference on page 836 for details (The Cat
disease) cerebellar atrophy, Purkinje cell loss, and With a Head Tilt, Vestibular Ataxia or Nystagmus).
neuroaxonal dystrophy are the predominant patho-
logical changes.
Clinical signs
Clinical signs may reflect either primary ear, vestibu-
lar or auditory dysfunction.
In this age cat, other inflammatory central nervous
A painful external ear and/or pain on opening the
system abnormalities, such as toxoplasmosis infection
mouth are often present.
should be considered. CSF analysis and serologic
testing help to differentiate it from inherited cerebellar Head tilt and nystagmus are the most common
degeneration. vestibular signs. Vestibular ataxia (cat leans, drifts,
falls or rolls to side of head tilt) may occur in more A cat with polycythemia was presented for ataxia, pos-
severe cases. sibly due to increases in serum viscosity.
The facial nerve may be involved concurrently result-
ing in abnormalities of facial expression.
Clinical signs
Abnormal odors or discharge from the ear canal may
Clinical signs are usually acute in onset.
be present.
Head tilt, cerebellar ataxia (incoordination, swaying
Oropharyngeal exam occasionally reveals an ear polyp.
from side to side), hypermetria, intention tremor and
nystagmus are possible.
Diagnosis
Menace deficits with normal vision and papillary light
Otoscopic examination should be used to examine the reflexes may also be present.
tympanic membrane. This may be difficult in animals
with severe otitis externa prior to cleansing.
● The tympanic membrane is often discolored Diagnosis
(hyperemic), opaque and bulging outward with
Routine laboratory evaluations (CBC, serum bio-
middle ear disease. Clear to yellow fluid may be
chemical analysis, urinalysis) may show abnormalities
seen behind the membrane.
in platelets or red blood cell mass or evidence of under-
Diagnosis may also be supported by abnormalities on lying systemic disease.
bulla radiographs or advanced imaging studies
Coagulation studies and bleeding time assessment are
(MRI or CT).
useful in determining the cat’s coagulation ability.
● Often the bulla are fluid filled on either skull radi-
ographs or advanced imaging studies. Advanced imaging studies may show evidence of
hemorrhage or infarction in the cerebellum.
Definitive diagnosis is made through culture of the
organism via a myringotomy or at surgical exploration. CSF analysis may show evidence of hemorrhage, how-
ever, should be performed with caution or avoided in
animals with coagulation or platelet problems.
VASCULAR DISEASES*

● Acute onset of cerebellar signs. Rule out other inflammatory, neoplastic and traumatic
● Head tilt, nystagmus, ataxia, hypermetria, causes of cerebellar disease.
and other cerebellar signs.
Treatment
Pathogenesis Treatment should be directed at the underlying coagu-
lation or bleeding disorder abnormality.
Injury to cerebellar tissue can occur as a result of
thrombosis or hemorrhage. Rarely, if a hematoma is present, surgical removal may
be helpful.
Diseases that predispose to hypercoagulability or vas-
culitis predispose to vascular thrombosis.
Hemorrhage can occur as a result of thrombocytope- Prognosis
nia or coagulation abnormalities.
Prognosis depends upon the ability to treat the underly-
Thrombosis leads to ischemia and cellular death. ing disease process and the degree of cerebellar damage.
THIAMINE DEFICIENCY* TOXINS*

● Initially, lethargy, inappetence and ataxia. ● Metronidazole toxicosis results in ataxia,
● Later signs include weakness, ventral paresis, seizures and cortical blindness.
flexion of the neck, dilated pupils, stupor ● Bromethalin toxicosis in the early stages
and coma. may also result in ataxia. Signs progress to
paresis, depression, tremors, seizures and
See main reference on page 848 for details (The Cat decerebrate posture.
With a Head Tilt, Vestibular Ataxia or Nystagmus). ● Ivermectin toxicosis has resulted in
generalized ataxia, tremor, weakness,
incoordination, and miosis in a kitten.
Pathogenesis
● Griseofulvin therapy resulted in ataxia in
Occurs in anorexic cats or cats that are fed all-fish a 12-week-old kitten.
diets containing thiaminase. ● Aminoglycosides, administered either
systemically or topically, may cause
This deficiency results in polioencephalomalacia of the
vestibular signs including ataxia.
oculomotor and vestibular nuclei, the caudal colliculus
● Chlorhexidine solution used to clean the
and the lateral geniculate body.
external ear may result in vestibular signs
including ataxia.
Clinical signs
Early non-specific signs are typically lethargy and Pathogenesis
inappetence.
Metronidazole toxicosis has been reported to result in
The earliest localizing sign is bilateral vestibular ataxia in cats.
ataxia, which appears as an abnormal broad-based ● Usually, this is associated with high doses of the
stance, loss of balance and vertigo. drug.
● As metronidazole is metabolized by the liver, how-
There is weakness and an inability or reluctance to
walk. The cat sits crouched with ventral flexion of ever, toxic serum levels can occur with appropriate
the neck. doses in animals with liver dysfunction.
Pupils are dilated and non-responsive or poorly Bromethalin toxicity results in vacuolization of the
responsive to light reflexes. nervous system, most likely due to a lack of intracellu-
lar energy.
vocalization, opisthotonos, and death.
Clinical signs
Episodes of spastic opisthotonos or ventroflexion of
the neck and generalized muscle spasm may occur Ataxia is usually the initial clinical sign of metronida-
especially when the cat is lifted or stressed. They may zole toxicity.
be interpreted as seizures, but true seizure activity ● Paresis is usually present, and seizures and corti-
rarely occurs. cal blindness may also be noted.
● These signs in association with metronidazole
administration should raise concern for toxicity.
Diagnosis
The early stages of bromethalin toxicosis may also
No antemortem diagnostic test is available.
result in ataxia.
Diagnosis is based on clinical signs and rapid ● Signs progress to paresis, depression, tremors,
response to thiamine. seizures and decerebrate posture.
Ivermectin toxicosis has resulted in generalized Prognosis

ataxia, tremor, weakness, incoordination and miosis in
a kitten. With metronidazole toxicity, a complete recovery is
possible after discontinuation of the drug if the signs
Griseofulvin therapy resulted in ataxia in a 12-week- are not severe.
old kitten.
● Clinical signs remained static up to 4 months after
Prevention
the initial presentation.
Avoid exposure to these products.
Aminoglycosides, administered either systemically or
topically, may cause vestibular signs including vestibu-
lar ataxia (cat leans, drifts, falls or rolls to side of the IDIOPATHIC ENCEPHALOPATHY*
head tilt), head tilt and nystagmus.
● Streptomycin and gentamicin have the most pro- Classical signs
nounced effects on the vestibular receptors, while
● Ataxia, paresis, and “head shaking” in
neomycin, kanamycin and amikacin preferentially
young cats up to 3 years old in the UK.
damage auditory receptors.
● Ataxia of the pelvic limbs was the initial sign.
Chlorhexidine solution used to clean the external ear
may result in vestibular signs.
Pathogenesis
Diagnosis Pathogenesis is unknown, although a viral etiology was
Serum concentrations of metronidazole will be in the suggested but not proven.
toxic range if measured soon after clinical signs Wallerian degeneration was noted primarily involving
begin. the spinocerebellar pathways and the ventral funiculus
● If there is a delay in collecting blood for drug of the spinal cord.
concentrations after the initiation of clinical
signs, serum concentrations of metronidazole may
decrease into the normal range even as the clinical
Clinical signs
signs remain persistent. An encephalomyelopathy of young cats reported in the
United Kingdom had clinical signs of ataxia, paresis
Diagnosis of other toxicities is supported by a history
and “head shaking”.
of exposure.
Cats 3–12 months old were affected, however, the dis-
Differential diagnosis ease was seen in cats up to 3 years of age.
Other diseases causing signs of vestibular disease Ataxia of the pelvic limbs was the initial clinical sign
include otitis interna, middle ear polyps in cats, and noted.
neoplasia (squamous cell carcinoma of the middle ear).
These can usually be differentiated from toxicity on the Diagnosis
basis of history, otoscopic examination and imaging of
the bulla. Diagnosis was made at necropsy.
Treatment Differential diagnosis

There is no specific treatment for metronidazole toxicity. Diseases causing peripheral vestibular disease should be
● Discontinuation of the drug is imperative. A com- considered including otitis interna and middle ear polyps.
plete recovery is possible.
No specific treatment is available for the other
Treatment
toxicities. No treatment was attempted.
RECOMMENDED READING
Baroni M, Heinold Y. A review of the clinical diagnosis of feline infectious peritonitis viral meningo-
encephalomyelitis. Prog Vet Neurol 1995; 6: 88.
Inada S, Mochizuki M, Izumo S, et al. Study of hereditary cerebellar degeneration in cats. AJVR 1996; 57: 296–301.
Kornegay JN. Feline infectious peritonitis: The central nervous system form. J Am Anim Hosp Assoc 1978; 14: 580.
March PA. Degenerative brain disease. Vet Clinic North Am 1996; 26: 945–971.
Nowotny N, Weissenböck H. Description of feline nonsuppurative meningoencephalomyelitis (“staggering disease”)
and studies of its etiology. J Clin Microbiol 1995; 33: 1668–1669.
Palmer AC, Cavanagh. Encephalomyelopathy in young cats. JSAP 1995; 36: 57–64.
Saxon B, Magne ML. Reversible central nervous system toxicosis associated with metronidazole therapy in three
cats. Prog Vet Neurol 1993; 4: 25–27.
Vandevelde M, Braund KG. Polioencephalomyelitis in cats. Vet Pathol 1979; 16: 420–427.
44. The cat with generalized weakness
Rodney S Bagley, Jacquie Rand, Terry King and
Fiona Campbell
KEY SIGNS
● Weakness.
● Inability or reluctance to walk or jump.
● Stiff, stilted gait.
● Ventroflexion of the neck.
MECHANISM?
● Diffuse loss of muscle strength results in generalized weakness. Diseases of the peripheral
nervous system, neuromuscular junction and muscle often result in generalized weakness.
Systemic diseases affecting metabolism of or perfusion to, the muscles may also result in
weakness.
WHERE?
● Peripheral nervous system, neuromuscular junction and muscle.
WHAT?
● Diseases include the peripheral neuropathies, neuromuscular junctionopathies (myasthenia
gravis) and myopathies. One of the most common causes of weakness is hypokalemic
myopathy.

Diseases causing generalized weakness
DEGENERATIVE
● Degenerative neuropathies (p 963)
Weakness with decreased to absent spinal reflexes. Dropped hock appearance in young Birman
cats, beginning 8–10 weeks of age. Storage disease may be associated with aneuropathy. These
diseases are often breed-specific with clinical signs beginning in cats less than 1 year of age.
● Degenerative motor neuronopathies (p 964)
Progressive weakness and muscle atrophy in adult cats, decreased to absent spinal reflexes, tremor
especially of head and tongue, cervical ventroflexion and dysphagia.
continued
941
continued
● Degenerative myopathies (X-linked muscular dystrophy, hereditary myopathy, Nemaline

rod myopathy) (p 964)
Any breed may be affected; inherited myopathy occurs in Devon Rex. Signs begin 2–24 months of
age, weakness and reduced activity, stiff, choppy gait, increase in muscle mass and hypertrophy of
the tongue (x-linked muscular dystrophy), ventral flexion of neck and dorsal protusion of scapula
(hereditary myopathy of Devon Rex).
METABOLIC
● Hypokalemic myopathy*** (p 945)
Typically older cats or Burmese < 1 year of age. Signs include weakness, inability or reluctance to
walk or jump, stiff, stilted gait, neck ventroflexion and sensitivity to palpation of larger muscle
groups.
● Diabetic neuropathy** (p 948)
Often presents as a “dropped-hock” appearance in older cats with clinical signs of diabetes
(polyuria, polydipsia, weight loss), subtle generalized weakness, reduced activity, difficulty jumping
and some cats have a classic plantigrade stance.
● Primary hyperoxaluria (p 967)
Uncommon clinically in cats. Domestic short-hair cats 5–9 months old. Generalized weakness,
with or without concurrent signs of renal failure.
● Polymyopathy* (p 961)
Signs include ventral flexion of the neck, apparent muscle pain, muscle weakness and a stiff gait.
Age of onset varies from 3 months to 13 years and most are domestic short- or long-haired cats.
Abnormal systemic metabolism affects muscle or nerve function. Concurrent hypokalemia is com-
mon. Signs may include weakness, ventral neck flexion and reduced physical activity. Typical
signs of hyperthyroidism are weight loss, polyphagia, irritability or restlessness.
● Hyperlipidemia (p 968)
Lipid granulomas may compress the peripheral nerve. Typical signs include hyperlipidemia and
lipemia retinalis in association with peripheral neuropathies involving individual peripheral, cranial
or sympathetic nerves.
● Hypernatremic myopathy (p 968)
Rare disease with signs similar to hypokalemic myopathy. Ventral neck flexion, weakness, reduced
physical activity and a “dropped-hock” appearance may occur.
● Hypocalcemia (p 962)
Most often occurs after thyroidectomy. Muscle weakness, tetany and tremors are typical.
Preparturient hypocalcemia presents as anorexia, lethargy, trembling, muscle twitching and weak-
ness.
● Hypoglycemia* (p 956)
Most often associated with insulin overdose in diabetic cats, but also rarely caused by an insuli-
noma in older cats. Signs include trembling, weakness, dilated pupils, reduced alertness, and if
severe, seizures progressing to coma.
44 – THE CAT WITH GENERALIZED WEAKNESS 943
● Reduced tissue oxygenation* (p @)

Any cause of substantially reduced tissue oxygenation will cause weakness. Examples include
severe anemia, methemoglobinemia associated with acetaminophen (paracetamol) toxicity, cardiac
disease, hydrothorax including pyothorax and chylothorax, and severe bronchopulmonary disease
or obstructive upper respiratory disease.
NUTRITIONAL
● Thiamine deficiency* (p @)
tic ventroflexion of the neck or opisthotonos, dilated pupils, stupor and coma.
INFECTIOUS
● Acute sepsis (p @)
Toxemia and reduced tissue oxygenation from acute bacterial sepsis may cause weakness and
depression, resulting from bacteremias via the uterus (pyometritis), thorax (pyothorax), abdomen
(peritonitis), skin (subcutaneous abscess). Pyrexia or hypothermia may be present. Signs referable
to the infection site (dyspnea, vaginal discharge or uterine distention abdominal guarding, skin
abscess) are often evident.
● Toxoplasmosis* (p @)
Protozoan organism that commonly affects the muscle or peripheral nerve. Most cats are asym-
tomatic. Signs are most severe in cats under 1 year of age and especially in young kittens. They
include lethargy, anorexia, dyspnea, icterus, uveitis, retinal hemorrhage and central nervous system
signs. Weakness or stiffness may occur with signs of spinal cord, peripheral nerve or muscle
involvement.
● Feline immunodeficiency virus (p @)
A subclinical myopathy has recently been described. Diagnosis is based on a positive FIV anti-
body test and inflammatory changes on muscle biopsy, in the absence of Toxoplasma gondii organ-
isms. Some cats had elevated CK and EMG abnormalities.
Inflammatory:
● Myasthenia gravis* (p @)
Typically adult cats or Siamese < 1 year of age. Signs include generalized weakness induced by
movement, a stiff, stilted gait prior to collapse, ventral neck flexion and a decreased palpebral
reflex.
● Polyneuritis (p @)
A rare cause of weakness with decreased spinal reflexes and conscious proprioceptive deficits.
● Polymyositis* (p @)
Primary inflammation of the muscles resulting in loss of muscle strength and neck ventroflexion.
Idiopathic:
● Idiopathic peripheral neuropathy* (p @)
A primary neuropathy without a definable cause. Signs include marked weakness with conscious
proprioceptive deficits and decreased spinal reflexes. Lower motor neuron tetraparesis is the pre-
dominant sign. Signs are similar to dogs with polyradiculoneuropathy (Coon Hound paralysis).
continued
continued
● Chronic relapsing polyneuropathy* (p 966)

Peripheral neuropathy of cats which has no definitive cause. Marked weakness with decreased
spinal reflexes and conscious proprioception. Signs similar to polyradiculitis neuropathy (Coon
Hound paralysis) but cats recover then relapse months later.
● Myotonia (p 967)
A disease associated with excessive muscle contraction. Signs include stiffness and muscle spasm,
short, stilted gait and increased muscle size.
● Dysautonomia* (p 961)
A disease primarily seen in younger cats (< 3 years) in Britain. Clinical signs are often acute in
onset and reflect autonomic system dysfunction. They include depression, anorexia, dilated pupils,
megacolon, constipation, xerostomia, keratoconjunctivitis sicca, prolapsed third eyelids, brady-
cardia, loss of anal reflex, incontinence and weakness.
TOXICITY
● Organophosphate toxicity** (p 947)
Toxicity usually occurs from misuse of flea and tick products and is associated with muscle weak-
ness. Signs include acute onset of miosis, salivation, urination, defecation and muscle weakness.
Rarely, persistent weakness occurs without associated autonomic signs. Cats may attempt to walk
a few steps, then collapse in sternal recumbency mimicking cataplexy/narcolepsy.
● Snakebite envenomation from Australian snakes** (p 950)
Australian snake venoms are predominately neurotoxic and usually strongly coagulant. Usually
there is no local reaction at the site of venom injection. Generalized muscle weakness and
dilated pupils that are poorly responsive to light are features. Complete flaccid paralysis is a
common finding. Vomiting and rapid respiration are present in 30% of cases. Excessive bleed-
ing from venepuncture sites may be evident. Hypothermia is a poor prognostic sign.
● Snakebite envenomation from USA snakes** (p 949)
Coral snake envenomation is most often seen in the southeastern US. Clinical signs are of a pro-
gressive flaccid paralysis. Palpebral reflexes may be diminished, as is rectal temperature. Recovery
rates have been good in a small number of reported cats.
● Tick toxicity** (p 953)
In Australia, toxin from the Ixodes tick affects muscle and nerve transmission and causes acute
onset of flaccid paralysis, beginning in the hindlimbs and ascending and acute onset of dypsnea. In
North America, Dermacentor and Argas ticks may also cause paralysis.
● Red-back spider envenomation (Latrodectus mactans hasselti; Australia) (p 974)
Envenomation occurs from the bite of the female red-back spider and often there is moderate to severe
pain, erythema, edema and localized swelling at the bite site. Venom causes depletion of acetylcholine
reserves at motor nerve endings, which may result in a patchy paralysis of voluntary muscle. The spi-
der is found Australia-wide, avoiding only the hottest desert habitats and cold alpine altitudes.
● Ciguatoxin intoxication (p 971)
Signs begin within 3–6 hours of ingestion of a toxic meal of reef fish (toxin found in large carniv-
orous fish species). Toxins affect neuromuscular transmission and hindleg paresis and vomiting are
the most prominent. Cardiovascular shock and/or respiratory distress may precede coma and death
within 24 hours of ingestion.
● Tetrodotoxin intoxication (p 973)

Tetrodotoxin is produced by Vibrio bacteria in the intestines of marine fish including toadfish,
pufferfish, newts and the blue-ringed octopus and accumulates in tissues. The toxins affect neuro-
muscular transmission. Signs begin 10–40 minutes after ingestion. Initial signs are gastrointestinal–
drooling, vomiting and diarrhea. Neuromuscular signs follow with weakness and ataxia progressing
to flaccid hindlimb paralysis. Pupillary dilation is usually a feature. With severe toxicity, cardio-
vascular shock and labored respiration often precede convulsions and death within hours.
An evaluation for underlying metabolic disease is

INTRODUCTION imperative in determining the cause of weakness.
Accurate diagnosis often requires evaluation with elec-
MECHANISM? trodiagnostics, and muscle and nerve biopsy.
Loss of muscle strength causes generalized weakness.
Fibrillation potentials, positive sharp waves, and pro-
The gait may have a stiff, stilted appearance. Loss of
longed insertional activity are abnormal electromyo-
cervical muscle strength results in an inability to hold
graphic findings, and occur when there is myocyte
the head up, which appears as ventroflexion of the
inflammation and abnormal membrane electrical activ-
neck, and is a common sign of weakness in cats.
ity. This occurs when there is muscle inflammation,
degeneration or denervation.
WHERE?
Disease either of the peripheral nervous system, neuro- DISEASES CAUSING GENERALIZED
muscular junction and/or muscle often results in gener- WEAKNESS
alized weakness.
Systemic diseases affecting metabolism or perfusion to HYPOKALEMIC MYOPATHY***
the muscles may also result in weakness.
Classical signs
● Aged cats or Burmese < 1 year.
WHAT? ● Ventral neck flexion.
Diseases include the peripheral neuropathies, neuro- ● Stiff, stilted gait.
muscular junctionopathies (myasthenia gravis) and ● Reluctance to walk or jump and physical
myopathies. The most common cause of generalized inactivity.
weakness is hypokalemic myopathy. In some geogra- ● +/- Sensitivity to palpation of larger
phic locations, tick toxicity and snakebite are relatively muscle groups.
common.
Hypoglycemia from an insulin overdose is a relatively
With Neck Ventroflexion).
common cause of metabolic weakness. Causes of
reduced muscle oxygenation include severe anemia,
methemoglobinemia associated with acetaminophen Pathogenesis
(paracetamol) toxicity, cardiac disease, hydrothorax
Potassium is important in maintaining normal muscle
including pyothorax and chylothorax, and severe bron-
cell membrane potentials.
chopulmonary disease or obstructive upper respiratory
disease. Most of these causes of weakness have other Potassium depletion can result in alterations in muscle
prominent signs such as pale or cyanotic mucous mem- cell membrane potentials, muscle cell glycogen content
branes, dyspnea or heart murmur. and synthesis, and blood flow to muscle.
Hypokalemia results in hyperpolarization of muscle Diagnosis

cell membranes which then require greater stimulus
for depolarization, leading to generalized muscle weak- Diagnosis is made by finding decreased serum potassium
ness. concentrations (usually < 3.5 mmol/L) in association with
clinical signs. The severity of signs varies between cats
Hypokalemia occurs when the dietary intake is insuf- when potassium is 2.5–3.5 mmol/L. Below 2.5 mmol/L
ficient to replace urinary and fecal loss. and especially below 2.0 mmol/L, signs are life threat-
A major contributing factor to hypokalemia in ening, with death occurring from respiratory muscle
older cats is the inability of the kidney to conserve failure.
potassium. Serum creatine kinase (CK) may be elevated reflecting
Acidification of diets to prevent struvite urolithias the mypoathy associated with hypokalemia.
increases renal and fecal potassium loss. Electrodiagnostic evaluation is rarely performed.
Diets deficient in potassium may induce signs. Clinical Abnormalities that may be found include increased
signs occurred in one group of cats fed a vegetarian insertional activity, fibrillation potentials and positive
diet. sharp waves and some bizarre high-frequency dis-
charges.
Burmese cats have an inherited hypokalemic myopa-
thy producing signs of periodic muscle weakness, with Muscle biopsies often have minimal change present.
signs first evident before 12 months of age, usually Mild myonecrosis is possible.
between 4–12 weeks.
Clinical signs Myasthesia gravis, polymyositis and organophosphate

toxicity can all cause similar clinical signs. Hypokalemia
Signalment is typically aged cats > 8 years or young is readily differentiated from these on serum potassium
Burmese < 1 year (usually 2–6 months). concentration and response to treatment.
Typically there is a history of acute onset of weakness. Rarely snake bite or tick paralysis may cause weakness
However, decreased activity and inappetence are often similar to severe acute signs of hypokalemia. Other
present for weeks to months prior to presentation. clinical signs, history and serum potassium concentra-
Clinical signs include ventral neck flexion, stiff, tion allow differentiation. Typically, cats with bites
stilted gait and a reluctance to walk or jump. Typically, from Brown or Tiger snakes have increased plasma
weak cats do not walk far, but soon sit or lie, flopping (CK) activity and increased clotting times. Cats with
down, instead of carefully sitting as normal cats do. tick bite have increased respiratory effort and a tick is
Sensitivity to palpation of larger muscle groups may be usually found with careful searching.
noticed.
Dyspnea occurs when the potassium is very low
(2.0–2.5 mmol/L), because of weakness of the respira-
Treatment
tory muscles. It may occur after fluid administration Supplementation with potassium is essential. Oral sup-
because volume dilution and increased urinary potas- plementation is more effective and is associated with
sium loss induced by diuresis may lead to further wors- fewer complications than intravenous administration.
ening of the hypokalemia. Concurrent and intravenous administration should be
reserved for severely weak cats.
Young Burmese cats are susceptible to this disease,
and potassium depletion may have played a role in the Caution should be used when administering potas-
previously described myopathy of Burmese cats. sium intravenously in fluids, as further decreases in
Transient episodes of weakness may occur beginning serum potassium concentration may occur as a result of
between 2–12 months of age. dilution and enhanced loss of potassium in urine.
Increased urinary potassium loss occurs secondary to

ORGANOPHOSPHATE TOXICITY**
renal sodium and water loss, when fluids are adminis-
tered in excess of maintenance and induce diuresis.
Classical signs
Clinical signs may then be exacerbated.
● Acute onset of miosis, salivation, urination,
In severely weak cats, use a low volume of fluid
defecation and muscle weakness.
with a high potassium concentration (e.g. 160 mmol
● Rarely, lethargy, anorexia and persistent
(Eq)/L at 2 ml/kg/h. Do not exceed 0.5 mmol (Eq)/kg/h
weakness without associated autonomic
as cardiac arrest may occur.
signs.
If IV fluids are indicated because of dehydration, the
rate of administration should not induce diuresis, as
catastrophic decreases in potassium can occur. Until Clinical signs
potassium is > 3.5 mmol (Eq)/h, maintenance fluid rates
(e.g. 10 ml/cat/h) are recommended with potassium Organophosphate intoxication potentiates the effect
supplementation (80–160 mmol (mEq)/L of fluids) of acetylcholine at the neuromuscular junction and
together with oral potassium supplementation (5–8 mg/ other synapses, by binding with and inactivating
cat PO q 12–24 h). Do not exceed 0.5 mmol (Eq)/kg/h acetylcholinesterase. This leads to increased acetyl-
of potassium in intravenous fluids. choline concentrations at the neuromuscular junction,
increased receptor stimulation and fatigue. Chronic
Do not give fluids if the cat is not dehydrated or is not exposure can result in peripheral neuropathies, as
severely weak. Oral therapy (5 mg/cat bid to tid) is cats are one of the species most prone to delayed neu-
more effective. rotoxicosis.
Endotracheal intubation and ventilatory support is A delayed neurotoxicity in cats is reported associated
required if the cat is in respiratory muscle failure, and with the use of chlorpyrifos spray for household appli-
support may be required for 1–2 days. cation against fleas. There is individual variation in
Do not give steroids as these increase urinary potas- sensitivity to chorpyrifos, and signs of toxicity have
sium excretion. occurred even when used according to label instruc-
tions. Toxicity has also been reported with flea collars
Oral supplementation (potassium gluconate) is used containing chlorpyrifos.
for long-term management. An empirical dose of 2–6
mmol (mEq)/cat/day is usually effective. Regular mon- Cats with organophosphate intoxication may have
itoring of serum potassium is required to determine the acute signs including miosis, salivation, urination,
effective maintenance dose for individual cats. defecation and muscle weakness.
Acute signs of fenthion toxicity are muscle weakness
Prognosis with few autonomic signs.
Prognosis is excellent provided respiratory paralysis A more persistent weakness without associated auto-
does not occur. nomic signs can occur with chronic organophosphate
toxicity. Cats may attempt to walk a few steps, then
Signs resolve in 24 hours to 3 days. collapse in sternal recumbency mimicking cata-
If respiratory paralysis occurs, intensive care and venti- plexy/narcolepsy. Typically, they are also lethargic and
latory support are required for survival. inappetent.
● Postural reactions and spinal reflexes may be depressed
in some cats, but may be normal in other cats.
Prevention
● The pupils may be bilaterally dilated and poorly
As many older cats may have underlying renal disease, responsive to light stimulation.
periodic evaluation of renal function and serum potas- ● Ventroflexion of the neck and muscle tremors may
sium concentration is suggested. be evident.
Diagnosis Diazepam should be avoided in these cats as it may

result in generalized muscle tremor, hypersalivation,
A presumptive diagnosis is based on the presence of miotic pupils and vomiting similar to acute mus-
consistent signs and a history of exposure to an carinic signs of organophosphate toxicosis.
organophosphate.
Concentration of serum cholinesterase activity may DIABETIC NEUROPATHY**
lend support to the diagnosis, but may be non-diagnostic
for chronic organophosphate toxicity. Values less Classical signs
than 500 IU/L (normal 900–1200 IU/L) are considered
consistent with organophosphate toxicity. ● Subtle generalized weakness and reduced
activity, difficulty jumping.
Electromyographic changes are occasionally present ● Some cats have a classic plantigrade
and include fibrillation potentials, positive sharp waves stance in the pelvic limbs.
and bizarre high-frequency discharges. A decremental
response to repetitive nerve stimulation may be present.
Pathogenesis
Beware that edrophonium (used to test for myasthe-
nia gravis) may produce an acute worsening of signs. The cause of the peripheral neuropathy is multifactor-
(Treatment with atropine (0.05 mg/kg IV) may help ial, including diabetes-associated metabolic changes in
the associated parasympathetic signs). the nerve metabolism and/or vascular abnormalities
resulting in nerve ischemia.
Clinical signs
Rule out other diffuse causes of weakness. For the acute
form, other acute poisonings or toxicities such as snake Many diabetic cats prior to initiation of treatment, or if
bite (increased CK, prolonged clotting times) or poorly controlled, have subtle generalized weakness,
hypoglycemia (low plasma glucose usually in an insulin- usually evident as reduced activity, reluctance to move
treated diabetic cat) may appear similar. Differentials and difficulty jumping.
for the chronic form include thiamine deficiency Some affected cats have a classic plantigrade stance
(response to therapy), polymyositis (increased CK, in the pelvic limbs, suggesting sciatic (tibial) nerve
abnormal EMG and muscle biopsy), hypokalemic dysfunction and tarsal extensor muscle weakness.
myopathy (low plasma potassium), hypernatremia (very
rare, hypernatremia), polyneuropathy (abnormal EMG
and decreased nerve conduction velocities), hyperthy- Diagnosis
roidism (other clinical signs and elevated plasma thyrox- Clinical signs of polyuria, polydipsia, and weight
ine), and myasthenia gravis (IV edrophonium/Tensilon loss, together with hyperglycemia (usually blood glu-
test, anti-acetylcholine receptor antibodies). cose is > 17 mmol/L (309 mg/dl) and glucosuria, are
usually diagnostic for diabetes.
Treatment Electromyographic abnormalities include evidence of
Treatment includes protopam chloride (2-PAM) (20 denervation (fibrillation potentials and positive sharp
mg/kg q 12 h IV) which reactivates cholinesterase and waves) and decreases in nerve conduction velocities.
diphehydramine (1–2 mg/kg PO q 8–12 h) which
Nerve biopsies may show axonal degeneration and/or
reduces muscle fasciculations.
demyelination. These changes, however, are not spe-
Atropine (0.2–0.4 mg/kg) can be given with acute toxi- cific for diabetic neuropathy.
city to decrease autonomic signs. Current recommen-
dations are that it only be used if marked bradycardia is
present, because it may precipitate respiratory arrest.
Salivation and defecation are not life threatening and Traumatic rupture of the gastrocnemius tendon may
generally do not require atropine. cause similar signs.
Treatment Diagnosis
Twice daily insulin therapy is usually required to A presumptive diagnosis is based on appropriate clini-
achieve good glycemic control. See page 237 (The Cat cal signs and is supported by finding small puncture
With Polyuria and Polydipsia). wounds.
Treatment of the hyperglycemia may result in improve- Serum CK is often elevated.
ment of sciatic nerve function if substantial peripheral
Electrodiagnostic studies may reveal decreased or
nerve damage has not occurred prior to diagnosis and
absent motor unit potentials with electrical stimula-
therapy.
tion.
ENVENOMATION BY SNAKES FOUND

IN THE USA**
Other toxic neuropathies and myopathies may present
Classical signs with similar clinical signs.
● Clinical signs are usually rapid in onset
(within 24 hours of envenomation).
● Progressive lower motor neuron (flaccid) Treatment
paralysis. General supportive care is important including keep-
● Death is usually the result of respiratory ing the cat in a warm, comfortable environment and
muscle paralysis. managing hydration status.
In the small number of cats reported with Coral snake
Pathogenesis envenomation, recovery rates have been good, usually
within 2–5 days.
Coral snake envenomation is most often seen in the
southeastern US. If respiratory paralysis results, mechanical ventilation
may be required.
Envenomation from Coral snakes results in a blockage
of transmission at the neuromuscular junction. Antivenom is available for Coral snake envenomation,
however, it may not neutralize all toxin present, and is
The exact mechanism of action of the toxin is not com- relatively expensive.
pletely defined.
Aspiration pneumonia may be a complicating factor
that will require standard treatment for aspiration
Clinical signs pneumonia.
Signs usually are seen within 2–4 hours following

envenomation, but may be delayed for several hours.
Prognosis
Cats present with a rapidly progressive lower motor
Cats reported with Coral snake envenomation have had
neuron (flaccid) paralysis.
a reasonably good prognosis for recovery.
Rectal body temperatures may be slightly decreased.
Respiratory paralysis may result in death unless respi-
Cranial nerve dysfunction (decreased palpebral rator support is available.
reflexes) may result.
Aspiration pneumonia may complicate the clinical
Respiratory paralysis can occur and result in death. signs.
Physical examination may reveal small puncture wounds Spontaneous recovery in instances with mild clinical
or the presence of small amounts of blood on the fur. signs is possible.
causes continuous bleeding from sites including

SNAKEBITE ENVENOMATION WITH
trauma sites, gastrointestinal tract, and lungs mani-
AUSTRALIAN SNAKES**
festing as hematemesis, hematuria, hemoptosis, etc.
● Coagulant manifestations often precede neurotoxin
Classical signs
signs.
● Australian snake venoms are ● Antitoxin effectively blocks the clotting mechanism
predominately neurotoxic and usually activation.
strongly coagulant.
Rhabdomyolysis (tiger, mulga, small-eyed) manifests
● Usually no local reaction at the site of
as myoglobinuria.
venom injection.
● Generalized muscle weakness and dilated Hemolysins (taipan, black) cause intravascular haemol-
pupils that are poorly responsive to light ysis and may manifest as jaundice, anemia, hemoglo-
are features. binuria and perhaps kidney tubular necrosis.
● Complete flaccid paralysis is a common
Hyaluronidase in the venom is responsible for the rapid
finding.
entry of the venom into the circulation.
● Vomiting and rapid respiration are present
in 30% of cases. The lack of local reaction at the bite site is probably due
to the low quantity of proteolytic enzymes in Australian
snake venom.
Pathogenesis
Clinical signs
Bites from Brown snakes (Pseudonaja sp.), Tiger
snakes (Notechnis scutatus), Taipan (Oxyuranus There is marked variation in type and severity of signs but
s. scutellatus) and Death Adders (Acanthophis antarcti- flaccid paralysis and dilated pupils that are poorly
cus) can cause ataxia, paralysis and dilated pupils. responsive are consistent findings, that is, neurological
signs predominate.
Neurotoxins act specifically at the neuromuscular
junction to paralyze all skeletal voluntary muscle. Onset is usually sudden.
Postsynaptic neurotoxins (tiger, brown, taipan, death Dilated pupils, ataxia to paresis, trembling, flaccid
adder) cause a non-depolarizing block of neuromuscular paralysis, vomiting, diarrhea, respiratory distress, hypo-
transmission by occupying acetylcholine receptors on thermia, weakness, pallor, jaundice, dark urine and bleed-
the motor endplate. Flaccid paralysis ensues and death ing from multiple sites may all be present.
is possible from respiratory failure.
Less commonly there is a history of initial collapse fol-
Presynaptic neurotoxins (tiger, brown, taipan) block lowed by apparent full recovery followed by a steady
acetylcholine release into the neuromuscular junction progression of clinical signs over the ensuing hours,
after depolarization. This action is delayed, becoming which may take from 5 minutes to 24 hours in the cat.
evident after 30–60 minutes.
The bite site may not be found unless there is bleeding
Increased catecholamine release (stress, exercise, nerve from the site.
stimulation) enhances the rate of intoxication whereas
Multiple bite sites usually result in the introduction of
low temperatures delay this process.
large quantities of venom.
Antitoxin cannot reverse presynaptic binding of
toxin. Diagnosis
The clotting mechanism is activated via initiation of A history of being bitten by a snake and finding the
the conversion of prothrombin to thrombin and fib- snake greatly aids diagnosis, but more often the bite is
rinogen to fibrin (tiger, brown, taipan, black). This unobserved.
Table 44.1 Comparison of main actions of snake venoms

Neurotoxin Coagulant Myotoxin Hemolytic
Tiger +++ +++ +++ +
Death Adder +++ + − +
Brown +++ ++ ++ − +
Black + ++ +++ +++
Copperhead ++ ++ +++ ++
Taipan +++ ++ ++ +++ +
Mulga ++ +++ +++ +
Small Eyed +++
Table 44.2 Comparative frequency of commonly observed signs of snakebites

Animal
Snake specified- specified
all animals (cats)
Tiger Brown Black Copperhead

Sudden collapse + ++ + +
soon after bite,
temporary recovery
then relapse
Neurological signs, ++++ ++++ ++ ++ ++++ ++++
weakness, ataxia,
flaccid paralysis
Excitement, trembling, +++ +++ +++ +++ ++
salivation, vomiting,
defecation, muscle spasm
Pupils dilated, pupillary ++++ +++ +++ +++ ++++
light reflex slow or absent
Local swelling + + +++ ++ ++
Hemoglobuinuria, ++ + + +
Myoglobinuria, or jaundice
Non clotting blood, extended ++ ++ ++ ++
coagulation time,
hematemesis, hematuria
+ 1–10% of animals show these signs; + + 11–30% of animals show these signs; + + + 31–75% of animals
show these signs; + + + + 75–100% of animals show these signs.
Typically the cat is presented with signs of a sudden

urine (most reliable if clinical signs are present), or
onset of paralysis, mydriasis and has evidence of
blood is useful, but adds to the cost of treating the
extended clotting times.
cat. Knowledge of the test limitations is essential.
Identification of the snake venom using a snake venom Knowledge of the types of snakes found in the area aids
detection kit to test samples from swabs of bite site, selection of antivenom.
Table 44.3 Clinical pathology

ACT Fibrinogen CPK Hb’uria Mb’uria
Brown Increased Decreased - - -
Mulga - - Increased Increased Increased
Black - - Increased Increased Increased
Taipan Increased Decreased Increased - Increased
Tiger Increased Decreased Increased - Increased
Small-eyed - - - Increased
Death Adder - - - - -
ACT - activated clotting time
CPK - creative phospholanese
Hb’uria - hemoglobinuria
Mb’uria - myoglobinuria
Increased creatine phosphokinase (tiger snake even- Organophosphorus poisoning especially in the early
omation) may be found on biochemistry analyis. stages may look similar (vomiting, salivating) Muscle
weakness may be a more predominant clinical presen-
Evidence of neurological signs plus coagulant or myo-
tation. Cats also may appear flaccid.
lysis or hemolysis signs suggests snake envenomation.
Treatment
Prompt administration of adequate amounts of the
Tick paralysis may result in similar clinical signs of
appropriate antivenom is the mainstay of treatment.
flaccid paralysis. Cranial nerve involvement is unusual
in tick paralysis, and when present is often unilateral Identification of the snake is often helpful when plan-
and associated with a tick on the head. Diagnosis is ning treatment, because both monovalent and polyva-
facilitated by finding a tick on the cat at the time of lent antivenoms are available. Polyvalent antivenom
presentation. may be necessary if the snake can not be identified.
Ciguatera and tetrodotoxin result in hindleg paresis Dosages are often standardized and dispensed as one
and vomiting in a cat with access to reef fish or toad- dose. Anaphylactic reactions are possible, so caution
fish, puffer fish, newts or blue ringed octopus. should be used when administering these products.
Red-back spider bite may result in initial vomiting fol- Choice of antivenom and dosage when the snake has not
lowed by agitation, muscle weakness and incoordina- been identified varies on locations around Australia.
tion. Muscular tremors and tachycardia may be present. ● Polyvalent antivenom.
● QLD north of Rockhampton – Brown 1000 U and
Thromboembolism is usually present in only one body
Death Adder 6000 U.
area (either both pelvic limbs or a thoracic limb). Cats
● QLD south of Rockhampton – Tiger 3000 U and
usually show clinical signs of pain. Affected muscles are
Brown 1000 U and Death Adder 6000 U.
usually firm and painful, with lack of evidence of perfu-
● Tasmania – Tiger 6000 U, Victoria – Tiger 3000 U
sion (cold to touch, discolored, absent peripheral pulses).
and Brown 1000 U.
Acute-onset sepsis results in profound weakness, ● NSW, SA, WA, NT – Tiger 3000 U and Brown
hypothermia, tachypnea, bradycardia and hypotension 1000 U and Death Adder 6000 U.
evidenced as poor pulses, pale mucous membranes,
Antivenom is given diluted in 100 ml saline slowly over
increased capillary refill time.
15–30 minutes after premedication with chlorpheni-
Botulism and polyradiculoneuritis:may result in a ramine (1 mg/kg IM), dexamethasone (2 mg/kg IV),
similar progressive flaccid paralysis. Both are relatively and epinephrine (0.05 mg/kg SC). Wait 20 minutes
uncommon in cats. after premedication before giving antivenom.
Table 44.4 Choice of antivenom dosage when snake has been identified
Recommended antivenom for
veterinary use Initial dose (Units)
Tiger snake Tiger snake antivenom 3000
Death Adder Death Adder snake antivenom 6000
Taipan Taipan snake antivenom 12 000
Brown Brown snake antivenom 1000
Black Tiger snake antivenom 3000
Mulga Tiger snake antivenom 9000
Maintenance of airway and breathing may involve Pathogenesis

intubation and mechanical ventilation if there is respiratory
paralysis. Oxygen therapy is indicated if there are mod- Worldwide, 43 species of ticks have been reported to
erate respiratory efforts. cause paralysis in domestic animals.
Packed cell volume, total protein, urea and activated In North America, Dermacentor andersoni, Dermacentor
clotting time are minimal diagnostic requirements. variabilis, and Argas (Persicargas) radiatus are the
species of ticks most commonly associated with
Fluid therapy is needed for resuscitation, rehydration, paralysis.
and maintenance (see treatment of dehydration, page
557, in The Cat With Polycythemia). Blood and plasma In Australia, the paralysis tick is Ixodes holo-
products may be necessary to control coagulation. cyclus, which is found along the eastern coast of
Australia.
Monitor respiration (spO2), ventilation, (ET, CO2,
blood gases), and circulation (heart rate, blood pres- Ixodes holocyclus is a three-host tick: larvae, nymphs
sure, pulses, capillary refill time, electrocardiogram) and adult females engorge on a host over several days
before detaching to develop to the next stage in the
Monitor blood parameters (packed cell volume, total environment.
protein, BUN, potassium, CK, creatinine).
Native hosts of Ixodes holocyclus, bandicoots and pos-
Monitor urine output to ensure that 1–2 ml/kg/h is sums, rarely develop disease.
being produced.
Ixodes holocyclus produces disease in accidental hosts,
Nutritional support should be provided as recovery including cats and dogs.
can be slow.
Most cases of tick toxicity occur during spring and
Nursing includes soft bedding, warmth, bladder and bowel early summer.
control, analgesia, physiotherapy, catheter care, eye care.
Usually a single adult female tick will cause disease;
Anticipate respiratory failure requiring mechanical rarely, large numbers of larvae or nymphs will cause
ventilation, DIC, renal failure, aspiration, corneal disease.
ulceration, sudden death as complications.
The tick must feed on the host for at least 5 days before
TICK TOXICITY** disease develops.
The toxin produced by the tick acts to:
Classical signs ● Inhibit the release of acetylcholine from the
● Acute-onset flaccid paralysis, beginning in neuromuscular junction to produce flaccid

the hindlimbs and ascending. paralysis.
● Block potassium efflux from cardiac myocytes to
● Acute-onset dyspnea.
produce heart failure.
Clinical signs ● One (or more) adult female Ixodes holocyclus tick(s)
or other paralysis ticks are found on the animal.
Acute onset of paresis/ataxia of the hindlimbs is the ● A “crater”, the feeding lesion which remains after
most consistent clinical sign. This rapidly progresses over the tick has detached, is found on the animal.
several hours to flaccid paralysis and ascends to involve – Multiple larval or nymphal Ixodes holocyclus
the forelimbs and results in lateral recumbency. ticks are found on the animal.
Dyspnea accompanies paralysis, and severe dyspnea – A tick or “crater” is not found but the animal
with forced expiration and cyanosis occurs responds to specific treatment for tick toxicity.
terminally.
A change in voice and inappetence may occur early in Differential diagnosis
the course of disease. Various snake envenomations may present similarly
Pupils are dilated and become non-responsive to light. but are not usually associated with dyspnea.
The nictitating membrane may protrude across the Visualization of the Ixodes holocyclus tick or other
globe. paralysis ticks are diagnostic. The brown dog tick,
The gag reflex is impaired and drooling of saliva Rhipicephalus sanguineus, is found in some of the
occurs. same areas as Ixodes holocyclus, but it very rarely par-
asitizes cats and is not associated with paralysis.
Regurgitation/vomiting can occur rarely at any stage.
Death can occur within 24–48 hours of onset of Treatment
signs.
Treatment involves removing the tick(s), administration
Scoring systems to describe the progressive stages of of specific antitoxin serum and supportive care.
paralysis and respiratory compromise are as follows:
● Gait score system. With Ixodes holocyclus (Australia), often clinical signs
– Score 1: Can walk: able to stand from recum- will progress during the first 24 hours of treatment due
bency and ambulate. to the delayed onset of the toxin’s action. In USA, signs
– Score 2: Cannot walk: requires aid to stand but usually resolve rapidly after tick has been removed, and
can maintain stance. supportive therapy is rarely necessary.
– Score 3: Cannot stand: unable to maintain a The tick can be removed manually using curved forceps
standing position. or a pair of partially opened scissors to lever out the tick
– Score 4: Cannot right: unable to maintain sternal while avoiding any pressure on the tick’s body. Search
recumbency. thoroughly for additional ticks. Apply tickicides
● Respiratory score system.
(fipronil, pyrethrins) to kill any additional unseen ticks.
– Score A: Normal character and rate (less than 30
breaths per minute). Tick Antitoxin Serum (TAS) for treatment of Ixodes
– Score B: Normal character and increased rate Holocyclus toxicity is manufactured from canine serum
(greater than 30 breaths per minute). so there is a risk of anaphylaxis when administered to
– Score C: Altered character with expiratory cats. TAS can also produce a vagally mediated sys-
sigh/grunt (undefined rate). temic reaction seen clinically as bradycardia, hypoten-
– Score D: Cyanosis and severe dyspnea. sion and circulatory shock (B-J reaction). To minimize
these risks give:
● Acepromazine (0.03 mg/kg SC or IM) to relieve
Diagnosis anxiety and respiratory distress. Wait 20–30 min-
Diagnosis is made when clinical signs typical of tick utes before giving TAS.
toxicity are observed in an animal in an area where ● Atropine (0.04–0.1 mg/kg SC) to block the B-J
Ixodes holocyclus or other paralysis ticks are endemic reaction, reduce salivation, and produce bronchodi-
and either: lation. Wait 20–30 minutes before giving TAS.
● Prednisolone sodium succinate (5–10 mg/ kg IV) Cardiac effects may persist after limb paralysis has
to reduce the likelihood and severity of anaphy- resolved. Cats should not be stressed for 2–3 weeks after
laxis. Wait 10–30 minutes before giving TAS. recovery from paralysis. In dogs, stress may cause sud-
● Epinephrine 1:10 000 (3 ml SC) about 5 minutes den death up to 3 weeks after discharge from hospital.
prior to administration of TAS to reduce the likeli-
hood of anaphylaxis.
Prevention
● TAS (0.5–1 ml/kg) diluted 50:50 with 0.9% NaCl
and warmed to room temperature; either give Check daily for ticks.
slowly IV (over 20–30 minutes) or give IP.
Use a preventative product (fipronil, pyrethrins).
Supportive care.
● Oxygen therapy (oxygen cage, flow-by, nasal
MYASTHENIA GRAVIS*
catheter, or positive pressure ventilation) is indi-
cated for moderate to severe dyspnea.
Classical signs
● Furosemide (2–5 mg/kg IV) should be given to
reduce pulmonary edema in dyspneic animals and ● Adult cats or Siamese < 1 year of age.
repeated as necessary. ● Episodic muscle weakness induced by
● Metoclopramide (0.5 mg/ kg IM or IV) is indi- movement.
cated in vomiting animals to reduce the risk of ● Ventral neck flexion.
aspiration. ● Decreased palpebral reflex.
● Eye ointment should be applied to prevent corneal
desiccation.
● Nil per os is essential until the gag reflex returns. Pathogenesis
Then introduce oral fluids slowly.
There are two forms of this disease; a congenital
● Parenteral fluids are not routinely indicated and
form that is not associated with antibody production,
must be used with care due to the potential wors-
and an acquired form that is associated with anti-
ening of pulmonary edema. Colloid or heta/penta
bodies being produced against the acetylcholine
starch fluids may be used to maintain circulating
receptor.
fluid volume if the hematocrit is significantly
elevated. Crystalloids may be given after 24 hours The congenital form occurs Siamese cats. Abyssinian
at submaintanence rates if slow return of the gag cats and possibly Somali’s may be predisposed to the
reflex delays introduction of oral fluids. acquired form.
● If possible animals should be positioned sternally
The acquired form can occur idiopathically, or second-
to minimize pulmonary ventilation–perfusion mis-
ary to a variety of tumors (thymoma). With thymoma,
matching. Laterally recumbent animal should be
the tumor either produces excess antibody or antibody
positioned with the shoulders elevated to aid pha-
is produced against a similar antigen within the tumor
ryngeal drainage and turned every 2 hours to reduce
and in muscle.
ventilation–perfusion mismatching.
● Urine retention often occurs and manual expres-
sion of the bladder may be needed during recovery.
Clinical signs
● Stress must be minimized.
● Provision of a cool (not cold) environment may This is a rare disease in cats. Generally a disease of
alleviate signs. adult cats, except for the congenital form in Siamese
which presents at < 6 months of age.
Prognosis
Exercise intolerance and episodic weakness induced
Prognosis for gait scores 1–3 and respiratory scores by walking or playing are typical signs. The cat may
A–C is good. Gait score 4 and respiratory score D con- walk a few steps and flop down. Recovery occurs with
fers a guarded prognosis. rest.
Muscle tremors are usually episodic and occur in mus- organophosphate toxicity (decreased serum cholin-
cles that are being used. esterase activity).
A stiff, stilted gait is often noted prior to collapse.
Treatment
Weakness of facial muscle may also be seen, and this is
most evident as a decrease in the palpebral reflex and A long-acting anticholinesterase product (pyridostig-
narrowing of the palpebral fissure. This appears to be a mine Mestinon, 0.5–3 mg/kg PO q 8–12 hours) can be
more consistent finding in cats versus dogs. given to enhance the effect of ACH at the neuromuscu-
lar junction. Start at the lower dose and increase as
Megaesophagus is uncommon and may lead to aspira- required.
tion pneumonia.
Cats may be more sensitive to the effect of this drug,
One cat has been reported with a jaw-drop and dyspha- and therefore, slightly lower dosages than those used in
gia as the only clinical signs. dogs should be used initially.
Diagnosis Additionally, immunosuppressive therapy with corticos-

teroid (1–2 mg/kg PO q 12 hours) or plasmapheresis may
Diagnosis is based upon clinical signs of exercise- be needed to control clinical signs in acquired forms.
induced weakness that is resolved with edrophonium.
An edrophonium response test may suggest the Prognosis
disease if strongly positive. Edrophonium is an anti-
Prognosis for some animals is good, with occasional
cholinesterase that potentiates acetylcholine (ACH) at
spontaneous cures or remission. Recurrences may occur.
the neuromuscular junction. When given IV (0.1 mg/kg),
this drug can reverse the clinical weakness seen with Treatment responses may not be as dramatic in cats
myasthenia gravis for a short period of time. compared to dogs.
Electromyography and nerve conduction studies will Complicating factors include severe weakness with res-
be normal. A decremental response may be seen during piratory compromise and aspiration pneumonia sec-
repeated stimulation of a peripheral nerve in some, but ondary to megaesophagus.
not all cats.
Single fiber EMG is a relatively new technique that Prevention
may aid diagnosis of this disease in the future. Avoiding breeding from sires and dams known to pro-
Documentation of antibodies to the acetylcholine duce congenitally affected offspring. Advise pedigree
receptor in serum appears to be the most definitive analysis to remove carriers.
diagnostic test. In congenital disease, however, these
antibodies will not be present.
HYPOGLYCEMIA*
Differential diagnosis Classical signs

Rule out other inflammatory, toxic and degenerative ● Trembling, weakness are most common.
causes of muscle weakness and tremor. ● Dilated pupils.
● Reduced alertness or lethargy.
Other causes of ventral neck flexion and generalized
● If hypoglycemia is severe, seizures and
weakness include thiamine deficiency (response to
progression to coma may result.
therapy), polymyositis (increased CK, abnormal EMG
and muscle biopsy), hypokalemic myopathy (low
plasma potassium), hypernatremia (very rare, hype-
Pathogenesis
rnatremia), polyneuropathy (abnormal EMG and de-
creased nerve conduction velocities), hyperthyroidism Hypoglycemia can also occur secondary to some
(other clinical signs and elevated plasma thyroxine) and endocrine disorders such as hypoadrenocorticism, lack
of glucose production by the liver in liver failure from Surgical removal of an insulinoma will normalize
lack of iron, and with some tumors (liver, spleen, GI) serum glucose concentrations if there are no metas-
which may produce hypoglycemia through excess IGF-2 tases, and results in a better long-term outcome than
production. medical management. Post-operative pancreatitis may
be a complication.
Hypoglycemia is most often associated with insulin
overdose in diabetic cats, but is also rarely caused by Medical management of insulinoma or other tumor
an insulinoma in older cats. producing hypoglycemia is only palliative and con-
sists of frequent small meals low in carbohydrate,
Because the central nervous system (CNS) requires a
diazoxide (12.5 mg bid PO) and corticosteroids
constant supply of glucose, clinical signs of hypo-
(0.5–6 mg/kg/day in divided doses, beginning at
glycemia relate to CNS dysfunction and activation
lower dose) to increase blood glucose. The somato-
of the sympathetic nervous system.
statin analog octreotide (10–40 μg/cat SC bid–tid),
has also been used in cats. Small doses of glucagon
Clinical signs subcutaneously may be effective.
Signs include trembling, weakness, dilated pupils, In some instances of insulinoma, intravenous dextrose
reduced alertness, and if severe, seizures progressing to administration may actually bring about worsening
coma. signs, most likely because these tumors retain some
responsiveness to serum glucose concentrations and
Insulinoma occurs in aged cats. respond by increasing insulin secretion.
Diagnosis Prognosis
Diagnosis of hypoglycemia is based upon finding hypo- With insulinoma and other tumors producing hypo-
glycemia (blood glucose < 60 mg/dl: < 3.3 mmol/L) in glycemia, clinical signs may be controlled, however the
the face of clinical signs. long-term prognosis is poor unless the tumor can be
removed by surgery.
Concurrent serum insulin concentration will help in
determining the presence of an insulin-secreting tumor. Correction of any underlying disorders will determine
Non-pancreatic tumors producing hypoglycemia are the ultimate prognosis.
associated with low insulin concentrations.
Abdominal ultrasound may be helpful when assessing
the pancreas, liver and lymph nodes for presence of REDUCED TISSUE OXYGENATION*
tumor.
Classical signs
Differential diagnosis ● Palor, cyanosis, decreased capillary refill

times, tachycardia and/or, hypothermia.
Signs of hypoglycemia can mimic other seizure and ● Tachycardia, gallop rhythms, murmurs,
generalized weakness disorders. coughing and vomiting with cardiac
disorders.
● Tachypnea, panting and open-mouthed
Treatment
breathing with respiratory disorders.
Diabetic cats with clinical hypoglycemia are best treated ● Facial edema with acetaminophen toxicity.
with intravenous dexdrose (20–50%) 1⁄2–2 ml to effect.
Subsequent insulin doses need to be reduced by 50%. See main reference page 118 for details (The Cyanotic
Some cats are in remission and do not need insulin. Cat).
Pathogenesis Prognosis
Any cause of substantially reduced tissue oxygenation Depends upon the underlying cause.
will cause weakness. Examples include severe anemia,
methemoglobinemia associated with acetaminophen
TOXOPLASMOSIS*
(paracetamol) toxicity, cardiac disease, hydrothorax in-
cluding pyothorax and chylothorax, and severe broncho-
Classical signs
pulmonary disease or obstructive upper respiratory
disease. ● Most cats are asymptomatic.
● Signs are most severe in cats under 1 year
Clinical signs of age and especially young kittens.
● Lethargy, anorexia, dyspnea.
Signs may be generalized or localized and are most
● Uveitis, retinal hemorrhage.
easily seen in the mucous membranes, nail beds or
● ± Weakness.
conjunctiva.
Palor, cynaosis, decreased capillary refill times,
tachycardia and hypothermia are common associated Clinical signs
signs.
Most cats are asymptomatic.
Tachycardia, gallop rhythms, murmurs, coughing
Signs are most severe in cats under 1 year of age, espe-
and vomiting may accompany cardiac disorders.
cially young kittens, although any age of cat can be
Tachypnea, panting, and open-mouthed breathing affected.
may accompany respiratory disorders.
Lethargy, anorexia and dyspnea due to pneumonia are
Facial edema may be present with acetaminophen the most frequent signs of generalized infection.
toxicity.
Fever may be present.
Diagnosis Gastrointestinal or hepatic signs such as icterus, vomit-
ing and diarrhea and abdominal effusion may occur
PCVs and complete blood cell counts are used to deter-
as a result of diffuse organ involvement or from a
mine the presence of anemia.
granuloma.
Arterial blood gas analysis is used to determine relative
Toxoplasma gondii can affect any area of the nervous
tissue oxygenation.
system resulting in encephalitis, myelitis, peripheral
A pulse oximeter reading may aid in determining the neuropathy or myositis.
degree of oxygenation.
The organism damages the nerve and muscle either
Chest radiographs can be used to identify pulmonary primarily, or secondarily through associated inflam-
and cardiac diseases. mation.
In addition, an ECG and echocardiogram is useful Weakness may be present if the spinal cord, periph-
when evaluating for heart disease. eral nerves or muscles are involved.
Hyperesthesia on muscle palpation, stiff gait or shifting
Differential diagnosis leg lameness suggests myositis.
Other causes of weakness should not have cyanosis and Experimental innoculation with meospora coninum also
pallor. causes clinical signs in cats.
Treatment Diagnosis
Treat the underlying cause of the reduced oxygenation Diagnosis is based upon the presence of IgM anti-
and provide oxygen if signs are marked. bodies to Toxoplasmosa gondii, which appear within
1–2 weeks and persist for 3 months, but sometimes for If untreated, signs progress to semi-coma, persistent
years, or rising IgG titers which appear by the fourth vocalization, opisthotonos and death.
week of infection, increase over 2–3 weeks and persist
Episodes of spastic opisthtonos or ventroflexion of
for months or years. Visualization of the protozoan in
the neck and muscle spasm may occur especially when
biopsy specimens is also diagnostic.
the cat is lifted or stressed. They may be interpreted as
seizures, but true seizure activity rarely occurs.
Rule out other myopathies (hypokalemic, polymyopa- Diagnosis
thy) and inflammatory causes of muscle disease as well
Diagnosis is based on clinical signs and rapid
as other neuropathies.
response to thiamine.
Cats that have progressed to a comatose state have a
Treatment
poor prognosis.
Treatment for toxoplasmosis currently is clindamycin
(8–25 mg/kg, q 8–12 hours; do not exceed 50 mg/kg q
24 hours) for 14–28 days, however the addition of
trimethoprim sulfa drugs PO, IM or SC may provide Other encephalopathies and encephalitis are differenti-
a better clinical response. ated on history, CSF findings and lack of response to
thiamine.
Newer drugs, such as azithromycin and clarithro-
mycin (macrolides), are being tested in other species, Head trauma may appear similar to late signs of thi-
but are unproven in cats. amine deficiency, but can usually be differentiated on
history and evidence of trauma. Thiamine-deficient
Watch the literature for new recommendations.
cats are lethargic and inappetant days and weeks
before signs are severe.
THIAMINE DEFICIENCY*
Hydrocephalus can present with central blindness and
ataxia, but there is no response to thiamine.
Classical signs
Dysautonomia is a consideration in countries where it
● Initially, lethargy, inappetence and ataxia.
● Later, weakness, ventral flexion of the
troflexion of the neck may appear similar to thiamine
neck, dilated pupils, stupor and coma.
deficiency, but there is no response to thiamine.
See main reference on page 848 for details (The Cat Hypokalemic myopathy, myasthenia gravis, poly-
With a Head Tilt, Vestibular Ataxia or Nystagmus). myositis and organophosphate toxicity can all cause
ventral flexion of the neck. However, ventral neck flex-
ion in thiamine deficiency is the result of active muscle
Clinical signs
contraction associated with increased muscle tone
Early non-specific signs are typically lethargy and rather than passive ventroflexion from weakness.
inappetence. Thiamine deficiency responds to thiamine supplemen-
tation unless in terminal stages.
ataxia, which appears as an abnormal broad-based
stance, loss of balance and vertigo. Treatment
There is weakness and an inability or reluctance to Treatment is administration of thiamine dosed typically
walk. The cat sits crouched with ventral flexion of the at 5–30 mg/cat/day per os. Maximum dose up to
neck. 50 mg/cat/day.
Pupils are dilated and non-responsive or poorly Severely affected cats should receive at least 1 mg
responsive to light reflexes. parenterally.
Change the diet to one with adequate thiamine and sup- other myopathies and inflammatory causes of muscle
plement with thiamine for at least a week. disease.
Myasthenia gravis (positive tensilon test, anti-acetyl-
HYPERTHYROIDISM* choline receptor antibodies), chronic organophosphate
toxicity (history of exposure), and polymyositis (mus-
Classical signs cle biopsy) should be considered.
● Weakness and ventral neck flexion.
● Cats may progress to collapse with
Treatment
minimal exercise.
The weakness may improve with treatment for hyper-
See main reference page 304 for details (The Cat With thyroidism.
Weight Loss and a Good Appetite).
Correct hypokalemia.
Clinical signs
POLYMYOSITIS*
The metabolic effects of the hyperthyroid state may in
some way affect muscle and/or nerve function. Many of
Classical signs
these cats are also hypokalemic. Clinical signs of
hypokalemia may be precipiated by thyroidectomy ● Weakness and neck ventroflexion.
and be apparent on recovery from anesthesia.
Weakness and ventral neck flexion occurs in a few cats
Clinical signs
with hyperthyroidism.
Polymyositis may be idiopathic, immune-mediated
Cats may progress to collapse with minimal exercise.
or result from infections with Toxoplasma gondii or
Other typical signs of hyperthyroidism may also be feline immunodeficiency virus.
present such as weight loss, polyphagia, irritability or
Signs typically are of generalized muscle weakness
restlessness.
and neck ventroflexion.
Some cats are lethargic.
Megaesophagus may occur with smooth muscle
Intermittent vomiting or diarrhea occurs in many cats. involvement.
With practice, a palpable thyroid nodule is detected in Thymoma may be present in some cats, and myositis
most cats. may occur concurrently with myasthenia gravis.
Regurgitation and/or dyspnea may be present with
Diagnosis
megaesophagus and thymoma.
In some cats, electromyography shows evidence of
denervation.
Diagnosis
Diagnosis is made by demonstrating elevated serum
Serum CK may be elevated.
total thyroxine (T4) concentrations. When total T4 con-
centration is at the high end of normal, but signs are con- Abnormal spontaneous muscle electrical activity
sistent with hyperthyroidism, measurement of free T4 or consistent with myocyte inflammation and abnormal
a T3 suppression test may help to confirm the diagnosis. membrane electrical activity (e.g. fibrillation poten-
tials, positive sharp waves, complex repetitive dis-
Differential diagnosis charges) may be present on electromyography.
Differential diagnoses include other causes of Multifocal areas containing mononuclear cell infiltrates
hypokalemic myopathy such as chronic renal failure, are present in the muscle biopsy.
Differential diagnosis ● Bradycardia (90–120 beats/minute).

● Dysuria and/or distended bladder or incontinence
Hypokalemic myopathy is differentiated on the basis of with an easily expressive bladder.
hypokalemia. ● Generalized weakness.
Myasthenia gravis may occur concurrently with myositis.
Chronic organophosphate toxicity is differentiated Diagnosis
on the basis of a history of exposure and sometimes
reduced cholinesterase activity. Diagnosis is based primarily on clinical signs and evi-
dence of autonomic dysfunction. The indirect-acting
Treatment parasympathomimetic, physostigmine (0.02 mg/kg IV)
produces no ocular response, but direct-acting pilocar-
Corticosteroid treatment (1–2 mg/kg PO q 12 hours) pine (topically) results in immediate miosis, demon-
may improve clinical signs. strating post-glanglionic denervation hypersensitivity.
Normal cats do not demonstrate these responses.
DYSAUTONOMIA*

● Younger cats (< 3 years). Differential diagnoses are many, depending on the pre-
● Acute onset of depression and anorexia. dominant signs. Cats may present with a history of con-
● Dilated pupils, xerostomia, stipation or inability to urinate or dilated pupils,
keratoconjunctivitis sicca, prolapsed third suggesting disease of the colon, lower urinary tract or
eyelids. eyes. Typical cases which exhibit most signs are classi-
● Bradycardia. cal for dysautonomia.
● Megacolon, constipation, loss of anal
reflex.
Treatment
● Incontinence, dysuria or distended bladder.
● Weakness. No specific treatment is available, but supportive care is
important, such as syringe or tube feeding.
See main reference page 792 for details (The
Parasympathomimetic agents may improve some clini-
Constipated or Straining Cat).
cal signs.
● Pilocarpine ophthalmic drops (1%/1 drop q 6 h)
Clinical signs may result in pupillary contraction and increase
Disease is confined to Europe or occurs in imported salivation.
cats. The prevalence has decreased markedly and it is ● Bethanechol (1.25–5 mg PO q 8–12 h) may bene-
now uncommon. fit constipation and urinary retention.

● Metoclopromide (0.2–0.5 mg/kg PO SC q 8 h) may
Younger cats (< 3 years) are more often affected. improve gastric motility.
Clinical signs are often acute in onset over 48 hours Up to 70% mortality rate has been reported.
with all cats showing depression and anorexia.
Other signs reflect autonomic system dysfunction and
include: POLYMYOPATHIES
● Ocular signs such as fixed, dilated pupils without
blindness, prolapsed third eyelids and dry eyes Classical signs
(keratoconjunctivitis sicca develops). ● Ventral flexion of the neck.
● Gastrointestinal signs include regurgitation, ● Muscle weakness.
megaesophagus, constipation and megacolon, loss ● +/- Apparent muscle pain and a stiff gait.
of the anal reflexes, dry mouth (xerostomia).
Pathogenesis HYPOCALCEMIA
Unknown.
Classical signs
Clinical signs ● Weakness, tetany and tremors.
● Muscle fasciculation, cramping, rigidity and
Age of onset varies from 3 months to 13 years. twitching.
Most cats were domestic short- or long-haired cats.
Ventral flexion of the neck and weakness was com- Pathogenesis
mon. Decreases in calcium decrease the threshold for neu-
Apparent muscle pain and a stiff gait may also be seen. ronal and muscle depolarization.
Hypocalcemia most often results from iatrogenic
Diagnosis injury to the parathyroid gland during surgical
removal of thyroid tumors.
Serum CK was usually elevated.
Primary hypoparathyroidism is possible but rare.
Many of these cats had low serum potassium levels and
may have had hypokalemic myopathy. Some cats had Hypocalcemia associated with queening (eclampsia)
clinical signs resolve spontaneously, others seemed to is rarely reported but occurs.
benefit from corticosteroid therapy.
Clinical signs
Differential diagnosis Clinical signs include weakness, tetany and tremors.
Rule out other inflammatory, toxic and degenerative Spontaneous muscle depolarization can manifest as
causes of weakness. muscle fasciculation, cramping, rigidity and twitching.
Other causes of ventral neck flexion and generalized Queens with preparturient hypocalcemia present with
weakness include thiamine deficiency (response to ther- anorexia, lethargy, trembing, muscle twitching and
apy), polymyositis (increased CK, abnormal EMG and weakness. They resemble the clinical picture of
muscle biopsy), hypokalemic myopathy (low plasma hypocalcemia in cows, rather than the violent muscle
potassium), hypernatremia (very rare, hypernatremia), tremor of eclampsia in dogs.
polyneuropathy (abnormal EMG and decreased nerve
conduction velocities), hyperthyroidism (other clinical Diagnosis
signs and elevated plasma thyroxine), myasthenia gravis
(IV edrophonium/Tensilon test, anti-acetylcholine Diagnosis is confirmed by finding decreased (usually
receptor antibodies) and organophosphate toxicity less than < 1.5 mmol/L (6 mg/dl) serum calcium on
(decreased serum cholinesterase activity). serum biochemical analysis.
Treatment Differential diagnosis
Some cats had clinical signs resolve spontaneously, Rule out other inflammatory causes of muscle disease
others seemed to benefit from corticosteroid therapy and acute organophosphate toxicity (history of expo-
(1–2 mg/kg PO q 12 hours). sure, signs and low cholinesterase activity).
Treatment
Prognosis
Treatment involves calcium supplementation and vita-
Variable. min D therapy.
If clinical signs are present, rapid institution of treat- Pathogenesis

ment is indicated with 0.5–1.5 ml/kg IV of 10%
calcium gluconate. Infuse calcium slowly over The cause of many degenerative neuropathies is not
10 minutes while monitoring heart rate. Stop infu- known.
sion if bradycardia occurs.
Short-term maintenance involves either SC calcium Clinical signs
(1–2 ml of 10% calcium gluconate diluted 1:1 in 0.9%
saline q 8 hours) or IV calcium (10–20 ml of 10% cal- These diseases are often breed-specific with clinical
cium gluconate in 500 ml of 0.9% saline) with rate signs beginning in cats less than 1 year of age.
adjusted to maintain normocalcemia. Monitor calcium Weakness with decreased to absent spinal reflexes
2–3 times daily initially. are typical signs.
Longer-term maintenance includes oral calcium A degenerative polyneuropathy occurs in young
(25 mg/kg q 8–12 hours) and vitamin D. The active Birman cats.
form of endogenous vitamin D3 (called calcitriol or
1,25 dihydroxycholecalciferol) is used at 2.5–10 ng/kg Clinical signs begin at 8–10 weeks of age.
● The gait is characterized by a “dropped-hock”
q 24 hours or synthetic vitamin D3 (dihydrotachysterol)
at 0.02–0.03 mg/kg q 24 hours for 3 days, then appearance and hypermetria and ataxia.
0.01–0.02 mg/kg q 6–24 hours. Cats with Neimann–Pick type-A storage disease
Calcium should be monitored carefully, as hyper- may have alterations in peripheral nerves. These
calemia is nephrotoxic. diseases may have weakness as part of the clinical
● Adjustments to doses should be made every 1–3
syndrome.
days based on calcium concentrations. Other degenerative neuropathies may occur in a variety
If hypocalcemia is the result of thyroidectomy, calcium of breeds and at various ages.
and vitamin D therapy can be reduced gradually over
2–3 weeks, and stopped if calcium remains in the nor-
mal range. Diagnosis
A tentative diagnosis is based on finding signs of
Prognosis weakness in a young Birman cat. Electrodiagnostic
evaluations may reveal abnormalities such as fibrilla-
Acute hypocalcemia following bilateral thyroidectomy tion potentials, positive sharp waves, and decreased
can be fatal if not recognized early and appropriate nerve conduction velocities depending upon the patho-
therapy instituted. logic process present.
● In general, neuropathies with demyelination tend
Prevention to be associated more commonly with decreased

nerve conduction velocities, whereas neu-
When performing bilateral thyroidectomy, allow 3–4 ropathies with predominant axonal abnormalities
weeks between removal of each lobe. tend to be associated with fibrillation potentials
and positive sharp waves (denervation potentials).
DEGENERATIVE NEUROPATHIES Mild to moderate fibrillation potentials, consis-
tent with denervation, or decreasing nerve con-
Classical signs duction velocity may be found in some cases with
electromyography and nerve conduction velocity
● Weakness with decreased to absent spinal testing, respectively.
reflexes.
● “Dropped-hock” gait in young Birman cats. Histologic lesions involving the axon or the myelin
sheath may be present on peripheral nerve biopsy.
Differential diagnosis Histologic lesions were most severe in the ventral

spinal gray matter, consisting of neuronal cell loss and
Clinical signs may be similar to other diseases that gliosis. No effective treatment is known.
affect the lower motor neuron including motorneuro-
pathies, myopathies and some diseases of the neuro-
muscular junction. Differential diagnosis
Hypokalemic myopathy (low plasma potassium),
Treatment chronic organophosphate toxicity (history of exposure),
No effective treatment is known. myasthenia gravis (tensilon test, anti-acetylcholine
receptor antibodies, decreased serum cholinesterase
Clinical signs usually progress until euthanasia or death activity).
occurs months to years after initial onset of signs.
In rare instances, clinical signs may stabilize or even Treatment
improve.
No effective treatment is known.
Prognosis Clinical signs progress until euthanasia or death occurs
Many of these diseases are progressive, and treatments months to years after initial onset of signs.
either have not been attempted or have not been benefi-
cial. DEGENERATIVE MYOPATHIES (X-LINKED
MUSCULAR DYSTROPHY, HEREDITARY
DEGENERATIVE MOTORNEUROPATHIES MYOPATHY, NEMALINE ROD MYOPATHY)
● Progressive weakness and muscle atrophy ● Signs begin 2–24 months of age.
in adult cats. ● Weakness and reduced activity.
● Decreased to absent spinal reflexes. ● Stiff, choppy gait.
● Tremor, especially of the head and tongue. ● Increased muscle mass and hypertrophy of
● Cervical ventroflexion. the tongue (X-linked muscular dystrophy).
● Dysphagia. ● Ventral flexion of neck and dorsal
protrusion of scapula (hereditary myopathy
See main reference on page 903 for details (The Cat of Devon Rex).
With Neck Ventroflexion). ● Any breed may be affected; inherited
myopathy occurs in the Devon Rex.
Clinical signs
Degeneration of the lower motor neuron cell bodies in
the ventral horn of the spinal cord and occasionally the Pathogenesis
cranial nerve nuclei leads to chronic progressive signs. An X-linked muscular dystrophy similar to
All cats were adults. Duchenne’s and Golden Retriever myopathy has been
described in male cats. A membrane-associated protein
Clinical signs included progressive weakness and (dystrophin) is deficient or absent.
muscle atrophy, tremor, especially of the head and
tongue, ventroflexion of the neck and dysphagia. Cardiac muscle may also be affected.
A specific cause of the other myopathies has not been
Diagnosis completely established.
Mild to moderate fibrillation potentials, consistent
with denervation, were found in the appendicular Clinical signs
(limb) and paraspinal muscles with electromyography. X-linked muscular dystrophy:
● The gait is mildly stiff or stilted, and cats tend to ● Muscle biopsy shows muscle fiber hypertrophy,
bunny-hop to run. fiber splitting, myonecrosis, calcium deposition,
● Occasionally there is marked stiffness and reluc- internalized nuclei and occasional fiber-type group-
tance to move. ing.
● Cats often appear to have increased muscle mass,
Hereditary myopathy of Devon Rex cats:
especially of the neck and proximal limb muscles,
● Serum CK levels are normal.
and stand with adducted hocks.
● Occasional fibrillation potentials and positive
● The tongue is hypertrophied and may protrude
sharp waves are found with electomyographic
partially. Excessive drooling of saliva occurs.
examination.
● Dehydration may be a recurring problem because
● Muscle biopsies show variability in muscle fiber
the tongue hypertrophy makes it difficult to drink.
size, internal nuclei, myofiber necrosis, regenera-
Eating is also affected by the tongue hypertrophy.
tion and fibrosis.
● There may be a history of gagging, regurgitation
or vomiting of food. Nemaline rod myopathy:
● Additionally, these cats may have fatal complica- ● Nemaline rods are characteristic within muscle
tions when undergoing general anesthesia or from biopsies.
manual restraint, as a result of peracute rhabdo-
myolysis.
● Signs generally develop before 2 years of age, and
hypertrophy of the proximal limb muscles is evi- Polymyositis (increased CK, muscle biopsy), organo-
dent as early as 10 weeks. phosphate toxicity (history of exposure, reduced
cholinesterase activity), hypokalemia (serum hypo-
Hereditary myopathy in Devon Rex cats (see main
kalemia) and congenital myasthenia gravis (positive
reference page 900, The Cat With Neck Ventroflexion).
tensilon test) are all differentials for degenerative
● Occurs in young (3–23 months of age) Devon Rex
myopathies.
cats.
● Clinical signs include generalized muscle weak-
ness, ventroflexion of the neck and dorsal protru- Treatment
sion of the scapula.
No effective treatment is known.
● Difficulty maintaining a normal head position when
eating may result in obstruction of the pharynx Long-term fluid therapy (subcutaneous) may be
with food and laryngospasm, which may be fatal. required in cats with X-linked muscular dystrophy for
● Megaesophagus may be present in some cats. them to survive, as tongue hypertrophy limits fluid
intake.
Nemaline rod myopathy:
● Weakness begins between 6–18 months of age.
● Clinical signs progress to a choppy, hypermetric Prognosis
gait.
Clinical signs are progressive until euthanasia or
● The patellar reflex is decreased, however flexion
death.
reflexes are present.
With X-linked muscular dystrophy, subcutaneous fluid
administration may be required to maintain fluid bal-
ance. With support, cats may live many years after
Diagnosis
diagnosis. Sudden death may occur in association with
These diseases usually require electrodiagnostic eval- anesthesia.
uation and muscle biopsy for definitive diagnosis.
With hereditary myopathy in Devon Rex cats, pro-
X-linked muscular dystrophy: gression of clinical signs occurs until 6–9 months of
● Increased serum creatine kinase (CK) and com- age. Clinical signs may stabilize after this time. Four in
plex repetitive discharges upon electromyo- six cats die suddenly of laryngospasm due to obstruc-
graphic (EMG) evaluation may be clues. tion of the pharynx with food.
With Nemaline rod myopathy, signs progress slowly Diagnosis

over the first year.
In cats with a suspected idiopathic peripheral neu-
Prevention ropathy, diagnosis is made on the clinical signs of
rapid onset of tetraparesis with loss of spinal reflexes.
Pedigree analysis and selected breeding are required to Muscle atrophy is evident within 7–10 days. One cat
remove the genes from the gene pool. was examined pathologically and had axonal degenera-
tion, fragmentation and loss of axons, as well as
IDIOPATHIC PERIPHERAL NEUROPATHY, demyelination and accumulation of macrophages in the
CHRONIC RELAPSING POLYNEUROPATHY, ventral nerve roots.
POLYNEURITIS
In chronic, relapsing polyneuropathy, electrodiag-
Classical signs nostic evaluation showed fibrillation potentials and
positive sharp waves in the limb and paraspinal mus-
● Lower motor neuron tetraparesis is the cles, as well as decreased nerve conduction velocities.
predominant sign.
● Marked weakness with conscious Demyelination and remyelination were present in nerve
proprioceptive deficits, and decreased biopsies.
spinal reflexes occur. In the cat with the acute, severe polyneuritis, patho-
logically there was extensive destruction of myelin
Pathogenesis associated with macrophages.
Nine cats have been reported with a suspected idio-

pathic peripheral neuropathy similar to polyradicu- Differential diagnosis
loneuritis (Coon Hound paralysis) in dogs.
Rule out other inflammatory, degenerative and toxic
Additionally, a chronic, relapsing polyneuropathy causes of muscle or neuromuscular disease.
has been reported in one cat and eluded to in other
publications. Snake bite (appropriate geographic location, increased
CK and clotting times), tick paralysis (geographic loca-
A cat has been reported with severe, acute polyneuritis tion, abnormal breathing and tick), botulism (gastro-
without evidence of an infectious etiology. intestinal signs) all cause marked tetraparesis but have
other differentiating signs, disk prolapse may cause
Clinical signs tetraparesis but cats are not flaccid in all four limbs,
traumatic spinal cord injury, diffuse hemorrhage in
In cats with a suspected idiopathic peripheral the spinal cord and around the nerve roots appear
neuropathy, clinical signs were similar to those dogs clinically similar.
reported with polyradiculoneuropathy (Coon Hounds
paralysis) with paraparesis to tetraparesis, rapid muscle
atrophy and decreased to absent spinal reflexes. Treatment
In chronic, relapsing polyneuropathy marked lower Spontaneous recovery occurs in cats with idiopathic
motor neuron tetraparesis occurred, recovered sponta- peripheral neuropathy.
neously and reoccurred months later.
Good nursing care is essential to provide fluids, nutri-
Conscious proprioceptive abnormalities, depressed spinal tion and to prevent urine scalding and pressure sores.
reflexes and muscle atrophy were present in the limbs.
With chronic, relapsing polyneuropathy improve-
One cat was reported with a severe, acute polyneuritis ment, if not resolution of clinical signs, may occur in
with weakness, conscious proprioceptive deficits and some cats after corticosteroid therapy.
decreased spinal reflexes.
In the cat reported with acute, severe polyneuritis, no
Icterus and anemia were associated abnormalities. treatment was attempted.
Prognosis PRIMARY HYPEROXALURIA

In cats with a suspected idiopathic peripheral neuro-
pathy, seven cats recovered spontaneously and com- Classical signs
pletely without specific treatment within 4–6 weeks. ● Domestic short-hair cats, 5–9 months old.
● Generalized weakness, absent cutaneous
trunci reflex.
MYOTONIA ● Signs of renal disease may or may not be
present.
Classical signs
● Stiffness and muscle spasm.
● Short, stilted gait. Pathogenesis
● Increased muscle size. It is suspected that the systemic oxalosis damages the
peripheral nerves.
Pathogenesis
Cats with myotonia have sustained muscle contrac- Clinical signs
tion, which is initiated voluntarily or with stimulation, Primary hyperoxaluria was reported in a colony of
and sustained involuntarily. domestic short-haired cats.
Myotonia most often occurs as a congenital problem. Cats developed clinical signs between 5–9 months of
Excessive muscle contraction is thought to be due to an age.
abnormal muscle cell membrane, which supports In some instances, clinical signs of weakness occurred
persistent depolarization. prior to the onset of renal failure.
Postural reactions were depressed.
Clinical signs
Spinal reflexes were inconsistently affected.
Affected cats often have a stiff, stilted gait and have
large, bulky muscles on palpation. The cutaneous trunci reflex was absent in most cats.
Muscle dimpling may occur with direct muscle Other signs of renal failure such as inappetence, weight
percussion. loss, polyuria, polydipsia were sometimes present.
Diagnosis Diagnosis
Electromyography demonstrates the characteristic Positive sharp waves, milder fibrillation potentials, and
myotonic potentials, and muscle biopsies may be sup- occasional bizarre high-frequency discharges were
portive of the diagnosis. found with electromyographic examination.
Pathologically, the neurons in the ventral gray matter of
Differential diagnosis the spinal cord and their proximal axons were most
Rule out other myopathies such as X-linked muscular affected.
dystrophy (increased serum creatine kinase, typical ● Swollen axons were present in the ventral nerve
muscle biopsy findings). Myotonia has characteristic roots and dorsal root ganglion cells.
EMG findings.
Treatment
Rule out other congenital causes of weakness such
No treatment has been described in cats. as hypokalemic myopathy (Burmese, low plasma
potassium), degenerative myopathies (signs, muscle As a rule, slowly decreasing serum sodium concentra-
lesions on biopsy), and myasthenia gravis (some tions over 2–3 days is safe. Serum sodium measurements
recovery with rest, and improvement after IV edro- should be determined frequently to avoid rapid
phonium). decreases in sodium, which can result in life-threatening
cerebral edema.
Treatment
Long-term management is with a low-sodium diet
No treatment was attempted. (e.g. Hill’s Feline H/D) with water added in excess of
maintenance requirements.
HYPERNATREMIC MYOPATHY
HYPERLIPIDEMIA
Classical signs
● Ventral neck flexion, muscle weakness and Classical signs
a “dropped-hock” gait.
● Hyperlipidemia and lipemia retinalis.
● Peripheral neuropathies involving
Clinical signs individual peripheral, cranial or
sympathetic nerves.
Rare disease with signs similar to hypokalemic
myopathy.
Generalized progressive muscle weakness which may Clinical signs
include ventral neck flexion and a “dropped-hock”
Hyperlipidemia in cats is usually the result of primary
appearance to the gait.
idiopathic hyperlipidemia or occurs secondary to dia-
betes mellitus.
Diagnosis
Chronic weakness, paresis and decreased spinal
Finding elevated serum sodium > 165 (mEq) mmol/L) reflexes may occur as a result of neuropathies second-
in the presence of clinical signs. ary to hyperlipidemia.
The neuropathy results from compression of nerves by
Differential diagnosis lipid granulomata (xanthomas).
Hypokalemic myopathy (diagnosis based on finding Signs depend on where the xanthomas form. Peripheral
hypokalemia i.e. plasma potassium < 3.0–3.5 (mEq) neuropathies involving individual peripheral, cranial or
mmol/L). sympathetic nerves.
Polymyositis (increased serum CK and muscle lesions
on biopsy). Diagnosis
Myasthenia gravis (positive edrophonium tensilon test Diagnosis is presumptive based on persistent fasting
and anti-acetylcholine receptor antibodies). hyperlipidemia (present > 24 hours after feeding) in the
presence of clinical signs of neuropathy and weakness.
Chronic organophosphate toxicity (diagnosis based on
history and sometimes reduced cholinesterase activity). Definitive diagnosis is on biopsy of the granuloma or
autopsy.
Treatment
Treatment centers around decreasing serum sodium
through fluid management. If the hypernatremia has Diabetic neuropathy may appear similar and hyper-
evolved slowly, extreme caution should be exercised lipidemia also occurs with diabetes. Xanthomas have
when attempting to decrease serum sodium with fluid been reported associated with the hyperlipidemia of
therapy. diabetes, but are not thought to be the cause of most
diabetic neuropathies. Persistent hyperglycaemia above Hypothermia may be associated with up-regulation
16 mmol/L (288 mg/dl) is diagnostic of diabetes. of anti-inflammatory cytokine activity. Cardiac
insufficiency is common, and coagulopathies often
Other neuropathies (e.g. neoplastic, idiopathic, inflam-
ensue.
matory) are not associated with persistent fasting
hyperlipidemia. Bradycardia is an inappropriate response to critical
illness, and its mechanism is unknown. Increased vagal
tone, sympathetic stimulation, and induction via hypo-
Treatment
thermia have all been postulated to be involved. It may
Feeding a low-fat diet resulted in resolution of the neu- be exacerbated by hypoglycemia or hyperkalemia
ropathy in 2–3 months in a few cats with peripheral which may accompany the septic state.
neuropathy.
Depression of myocardial function is exacerbated
Gemfibrozil (7.5–10 mg/kg daily) is indicated if by hypothermia, and continues after rewarming.
dietary therapy does not normalize triglyceride concen- Intracellular calcium overload contributes to diastolic
trations. dysfunction. Systolic dysfunction occurs secondary to
ischemia, myocardial edema or infarction.
Marine (fish) oils rich in omega-3 fatty acids may help
to decrease triglyceride concentrations. Cytokines increase vascular permeability and hypoal-
buminemia reduces oncotic pressure. When combined
with depressed myocardial function, the septic cat is
susceptible to fluid overload during treatment for
ACUTE SEPSIS
hypovolemia.
Classical signs Anemia results in local hypoxia and local lactic acidosis.
● Generalized weakness or flaccid paralysis.
● Hypothermia.
● Tachypnea. Clinical signs
● Bradycardia.
Depression and anorexia are typically present, and if
● Hypotension (poor pulses, pale mucous
sepsis is severe, the cat may be profoundly weak or
membranes, increased capillary refill
collapsed.
time).
Pyrexia or hypothermia may be present
Signs suggesting the infection site such as dyspnea,
Pathogenesis vaginal discharge or uterine distention, abdominal
guarding, or skin abscess are often evident.
Toxemia and reduced tissue oxygenation from acute
bacterial sepsis may cause weakness and depression. The classic signs of sepsis, labeled the “sepsis triad”
(fever, tachycardia, tachypnea) or the hyperdynamic
Toxemia may be associated with bacteremias originat-
phase, are rarely recognized.
ing in the uterus (pyometritis), thorax (pyothorax),
abdomen (peritonitis) or skin (subcutaneous abscess). Sepsis in cats often presents as the “shock triad”
(hypotension, bradycardia, hypothermia). Hypotension
Pyrexia or hypothermia may be present, and signs
is evidenced as poor pulses, pale mucous membranes
referable to the infection site are often evident includ-
and increased capillary refill time.
ing dyspnea, vaginal discharge, abdominal guarding or
skin abscess. Localized infection will often cause pyrexia, but sepsis
often presents at a stage where fever is no longer sus-
Hypothermia weakens the immune system, depres-
tained and hypothermia has developed.
ses the myocardium, bluntens the vasculature response
to catecholamines and reduces cellular function. Heart rate often follows temperature.
Diagnosis fresh whole blood if anemic, plasma if hypoalbumine-

mic, and give clotting factors via fresh whole blood or
Diagnosis is based primarily on clinical signs and fresh frozen plasma if coagulopathic. Do not use a glu-
history, especially if a site of infection is found. cose solution unless hypoglycemic.
Finding of the “shock triad” of hypotension, brady- Cardiac pumping support via use of positive
cardia, and hypothermia is highly suspicious. inotropes (dopamine, dobutamine, epinephrine) is
White cell count alterations are common. Neutro- essential.
philic leukocytosis with left shift may be evident, but Resuscitation goals are to restore oxygen delivery
with overwhelming sepsis, leucopenia with neutrope- through correction and maintenance of arterial pres-
nia or a degenerative left shift occur. Monocytosis sure, and adequate arterial oxygen content. The aims
occurs with long-standing or deep-seated infection. are to correct hypothermia, hypovolemia, bradycardia
Thrombocytopenia can be seen from day 1. and anemia. If perfusion is still inadequate, address
hypotension with inotropic and vasopressor support.
Red cell count changes include anemia from hemoly-
sis, or a falling PCV and schistocytes associated with Rewarm with warm intravenous fluids, warm humidi-
DIC. fied oxygen, forced air heating, incubators and circulat-
ing water blankets. Care is necessary as active external
Coagulation testing (PT, APTT, ACT, FDPs) may indi- rewarming can cause a paradoxical decrease in core
cate DIC. temperature, acidosis and shock, because of the return
Hypoalbuminemia is common. of cold blood with lactic acid from the periphery.
Icterus is common, and usually results from hemolysis Bradycardia is treated with adequate warming, fluid
rather than cholestasis. bolus, atropine (0.04 mg/kg IV), and a positive
inotrope/chronotrope.
Hypovolemia is treated with crystalloids (55–60 ml/kg
bolus rate IV) and colloids (5 ml/kg bolus rate IV). Adjust
Rule out other causes of acute muscle weakness such as fluid rate to maintain envolemic status. Monitor respira-
metabolic, inflammatory or toxic causes. tory rate and depth, and lung sounds carefully because
pulmonary edema and pleural effusion are common.
Identification of a focus of infection such as peritonitis,
pyothorax, pyometritis, pyelitis or subcutaneous Hypotension refractory to fluid therapy is treated with
abscess helps to differentiate sepsis from other causes exogenous catecholamines, but many patients become
of weakness. refractory after 72–96 hours.
● Dopamine (5–20 μg/kg/min CRI) has positive
Weakness with hypothermia, hypotension and
inotropic, chronotropic and some vasoconstrictor
bradycardia are pathognomonic.
effects, and has few adverse side effects.
● Dobutamine (5–20 μg/kg/min CRI) increases car-
diac output and oxygen delivery. Seizures occur
Treatment
with continued (> 24 hours) use.
The basis of therapy is ventilation, infusion, and ● Epinephrine (0.05–0.1 μg/kg/min CRI).
pumping (VIP), together with early antimicrobial ● Vasopressin.
treatment.
Anemia requires red cell transfusion if the PCV is less
Ventilation reduces the work of breathing, and than 20%.
includes oxygen, PEEP, intubation and/or mechani-
Pain control helps maintain mental well-being, and is
cal ventilation as necessary.
titrated to effect as responses are variable and affected
Infusion of fluids is essential. Colloids rapidly by underlying hepatic and renal dysfunction:
increase intravascular volume, and can be combined ● For mild to moderate pain use butorphanol
with crystalloids to support interstitial volume. Use (0.2–0.8 mg/kg IV q 2–6 h).
● For severe pain use methadone (0.2–0.4 mg/kg IM Prognosis worsens if shock signs (hypotension) do not
q 4–6 h), or morphine (0.1 mg/kg IM q 2–6 h respond to resuscitation within a few hours.
or 0.12 mg/kg/h CRI) with or without diazepam
Severe hypothermia (T < 35˚C), or neutropenia (neu-
(0.2 mg/kg IV).
trophil count < 1.0 × 109/L) are poor prognostic signs.
Hypoglycemia is treated with 21⁄2–5% dextrose added to
IV fluids and/or boluses of dextrose at 0.25–0.50 g/kg
increments.
MYOPATHY
Hyperglycemia is treated with low doses of regular
insulin IV as CRI of 40–60 mU/kg/h. Classical signs
Hyperkalemia is treated by adding 2 g potassium ● Subclinical myopathy evident on muscle
(26.8 mmol) per IL fluids, with a maximum CRI of biopsy.
0.5 mEq/kg/h.
Hypocalcemia. If not giving blood products, use lac-
Inappetent Cat).
tated Ringer’s solution (Hartmann’s) as the IV fluid, and
give a slow IV bolus of calcium gluconate (20 mg/kg).
Clinical signs
Hypomagnesemia. Administer Plasma-Lyte 148
which is compatible with blood. A subclinical myopathy has been shown to occur in
experimentally infected FIV cats.
Antimicrobial therapy. Early identification of the most
likely pathogen is advantageous. Use antibiotic combi-
nations (≥ two antimicrobials is now routine) to gain Diagnosis
synergy, spectrum and reduced emergence of resistance.
A presumptive diagnosis is based on evidence of a sub-
● Acceptable combinations while awaiting culture
clinical myopathy in a FIV positive cat where other
results include:
potential causes of myopathy have been excluded.
– Ampicillin (20–50 mg/kg q 6 h), gentamicin
(6 mg/kg q 24 h) and metronidazole (20–40 mg/ Some cats had elevated CK levels and changes on
kg q 24 h). EMG evaluation.
– Cephazolin (20–40 mg/kg q 8 h), gentamicin
Muscle biopsies may show inflammatory changes.
(6 mg/kg q 24 h) and metronidazole (20–40 mg/
● Predominant histologic characteristics were perivas-
kg q 24 h).
cular and pericapillary lymphocytic infiltration and
– Enrofloxacin (5–11 mg/kg q 24 h), metronida-
myofiber necrosis, phagocytosis and regeneration.
zole (20–40 mg/kg q 24 h).
OR
– Ticarcillin/clavulanate (30–50 mg/kg q 8 h) ± CIGUATOXIN INTOXICATION
gentamicin (6 mg/kg q 24 h)
OR Classical signs
– Enrofloxacin (5–11 mg/kg q 24 h)
● Signs begin within 3–6 hours of ingestion
– Ampicillin, cephazolin, or ticarcillin/clavulanate
of a toxic meal of reef fish.
as above.
● Hindleg paresis and vomiting are the most
– CAUTION: do not use gentamicin if there are
prominent.
signs of renal dysfunction. Enrofloxacin has been
● Cardiovascular shock and/or respiratory
associated with blindness which is often irre-
distress may precede coma and death
versible.
within 24 hours of ingestion.
Prognosis
Prognosis is guarded to poor, and a successful out-
Pathogenesis
come relies on early intervention, and detection and Ciguatoxin is the main toxin that accumulates in the
elimination of the site of infection. flesh and viscera of large carnivorous species of fish
associated with coral reefs (mostly coral trout, Cardiovascular effects are biphasic. Low doses of toxin
Spanish mackerel, barracuda). tend to induce hypotension, hyperventilation, brady-
cardia and atrioventricular block. As toxin absorption
A marine benthic dinoflagellate, Gambierdiscus toxi-
increases, the higher doses cause hypertension, tachy-
cus, is believed to produce a precursor to ciguatoxin,
cardia, respiratory depression and perhaps cardiac
gambiertoxin, which undergoes biotransformation
arrest.
within the stomach of herbivorous fish. The resultant
ciguatoxin is absorbed from the stomach and Recovery is slow and signs may persist for 1–2 weeks.
sequestered in the muscles and viscera (potency
increases tenfold in the process).
Diagnosis
Ciguatoxin is heat stable and not affected by cooking.
History of access to coral reef fish.
Ciguatoxin is lipid soluble and may cross the
Presence of gastrointestinal signs along with neuro-
blood–brain barrier, which accounts for the CNS effects.
logical signs is supportive.
An associated toxin, maitotoxin, is water soluble and is
A rapid calorimetric immunoassay (the “stick test”)
believed to account for the gastrointestinal effects.
conducted on the fish flesh is inexpensive and quick
Ciguatoxin interferes with the sodium channels and of use in ciguatera endemic regions.
located on the cell membrane of neurons. In the muscle
sarcolemma it increases sodium permeability of the
cell membrane. Increased sodium permeability
enhances activation. Rule out other causes of neurological signs, especially
tick paralysis and brown snake envenomation. Cats
Cardiac effects are the most life threatening and
with ciguatoxicity typically have gastrointestinal signs,
involve arrhythmias and negative inotropy. Focal
a history of access to reef fish, a lack of voice involve-
myocardial necrosis is evident histologically.
ment (typical in tick paralysis), and no coagulation
Centrally mediated interference with phrenic nerve defects (typical in brown snake).
conduction may lead to respiratory failure and death.
Rule out toadfish (tetrodotoxin) poisoning largely via
history of access as well as pupillary dilation and
Clinical signs voice changes are more typical of tetrodotoxin.
Cats fed reef fish are at risk of poisoning, as are humans,
even though incidences are low. Cats fed viscera and Treatment
liver of these fish may consume a lethal meal because
No specific treatment is available. Symptomatic and
ciguatoxin levels are 50 times greater than in fish flesh.
supportive measures including maintenance of body
Signs begin within 3–6 hours of ingestion of a toxic fluids and artificial respiration may be required.
meal and may last up to 14 days.
Gastric lavage and/or induction of emesis in the early
Neurological signs include hindlimb paralysis stages of intoxication may decrease the severity of signs.
extending to forelimbs in severe cases, and ataxia.
Atropine (up to 1 mg/kg) helps control the gastroin-
Gastrointestinal signs include hypersalivation and
testinal signs as well as reduces the bradycardia
vomiting.
and hypotensive components of the cardiovascular
Less severe cases may have some mild gastrointestinal effects.
signs and mild paresis.
Lignocaine by constant rate infusion (400 μg/kg/min)
Respiratory difficulty and arrhythmias may also has been shown to alleviate the cardiovascular effects
occur. Death from respiratory failure can occur several of ciguatoxin in the cat, probably by blocking the
days later. sodium channels.
Calcium gluconate (200 μg/kg/min CRI) infusion has as flaccid paralysis especially of the hindlimbs and
been found to be of value in offsetting cardiac effects. diaphragm.
Proprandol (beta-blocker) at 1 mg/kg IV has been Although cardiac muscle is less sensitive than nerve or
used to control severe tachycardias. skeletal muscle tissues, severe intoxication can cause
bradycardias, heart block and asystole as well as ven-
Mannitol (1 g/kg) infusions have not been shown to
tricular fibrillation.
be successful in the cat, despite its reputation as the
treatment of choice in humans, presumably through its
effect as a free radical scavenger.
Clinical signs
Current research is centered on production of an anti-
Signs begin 10–40 minutes after ingestion.
toxin using monoclonal antibodies.
Pawing at the mouth and licking of the lips probably
equates to human reports of paraesthesia or numbness
TETRODOTOXIN INTOXICATION
around the mouth and lips with a tingling (prickling)
sensation.
Classical signs
Drooling, vomiting and diarrhea are usually followed
● Signs begin 10–40 minutes after ingestion.
by muscular weakness and ataxia. Voice loss and
● Initial signs are gastrointestinal – drooling,
dyspnea occur once muscular weakness is evident.
vomiting and diarrhea.
● Neuromuscular signs follow with Flaccid paralysis, especially of the hindlimbs, develops
weakness and ataxia progressing to flaccid rapidly following initial signs of weakness and ataxia.
hindlimb paralysis.
Bradycardia, cyanosis and hypotension are variable.
● Pupillary dilation is usually a feature.
● With severe toxicity, cardiovascular shock Pupillary dilation is usually a feature.
and labored respiration often precede
Death may ensue with terminal convulsions, labored
convulsions and death within hours.
breathing, tachycardia and hypotension evident.
Tetrodotoxin accumulates in the flesh and viscera of Diagnosis is usually based on a history of rapid onset
toadfish (Sphaeroides hamiltoni) and puffer fish, of neurological signs after access to a toxin source.
newts and the blue ringed octopus. It is produced in
No routine diagnostic laboratory tests are available.
the intestines of these species by Vibrio bacteria.
Autopsy tissue samples can be tested by gas chro-
Tetrodotoxin is heat stable and is not affected by
matography for toxin.
cooking.
Tetrodotoxin is a powerful vasopressor and neuro-
toxin. It exerts its action by inhibiting the excitability
of neurones by blocking the sodium channels and Ciguatoxicosis typically causes similar signs although
decreases sodium permeability of the cell membrane slower in onset and longer in duration and usually less
(ciguatoxin has the opposite effect). intense and less acutely life threatening. Pupillary
dilation is not a feature of ciguatoxin.
Tetrodotoxins function similarly to local anesthetics
and prevent depolarization of excitable tissues. Tick paralysis signs are less intense and more slowly
progressive and the presence of a tick is diagnostic.
Tetrodotoxin affects skeletal muscle membranes and
vasomotor nerves, causing hypotension. Reduced Brown snake envenomation typically includes coagu-
neuromuscular junction impulse conduction manifests lation deficits.
Treatment The toxin action on the presynaptic terminal of the

neuromuscular junctions results in initial outpouring
Gastric lavage and administration of activated charcoal of the neurotransmitters (acetylcholine and norepi-
are useful to remove unabsorbed toxin. nephrine) followed by depletion of acetylcholine
reserves at motor nerve endings. This may result in
Airway maintenance, oxygen therapy and mechanical paralysis of voluntary muscles.
ventilation may be required.
The accompanying widespread release of cate-
Hypotension is treated with fluid resuscitation (up to cholamines causes hypertension.
50–60 ml/kg of crystalloid replacement fluids) with or
without peripheral vasoconstriction via norepineph-
rine (0.2 μg/kg/min) or dopamine (5–10 μg/kg/min Clinical signs
CRI) Erythema, edema and localized swelling at the bite
Etamiphylline (210 mg IM per cat), a cardiac and res- site occur within seconds to minutes after the bite.
piratory stimulant, has benefited some cases. The pain increases in intensity within 5–15 minutes,
causing generalized hyperaesthesia, vocalization, chew-
ing or licking at the bite site and holding of the affected
RED-BACK SPIDER ENVENOMATION limb off the ground; swelling of the limb may occur.
(AUSTRALIA) (LATRODECTUS MACTANS
Pain may appear widespread for example abdominal
HASSELTI) AND BLACK WIDOW SPIDER
pain, causing abnormal postures such as hunched
ENVENOMATION (USA) (LATRODECTUS
appearance, and may occur within 30–60 minutes of
MACTANS)
the bite.
Classical signs Malaise, depression and vomiting may ensue.
● Pain and swelling initially localized to the Restlessness, tremors and weakness especially of the
area of the spider bite. Pain may spread to affected limb are common, and usually occur within
remote areas over 30–60 minutes and may 3 hours, but could be up to 24 hours
include abdominal pain.
Tachycardia and hypertension occur in several cases.
● Vomiting is a variable sign.
● Agitation, muscle weakness, and
incoordination occur later (1–24 hours). Diagnosis
● Muscular tremors and tachycardia.
A presumptive diagnosis is based on the history of sud-
den onset of severe pain in a cat with access to spi-
ders or finding a collapsed cat with no coagulation
Pathogenesis
defects near where red-back or black widow spiders
Pain is produced at the spider bite site and beyond via have been found.
an unknown mechanism which is presumed to be
related to the presence of algesic agents (e.g. hista-
mine, 5-hydroxytriptamine, bradykinin). These act
directly on nociceptors to promote the formation of Snake bite envenomation typically displays coagula-
prostaglandins and other inflammatory mediators tion defects as well as flaccid paralysis without obvi-
which may act in synergism with the venom compo- ous pain. Hindleg paralysis associated with poor
nents to enhance pain production. circulation is a feature. Cold, purple-blue skin and
absent pulses are typical.
Venom is a protein (alpha-latrotoxin) of 130 000 dal-
tons molecular weight, which is predominantly neu- Trauma can usually be differentiated if other injuries
rotoxic in action. are evident.
Polymyositis or polymyopathy tends to be more gen- Administer red-back spider antivenom (500 units IM
eralized and much less intense; there is less rapid pro- or diluted 1:50 slowly IV or black widow spider
gression and no localization to an area. antivenom (equine origin) used similarly. Repeat the
dose if no appreciable response is observed in
Acute abdomen typically is more confined to the
1–2 hours. The efficacy may be reduced if given after
abdomen and is not accompanied by weakness unless
paralysis occurs.
advanced. Diagnostic tests such as abdominal ultra-
sound, abdominocentesis and/or diagnostic peritoneal Administer pain relief with opioids (e.g. buprenor-
lavage may be necessary to help differentiate. phine 0.1–0.5 mg/kg ) each 4–8 hours as needed.
Fluid and electrolyte therapy is necessary, especially
Treatment correction of calcium and potassium deficits.
Replacement isotonic crystalloid fluids should be used
Supplemental oxygen by mask, head box, or nasal
and these may need to have 20–80 mEq/L potassium
tube should be administered at 100–200 ml/kg, if the
added, depending on the serum potassium concentra-
cat is dyspneic or distressed.
tion. Calcium supplementation may be necessary and if
Ice packs may aid local pain relief. Pressure bandages serum levels can be monitored, increments of 5–10 mg/kg
may enhance pain and probably do little to restrict of calcium gluconate may be given each hour added to
venom movement once systemic signs are present. This IV fluids.
is because there is usually a 1⁄2–3-hour lag between the
Rest, warmth and close observation are important.
bite and the onset of systemic signs.
RECOMMENDED READING
Atwell RB, Campbell FE. Reactions to tick antitoxin serum and the role of atropine in treatment of dogs and cats
with tick paralysis caused by Ixodes holocyclus; a pilot survey. Aust Vet J 2001; 79: 394–397.
Dow SW, LeCouteur RA, Fettman MJ, Spurgeon TL. Potassium depletion in cats: Hypokalemic polymyopathy. J Am
Vet Med Assoc 1987; 191: 1563–1568.
Gerritsen RJ, van Nes JJ, van Niel MHF, et al. Acute idiopathic polyneuropathy in nine cats. Vet Quart 1996; 18:
63–65.
Sharp NJH, Nash AS, Griffiths IR. Feline dysautonomia (the Key–Gaskell syndrome): A clinical and pathological
study of forty cases. J Small Anim Pract 1984; 25: 599–615.
Shelton GD. Neuromuscular disorders. In: August JR (ed) Consultations in Feline Medicine, 2nd edn. Philadelphia,
WB Saunders, 1994, pp. 405–412.
Shelton GD. Diseases of the muscle and neuromuscular junction. In: Sherding RG (ed) The cat diseases and man-
agement, 2nd edn. New York, Churchill Livingstone, 1994, pp. 1569–1576.
45. The cat with lameness
Maurine Thomson
KEY SIGNS
● Difficulty walking.
● Limping.
● Inability or reluctance to bear weight on limb.
MECHANISM?
● Structural or functional disorder of one or more limbs resulting in an altered gait or stance.
WHERE?
● Generally a disorder of the musculoskeletal system, occasionally neurological, metabolic or
referred pain.
WHAT?
● Most lameness in cats is associated with trauma, particularly cat fight injuries or motor vehicle
accidents.

Diseases causing lameness
DEGENERATIVE
● Degenerative joint disease* (p 981)
Less common in the cat than dog, and often asymptomatic. Usually secondary to external joint
trauma.
● Intervertebral disc disease* (p 982)
Rare in the cat, can cause paresis or lameness.
ANOMALY
● Hip dysplasia (p 987)
Rare in the cat compared to the dog, and occurs mainly in Persians. Usually asymptomatic
in cats.
976
45 – THE CAT WITH LAMENESS 977
● Osteochondrosis dissecans (p 988)

Rare in the cat, reported in the shoulder joint.
● Femoral neck metaphyseal osteopathy (p 988)
Similar appearance to Legg–Calve–Perthes disease in dogs. Occurs rarely, exclusive to young male
cats less than 2 years of age.
● Feline mucopolysaccharoidosis (p 988)
Rare inherited disorder of Siamese cats, which may cause a stiff gait.
● Osteogenesis imperfecta (p 989)
Rare inherited disorder of osteogenesis, which is characterized by brittle bones, which fracture
readily with minor trauma.
● Scottish fold osteochondrodysplasia (p 989)
Occurs in Scottish folds resulting in periarticular exostoses and ankylosis.
● Pectus excavatum (p 989)
Congenital abnormality resulting in dorsal to ventral narrowing of the thorax. May be associated with
limbs splaying laterally and impaired ambulation.
● Spina bifida (p 989)
Characterized by a closure defect in the neural arches, and is inherited with the gene for tailless-
ness in Manx cats; causes variable neurological deficits.
NUTRITIONAL
● Hypervitaminosis A (p 990)
Seen occasionally in cats on all-liver diet. Causes joint ankylosis and spinal pain.
● Nutritional hyperparathyroidism* (p 990)
Due to diet low in calcium. Seen in young kittens on an all meat diet. Causes osteopenia and
pathological fractures.
● Rickets (p 991)
Seen in young cats fed diet with calcium:phosphorus imbalance and vitamin D deficient. Causes
osteopenia and thickening of physeal growth plates.
NEOPLASTIC
● Neoplasia (primary neoplasia of bone, synovium, connective tissue or spinal cord
and secondary metastatic neoplasia to digits from lung carcinomas) (p 977)
Rare in cats. Generally occurs in older cats and may present acutely or with an insidious onset of
lameness. There is usually swelling at the site of the neoplasia.
INFECTIOUS
● Cellulitis and soft tissue abscesses*** (p 979)
One of the most common causes of lameness in the cat, secondary to cat fight wounds. Usually
acute onset of lameness, with variable signs of systemic illness.
● Bacterial septic arthritis or osteomyelitis (p 983)
Usually secondary to bite wound or hematogenous spread from septic foci. See lameness and typi-
cal discharging sinus.
continued
continued
● Localized tetanus (p 985)

Occasionally causes paresis or paralysis of a solitary limb in the initial stages, but usually
advances to generalized tetanus.
● Viral arthritis (p 983)
Can occur secondary to calici virus exposure or vaccination; also coronavirus.
● Fungal infections (p 984)
Histoplasmosis, Coccidiomycosis, Sporotrichosis usually cause non-healing lesions, draining
sinuses or osteomyelitis.
More often causes CNS signs such as ataxia, and paresis but can cause stiff gait, shifting lameness
and muscle and joint pain.
● Neospora caninum (p 985)
Causes encephalomyelitis with ataxia and paresis and polymyositis.
IMMUNE MEDIATED
● Feline progressive polyarthritis (erosive) (p 985)
Rare disease; proliferative subtype occurs as acute onset in 1–5-year-old male cats, deforming sub-
type occurs as chronic onset in older cats. Usually several joints affected, most commonly carpus
and tarsus. Proliferative subtype often has systemic signs of illness. Deforming subtype may be
FeLV positive.
● Immune-mediated polyarthritis (non-erosive) (p 985)
Rare disease, due to deposition of immune complexes in the synovial membrane. Usually carpus
and tarsus affected. May be idiopathic or associated with SLE or chronic infection.
TRAUMA
● Fractures, luxation, muscular contusions*** (p 980)
Very common cause of presenting lameness.
● Cruciate rupture (p 982)
Occurs much less frequently in the cat than the dog, and usually less symptomatic.
● Patellar luxation (p 983)
Occurs only rarely in the cat, predisposition in Devon Rex cats.
The severity of the lameness will vary with the severity

INTRODUCTION and type of the injury or insult, varying from a mild to
a non-weight-bearing lameness.
MECHANISM? Generally periosteum has the densest nerve supply of the
deep tissues, and has the lowest pain threshold, followed
Lameness can occur in any limb, and is defined as
by the joint capsule, tendon, fascia and muscle.
interference in the normal locomotion of the cat. It is
usually pain related, and is secondary to tissue injury Mechanical lameness can result from an abnormal limb
which has caused structural alteration, edema and conformation such as shortening, angulation or a rota-
inflammation. tional abnormality.
Referred pain is pain felt in a part of the body other Many bacteria are present in the oral cavity of cats,
than that where the cause of pain is located. but Pasteurella, Bacteroides and Fusobacterium are
the most common organisms responsible for abscess
Signs of weakness can be confused with lameness. See
formation, though a mixture of anaerobes and aerobes
The Cat With Generalized Weakness (page 941).
may also be present.
Paresis and ataxia can also be confused with lameness.
The Weak and Ataxic or Paralyzed Cat See (page 908). Infection may take the form of a discrete abscess or a
diffuse cellulitis.
WHERE? Occasionally L-forms of bacteria which lack bacterial
The origin of the lameness may be from bone, muscle, walls are involved.
joint or neurological.
Diagnosis requires a good physical examination and Clinical signs
orthopedic examination to localize the lameness in the Acute lameness.
affected limb or limbs.
Soft tissue swelling and pain at the affected site.
WHAT? Often a small scab and evidence of a bite wound can
identify the area of penetration.
The most common causes of lameness in the cat are
cellulitis or an abscess from a cat bite injury, and motor Associated with variable signs of systemic illness,
vehicle trauma resulting in fracture or luxation. including depression, pyrexia and anorexia.
The site of the injury is generally localized by palpation L-forms produce a syndrome of fever and persistently
of pain and swelling at the affected site. draining, spreading cellulitis and synovitis that often
involve extremities. Lesion is unresponsive to most
Cellulitis is often associated with pyrexia and lethargy.
antibiotics except tetracycline group.
Motor vehicle trauma is often associated with other
signs of external injury such as grazes or scuffed nails,
Diagnosis
with or without dyspnea or internal injuries.
History of a cat fight.
DISEASES CAUSING SIGNS Clinical signs of penetrating injury.
OF LAMENESS
Abscess formation can be demonstrated by aspiration
of purulent material.
CELLULITIS/SOFT TISSUE ABSCESS***
L-form bacteria produce a discharge containing pre-
Classical signs dominantly macrophages and neutrophils, but organ-
isms cannot usually be detected cytologically or grown
● Acute lameness of affected limb. on culture. Response of syndrome only to tetracycline
● Pain and soft tissue swelling at site of injury. group antibiotics suggests diagnosis.
● Often associated with pyrexia, anorexia,
lethargy.
● Wounds in close proximity to a joint can Differential diagnosis
cause septic arthritis. Soft tissue injury caused by another form of external
injury.
Pathogenesis Foreign body reaction.
Occurs secondary to a penetrating bite wound, Osteomyelitis often causes swelling and sinus forma-
and is one of the most common causes of lameness tion. Rare in the cat and usually associated with an
in the cat. open fracture or bite wound.
Treatment Hindlimb lameness in young cats less than 7 months

of age is usually due to disruption of the growth plate
Abscess formation generally requires lancing, and to the femoral head rather than hip luxation.
flush with weak solution of chlorhexidine, followed
by course of antibiotics sensitive to Pasteurella, i.e. Type and location of the fracture or luxation will
amoxycillin and clavulonic acid 12 mg/kg for 5 days. depend on the type of forces that have occurred at the
time the injury was sustained.
Rarely there may be extensive regions of necrosis,
which may require debridement and delayed closure.
Cellulitis treated by broad-spectrum antibiotics, i.e. Clinical signs
amoxycillin and clavulonic acid, or cephalosporins.
Acute lameness of the affected limb.
Osteomyelitis may be a rare secondary complication
Pain and swelling localized by physical examination.
resulting in sinus formation after initial healing of the
abscess. Most common sites of fractures are femur, humerus,
pelvis, tibia and radius.
L-form bacteria respond rapidly to tetracycline (22 mg/kg
tid PO) or doxycycline (5 mg/kg bid PO). Hip luxation is the most common form of joint disrup-
tion in the mature cat.
Pain localized to the hip in young cats is more likely due
Prognosis to separation of the femoral head.
Normally excellent, and resolves after initial treatment. Fracture/luxation injuries may be open or closed.
With extensive injury the prognosis is still excellent, Open shearing injuries of the carpus and tarsus often
although it may require more prolonged treatment. occur due to the minimal degree of soft tissues cover-
ing over these regions.
With septic arthritis some degree of degenerative joint
disease will occur, although cats tolerate this with less
clinical symptoms than dogs.
Diagnosis
Usually history of trauma.
FRACTURES, LUXATION, MUSCULAR Localization by physical examination.
CONTUSIONS***
Radiography is normally required to demonstrate exact
type and location of the fracture or luxation.
Classical signs
● Acute, usually non-weight-bearing
lameness of affected limb or limbs. Differential diagnosis
● Soft tissue swelling at the site of injury.
Cellulitis can cause a similar degree of soft tissue
● Abnormal movement or angulation of the
swelling and lameness. Usually differentiated by evi-
affected bone or joint.
dence of penetrating wound and pyrexia.
Neoplasia of a bone or joint can present suddenly if
associated with a pathological fracture. Very rare in the
Pathogenesis
cat, and usually differentiated on radiographs.
Usually due to external trauma from a motor vehi-
Nutritional hyperparathyroidism in the young cat can
cle accident.
present suddenly due to spontaneous fractures.
Can also occur from other external trauma such as dog Radiographically will see generalized osteopenia, with
attack, malicious attack or fall. history of poorly balanced diet.
Treatment Can occur secondary to septic arthritis from hematoge-

nous spread or direct contamination.
Will depend on the location and extent of the injury.
Occasionally occurs in association with acromegaly
Simple fractures in young animals may be amenable to from excess growth hormone.
external coaptation, i.e. splints or casts.
More extensive fractures generally require some form Clinical signs
of internal fixation. See relevant textbooks dealing with Insidious lameness which may be exacerbated by
orthopedic diseases and management. strenuous activity.
Joint sprains or other soft tissue injuries usually Usually some degree of joint thickening and reduced
respond well to brief periods, i.e. 2 weeks or less, of range of motion on physical exam.
immobilization, or simple rest.
Often does not cause any clinical signs of lameness and
may be incidental finding.
Prognosis
Depends on the location and degree of severity of the Diagnosis
injury. History of insidious or vague intermittent lameness.
With appropriate treatment most injuries have a very Radiographs demonstrate signs of osteoarthritis such as
good prognosis for return to normal function. osteophytes, periosteal proliferation and periarticular
Excision arthroplasty in the cat for treatment of femoral joint thickening.
head separation or fracture has a very good to excellent
prognosis following surgery. Differential diagnosis
Cats are generally less symptomatic for osteoarthritis fol- Joint neoplasia, which is very rare in the cat. Usually
lowing joint trauma than are dogs. expect more extensive swelling and consistent lameness.
Treatment
DEGENERATIVE JOINT DISEASE*
Most cats are not symptomatic for osteoarthritis, or
Classical signs if associated with a sudden exacerbation of the joint
normally respond well to conservative management.
● Chronic, insidious lameness of the affected This involves rest and short-term non-steroidal anti-
limb. inflammatory drugs, i.e. aspirin 10 mg/kg every 48
● Lameness may be worse after sleeping, or hours or corticosteroids, i.e. prednisolone 0.25 mg/kg
when first rising. daily, or other non-steroidal anti-inflammatory drugs,
● May have thickening of the affected joint, e.g. carprofen, ketofen or meloxicam depending on
with decreased range of movement. availability and registration for use in cats.
● Much less common in the cat than the dog.
Encourage weight loss in fat cats.
Pathogenesis In severe cases of osteoarthritis associated with ero-

sive arthritis or joint instability, arthrodesis may be
Generally secondary to joint trauma such as open warranted.
fracture, or penetrating bite wound.
Can occur secondary to joint conformational abnor-
Prognosis
mality such as hip dysplasia in Persian cats, patellar
luxation or cruciate rupture. Generally very good when single joint is involved.
May be part of an immune mediated polyarthritis, e.g. With severe polyarthritis long-term prognosis is
systemic lupus erythematosus. poor, with most cases relapsing after therapy.
INTERVERTEBRAL DISC DISEASE* Pathogenesis

Usually due to external trauma such as a fall, hyper-
Classical signs extension injury of the stifle, or excessive internal
● Much rarer in the cat than the dog. rotation of the tibia.
● Usually results from traumatic herniation Generally causes rupture of the anterior cruciate, rarely
of the disc. is the caudal cruciate involved, unless there has been
● Clinical signs vary with the location of the major stifle disruption.
disc herniation.
● Signs may be acute or progressive in
onset. Clinical signs
Acute lameness of the affected hindlimb.
Generally there will be stifle swelling and pain present
Pathogenesis on joint palpation.
Usually results from traumatic herniation of the disc, A positive cranial drawer sign or tibial thrust is gener-
resulting in acute spinal cord compression. ally evident on palpation, though pain may prevent an
adequate examination of the joint.
Much rarer in the cat than the dog.
Chronic cases may show a mild intermittent lameness
as opposed to the acute injury.

Location of the site of herniation dictates type of clini- By identification of a positive cranial drawer sign
cal signs seen. and pain in the stifle.
Usually associated with paresis of the hindlimbs. See
The Weak and Ataxic or Paralyzed Cat (page 908). Differential diagnosis
Traumatic disruption of all stifle ligaments due to
excessive trauma. Usually palpation will reveal laxity
Diagnosis in a mediolateral direction also if the collaterals have
been disrupted.
Lesion identified by neurological examination.
Confirmation of disc herniation by radiographs, myel- Treatment
ography or CT imaging.
Conservative therapy with rest and anti-inflamma-
tories is generally sufficient for return to normal
function in most cats.
CRUCIATE RUPTURE Degenerative joint disease will usually occur, but this
does not normally cause clinical signs of lameness.
Classical signs
In refractory cases the stifle can be stabilized with
● Acute onset of hindlimb lameness. an extra-articular surgical technique. See relevant
● May have thickening of the affected joint texts on surgical management of cruciate disease.
due to synovitis, with pain evident on
palpation of the stifle. Prognosis
● Positive cranial drawer sign or tibial thrust.
● Much less common in the cat than the dog. Generally the prognosis is very good to excellent with
both conservative and surgical management.
Type of surgery varies with the severity of the disease,

PATELLAR LUXATION
ranging from lateral imbrication, deepening of the
trochlear groove and transposition of the tibial tuberosity.
Classical signs
● Can be congenital or acquired secondary to
trauma. Prognosis
● Much rarer in the cat than the dog, though Generally excellent, despite the progression of some
a predisposition occurs in purebred cats degree of degenerative joint disease.
such as the Devon Rex.
● Lameness may be worse after sleeping, or
when first rising. BACTERIAL SEPTIC ARTHRITIS
● May have thickening of the affected joint, OR OSTEOARTHRITIS
with decreased range of movement.
VIRAL ARTHRITIS
Pathogenesis
The congenital form occurs secondary to malalign- Classical signs
ment of the quadriceps mechanism, generally resul- ● Lameness may be of a single limb or
ting in a medial luxation of the patella. multiple.
Varying degrees of deformity of the trochlear groove
● If all limbs involved will be reluctant to
and tibial tuberosity can occur depending on the sever- ambulate at all.
ity of the luxation.
● Can cause erosive or non-erosive signs
radiographically.
The acquired form can occur secondary to external ● Considered rare in the cat as a cause of
joint trauma from a fall or motor vehicle accident. lameness.
Clinical signs
Pathogenesis
The congenital form is characterized by varying degrees
of lameness depending on the severity of the condition. Bacterial:
The lameness if often insidious and intermittent. ● Generally from a blood-borne infection that arises
from a septic foci elsewhere in the body.
Usually occurs in young, purebred cats. ● Can occur from direct bite wound or open joint
The acquired form can occur at any age, usually pre- injury.
senting with an acute lameness. ● Rarer in cats than dogs.
● Can occur in kittens secondary to umbilical vein
Palpation of the stifle will demonstrate luxation of the infections.
patella. ● Pasteurella species are most commonly identified.
● Can be due to bacterial L forms, which are mutant
Diagnosis bacteria, which have lost their cell wall.
Palpation of the stifle demonstrates patellar luxa- Viral:
tion, usually in a medial direction. ● Calicivirus polyarthritis can occur uncommonly in
Lameness present in the affected limb, which varies young kittens following natural exposure or after
with the severity of the underlying disease. live attenuated vaccination.
● Lameness usually occurs 7–10 days after mild res-
piratory tract signs, though can occur in the absence
Treatment of respiratory signs.
In cats with clinical disease surgery is generally ● Coronavirus has also been associated with
warranted. polyarthritis.
● The effusive form of feline infectious peritonitis

TOXOPLASMOSIS
(FIP) virus occasionally causes lameness, with leak-
age of fluid into joint spaces.
Classical signs
● The granulomatous form of FIP may cause paresis
or paralysis as a result of spinal cord inflammation. ● More commonly causes CNS signs such as
ataxia and paresis.
Mycoplasma:
● Can cause a stiff gait, shifting leg
● M. gatae is linked to arthritis and tenosynovitis in
lameness, hyperaesthesia on muscle
older cats.
palpation and joint pain.
● Mycoplasmal infection may incite an antigenic
response resulting in the formation of immune-
mediated disease such as rheumatoid-like (deform-
With Signs of Acute Small Bowel Diarrhea) and page
ing) arthritis.
958 (The Cat With Generalized Weakness).

Acute onset of lameness in one or several limbs. CNS signs seen most frequently, see The Paretic Cat
Usually associated with systemic signs such as (page 911).
pyrexia, lethargy. May cause shifting limb lameness.
May appear weak rather than lame if all four limbs Can cause arthritis and myositis.
involved.
Usually demonstrate joint pain on manipulation of Diagnosis
limbs.
High IgM titers suggest recent infection, but do not
confirm that T. gondii is responsible for the clinical
Diagnosis signs in a given cat.
Radiographic signs may demonstrate changes of ero- The organism can sometimes be seen in a muscle
sion and periosteal proliferation in advanced cases, but biopsy or very rarely in CSF.
may show no abnormalities initially.
Arthrocentesis generally required for cytology and cul- FUNGAL INFECTIONS
ture and sensitivity.
Classical signs
Differential diagnosis ● Cats less commonly affected than dogs.

● Lameness due to fungal osteomyelitis.
Weak or paretic cat can appear similarly. See The Weak ● Can be a single bone involved, or more
and Ataxic or Paralyzed Cat (page 908). commonly multiple sites affected.
Immune-mediated polyarthritis. ● Spores usually inhaled from the soil.
See main references on page 368 for details (The Pyrexic

Treatment Cat) and page 401 (The Cat With Enlarged Lymph
Antibiotics for bacterial infection depending on results Nodes).
of culture and sensitivity.
L form infections respond well to 10–14-day course of Clinical signs
tetracycline or doxycycline.
Occurrence tends to be location dependent:
Calicivirus is often self-limiting, and cats recover ● Coccidioides: south-western USA, Mexico, Central
well. and South America.
● Blastomyces: small area of distribution mainly in Clinical signs

North America and near fresh water.
● Histoplasma: widespread in temperate and subtrop- Occurs following penetrating trauma and tissue
ical regions of the world, not Australia. devitilization.
● Cryptococcus: worldwide distribution. Retrograde axonal transport of the Clostridium tetani
● Sporotrichosis: worldwide distribution. neurotoxin occurs.
Result in non-healing tumor-like lesion of the distal Can see paresis or paralysis of a solitary limb in the
limbs and draining sinus tracts (sporothrix) or lameness initial stages.
due to fungal osteomyelitis.
Generally advances to generalized tetanus.
Radiographically, see tumor-like lesions present in the
bone with bone bony destruction and proliferation seen.
Diagnosis
Diagnosis History of recent wound and clinical signs.
Organism is often evident in cytological preparation of EMG findings characteristic with persistent electrical
aspirates or discharge from lesion or in a biopsy section. motor unit discharges following needle insertion or tap-
Positive fungal titer may aid diagnosis. ping of muscles.
Serum antibody titer to tetanus toxin compared with
NEOSPORA CANINUM control cats may aid diagnosis.
Classical signs
IMMUNE-MEDIATED POLYARTHRITIS
● Neurological signs such as ataxia and
(NON-EROSIVE)
paresis.
● Polymyositis frequently present.
Classical signs
● Are considered rare diseases in the cat.
Clinical signs ● Can be acute or chronic onset.
Polymyositis and encepalomyelitis with ataxia and ● Often associated with other systemic signs
paresis are seen most frequently. such as lethargy, pyrexia and anorexia.
● Can cause erosive or non-erosive signs
radiographically.
Diagnosis
Serum titers and muscle biopsy results are the most
Pathogenesis
common methods of diagnosis.
Erosive form (feline progressive polyarthritis):
● Chronic progressive polyarthritis has prolifera-
LOCALIZED TETANUS
tive and deforming subtypes.
● Proliferative form occurs in male cats aged
Classical signs
1–5 years.
● Retrograde axonal transport of the toxin ● Deforming type occurs more rarely in older cats.
from an infected focus. ● Severe subchondral bone destruction may occur,
● Can cause paralysis of single limb. leading to joint instability and deformity.
● Usually progresses to generalized tetanus. ● Radiographic signs are similar to those of rheuma-
toid arthritis in other species.
See main references on page 1340 for details (The Cat ● Often associated with feline leukemia virus-
With an Abnormal Third Eyelid). positive cats.
● Mycoplasmal products have been postulated to Differential diagnosis

chronically stimulate immune-mediated diseases
such as deforming arthritis. Infectious arthritides, such as viral infections.
Non-erosive form: (immune-mediated polyarthritis). Causes of weakness and paresis in the cat. See The
● Can be due to systemic lupus erythematosus, chronic
Weak and Ataxic or Paralyzed Cat (page 908).
infection elsewhere, or idiopathic.
● Due to deposition of immune complexes in the syn-
Treatment
ovial membrane which incites an inflammatory
response. Remove the cause if secondary to drug administration
● The inciting agent is usually not identified, but if or chronic infection.
the cat is on medication this may be a potential Treatment consists of immunosuppressive doses of cor-
source and should be discontinued. ticosteroids for several months, or in combination with
chlorambucil at 1.0–1.25 mg/cat once daily, and pred-
Clinical signs nisolone 10–20 mg twice daily until resolution of clin-
ical signs, then slowly taper the dose of prednisolone
Deforming type of progressive polyarthritis has a over 2–4 months. Continue the chlorambucil at the
chronic onset. All other forms tend to be acute onset same dose every other day. Combination of pred-
of lameness and stiffness. nisolone and gold salts (aurothioglucose 1 mg/kg by
Often affects carpus and tarsus more severely than injection once a week) has also been used.
other joints.
Prognosis
Diagnosis Good initial response to drugs, but greater than 50% of
cases are likely to relapse, becoming more refractory to
Radiographic signs in erosive forms show marked treatment.
destruction and deformity of the distal joints often
resulting in luxation or subluxation but with minimal
periosteal proliferation. NEOPLASIA (PRIMARY NEOPLASIA OF
BONE, SYNOVIUM, CONNECTIVE TISSUE
The proliferative form is characterized by periarticu- OR SPINAL CORD AND SECONDARY
lar soft tissue swelling in the early stages, then pro- METASTATIC NEOPLASIA TO DIGITS FROM
gressing to extensive periarticular proliferation. This LUNG CARCINOMAS)
is most frequently seen in the carpi, tarsi and smaller
distal joints. Classical signs
Arthrocentesis preferably done on two or more joints. ● Rarer in the cat than dog.
Joint fluid is generally slightly increased in amount, ● May be acute or insidious onset of
slightly turbid, and with reduced viscosity. Cytology typ- lameness.
ically reveals a non-septic purulent inflammation, with ● Usually associated with swelling at site of
cell counts in the range of 4000–70 000 nucleated neoplasia.
cells/μl, and predominantly non-degenerative neu-
trophils. A variable number of small and large mononu-
clear cells may also be present. Pathogenesis
Joint cultures are negative for bacteria and Primary bone tumors are rare in the cat. Osteosarcoma
Mycoplasma. is the most commonly identified tumor.
Rheumatoid factor, ANA and LE cell tests are consis- Generally occurs in cats older than 10 years.
tently negative.
Primary bone tumors are much less metastatic in the cat
Hematological parameters are generally unremarkable. than the dog.
Metastatic spread from carcinomas to bone is very rare Primary bone tumors in the cat are a lot less aggres-
in the cat, compared to the dog. sive than in the dog and generally not followed with
chemotherapy.
Can get carcinomas of the digits secondary to primary
lung tumors.
Joint neoplasias are very rare in the cat, and are due to
HIP DYSPLASIA
synovial cell sarcomas or other soft tissue sarcomas.
Multiple cartilaginous exostoses or feline osteochondro- Classical signs
matosis can transform to a malignant disease in the cat.
● Usually occurs in Persian and long-haired
Lameness can also occur from nerve sheath tumors of the cats.
plexus or spinal cord, but these are very rare in the cat. ● Usually asymptomatic in cats compared to
dogs.
Clinical signs ● Generally requires only conservative
management.
Can be acute or insidious onset of lameness.
Rarely can be associated with pathological fracture.
Pathogenesis
Usually thickening identified at site of disease, which
may or may not be painful. Congenital disorder of Persian and other long-haired
cats.
Diagnosis Radiographically, see luxation of the coxofemoral joint,
with varying degrees of osteoarthritis present.
Radiographically, will see bone lysis in the meta-
physeal region of long bones, or joint thickening and
proliferation.
Clinical signs
Histopathology is required for definitive diagnosis.
Usually no clinical signs of lameness are seen.
Thoracic radiographs should be taken to demonstrate
primary lung tumor if multiple digits are swollen, or Pain may be exhibited on flexion and extension of the
prior to amputation to rule out metastatic disease. hip joints.
Occasionally may show signs of a stiff gait or lame-
Differential diagnosis ness, which is exacerbated by excessive activity.
Osteomyelitis.
Septic arthritis. Diagnosis
Pain on manipulation of the hip joints in a long-haired
Treatment cat.
If no evidence of metastatic disease, amputation is the Radiographic evidence of hip laxity and osteoarthritis.
treatment of choice.
If a solitary tumor of a digit is present, often this can be
removed and the limb saved. Treatment
Usually conservative management consisting of rest,
Prognosis weight loss and intermittent anti-inflammatory drugs is
all that is required in symptomatic cats.
If no evidence of metastatic disease, then amputation is
often curative, with median survival times greater than If lameness persists femoral head and neck arthroplasty
2 years. results in an excellent prognosis.
OSTEOCHONDROSIS DISSECANS Clinical signs

Vague, progressive hindlimb lameness.
Classical signs
May be bilateral.
● Onset of forelimb lameness in the cat less
than 1 year of age.
Diagnosis
Pathogenesis Radiographically, see radiolucency of the femoral
neck and proximal femoral metaphysis.
Very rare in the cat.
Has been reported as cause of shoulder lameness.
Occurs due to a defect in osteochondral ossification.
Traumatic fracture of the femoral neck.
Clinical signs
Treatment
Insidious forelimb lameness in cats less than 1 year of
age. Femoral head and neck osteotomy.
Pain identified on full extension and flexion of the

shoulder joint. Prognosis
Excellent.
Diagnosis
Radiographically a thickened flap of cartilage or joint FELINE MUCOPOLYSACCHARIDOSIS
mouse can be identified in the shoulder joint.
Classical signs
Treatment ● Rare inherited disorder in Siamese and
Surgical removal of the cartilaginous flap. Siamese cross cats.
● Causes a stiff gait and paraparesis.
Prognosis ● Cats also have a broad maxilla, corneal
clouding, pectus excavatum and
Excellent. neurological abnormalities.
FEMORAL NECK METAPHYSEAL Clinical signs

OSTEOPATHY Rare inherited disorder that occurs as a result of a lyso-
somal enzyme deficiency in Siamese and Siamese cross
Classical signs cats.
● Onset of hindlimb lameness in the cat less Usually present at less than 6 months of age.
than 1 year of age.
Typically have dysmorphic facial features (a broad
maxilla), plump paws (from thickened skin) and
corneal clouding.
Pathogenesis
Generally exhibit a stiff gait and paraparesis with dif-
Uncommon condition.
fuse neurological signs.
Reported in male cats less than 2 years of age.
Also present with a chronic mucoid ocular discharge
Idiopathic necrosis of femoral neck. and chronic respiratory tract infections.
Constellation of clinical signs suggests the diagnosis. Inherited disorder of fold-ear cats.
Radiographs show dysplastic femoral heads and necks Get shortening of the coccygeal vertebrae, metacarpal
and subluxated hip joints. and metatarsal bones and phalanges.
Excessive granulation of neutrophils, and vacuolation They may develop periarticular exostoses and joint
of lymphocytes are suggestive. ankylosis.
Positive urine toluidine test for sulfated beta glycos-
aminoglycans is consistent with diagnosis. PECTUS EXCAVATUM
Definitive diagnosis is via enzyme assays of leukocytes
Classical signs
and skin fibroblasts to demonstrate deficient beta glu-
curonidase activity. ● A congenital disorder characterized by
dorso-ventral flattening of the thorax.
● Kittens and cats show variations in
OSTEOGENESIS IMPERFECTA
respiratory and cardiovascular
abnormalities.
Classical signs
● Also associated with lateral limb deviation.
● A defect in osteogenesis results in multiple
spontaneous fractures.
Clinical signs
● Present with multiple sites of bony pain
due to fractures, or unwilling to ambulate. A deformity of the sternal and costal cartilages result-
● Lameness generally of young cats. ing in narrowing of the thorax.
Occurs as a congenital abnormality of cats, with the
Clinical signs specific cause unknown.
A heritable disease with failure of osteoprogenitor cells Can be associated with the so-called “wimmer’s”syn-
to develop into mature osteoblasts. drome, in which there is lateral deviation of the limbs
and impaired ambulation.
Results in bones that are very brittle and fracture
spontaneously. Kittens and young mature cats < 1 year of age may
show respiratory and cardiovascular abnormalities
Spontaneous fractures can occur in any bones, although
associated with flattening of the thorax.
the long bones are more commonly affected.
Diagnosis
Diagnosis
Based on clinical signs and radiographic findings of
Radiographically the cortical bone is very osteopenic, dorso-ventral flattening of thorax and lateral deviation
with multiple fractures present. of limbs.
SCOTTISH FOLD SPINA BIFIDA

OSTEOCHONDRODYSPLASIA
Classical signs
Classical signs
● Congenital disorder caused by a closure
● Disease affecting cats with at least one defect of the vertebral arches.
fold-eared parent. ● Inherited with the gene for taillessness in
● Lameness generally occurs at 5–6 months Manx cats.
of age.
(continued)
Classical signs—Cont’d They often display an abnormal posture with a stiff

neck and gait.
● Varying degrees of severity of the
condition exist.
Diagnosis
See main references on page 920 for details (The Weak
Radiographically there is ankylosis of cervical and
and Ataxic or Paralyzed Cat).
cranial thoracic vertebra, and new bone proliferation
around shoulder and elbow joints.
Clinical signs History of diet almost exclusively of liver.
Improper closure of the neural tube during embryogenesis
occurs, with varying severity of neurological signs seen
affecting hindlimb function and urinary and fecal control. Treatment
In the Manx cat it is often associated with sacral Correction of the diet, ideally on a balanced commer-
dysgenesis. cial diet.
May require short-term analgesics.
Diagnosis
Prognosis
Based on clinical signs, radiographic findings.
Correction of the diet halts the progression of disease,
and some remodeling of existing bone may occur.
HYPERVITAMINOSIS A However, bony changes are often permanent and pain
may persist.
Classical signs
● Due to excessive intake of vitamin A, NUTRITIONAL HYPERPARATHYROIDISM
usually from an all-liver diet.
● Lameness occurs due to bony exostoses Classical signs
around the cervical vertebrae and ● Lameness present in multiple sites in
ankylosis of joints. young kittens.
● Due to a diet deficient in calcium, such as
an all-meat diet.
Pathogenesis
Due to excessive vitamin A intake over several months, Pathogenesis
usually from an all-liver diet.
Due to increased parathyroid hormone from persistent
Causes bony exostoses of spine and osseous hyper- hypocalcemia, either from an absolute dietary calcium
plasia and proliferation at joint margins, particularly deficiency or secondary to excessive phosphorus intake
the shoulder and elbow joints. relative to calcium.
Excess vitamin A causes increased reactivity of the Causes generalized osteopenia.
periosteum, resulting in bony proliferation at sites of
joint capsule and soft tissue attachments to bone. Most commonly seen in kittens on an all-meat diet.
Occurs with an all-meat diet even if the kittens have
access to milk.
Clinical signs
Clinical signs
Cats are often reluctant to move around, and are very
painful. Osteopenia can result in spontaneous fracture.
Diagnosis Results in osteopenia and widening of the growth

plates.
History of inadequate diet.
Radiographs demonstrate diffuse osteopenia, with or Clinical signs
without folding fractures.
Osteopenia can result in spontaneous fracture.
Treatment Abnormalities of the growth plate with rickets can
cause angular limb deformities.
Correct the diet by adding calcium, or more appropri-
ately, change to a balanced commercial diet formulated
for kittens. Diagnosis
Confine if multiple folding fractures are evident. Diffuse osteopenia, and may see pathological fractures.
With rickets see widened growth plates and osteopenia.
Prognosis
Very good if fractures have not resulted in malunion. Treatment
Residual deformity of the spine and pelvis may result in Correct the diet by feeding a balanced commercial diet,
chronic partial bowel obstruction with constipation. and adequate exposure to light.
May require confinement if multiple fractures have
RICKETS occurred.
Classical signs
Prognosis
● Lameness present in multiple sites in
young kittens. Usually excellent prognosis if there is not abnormal
● Due to a diet deficient in vitamin D or limb angulation. Correction of the diet corrects the
insufficient mineral content, such as an all- underlying osteopenia and growth plate defect.
meat diet.
Pathogenesis
Diet deficient in vitamin D or with insufficient mineral
content causes the cartilaginous matrix of the growth
plate not to calcify.
RECOMMENDED READING
Bojrab MJ. Disease Mechanisms in Small Animal Surgery, 2nd edn. Lea and Febiger, Philadelphia, PA, 1993.
Carro T. Polyarthritis in cats. Comp Continu Edu Pract Vet 1994; 16: 1, 57–67.
Greene CE. Infectious diseases of the dog and cat, 2nd edn. Philadelphia, PA, WB Saunders, 1998.
Slatter D. Textbook of Small Animal Surgery, 3rd edn. WB Saunders, Philadelphia, PA, 2003.
Withrow SJ, MacEwen EG. Small Animal Clinical Oncology, 3rd edn. Philadelphia, WB Saunders, 2001.
CHAPTER NUMBER - CHAPTER TITLE
PART 12
Cat with behavioral problems
46. The cat with aggression

Kersti Seksel
KEY SIGNS
● Body position, piloerection.
● Hissing, spitting.
● Spraying.
● Scratching, biting.
MECHANISM?
● Aggression is a threat, challenge or attack that is directed towards one or more individuals.
● It can be intra- (members of the same species) or interspecific (members of other species).
● Aggression may be normal or abnormal depending on the context.
● Aggression can be overt (active, e.g. obvious distance increasing signals) or covert (passive,
e.g. blocking access).
● Several types of aggression may occur concurrently (see list below).
WHERE?
● The hypothalamus and amygdala are involved in defense and aggression.
● Monoamines and androgenic steroids act as modulators of established offensive and defen-
sive aggressive behaviors.
992
46 – THE CAT WITH AGGRESSION 993
WHAT?
● Currently 11 diagnostic categories of feline aggression are recognized and they may co-occur.
The actual prevalence of each category is unknown.
● Most causes of aggression are the result of the interplay between environmental and genetic
factors, as well as previous experiences (learning).
● Medical conditions and drugs have also been associated with feline aggression.

Diseases causing aggression
● Play aggression** (p 995)
Aggression usually exhibited by young cats with no contact with other cats in early development.
Often directed towards humans, but can be other cats or animals. May involve stalking,
chasing, pouncing and biting (usually inhibited) but rarely vocalization and is directed towards
moving objects.
● Redirected aggression** (p 996)
Aggression directed towards another cat or a human when the original target of the aggression is
not accessible. It is of sudden onset, can be prolonged in duration and usually alters the behavior
of the victim.
● Intercat, intermale aggression** (p 998)
Aggression directed by an entire male cat towards another entire male cat in response to its pres-
ence in the near proximity, and is more common during the breeding season.
● Fear aggression** (p 999)
Aggression seen in a confined or cornered animal, and it is usually preceded by attempts
to escape. Cats can be fearful of people, places, other cats, or various stimuli such as noises
or odors.
● Aggression when patted** (p 1000)
Exhibited towards humans after tactile stimulation of variable duration. It can occur even if the cat
seeks the initial attention.
● Impulse control or status-related aggression** (p 1002)
Aggression directed towards people when the cat is actively or passively prevented from
controlling an interaction or situation. The cat may even initiate contact and demand attention
but then attack.
● Territorial aggression* (p 1003)
Aggression exhibited in response to an intruder, another cat or person, coming into an area in
which the cat has established itself. The cat does not try to avoid encounters with the intruder.
● Pain aggression* (p 1004)
Aggression exhibited in response to a painful stimulus.
● Predatory aggression (p 1005)
Aggression exhibited in response to a natural prey object.
continued
994 PART 12 CAT WITH BEHAVIORAL PROBLEMS
continued
● Maternal aggression (p 1006)

Aggression exhibited in response to the proximity of any human or animal which is perceived as
threatening the kittens.
● Idiopathic aggression (p 1007)
Unprovoked and unpredictable aggression. No underlying cause can be identified and diagnosis is
by exclusion. Very rare in cats.
INTRODUCTION
WHAT?
There are 11 diagnostic categories of aggression – play,
MECHANISM?
redirected, intercat/intermale, fear, aggression when
patted, status related, territorial, pain, predatory, mater-
As a behavioral event, aggression can be both a
nal or idiopathic.
description and a diagnosis.
Most causes of aggression are the result of the inter-
Aggression is a non-specific sign. It may be passive
play between environmental and genetic factors and
(covert) or active (overt) and involve a threat, chal-
previous experience (learning).
lenge or an actual attack.
Medical conditions such as toxoplasmosis, ischemic
Signs may be visual (changes in body posture, piloerec-
vascular problems, hepatoencephalopathy, encephali-
tion), auditory (hissing, spitting), or olfactory (spraying,
tis, meningioma, lead poisoning, arthritis, sensory (hearing
scratching) and may involve use of teeth and/or claws.
and/or sight) deficits, hyperthyroidism, epilepsy, feline
Covert or passive aggression may involve behaviors lower urinary tract disease, feline immunodeficiency
such as staring or sitting in doorways and blocking virus, and rabies have all been associated with feline
access, and as such is often missed by the owners. aggression.
Overt or active aggression may involve more obvious The use of medications such as anesthetic agents and
visual signs such as hissing, spitting growling, swatting corticosteroids has been linked with feline aggression.
and actual fighting.
Careful history taking and physical examination is
Excitation of the ventromedial hypothalamus (VMH) essential in making a diagnosis.
and amygdala leads to a defensive response. ● A complete description of physical location,
● The medial amygdaloid nucleus is involved with body posture, vocal and physical signals, and the
intraspecies aggression. behavior sequences are essential data to make an
● Stimulation of lateral amygdala facilitates preda- accurate diagnosis.
tory attack and defensiveness. More defensive ● Diagnosis may involve complete blood work and
cats have less predatory aggression. radiography to rule out contributing medical factors.
In most behavioral conditions, the underlying patho- Behavior-modifying drugs are increasingly being
genesis is unknown but is likely to be neurochemically used in the treatment and management of behavior
complex. problems in cats. The rationale for using psychotropic
medication is based on their purported neurochemical
WHERE? actions in the brain. Most drugs in common use are not
registered for this purpose in cats. Drugs should always
The hypothalamus and amygdala are involved in
be an adjunct to behavior modification therapy not a
defense and aggression.
replacement.
Monoamines and androgenic steroids act as modula- ● Many classes of medications have been used in
tors of established offensive and defensive aggressive the treatment of behavior problems including anti-
behaviors. histamines, anxiolytics, antidepressants and anti-
convulsants. Medications that may have anxiolytic Diagnosis

actions include the benzodiazepines, tricyclic anti-
depressants (TCAs), antihistamines, azaperones, Based on careful complete behavioral history and thor-
barbiturates, selective serotonin re-uptake inhibitors ough physical examination. Key features include:
● A young cat, that lacked contact with its mother
(SSRIs) and beta blockers.
or conspecifics (other members of its own species)
in the socialization period may be more likely to
CATEGORIES OF AGGRESSION exhibit this type of aggression.
● The behavior occurs when the target is moving at
the time the aggression occurs.
PLAY AGGRESSION**
● The cat does not vocalize and the bites are usually
inhibited.
Classical signs
● Aggression involves stalking, pouncing,
chasing, hiding, laying in wait but rarely Differential diagnosis
vocalizing. Other types of aggression need to be considered.
● May involve biting as well as scratching. ● Predatory aggression may have similar signs and
vocalization rarely occurs in either type of aggres-
sion, however in cases of play aggression, the tar-
Pathogenesis
get is not normally considered prey.
As with most behavioral conditions the underlying ● Redirected aggression may have some signs in
pathogenesis is as yet unknown, but is likely to be neu- common but a lack of history of precipitating events
rochemically complex. and an early environment lacking in social contact
will suggest play aggression. Additionally, cats with
Young cats, possibly orphaned, hand raised or early
play aggression will stalk and lay in wait for their
weaned are most likely to exhibit this type of aggres-
victim whereas this is not usually seen in redirected
sion due to lack of appropriate socialization. Social play
aggression.
is seen between 4–12 weeks of age, and by 14 weeks of
● Status-related aggression may have similar signs
age is replaced by social fighting.
but this is usually seen in cats after social maturity
It is likely to be associated with owner-facilitated (after 2–4 years of age).
learning (that is the owner encourages rough play or
Cats may exhibit several types of aggression concurrently.
attacks) and long-term potentiation or early orphaning
and the absence of appropriate stimuli during the sensi-
tive period for modulating responses. Treatment
The cat should be provided with appropriate toys
Clinical signs
that dangle or move and can be kept at a distance from
The cat may stalk, chase, pounce and lay in wait for people, for example cat dancers™, cat wire toys, or cat
people passing by and rarely vocalizes. The cat may tracks™ on which to pounce and direct these behav-
also bite but the bites are usually inhibited. iors.
● The toys need to be changed at regular intervals,
Targets are usually moving objects or people and
even daily, for the cat to maintain interest.
may be another cat or other animal in the household,
● The cat may need to be taught how to play, and then
especially an older one, in the household.
encouraged to play with toys.
Young cats, especially early weaned, are more likely
Rough play, especially using hands or other body
to show this type of aggression and it may be normal
parts, should be discouraged.
behavior.
● Whenever the cat plays in this manner, play should
It is sometimes difficult to recognize play aggression as be interrupted or suspended.
some cats play more roughly than others and do not ● The cat’s attention should be directed to appropriate
retract their claws when they swat. toys instead.
Direct punishment, such as smacking, may actually The first episode is triggered by a stimulus that the
encourage the behavior and is generally unhelpful and cat is thwarted in its attempts to respond to and may
may lead to other problems, such as fear aggression. be missed.
● The cat is highly aroused and directs its attention onto
Indirect punishment not connected with the owner,
the next person or cat it sees. For example, a cat sees
such as clapping hands, may help to distract the cat and
another cat through the window, it is highly aroused
the owner can then divert attention to a favorite toy.
but is thwarted in its attempts to reach it. Another cat
Provision of a regular routine that involves interac- in the household then enters the room and the cat redi-
tive play time involving toys 2–3 times daily for 5–10 rects the aggression to the second cat.
minutes is important to provide a natural outlet for the
In the second, and subsequent episodes, the initial
behavior.
stimulus no longer has to be present to elicit the
A second kitten, preferably one that is not very young, aggression, just the target of the first attack.
may help to teach appropriate behavior.
Additionally, the behavior of the target also changes.
Often this results in a prolonged conflict, with the sec-
Prognosis
ond cat now acting warily, running away, and showing
Generally favorable if owners are prepared to put in the avoidance behavior, whenever the first cat enters the
time. room or approaches.
Generally decreases with age. The cat is highly aroused and may growl, hiss, pace,
lash its tail, piloerect, have dilated pupils and inflict
serious bites if approached or handled.
REDIRECTED AGGRESSION**
Diagnosis
Classical signs
Possible history of previous encounter with another cat
● Sudden onset of aggression.
or thwarted access to some arousing stimuli (e.g. sight,
● The original target of the aggression (e.g.
sound or smell of another cat or animal, e.g. possum).
other animal or cat outside) is not
accessible. Sudden onset of aggression.
● The cat then directs its aggression towards
Physical examination reveals no evidence of problems,
an unrelated target, a person or another
e.g. pain, middle cerebral artery infarct.
cat, that enters the area soon after.
Pathogenesis
Other types of aggression should be considered.
As with most behavioral conditions underlying patho- ● Intercat, intermale aggression is usually directed
genesis is unknown, but is likely to be neurochemically between entire males in the breeding season.
complex. The ventromedial hypothalamus likely to be ● Territorial aggression is commonly directed
involved and long-term potentiation involving excita- towards a new cat introduced into the household or
tory amino acids and post-synaptic second messenger a visitor. The cat does not try to avoid the perceived
systems may be involved in the repeated displays. intruder and may directly approach.
● Fearfully aggressive cats usually show classic
Cats have been used as models for “kindling”. Once stim-
body postures (lowered body position, piloerection,
ulated, the cells then have a very low threshold for stimu-
flattened ears, etc.) and will give many warning sig-
lation and cats stay reactive and aroused for up to 24 hours.
nals to try to avoid conflict.
● Status-related aggression is usually not of sudden
Clinical signs onset and the cat may initiate contact or attention
but then threatens or attacks.
The eliciting factors of the aggression are different in
the initial and subsequent episodes. Cats may exhibit several types of aggression concurrently.
Treatment ● Benzodiazepines, such as diazepam (0.2–0.4 mg/kg

PO q 12 h – average 1–2 mg/cat PO q 12 h), may be
It is inadvisable to approach any highly aroused cat, necessary for the victim. Care as it can lead to
especially to try to calm or reassure it. The cat should hyperexcitement and has been associated with
be left alone until it is calmer. This may be 24 hours. hepatopathy.
If another cat is involved, then the cats should initially ● Azaperones – Buspirone has been reported to
be separated regardless of whether it is the victim or be helpful in some cases (0.5–1.0 mg/kg PO q
the instigator (the thwarted one). 8–12 h).
● They should be placed in separate rooms so that ● Blood biochemistry analysis should be done prior
they can hear and smell each other, but no visual to medication to determine a baseline especially
contact occurs. for liver and kidney parameters as all are meta-
● The cats should be rotated around all the rooms bolized by the liver and excreted through the renal
until they have distributed their scent in all rooms. system. These parameters should be checked every
● While separated a regular routine should be 6–12 months depending on the age and general
established with each cat so that feeding and play- health status of the cat.
ing occur at a set time each day. Ideally the cats are ● The cats may require medication for a prolonged
fed 5–6 small meals each day. period – up to 6–12 months – and then should be
slowly weaned off.
Treatment then involves slowly reintroducing the cats
to each other (the same way a new cat is introduced The synthetic pheromone, Feliway®, can also be bene-
into the household). ficial. It should be sprayed on 4–6 prominent objects in
● The aim is for them to have a positive association each room at cat nose height for a period of 30–45 days
with each other. This essentially means that “good” and is said to decrease anxiety. A Feliway® diffuser
things such as play or feeding only happen in the plugged into the room in which the cat spends most of its
presence of the other cat. time can also be very helpful. Treatment should continue
● The cats are then slowly reintroduced. Initially they for at least 1 month.
are only in the same room during meal times and If aggression is directed towards a person, the cat
are separated at other times. They are placed in should be avoided in all stimulating circumstances.
cages (or on a cat harness and lead) at opposite ends ● Whenever the cat is calm desensitization and
of the room and are fed at this time. This should counter-conditioning can be used. This means
create a positive association with food and the pres- rewarding the cat (this may involve feeding or
ence of the other cat. playing) for being relaxed in the person’s presence
● If no hissing or spitting occurs and the cats eat the
and walking away if the cat starts to become
food, the cages are gradually brought closer and aroused.
closer to each other over a period of days and meals. ● Punishing the cat will exacerbate the problem as
This may take several weeks or even months. it may lead to even greater arousal.
● Then one cat at a time is allowed out of its cage
to explore and if no aggression occurs then both are
allowed to interact under supervision.
● The re-introduction needs to be slow. Prognosis
Anxiolytic medication may also be needed to treat one Generally good if it is a single event and people can
or both cats. recognize the initiating stimuli and avoid them.
● Tricyclic antidepressants (TCAs) such as
Poor if the aggression is intense, of long duration
amitriptyline (0.5–1 mg/kg PO q 12–24 h, average
and there are multiple stimuli that cannot be identified.
5–10 mg/cat PO q 24 h) or clomipramine (0.5 mg/kg
PO q 12 h) or selective serotonin re-uptake Even though the aggression is of sudden onset it may
inhibitors (SSRIs) such as fluoxetine (0.5 mg/kg take weeks, or even months, for the cats to be success-
PO q 24 h) may be useful for the aggressor. fully reintroduced.
season) and thorough physical examination to rule out

INTERCAT, INTERMALE AGGRESSION**
any concurrent medical conditions.
Classical signs
● Usually seen in entire males at around 2–4 Differential diagnosis
years of age.
Other types of aggression need to be considered.
● May be associated with social role (status)
● Territorial aggression is commonly directed
in neutered cats and tends to appear later.
towards a new cat introduced into the household or
a visitor and is not associated with breeding.
Pathogenesis ● Status-related aggression is more often displayed
Male–male aggression involves hormonal changes towards people and the cat may initiate contact
associated with sexual maturity and neurochemical and then threaten or bite if it cannot control the
changes associated with social maturity. The brain is situation.
masculinized prenatally and the production of tes- Need to recognize what is normal male–male aggres-
tosterone later leads to presence of male behaviors. sion as this may not require treatment.
Aggression also involves limbic system changes and
changes in the serotonin system. Cats may exhibit several types of aggression concur-
rently.
In entire males, intermale aggression usually starts when
they reach social maturity, at around 2–4 years of age,
but may be seen after sexual maturity at 1–3 years of age.
Treatment
In neutered cats, it occurs later and is associated with
Prepubertal and post-pubertal castration reduces or
their social role or status. It is less likely to occur in cats
stops the frequency of fights in about 90% of cases
that were well socialized as kittens.
between entire males.
Clinical signs Treatment may involve changing the social environ-

ment as well as the neurochemical one. Cats in the same
Very common. household should be reintroduced slowly as described
Usually seen in entire males around 2–4 years of age, above for redirected aggression (page 997). It is impor-
but may occur as early as 1 year of age. tant not to try to introduce them too fast or too soon.
● Behavior may be normal male–male aggression Anxiolytic medication may also be needed to treat one
associated with mating. It increases during breeding or both cats to alter the neurochemical environment.
season and with overcrowding. ● Tricyclic antidepressants (TCAs) such as
● In male–male aggression the cat flattens its ears, amitriptyline (0.5–1 mg/kg PO q 24 h, average
howls, hisses, piloerects and uses both the teeth and 5–10 mg/cat PO q 24 h) or clomipramine (0.5 mg/kg
claws in fights. PO q 24 h) or selective serotonin re-uptake
In social aggression the signs depend on the mode and inhibitors (SSRIs) such as fluoxetine (0.5 mg/kg
may be active (threatening) or passive (blocking PO q 24 h) may be useful for the aggressor.
● Benzodiazepines, such as diazepam (0.2–0.4 mg/kg
access). Outright fighting is rare. Cats that have been
well socialized before 12 weeks of age are less likely to PO q 12 h average of 1–2 mg/cat PO q 12 h), may be
fight or inflict serious damage. necessary for the victim. Care as it can lead to hyper-
● May be associated with social role (status) in excitement and has been associated with hepatopathy.
● Azaperones – Buspirone has been reported to be
neutered cats and tends to appear later.
helpful in some cases (0.5–1.0 mg/kg PO q 8–12 h).
● Blood biochemistry analysis should be done prior
Diagnosis
to medication to determine a baseline especially for
Diagnosis is based on a complete behavioral history (an liver and kidney parameters as all are metabolized
entire male cat showing aggression during breeding by the liver and excreted through the renal system.
These parameters should be checked every 6–12 friendly cats, and is affected by the temperament of the
months depending on the age and general health tom. This may account for some fearful behavior seen
status of the cat. in cats.
● The cats may require medication for a prolonged
Inadequate or lack of socialization and handling prior
period – up to 6–12 months – and then should be
to 12 weeks of age may also contribute to the cat’s
slowly weaned off.
responses to people.
The synthetic pheromone, Feliway, can also be bene-
Inadequate or lack of socialization with other cats early
ficial. It should be sprayed on 4–6 prominent objects in
in life may contribute to the cat’s responses to other cats.
each room at cat nose height for a period of 30–45 days
and is said to decrease anxiety. A Feliway® diffuser in Cats learn to be fearful of certain situations, espe-
the room where the cats spend most of their time has cially if they have had a bad experience with no oppor-
also proved useful. tunity to escape (e.g. rough handling, noises, smells at
veterinary hospitals).
Prognosis Inappropriate punishment can also cause fear and
lead to aggression.
Intermale aggression generally responds well to
treatment. It may also be exacerbated by accidental reinforcement,
that is attempting to calm an anxious cat by speaking
Social aggression can be more difficult to treat espe-
softly or stroking and hence rewarding the fearful or
cially if it is very long-standing and getting worse.
aggressive behavior.
Clients need to be able to recognize it early but this is
often difficult with passive (covert) aggression where
the cat just blocks access to areas.
Clinical signs
The prognosis is relatively good with early interven-
Fearful cats will typically hiss, spit, growl, swat, pilo-
tion, and if the cats share the area and different times.
erect, flatten their ears against the head and show a low,
hunched or crouched body position. Additionally, they
FEAR AGGRESSION** may try to flee or attack, depending on the circum-
stances. Pupillary dilation is common and the mouth
Classical signs is open with teeth bared.
● Cats can be fearful of people, places, other Often the behavior is a combination of offence and
cats, or various stimuli such as noises or defense.
odors.
The fearful cat generally will initially attempt to
● The aggression exhibited may be a
avoid the stimulus if that is an option and many warn-
combination of offence and defense.
ing signals are given.
Aggression is usually the last resort but is violent and
Pathogenesis
may become learnt.
As with most behavioral conditions the underlying
pathogenesis is unknown, but is likely to be neuro-
Diagnosis
chemically complex. The amygdala and long-term
potentiation are involved in learning fear, while the The diagnosis is based on a complete behavioral history
forebrain is involved in unlearning fear. The locus and a thorough physical examination to rule out med-
ceruleus (LC), the principal norepinephric nucleus, is ical causes.
involved with supplying the limbic system and hence
A history of exposure to a fear-provoking stimulus,
the “emotional” signs seen with fear.
combined with a description of body language (ears
Genetically two types of cat personality are recog- back, “Halloween” cat) and aggression typify fear
nized – either timid and fearful cats or confident, aggression.
Differential diagnosis ● Tricyclic antidepressants (TCAs) such as

amitriptyline (0.5–1 mg/kg PO q 12–24 h, average of
Other types of aggression should be considered. 5–10 mg/cat PO q 24 h) or clomipramine (0.5 mg/kg
● Redirected aggression may have some signs
PO q 24 h) or selective serotonin re-uptake
in common but different body language and his- inhibitors (SSRIs) such as fluoxetine (0.5 mg/kg
tory of fear-provoking events will suggest fear PO q 24 h) may be necessary.
aggression. ● The cat may require medication for a prolonged
● Although some of the signs are similar cats that
period (up to 6–12 months). Attempts to wean off
exhibit play aggression generally have a more medication should be slow and some cats may need
confident body posture and behavioral history life-long treatment.
and context of the aggression are different. There ● Blood biochemistry should be done prior to
is no stalking or pouncing involved in fear medication to determine a baseline especially for
aggression. liver and kidney parameters as all medications are
● Territorial aggression is usually directed towards
metabolized by the liver and excreted through the
another cat or person and the cat is confident and renal system. If long-term or life-long medication is
approaches the intruder and threatens. Fearfully needed then repeat blood test should be done at
aggressive cats will try to avoid contact. 6–12-month intervals depending on the age and
Cats may exhibit several types of aggression concurrently. general health status of the cat.
The synthetic pheromone, Feliway®, can also be
Treatment beneficial. It should be sprayed on 4–6 prominent
objects in each room at cat nose height for a period of
Depending of the severity of the problem the cat may 30–45 days and is said to decrease anxiety. A Feliway®
need no treatment or may need behavior modification, diffuser in the room in which the cat spends most of
such as desensitization and counter-conditioning, in its time has also proved useful.
combination with psychopharmacological intervention
in severe or long-standing cases. Punishment, or forced restraint will aggravate the
situation and should be avoided. It may increase the
Behavior modification involves desensitization anxiety and impede learning.
and counter-conditioning by slowly introducing the cat
to the fearful situation in a gradual, controlled sequence. Prognosis
● First, the cat is offered a tasty treat such as veg-
emite, chicken, cheese or dehydrated liver. If the cat Prognosis is good if the behavior is of recent onset, the
eats then it is usually a good indication that it is not cat is adult and the fear-eliciting stimuli can be defined.
too anxious. Prognosis worsens if the problem is of long duration
● Then, while the cat is eating, the fearful stimu- or the cat stays aroused or reactive for long periods
lus, such as a person, is gradually introduced at after exposure to the fear-provoking stimulus.
a distance. The initial distance should be great
enough not to cause any fearful response from the The prognosis may be poor if the cat is genetically
cat. timid and there has been no early exposure during the
– If the cat continues to take food the person sensitive period (before 12 weeks of age).
approaches the cat very slowly.
– The time frame for the gradual approach may AGGRESSION WHEN PATTED**
vary from days to months depending on the
severity of the problem. Classical signs
● The cat should not be forced into the fearful situa-
tion as that will exacerbate the fear.
● The cat may suddenly bite or scratch
people after tactile stimulation of variable
Anxiolytic medication may also be needed to treat the duration.
cat to alter the neurochemical environment.
Pathogenesis no stalking or pouncing involved and the aggression

only occurs when the cat is being petted or soon
As with most behavioral conditions underlying patho- after the petting stops.
genesis is unknown, but is likely to be neurochemically ● Status-related aggression has similar signs but will
complex. Long-term potentiation, exitatory amino also be exhibited in other contexts, not just associated
acids, “kindling”, and increased arousal are all con- with petting and it may also involve passive aggres-
tributing factors. sion such as blocking access to rooms, etc.
Some cats have a very low tolerance to being patted ● Pain needs to be considered as an underlying or
or stroked. The cat may even seek out attention and concurrent factor. However, pain aggression may be
jump on the owner’s lap, but still not tolerate long peri- exhibited in other contexts, not just associated with
ods of stroking. petting.
The behavior is reported to be more common in Cats may exhibit several types of aggression concurrently.
unneutered males and is thought to relate to social
grooming behavior. Treatment
It can be a manifestation of status-related aggression. Many of these cats can be taught to gradually toler-
ate longer periods of stroking.
Clinical signs Initially determine how long the cat can tolerate
attention.
The cat may swipe or bite if the petting stops, or if ● If the cat usually tolerates a short period of stimula-
the stroking is carried out for a prolonged period. tion, e.g. 3 minutes, but not 4 minutes the cat should
● Some cats appear to be content just sitting on a lap
be slowly stroked for only 2 minutes, that is the period
as long as no stroking or other tactile stimulation should always be below the cat’s current threshold
occurs. for non-tolerance of stimulation. The cat should
The cat may stiffen, or lash with the tail and may or then be rewarded with food treats.
may not give a warning bite while being patted. ● The time can be gradually increased over a period
of days/weeks until the cat tolerates longer and
Owners are most commonly bitten or scratched on the longer periods. Always stop the stroking prior to
hands and arms. the cat showing signs of arousal.
● The training session should be held at predictable
Diagnosis times each day.
Based on the behavioral history of sudden aggression Punishment is not effective as it tends to lead to more
during petting with no obvious warning but the owner aggression as the cat is already aroused and over-
learns to recognize the signs of twitching and stimulation. stimulated.
Thorough physical examination is essential to rule Anxiolytic medication may also be needed to treat the
out medical causes such as pain due to arthritis, etc., cat to alter the neurochemical environment.
that may cause the cat to resent being handled or der- ● Tricyclic antidepressants (TCAs) such as
matological conditions that may cause irritability or amitriptyline (0.5–1 mg/kg PO q 12–24 h, average
inflammation of the skin. of 5–10 mg/cat PO q 24 h) or clomipramine
(0.5 mg/kg PO q 24 h) or selective serotonin re-
uptake inhibitors (SSRIs) such as fluoxetine
(0.5 mg/kg PO q 24 h) may be necessary.
Other types of aggression such as: ● Blood biochemistry analysis should be done prior
● Although some of the signs are similar cats that to medication to determine a baseline especially for
exhibit play aggression generally have a more liver and kidney parameters as all are metabolized
confident body posture and the behavioral history by the liver and excreted through the renal system.
and context of the aggression are different. There is These parameters should be checked every 6–12
months depending on the age and general health It can also involve behaviors such as soliciting atten-
status of the cat. tion by biting.
● Some cats may require medication for a prolonged
period (up to 6–12 months or even life-long) and
Diagnosis
then should be slowly weaned off if possible.
● Feliway® sprayed on hands before handling may Diagnosis is based on a complete behavioral history
also help decrease arousal. that indicates the aggression occurs in contexts where
the cat is displaying assertive or controlling behaviors.
Prognosis Thorough physical examination is essential to rule
out medical causes such as pain, for example due to
Some cats never learn to like being stroked, and the
arthritis, or dermatological conditions that may cause
safest option is to leave them alone.
irritability or inflammation of the skin that may also
Punishment tends to aggravate the situation and should elicit aggression.
be avoided.
STATUS-RELATED AGGRESSION**
Other forms of aggression including:
● Territorial aggression is usually seen in a different
Classical signs
context and is directed towards another cat or per-
● The cat may try to control territory or son that approaches the defined territory and the cat
people by blocking access to an area. threatens.
● The cat may bite when approached or ● Aggression when patted may be a part of status-
handled yet solicit attention and then bite if related aggression however, that is the only con-
it is or is not given. text in which the behavior is elicited.
● Biting may also occur when the attention ● Although some of the signs are similar in cats that
ceases. exhibit play aggression the behavioral history and
context of the aggression are different. Additionally
in play aggression the cat is younger and there is
Pathogenesis
generally stalking or pouncing involved.
The behavior is about the cat’s need to control specific
Many cats can exhibit several types concurrently.
situations or interactions and may indicate an underling
anxiety. It involves overt as well as covert behaviors.
See expanded section on aggression when patted Treatment
(page 1000).
Identify and then avoid all situations that may be
As with most behavioral conditions underlying patho- provocative, e.g. approaching, stroking, handling.
genesis is unknown, but is likely to be neurochemically
Instigate a behavior-modification program where
complex. The hypothalamus is the primary area
the cat is taught to earn all attention or rewards by
involved with threat displays. There may be genetic as
deferring to the owner.
well as learnt components.
● It has to come or sit at the owner’s request, prior
It may be associated with lack of impulse control. to any interaction with the owner.
● It is not allowed to initiate any interaction. If the
cat does solicit attention the owner should com-
Clinical signs
pletely ignore the cat or walk away.
The cat may bite when the owner attempts to ● No reward/attention is given until the cat defers
approach, lift, move or handle the cat (overt aggression). and responds to the command (e.g. sit or come).
The cat may also block access to areas for example Desensitization and counter-conditioning to handling,
by sitting in doorways and staring (covert aggression). moving, etc., can be done and the cat rewarded for
appropriate acceptable behavior – see aggression when Pathogenesis

patted for details (page 1000).
● If the cat shows any sign of aggression then move
As with most behavioral conditions the underlying
away and stop all interactions. pathogenesis is unknown. There is often an underlying
● Physical punishment should be avoided as that
anxiety component.
will exacerbate the problem. The cat’s territory may be patrolled and can be marked
● Anxiolytic medication may also be needed to treat by rubbing, bunting and/or spraying to maintain social
the cat to alter the neurochemical environment. distance and define hierarchy.
– Tricyclic antidepressants (TCAs) such as
amitriptyline (0.5–1 mg/kg PO q 24 h, average The aggression can be intra- and interspecific (between
of 5–10 mg/cat PO q 24 h) or clomipramine members of the same species or between other species),
(0.5 mg/kg PO q 24 h) have proven useful in including people.
some cases.
– Selective serotonin re-uptake inhibitors (SSRIs) Classical signs
such as fluoxetine (0.5 mg/ kg PO q 24 h) have
also proved useful and can be easier to administer The cat exhibits aggression to anyone approaching
as they are available in a liquid formulation. or entering its territory and may attack.
– Benzodiazepines are generally not recom- The behavior may be more marked in entire toms in
mended as they may disinhibit aggression. the breeding season.
– Blood biochemistry analysis should be done prior
to medication to determine a baseline especially Aggression decreases with increased distance away
for liver and kidney parameters as medications are from the territory.
metabolized by the liver and excreted through the It is often seen when a new cat is introduced into the
renal system. These parameters should be household or the cat returns from a visit to a cattery
checked every 6–12 months depending on the age or veterinary hospital and now is not recognized by
and general health status of the cat. the other cat.
The cat may require life-long medication or for pro-
longed periods of up to 6–12 months. Attempts to slowly Diagnosis
wean off medication may be made.
Diagnosis is based on a complete behavioral history
Prognosis and a thorough physical examination.
The behavior can usually be managed, not cured,

with owner education and compliance. Differential diagnosis
The prognosis is poor if the eliciting stimuli cannot Other types of aggression should be considered including:
be defined, the attacks are severe or people cannot ● Status-related aggression and territorial aggres-
read the cat’s body language. sion may co-exist, however, the contexts in which
territorial behavior is elicited will be different.
Punishment tends to aggravate the aggression and ● Intercat intermale aggression is seen in entire
should be avoided at all times. males during the breeding season, whereas territo-
rial aggression may be seen at other times and may
TERRITORIAL AGGRESSION* be exhibited by males and females.
Classical signs
● The aggressive behavior is directed Treatment
towards intruders approaching or entering
into the cat’s established domain. Avoid situations that may be provocative to avoid
reinforcing the behavior.
● If directed towards another cat within the home they

PAIN AGGRESSION*
may need to be separated - see section on redi-
rected aggression on how to reintroduce (page 997).
Classical signs
Anxiolytic medication may also be needed to treat the
● The cat responds to being handled or
cat to alter the neurochemical environment.
approached in an aggressive manner.
● Tricyclic antidepressants (TCAs) such as
● History of a painful stimulus or elicitation
amitriptyline (0.5–1 mg/kg PO q 12–24 h – average
of pain.
of 5–10 mg/cat PO q 24 h) or clomipramine
(0.5 mg/kg PO q 24 h) or selective serotonin re-
uptake inhibitors (SSRIs) such as fluoxetine
(0.5 mg/kg PO q 24 h) have proved useful in man- Pathogenesis
aging the behavior of the aggressor. This is a defensive behavior and can become fear
● Benzodiazepines, such as diazepam (0.2–0.4 mg/kg
aggression if associated with long-term painful treat-
PO q 12 h – average of 1–2 mg/cat PO q 12 h), may ment or chronic pain.
be necessary for the victim to alter its behavior.
Care with benzodiazepines as they may disinhibit Any source of pain or painful stimulus can lead to the
aggression. cat exhibiting aggression. The stimulus may range from
● Blood biochemistry should be done prior to med- actual handling of a painful area to just patting, groom-
ication to determine a baseline especially for liver ing or trying to medicate the cat.
and kidney parameters. The cat may require med- As with most behavioral conditions the underlying
ication for a prolonged period of up to 6–12 months pathogenesis is unknown. Long-term potentiation asso-
and then should be slowly weaned off. ciated with true pain or circumstances in which the pain
The synthetic pheromone, Feliway®, can also be ben- was originally elicited is likely to be involved.
eficial. It should be sprayed on 4–6 prominent objects
in each room at cat nose height for a period of 30–45 Clinical signs
days and is said to decrease anxiety. A Feliway® dif-
The cat may show signs of offensive (distance increas-
fuser placed in the room that the cats spend most of
ing signals or postures such as staring, swatting with the
their time has also proved helpful.
front paw, growling) or defensive (signals or postures
The cats may need to be permanently separated or such as arched back, piloerection, flattened ears, hiss-
one of the cats may have to be rehomed if the problem ing) aggression and/or avoidance with handling.
is very severe or long-standing.
The signs may be exhibited prior to any manipulation
If directed towards people deny the cat access to or when the cat is approached.
areas that may be guarded. If the cat shows any
signs of aggression then move away and stop all inter- Diagnosis
actions.
Diagnosis is based on a complete behavioral history
Physical punishment should be avoided as it will and a thorough physical examination.
exacerbate the problem.
Hematological and biochemistry analysis and imaging
techniques such as X-ray may be required to make a
Prognosis diagnosis.
May be difficult to treat if long-standing or severe
but it can usually be managed with environmental Differential diagnosis
manipulation.
Other types of aggression should also be considered but
Prognosis is worse if directed towards other cats and is the diagnosis should be able to be made on physical
long-standing and severe. examination and history.
● Status-related aggression or aggression when

PREDATORY AGGRESSION
patted may have similar signs, however, the history
of any painful stimulus or elicitation of pain
Classical signs
should delineate the problem.
● Fearful behavior or aggression may be sec- ● The cat exhibits signs of predatory
ondary to pain. The behavior can then become behavior such as stalking in silence,
learnt. a lowered body posture, crouching and
sudden lunge or pounce when target
Cats may exhibit several types of aggression concur-
moves suddenly but it is directed towards
rently.
non-prey.
Treatment
Pathogenesis
Relieve the source of the pain (appropriate analgesics
Predatory aggression needs to be differentiated
or anti-inflammatory medication as indicated).
from predatory behavior, which is normal and
Treat the anxiety associated with the pain (anxiolytics, instinctive. The focus of predatory aggression (e.g.
e.g. diazepam, tricyclic antidepressants, e.g. amitripty- non-prey item, body part) and outcome (do not eat) are
line – see page 1001 for dose rates). different.
Avoid all accidental reinforcement by patting, telling The cat shows all the contextual behaviors of pre-
the cat “it’s okay” in an effort to calm, especially when datory behavior, stalking in silence, lowered body
the cat is aroused. This may reward aggressive behav- posture, crouching and sudden lunge or pounce when
ior and may prolong the response. target moves suddenly, but it is out of context.
Avoid all potentially painful situations. There are no warning signs and may be directed
towards people as well as other animals.
Some learnt aggression may result. The cat has associ-
ated previous handling with pain, so desensitization As with most behavioral conditions the underlying
and counter-conditioning may also be necessary so pathogenesis is unknown. The hypothalamus is in-
that the cat learns to relax when handled. volved with active biting and attack. Experimentally
● Offer treats when the cat remains relaxed when stimulation of the lateral amygdala facilitates preda-
approached or gently handled. tory aggression. More defensive cats appear to show
● Gradually increase the amount of time and the area less predatory aggression.
that is being manipulated, rewarding for relaxed
and non-aggressive responses.
Clinical signs
Try to prevent the aggression developing by providing
The cat stalks and may lie in wait for the “victim”,
appropriate analgesia with all painful manipulations,
then pounces when the target moves.
especially surgery.
There are no preceding threats.
Avoid punishment as that may exacerbate the
aggression. Although the behaviors are the same as predatory
behavior (normal), the context in which the behaviors
Feliway® may help decrease arousal.
are exhibited make this behavior abnormal.
Prognosis
Diagnosis
Depends on adequacy of the pain relief, as well as dura-
Diagnosis is based on a behavioral history (of sudden
tion of pain and duration of the aggression but gener-
attacks with no preceding threats, that is usually dir-
ally good.
ected towards moving targets), which are not normal prey
Prevent occurrence if possible. and a thorough physical examination.
Differential diagnosis Distracters such as loud noises can be useful when the
owner sees the cat in pre-pounce mode. They should not be
Other types of aggression such as: used as a punishment as that may redirect the aggression.
● Predatory behavior that is directed towards prey
(rodents, birds and although it may be undesirable is This can be a dangerous situation especially when the
normal behavior and should be differentiated from targets are children and the elderly as the cat can
predatory aggression when non-prey are the targets. inflict severe damage. Euthanasia or re-homing
It is instinctive behavior hence difficult to modify. may need to be considered as options.
The cat may not eat the prey item even if caught.
● Play aggression has many of the elements of Prognosis
predatory aggression but the context is different. Good if the cat can be monitored and the behavior
It is also seen more in younger cats that are prac- redirected or the cat confined to prevent access to prey.
ticing their hunting skills and it is more easily
redirected. Not good if the target is a helpless individual and the
● Status-related aggression should also be consid- cat cannot be monitored.
ered however, the silent stalk and pounce is not seen
with status related aggression. MATERNAL AGGRESSION
Classical signs
Treatment ● The queen threatens when she, the kittens

or the nesting are approached. She will
For aggression directed towards prey. attack if cornered.
● Avoid all potentially problematical situations. ● It may involve aggression directed towards
● Confine cat indoors or to a specific area to prevent the kittens.
predation.
● Confine cat outdoors in wire-mesh enclosures, runs
and tunnels. These are being sold as ‘modular cat Pathogenesis
parks’ which are modular enclosures that can be joined
together to provide extensive outdoor enclosures for This occurs in the periparturient period and may
the cat. involve protecting the nest area as well as the kittens.
● Supervise when outside. This is normal behavior if the approach distance is
● Provide appropriate toys for mental stimulation long or generalized. It is due to hormonal influences
and ability to hunt. Vary these on a daily basis. on the hypothalamus, and associated with the pres-
● Put several bells at intervals on the cat’s collar to ence and the proximity of the kittens.
provide warning to prey.
The queen may be aggressive in the presence of male
For aggression directed towards non-prey. cats and this may be related to the fact that free-ranging
● Avoid all potentially problematical situations. males have been reported to commit infanticide.
● Confine cat to a specific room or area to prevent
access to victim, especially at times the cat is most The behaviors seen may also be anxiety related and
likely to exhibit this behavior. hence the neuropathology is the same.
● Put several bells on the cat’s collar at varying
intervals so that the victim has warning signal of the Clinical signs
cat’s presence. This is not always successful but
Generally the queen will hiss and give other long-dis-
worth trying.
tance signals when she, the kittens or the nesting area is
● Redirect the pounce onto toys. When the aggres-
approached.
sion is directed towards people, toys dangled at the
end of a fishing rod, to keep the cat at a distance It usually involves more threats than actual attack and
from the person, can be helpful. usually is directed toward unfamiliar individuals.
Attack tends to be a last resort and occurs if she is Pathogenesis

cornered.
This is a diagnosis of exclusion and very rare.
Some queens may cannibalize their own kittens and
this is considered to be abnormal. It may happen if the It is not well understood and reflects truly abnormal
queen is stressed or malnourished and the incidence has behavior.
been reported to increase if the litter is very large, it is As with most behavioral conditions the underlying
a second pregnancy, or the kittens are ill. However, it pathogenesis is unknown, but is likely to be neuro-
can be normal if the queen eats stillborn or aborted chemically complex. It is a very rare condition and may
fetuses. It may also occur during overzealous eating of reflect seizure activity.
the placenta after birth.
Clinical signs
Diagnosis
Sudden mood changes and aggressive episodes with
Diagnosis is based on the behavioral history of aggres- neither obvious provocation nor predicability.
sion in the presence of kittens and thorough phys-
ical examination to exclude pain or other causes of It has been described as “toggle-switch” aggression as
aggression. it may start suddenly as if a switch has been turned on.
It can stop just as suddenly and the cat may appear to
be unaware of any change in its behavior.
Other types of aggression should be considered such as Diagnosis
territorial, pain and status-related aggression, however
this type of aggression should be easily differentiated Diagnosis is based on a behavioral history of sudden
as it occurs only in queens with kittens in the peri- episodes of unpredictable aggression and thorough
parturient period. physical examination and rule out of all other causes,
both medical and behavioral.
Treatment
All other types of aggression as well as medical
Avoid approaching the queen during this period. causes, such as seizures, should be considered.
Separate the queen from other cats, especially males.
Spey the queen that exhibits infanticide. Treatment
It is difficult to treat using standard behavior-modi-
Prognosis fication techniques because it is truly unpredictable.
● Additionally, avoiding situations that may be
The aggression should resolve when the kittens are
removed from the queen but may recur with the next lit- provocative is not possible as there is no true provo-
ter. cation or obvious context.
Treatment with anticonvulsants such as diazepam or
IDIOPATHIC AGGRESSION phenobarbitone should be considered.
No physical punishment should be used.
Classical signs
● The aggression is unprovoked and Prognosis
unpredictable.
Poor as the underlying cause is not known.
RECOMMENDED READING
Beaver B. Feline Behavior: A Guide for Veterinarians. Philadelphia, PA, W.B. Saunders Company, 2003.
Landsberg G, Hunthausen W, Ackerman L. Handbook of Behavior Problems of the Dog and Cat. Oxford,
Butterworth-Heinemann, 2003.
Overall KL. Clinical Behavioral Medicine for Small Animals. St Louis, Missouri, Mosby, 1997.
Simpson BS, Simpson DM. Behavioral pharmacotherapy. In: Voith VL, Burchelt PL (eds) Readings in Companion
Animal Behavior. Trenton, NJ, Veterinary Learning Systems, 1996, pp. 100–115.
47. The cat with anxiety-related
behavior problems
Kersti Seksel
KEY SIGNS
● Over-grooming (including psychogenic alopecia, feline hyperesthesia and self-
mutilation).
● Pica.
● Inappropriate vocalization.
● Inappropriate elimination (spraying).
MECHANISM?
● Anxiety, fears, phobias, stereotypies and obsessive-compulsive disorder (OCD) are neuro-
chemically related but do not have the same underlying mechanism.
● Anxiety is the anticipation of future danger or misfortune.
● Obsessive-compulsive disorders are constant and repetitive behaviors that appear to serve no
obvious purpose and interfere with the animal’s normal functioning.
● Stress is thought to play a key role in the development of anxiety-related conditions.
WHERE?
● The prefrontal cortex, amygdala and limbic system, and hypothalamus (hypothalamic-
pituitary-adrenal axis) are involved in the regulation of fear.
● Serotonin, norepinephrine, dopamine and GABA are all involved in the development of fear and
anxiety.
● The anatomical focus of OCD is believed to be the limbic system.
WHAT?
● Anxiety-related disorders include excessive self-grooming, changes in appetite and inappropri-
ate elimination (spraying).
1009

Diseases causing anxiety–related behavior problems
PSYCHOLOGICAL
● Over-grooming (including psychogenic alopecia, feline hyperesthesia and self-
mutilation)** (p 1015)
Alopecia diagnosed by exclusion when no underlying medical problem is evident. Hair loss and
saliva discoloration are only evident on parts of the body that can be reached by the teeth and/or
tongue. Plucked hair has microscopic evidence of shear.
● Pica (eating non-food material)* (p 1018)
Ingestion of non-nutritive substances that appear to be of no benefit to the cat.
● Inappropriate vocalization** (p 1017)
Vocalization that is excessive in duration, intensity or frequency that is not associated with other
causes such as pain or symptoms of estrus.
● Inappropriate elimination – spraying*** (p 1012)
Marking of usually prominent vertical areas with or without urine, and often associated with overt
or covert intercat aggression.
Obsessive-compulsive disorders include stereotypies

INTRODUCTION and self-directed behaviors.
● They are constant and repetitive in form, appear to
MECHANISM? serve no obvious purpose, and interfere with the
animal’s normal functioning.
Anxiety, fears, phobias, stereotypies and obsessive-com- ● They are often derived from otherwise normal
pulsive disorder (OCD) are neurochemically related but behaviors like grooming, eating or walking but
probably do not have the same underlying mechanism. are abnormal in that they are excessive in duration,
OCD in humans is classified as a subset of anxiety- frequency or intensity in the context in which they
related disorders. Anxiety is thought to be the common are performed.
factor underlying stereotypic behaviors and OCD.
Stress or anxiety in cats may be manifest as a change in
Anxiety is the anticipation of future danger or appetite (e.g. a decrease in appetite or pica); grooming
misfortune without any obvious cause. The threat may (e.g. increased or decreased); elimination (e.g. spraying
be real or imagined and may be normal or abnormal or non-spraying marking); changes in social inter-
depending on the context. actions (e.g. vocalization); and physical activity (e.g.
● When it is out of context and occurs at a constant and increased or decreased).
elevated level then it is likely to become a problem.
Anxiety is usually accompanied by signs of hypervig- WHERE?
ilance (e.g. scanning), autonomic hyperactivity (e.g.
Positron emission tomography scans indicate biochem-
gastrointestinal upsets) and increased motor activity
ical and structural abnormalities in anxiety, panic
(e.g. pacing).
and OCD.
Anxiety disorders constitute more than 75% of prob- ● The prefrontal cortex, central nucleus of the
lems diagnosed in veterinary patients presented to amygdala, limbic system and hypothalamus (hypo-
behavior clinics. thalamic-pituitary-adrenal axis) are involved in the
47 – THE CAT WITH ANXIETY-RELATED BEHAVIOR PROBLEMS 1011
regulation of fear and anxiety. Long-term potentia- Medical conditions such as hyperthyroidism have
tion of fear and anxiety is a contributing factor. been associated with feline anxiety, as have some
● Serotoninergic, noradrenergic, dopaminergic and medications.
GABA-ergic systems are involved in the development
The longer that these conditions are unrecognized and
of fear and anxiety. The neurotransmitter serotonin
untreated, the more complex they become.
has been identified as a mediator of fear and anxiety.
● The locus coeruleus, which is part of the noradren- Diagnosis is based on a complete behavioral history
ergic system, is involved in the mediation of many and thorough physical examination. It may involve com-
of the physiologic reponses associated with anxiety plete blood work, dermatological and neurological work
such as hypervigilance. up, as well as radiography to rule out contributing or
● The anatomical focus of OCD is believed to be the lim- concurrent medical factors.
bic system. Computed tomography indicates that
the basal ganglia near the caudate nucleus are involved. CONDITIONS CAUSING ANXIETY-
● Dopaminergic, serotonergic and opioid pathways RELATED BEHAVIOR PROBLEMS
are thought to be involved in compulsive and self-
injurious behaviors.
● Aberrant serotonin metabolism and possibly INAPPROPRIATE ELIMINATION-
endorphin metabolism are thought to contribute. SPRAYING***
Increased dopamine in the basal ganglia and a rela-
tive increase in the serotonin metabolite 5-hydroxy Classical signs
indole acetic acid (5-HIAA) in the cerebrospinal ● Urination and/or defecation outside the
fluid (CSF) have also been detected. litter box.
Stress responses are modulated through altered chole-
cystokinin, opioid and dopaminergic mechanisms.
● Physiological measurements of stress include: incre-
Pathogenesis
ased catecholamine levels and resultant tachycardia Elimination problems are the most common behav-
(sympathetic autonomic nervous system); increased ioral problem reported in cats, accounting for between
corticosteroid levels resulting from stimulation of the 40–75% of behavioral problems.
pituitary-adrenal axis; decreased neutrophil/lym-
Both males and females, neutered and entire, present
phocyte ratios; and altered response to adrenocorti-
with elimination problems. They have been reported in
cotropic hormone (ACTH) stimulation test.
all breeds and across all age groups.
Production and release of substance P may also be
Cats that are urinating out of the litter box usually
responsible for some behavioral effects such as saliva-
squat, produce a large quantity of urine, use a hori-
tion and gastrointestinal distress.
zontal surface and often scratch afterwards. In contrast
to marking, urination outside of the litter box is associ-
WHAT? ated with the elimination of waste.
Anxiety can occur after sensitization to a specific Predisposing factors for inappropriate urination
stimulus and then become generalized to other situa- include:
tions. It may also be non-specific in origin. ● Medical conditions such as cystitis, diarrhea, con-
stipation, feline lower urinary tract disease and dis-
Anxious or stressed cats may exhibit a variety of
eases causing polyuria.
non-specific signs such as autogrooming, changed
● Litter box aversion may be due to a new type of
appetite or spraying.
litter or a dirty box. Aversion can also be induced
The following are the most common signs of anxi- by “catching” the cat in the litter box prior to per-
ety exhibited by cats. The actual prevalence of anxi- forming potentially unpleasant procedures such as
ety-related conditions is unknown but they are medicating or grooming.
probably the most common class of disorders in pet ● Litter box location preference can develop. Many
animals. cats prefer to eliminate in quiet or safe places where
they will not be disturbed, e.g. under beds, behind – Hormonal factors. Entire cats spray more than
furniture. They may have learnt to urinate in the neutered cats, and male cats spray more than
location where the litter box was originally placed, female cats.
even though the litter box has now been relocated. – Territorial, agonistic encounters or any highly
● Litter box location aversion can also develop if arousing circumstances.
the cat has an unpleasant experience while in the – Environmental stimuli such as the sight, sound
box. Cats that experience pain while urinating (e.g. or smell of another cat, within the household, as
with cystitis, arthritic pain) may develop an aver- well as outside.
sion to using the litter tray in that location. – Anxiety-related problems including separation
● Substrate preference. Some cats prefer to anxiety, changes in routine (for example, moving
scratch in soft textures or surfaces, others on hard. house), the introduction of a new spouse, new baby
● Substrate aversion. Some cats do not like getting or new cat in the area.
their feet wet or dirty so they will not use soiled lit-
Inappropriate defecation is associated with the
ter boxes. Every cat litter also has a different odor,
elimination of waste.
so many cats develop a preference or aversion to a
particular scent. Predisposing factors for inappropriate defecation
● Fear and anxiety. Separation anxiety can cause include:
elimination problems, and this is usually seen when ● Medical conditions such as cystitis, diarrhea and
the owner is absent. The cat may choose to eliminate constipation have been reported as associated factors.
on the objects associated with the owner, e.g. clothes, ● Cats that experience pain while defecating (e.g.
bedding, briefcases, shoes. It is usually seen after constipation, arthritic pain) sometimes develop an
separation greater than 12 hours, or immediately the aversion to using the litter box.
owner returns. Fearful cats may eliminate where they ● Factors, which predispose to inappropriate urination
are hiding, as often they are too frightened to go to also predispose to inappropriate defecation. These
the litter box. include litter box aversion, litter box location
preference, litter box location aversion, substrate
Spraying is a marking behavior, often associated
preference, substrate aversion, fear and anxiety.
with anxiety. It may be territorial, sexual or agonistic.
Rarely defecation may be a marking behavior.
In multi-cat households it is associated with overt or
covert aggression.
● Cats that spray usually stand, but may squat, usu- Clinical signs
ally produce only a small quantity of urine, fre-
The elimination of urine or feces in an inappropriate loca-
quently use vertical surfaces but may use horizontal
tion. The amount and frequency may also be altered.
surfaces and rarely scratch afterwards.
● It is estimated that 10% of castrated males and 5% Inappropriate elimination is a non-specific sign. It may
of spayed females spray at some time in their life. be associated with a medical condition, fear or anxiety,
Spraying appears to be more common in multi-cat or factors associated with the litter box.
households with a 100% chance of at least one cat
Inappropriate urination or defecation involves the
spraying in a household with more than 10 cats.
cat passing normal amounts of urine or feces outside
Male cats that live with a female cat are more
the litter box.
likely to spray than those living with another male
cat. Spraying or urine marking involves the cat passing
● Predisposing factors include: small amounts of urine usually on vertical objects,
– Medical conditions ranging from those associ- often in response to an anxiety-provoking stimulus.
ated with the urogenital system such as renal
calculi, renal failure and cystitis, as well as viral
Diagnosis
diseases such as FIV and FELV and impacted
anal glands. It is reported that up to 30% of cats Diagnosis is based on a complete behavioral history
that present for spraying may have a concurrent with a finding of inappropriate elimination. A thorough
medical condition. physical examination, hematological and biochemical
analysis, urinalysis, even radiography may be required appropriate openings, over the litter box is help-
to exclude medical causes. ful. Sometimes changing the type of litter box
also helps, such as one with higher or lower sides.
Careful questioning of the owner is important to differen-
– Make the location of the litter box more
tiate urine marking from inappropriate urination. Medical
acceptable to the cat. Place a litter box over the
problems need to be dealt with prior to, or at least con-
area being used by the cat. Then very gradually
currently with, any behavioral therapy that is instigated.
change the location of the litter box until it is in an
The treatment of a non-specific sign such as inappro- area that is more socially acceptable. This may
priate elimination is not acceptable and will ultimately mean gradual increments as small as 5 cm daily.
lead to treatment failures. – Decrease the attractiveness of the area the cat
prefers to use by changing its significance. Most
cats will not eliminate in their feeding or play
areas so try feeding the cat in this spot. Dry cat
Medical problems need to be dealt with prior to, or at food appears to work best as it takes longer to
least concurrently with, any behavioral therapy that is consume. Some very determined cats will eat
instigated. One or several of the following should be con- the food first, then eliminate in the area.
sidered as contributing to the possible underlying causes. Superglueing 8–10 pieces of dried cat food to an
● Medical conditions such as cystitis, diarrhea, consti- old saucer or piece of cardboard and placing it in
pation, feline lower urinary tract disease, diabetes, the cat’s favorite elimination spot will provide a
renal disease and urinary incontinence. long-term stimulus of food.
– Leave the cat’s toys or bedding in the area.
– Confine the cat to a small area to retrain the cat.
Treatment
Only allow access to larger areas gradually once
Treatment of inappropriate urination and/or defe- the cat uses the litter box consistently.
cation. – Make the area less accessible and less pleasant
to the cat by covering the area with thick plastic,
After addressing any medical problem, the treatment
aluminum foil, double-sided sticky tape, Snappy
involves: (1) Increasing the attractiveness of the area
trainers, sandpaper or place trays of marbles in
the owner wants the cat to use, and (2) Decreasing the
the area so the cat cannot get a solid surface on
attractiveness of the area that the cat wants to use.
which to stand.
● Litter box problems. To help make the litter box
– If the cat persists in urinating or defecating
more attractive to the cat:
in the bath tub sometimes leaving a few inches
– Change the type of litter. Alternatives include
of water in the bottom helps to control this behavior.
sawdust, soil, rabbit pellets, shredded newspaper
● For inappropriate elimination related to anxiety,
(or recycled-paper litter), clumping litters, sand
remove or minimize the cause of the anxiety if
or other type of commercial litter. Sometimes
possible. Provide a regular predictable routine,
a combination of substrates is effective. Cats
such as feed and play at a set time each day.
appear to prefer finely textured litter that is not
too heavy (fine sand consistency). Treatment of spraying.
– Try an empty litter box for those cats that prefer ● Owner education of normal cat behavior is impor-
smooth surfaces like bath tubs and sinks. tant so that they understand that the behavior can-
– Increase the frequency with which the litter box not always be eliminated but can be managed.
is cleaned and changed. ● Treatment of any concurrent or underlying medical
– Change the cleaning agent used to clean the lit- problem is essential.
ter box. Do not use disinfectants, try using soapy ● Remove or minimize the cause of the anxiety if
water or water only. possible. Provide a regular predictable routine,
– Increase the number of litter boxes (a good rule such as feed and play at a set time each day.
of thumb is one litter box per cat and one extra). ● Environmental manipulation: This can often be
– Cover the litter box to make it more private for the difficult to achieve in practice, although theoreti-
cat. Often just putting a cardboard box, with cally it should work well. It is rarely possible or
● Tricyclic antidepressants (TCAs) such as:

practical to remove the neighbor’s cat, the new baby,
– Amitriptyline (0.5–1 mg/kg PO q 12–24 h, aver-
or new spouse, or entirely prevent other anxiety-
age of 5–10 mg/cat PO q 24 h).
provoking circumstances such as moving house.
– Clomipramine (0.5 mg/kg PO q 24 h).
However, if possible:
– Nortriptyline (0.5–2.0 mg/kg PO q 12–24 h).
– Decrease the number of cats in the household.
● Selective serotonin re-uptake inhibitors (SSRIs)
– Decrease the access to windows and doors to
such as:
decrease the sight, sound and smell stimuli.
– Fluoxetine (0.5 mg/kg PO q 24 h).
– Change the amount of time spent indoors/outdoors.
– Paroxetine (0.5 mg/kg PO q 24 h) (2.5 mg/cat)
– Prevent access to arousing stimuli.
have been successful in controlling signs in some
– Make the sprayed areas less attractive to the cat
cases.
to spray on by making them feeding or play areas
– Fluvoxamine (0.25 mg/kg PO q 12 h) – concurrent
instead.
use with benzodiazepines should be avoided.
– Feliway®, the synthetic analog of the F3 fraction
● Benzodiazepines such as:
of the cheek gland pheromone of cats, may help
– Diazepam (0.2–0.4 mg/kg PO q 12 h, average
if sprayed daily for 30 days onto soiled areas.
of 1–2 mg/cat PO q 12 h) They affect depth
– A Feliway Diffuser® plugged into the room in
perception, so cats may fall off objects or miss
which the cat(s) spend most of their time has
objects when they jump until they learn to com-
proven to be helpful in decreasing spraying,
pensate. At therapeutic levels, there should be a
especially if inter-cat aggression is contributing
calming effect but little or no effect on motor or
to the spraying.
mental functions. Cats may stagger for the first
Surgery for spraying cats. 1–2 days, but this should then spontaneously
● Neutering the entire cat. Spraying is a marking resolve. If it does not, then the dose should
behavior and in 87% of entire male cats, castration be decreased or withdrawn, as the potential for
alone solves the problem. cumulative effects and toxicity due to the inter-
● Olfactory tractotomy is reported to be effective mediate metabolite may occur. Use with caution
in about 50% of refractory cases in males and in in aggressive animals as diazepam may lead to
most females. The surgical transection of the disinhibition and potentiate aggression. Adverse
olfactory tract causes anosmia (loss of sense of effects usually disappear with a decrease or
smell), which is thought to be an important factor withdrawal of medication. High doses have been
in spraying. This technique is rarely used or rec- associated with increased liver enzymes, hepato-
ommended now. toxicity and convulsions, especially in over-
weight cats.
Pharmacological treatments: These treatments are
– Oxazepam (0.2–0.5 mg/kg PO q 12–24 h) has
generally aimed at reducing the anxiety level of the
been successful in other cases and is useful if
cat by altering the neurochemical environment, and
diazepam produces excessive sedation.
should be used in conjunction with behavioral modi-
● Azaperones.
fication and environmental manipulation techniques.
– Buspirone (0.5–1 mg/kg PO q 8–12 h).
● Potential side effects should be explained to
● Antihistamines.
the owner prior to instigating any therapy, as most
– Cyproheptadine (0.4–0.5 mg/kg PO q 12 h) has
of the drugs are not registered for use in animals.
been reported to be successful in some cases of
Hematological and biochemical analysis should be
spraying.
carried out prior to instigating drug therapy.
Anxiolytic medication should always be gradually Cleaning the soiled areas with non-ammonia-based
withdrawn, never suddenly stopped. products such as enzymatic washing powders is
● Medications that influence serotonin metabolism, important. Products such as Anti-Icky Poo have
such as the selective serotonin reuptake inhibitors also been advocated as successful in eliminating
and the tricyclic antidepressants have been used in odors. Additionally, neutralizers such as Bac to
the treatment of anxiety-related disorders. Anxiolytic Nature used after cleaning can be effective in remov-
medication has also proved useful in some cases. ing the odor.
Punishment is not effective in changing behavior. It Grooming serves many purposes including cleaning,
serves to further increase the anxiety, as well as impede removal of parasites, thermoregulation and alleviation
learning of non-anxious behavior. of stress (e.g. after punishment, intercat aggression).
Multi-cat households: For treatment to be effective Self-licking, biting and hair loss are non-specific signs.
it is essential that a correct diagnosis is made and the
As with most behavioral conditions, the exact patho-
correct cat(s) treated. One way of trying to determine
genesis is unknown but likely to be complex.
which cat is spraying in a multi-cat household is to
● It may be a behavioral response to environmental
administer fluorosceine to each cat in turn. All cats
conditions which stress the cat and result in stereo-
should be tested, as it is not unusual for more than one
typic or obsessive-compulsive behaviors over time.
cat to spray. Place five or six fluorosceine strips (or liq-
– There are numerous reported causes of anxiety
uid) in a gelatin capsule and give once daily for 3–5
in cats which include any environmental
days until the cat(s) is identified. An ultraviolet light
changes such as: moving; a new baby or spouse;
will make it easier for the owner to detect fluorosceine
separation from the owner; too many cats in the
in urine. A washout period of 24–48 hours between
household or area; presence of new cats in the
each cat has been recommended. However, fluoro-
area; loss of territory; punishment from the
sceine is not an infallible way of detecting urine and a
owner; presence of attacking birds (e.g. magpies)
study has shown that the substrate as well as an indi-
and lack of stimulation.
vidual cat’s metabolism will affect detection rates.
● Lowered serotonin and increased dopamine
Additionally, fluorosceine may stain the substrate.
levels are associated with some obsessive-com-
pulsive disorders. Dopamine is also associated
Prognosis
with stress.
The prognosis is generally good for both inappro- Medical conditions such as flea allergy, dietary
priate elimination and spraying. However, it depends allergy, sensitivity to dust mites can trigger the initial
on owner commitment, the success in determining grooming episodes.
the underlying cause, and the ability to manage the
Currently feline hyperesthesia, over-grooming, self-
underlying problem. Prognosis also deteriorates
mutilation and psychogenic alopecia are considered
with increased length of time that the behavior is left
to be part of the anxiety response.
untreated and with recidivistic events.
Owner education of normal feline behavior is essential Clinical signs
to achieve compliance.
Hair can be removed by plucking, barbering or just by
licking and excoriation.
OVER-GROOMING (INCLUDING
Self-licking, biting and alopecia are seen wherever the
PSYCHOGENIC ALOPECIA, FELINE
cat can reach, especially around the sides and rump,
HYPERESTHESIA AND SELF-
back legs and groin. The head and back of neck may
MUTILATION)**
still have a normal hair coat.
● Usually the alopecia is non-symmetrical and the
Classical signs
skin may look normal.
● Hair loss and discoloration only on the ● The hair in the area is a ginger or rusty brown
parts of the body that can be reached by color due to the action of the saliva.
the teeth and tongue.
Microscopic examination of plucked hair shows evi-
● Plucked hair has evidence of shearing.
dence of shear.
● Ulceration and self-mutilation may occur.
In some cats, over-grooming becomes excessive and
self-mutilation and ulceration occur in the affected
Pathogenesis
areas. Secondary bacterial infections may then occur
Normal adult cats spend about 30–50% of their time necessitating treatment. Occasionally, the over-
awake grooming. grooming is so severe that ulcers develop in the mouth
(tongue, pharynx and hard palate) making eating diffi- Remove or minimize the cause of the anxiety if
cult or impossible. Bleeding may occur associated with possible.
hard palate ulcers.
Provide a regular predictable routine, such as feed
In feline hyperesthesia syndrome, cats may become and play at a set time each day. Treatment involves
agitated and aggressive and show skin rippling and altering the neurochemical as well as the physical envi-
muscle spasms, usually over the lumbar area after stim- ronment. Potential side effects should be explained to
ulation such as stroking. They may exhibit frenzied the owner prior to instigating any therapy, as most of
behavior such as licking or biting at the flanks, back or the drugs are not registered for use in animals.
tail or frantic running. ● Medications that influence serotonin metabolism,
such as the selective serotonin reuptake inhibitors
Diagnosis and the tricyclic antidepressants have been used in
the treatment of anxiety-related disorders. Anxiolytic
Diagnosis is based on a complete behavioral history,
medication has also proved useful in some cases.
and thorough physical examination including a com-
The comparative effectiveness of each medication
plete blood count and biochemistry panel.
remains to be evaluated and may depend on elicit-
No evidence of dermatological causes, such as atopy, ing causes.
external parasites, food allergy is identified. ● Tricyclic antidepressants (TCAs) have proved to
be effective.
Microscopic examination of plucked hair has evi-
dence of shear. Hair that is lost due to endocrine con-
age of 5–10 mg/cat PO q 24 h). Start at the low-
ditions has telogen bulbs visible.
est dose and increase after 10 days if no response.
– Clomipramine (0.5 mg/kg PO q 24 h).
Any skin disease causing pruritus should be eliminated. such as fluoxetine (0.5 mg/kg PO q 24 h) have
● External parasites, dermatitis of fungal or bacte- been successful in controlling signs in some cases.
rial origin are differentiated on the basis of derma- Toxicity has been reported in humans when used
tological examination. with cyclosporine.
● Food allergy is differentiated by use of a food ● Benzodiazepines, such as diazepam (0.2–0.4
trial for 6–8 weeks that leads to resolution of signs mg/kg PO q 12 h – average of 1–2 mg/cat PO q 12
when a novel protein such as venison or duck is h) are effective in some cats. Oxazepam (0.2–0.5
introduced. mg/kg PO q 12–24 h) is useful where diazepam
● Endocrine disorders are differentiated on the leads to excessive sedation.
basis of distribution of hair loss that is usually ● Blood biochemistry analysis should be done prior
symmetrical, as well as microscopic examination to medication to determine baseline concentrations
of hair indicating the presence of telogen bulbs. especially for liver and kidney parameters. The cat
● Feline hyperesthesia syndrome is a poorly under- may require medication for a prolonged period
stood condition which may be differentiated on the (up to 6–12 months) and then slow withdrawal of
basis of signs of extreme sensitivity to touch on medication should be attempted. If cats require
the dorsal region, skin rippling, biting or licking of longer-term or lifetime medication, biochemistry
the area with no obvious dermatological or neuro- parameters should be monitored every 6–12 months.
logical basis.
Punishment is not effective in changing behavior. It
● Pain associated with any condition including
serves to further increase the anxiety, as well as impede
trauma or infection is differentiated by response to
learning of non-anxious behavior.
analgesia or alleviation of pain.
Treatment Prognosis
Treatment of any concurrent or underlying medical Prognosis is variable and depends on owner commit-
problem is essential, such as elimination of fleas, or ment, success in determining an underlying cause, and
resolution of food allergy by changing the diet. management of the underlying problem. Prognosis
deteriorates with increased length of time the problem Hyperthyroidism is excluded based on a normal thy-
is left untreated. roxine (T4) concentration.
INAPPROPRIATE VOCALIZATION**
Classical signs Estrus is a normal behavior and may be differentiated
on the basis of the presence of classical behavioral
● Vocalization of increased duration,
signs of restlessness, frequent urination, spraying,
frequency or intensity.
rolling, lordosis, etc., during the breeding season. As
the cat is seasonally polyestrus these will recur on
average every 3 weeks for several months if the cat is
Pathogenesis
not mated.
Excessive vocalization may be a normal innate behav-
Oriental breeds tend to vocalize more than other
ior in some breeds such as the Siamese.
breeds and this is a normal behavior that is differenti-
Vocalization may indicate a need for social contact, ated on the basis of breed.
attention or food. This has been reported in cats that
Vocalizations that are a normal behavioral response
are on restricted-calorie diets.
to physical stressors such as cold and hunger are dif-
Septal, ventral hypothalamic lesions as well as hip- ferentiated on the basis of a thorough history and
pocampal abnormalities have been associated with response to removal of these stressors.
excessive vocalization.
Cognitive dysfunction (aging, senility) is differenti-
Anxiety resulting from social stressors such as the ated on the basis of age (cats are usually more than
presence of other cats, a change in routine, or after a 12 years of age) as well as the presence of other signs
move has been implicated as a trigger. which may include changes in sleep–wake cycles,
decreased social interaction with owners, disorienta-
Excessive vocalization may be a function of aging,
tion, and loss of previously learnt behaviors such as toi-
cerebral degeneration and alteration of neurotransmit-
let training. Cognitive decline is of gradual onset.
ter activity. It may be seen in aged cats exhibiting other
signs of senile behavior. Hyperthyroidism is differentiated on the basis of clas-
sical signs (weight loss, increased appetite, restlessness,
increased vocalization) and elevated T4 concentration.
Clinical signs
Feline hyperesthesia syndrome is a poorly understood
Vocalization is a non-specific sign.
condition which may be differentiated on the basis
With excessive vocalization associated with anxiety, of signs of extreme sensitivity to touch on the dorsal
the vocalization is of changed duration, frequency or region, which stimulates skin rippling, biting or licking
intensity. of the area and often frantic running. Diagnosis is based
on signs and lack of other dermatological or neurolog-
It may be nocturnal, or just more noticeable at night.
ical disease.
It is relatively common in older cats with decreased
Pain associated with any condition including trauma or
perceptual and locomotor abilities. It may also be due
urinary tract infection is differentiated by response to
to reduced cognitive function (senility).
analgesia or alleviation of pain.
● Vocalization may decrease with pain, so it is impor-
Diagnosis tant to know what is normal for the cat.
Diagnosis is based on a complete behavioral history Attention-seeking behavior is differentiated on the
documenting inappropriate vocalization. A thorough basis of a history that is suggestive that vocalization
physical examination, and hematological and biochem- only occurs in the presence of the owner when the
ical analysis must exclude medical causes. owner is not paying attention to the cat.
Travel can induce a panic or fear response in cats, and determine baseline values especially for liver and
this can be differentiated on the basis of history that the kidney parameters. The cat may require medica-
behavior occurs only in these circumstances. tion for a prolonged period (up to 6–12 months).
Gradual withdrawal of medication could be
attempted by reducing the dose by half every 2–4
Treatment
weeks once the symptoms have been successfully
Owner education of normal cat behavior is important controlled for 2–3 months.
so that they understand that the behavior cannot be
Punishment is not effective in changing behavior as it
eliminated but can be managed.
further increases anxiety and impedes learning of non-
Treatment of any concurrent or underlying medical anxious behavior.
problem is essential.
Remove or minimize the cause of the anxiety if possible. Prognosis
Provide a regular predictable routine, such as feed The prognosis is variable. It depends on owner com-
and play at a set time each day. mitment, the success in determining the underlying
cause and the ability to manage the underlying prob-
Environmental enrichment with toys that are changed
lem. Prognosis also deteriorates with increased length
daily, places to hide, and opportunities to play provides a
of time that the behavior is left untreated.
stimulating mental and physical environment for the cat.
Owner education of normal feline behavior is essential
Treatment may also involve altering the neurochemical as
to achieve compliance.
well as the physical environment.
● Medications that influence serotonin metabolism,
such as the selective serotonin reuptake inhibitors and PICA (EATING NON-FOOD MATERIAL)*
the tricyclic antidepressants have been used in the
treatment of anxiety-related disorders. Anxiolytic Classical signs
medication has also proved useful in some cases.
● Abnormal ingestion of non-nutritive
Potential side effects should be explained to the
substances.
owner prior to instigating any therapy, as most of the
drugs are not registered for use in animals.
● Tricyclic antidepressants (TCAs) such as: Pathogenesis
Plant eating may be due to lack of access to grass or
age of 5–10 mg/cat PO q 24 h) or clomipramine
vegetation, or be normal investigatory behavior. Young
(0.5 mg/kg PO q 24 h).
cats especially, may chew, but not necessarily ingest,
non-food substances as part of their normal exploratory
such as:
behavior.
– Fluoxetine (0.5 mg/kg PO q 24 h) have been suc-
cessful in controlling signs in some cases. It may represent obsessive-compulsive disorder
● Benzodiazepines such as: (OCD) with stereotypic chewing or mouth movements.
– Diazepam (0.2–0.4 mg/kg PO q 12 h, average of The chewing is carried out differently from eating food
1–2 mg/cat PO q 12 h) have been successful in items.
others cases. However, benzodiazepines can lead
Neurochemical and neuroanatomical changes are
to increased vocalization in some cats.
seen on positron emission tomography scans with
● The monoamine oxidase inhibitor (MAOI) selegi-
OCD.
line (deprenyl) at 0.5 mg/kg PO q 24 h has been
reported to be effective in some cases for cognitive Wool chewing is a ritualistic or stereotypic behavior.
dysfunction associated with senility. Generally these behaviors are more annoying than
● Blood biochemistry and hematology analysis damaging, unless they start interfering with the animal’s
should be done prior to beginning medication to normal functioning.
● More common in oriental breeds such as Siamese with their molars. Note that some cats just suck the
and Burmese, although it has been reported in all item, and this behavior may be of different origin.
breeds including crossbreeds.
Quite large quantities can be ingested.
● No sex predisposition for wool eating has been
● This is a problem if blankets, socks and sweaters
reported.
are eaten, as there is the potential for intestinal
● Behavior is reported to begin from 2–8 months of
obstruction.
age up to 1–2 years of age.
● It is reportedly more common in cats that are
entirely indoors. Diagnosis
● It can be triggered by stress.
● Hunger stimulates the behavior. Diagnosis is based on a behavioral history of obser-
● Postulated causes include: vation of the ingestion of non-food substances, and
– Early weaning (at 2–4 weeks); in contrast, feral exclusion of other underlying disease. A thorough
cats may suckle until 6 months of age. physical examination including a neurological exami-
– Insufficient handling of kittens before homing. nation should be performed.
– Insufficient fibre in the diet. A complete blood count, and biochemical analysis
– Separation anxiety. including measurement of electrolytes should be per-
– Having no opportunity to develop exploratory formed to exclude medical conditions.
and hunting behaviors.
– A malfunction in the neural control of appetitive Normal serum lead levels.
behavior. Normal thyroxine (T4) concentration.
● Some cats appear to grow out of it and the problem
resolves during early adulthood without treatment.
● Wool chewing and pica appear to be inherited. Differential diagnosis
Wool sucking may be different in that it occurs in Hyperthyroidism is differentiated on the basis of
very early-weaned cats. typical signs (weight loss, increased appetite, rest-
lessness, increased vocalization) and elevated T4
Ingestion of houseplants may occur in cats confined
concentration.
indoors with no access to grass or vegetation. Ingestion
of small amounts of grass or other vegetation is normal Lead poisoning is differentiated on the basis of signs
behavior in cats. of weight loss, inappetence and elevated blood lead
concentration.
Clinical signs Other neurological disease causing pica, such as
encephalitis (e.g. feline infectious peritonitis (FIP) or
Pica may include the ingestion of substances such as
neoplasia, should be excluded based on neurological
soil, rubber, paper, wood, string, houseplants, wool or
examination and other ancillary tests (e.g. CSF analysis).
fabric.
Dietary deficiencies are differentiated by examination
Individual cats tend to ingest one type of substance
of the diet.
only.
Intestinal parasites are differentiated by presence of
Fabric-eating cats appear to start by eating woollen fab-
eggs on fecal flotation.
rics. They may then proceed to other fabrics such as
cotton, silk and synthetics, but this is not always the case. Normal investigative behavior is differentiated on the
● Cats do not appear to like eating raw wool. It is pos- basis of which substances are ingested and the amount
tulated that they do not like the taste or texture of consumed. It is more common in young cats.
the lanolin.
Lack of access to grass or vegetation resulting in
While the cat is chewing it appears to be totally ingestion of small quantities of houseplants is usually
engrossed. They pull and tug on the wool, then grind confined to indoor cats.
Treatment Treatment with psychotropic medication may be

needed if a diagnosis of OCD is made. Potential side
Avoid allowing the cat access to potentially harmful effects should be explained to the owner prior to insti-
ingestible materials. gating any therapy, as most of the drugs are not regis-
Taste deterrents such as bitter apple or chilli can tered for use in animals. Anxiolytic medication should
prove effective and may be more potent if they are always be gradually withdrawn, never suddenly
paired with a distinctive scent such as eucalyptus oil stopped.
or cologne, to provide an additional (olfactory) cue that ● Premedication hematology and serum biochemistry
the material is to be avoided. Thus, the cat learns to analysis is recommended to provide baseline val-
associate the smell of the oil with an unpleasant taste ues, which is especially important if the cat has to
and eventually the scent alone is enough for the cat to stay on long-term or life-time medication. These
avoid the material. This appears to deter some cats if should be repeated every 6–12 months depending
the behavior is of recent origin. on the age and health status of the cat.
● Tricyclic antidepressants such as:
Provide a regular predictable routine to minimize – Amitriptyline (0.5–1 mg/kg PO q 12–24 h, aver-
stress. age of 5–10 mg/cat PO q 24 h). Start at the low-
● Provide set times to interact, play and feed the cat.
est dose and increase if no response seen after
Increase environmental enrichment by providing 10 days.
toys and mental stimulation. – Nortriptyline (0.5–1 mg/kg PO q 12–24 h). This
● Provide an indoor garden with grass, catnip and or is useful if cat is very sedated with amitriptyline.
cat mint as a safe source of vegetation, as well as – Clomipramine (0.5 mg/kg PO q 24 h).
environmental enrichment. ● Selective serotonin re-uptake inhibitors such as:
– Fluoxetine (0.5 mg/kg PO q 24 h) have proved
Other suggestions reported to help are: useful in some cases.
● Allow the cat access to dried food all day.
● A minimum treatment period of 6 months is rec-
● Increase the fiber content of the diet by adding
ommended as some medications may take 6–8 weeks
bran or vegetables. to reach therapeutic levels.
● Provide gristly meat and raw bones to chew on to
– Gradual weaning off medication can be
increase time spent chewing and eating. attempted when the behavior has been success-
● Give small strips of woolen fabric or sheepskin to
fully managed for 3 months. This can be
ingest with their meal. This must ONLY be done under achieved by halving the dose every 2–4 weeks as
veterinary supervision, and the owner warned that it long as the symptoms are still controlled.
could lead to constipation or intestinal obstruction.
Do not use direct punishment as this may increase anx-
Prognosis
iety and exacerbate the problem.
● Environmental punishments such as double-sided Treatment takes time and patience so owner commit-
sticky tape or Snappy trainers may help keep cats ment is essential.
away from some areas. A Snappy trainer is a stan-
Prognosis is guarded if an inherited predisposition
dard mousetrap with a red plastic paddle attached to
is suspected. However, most cases can be success-
the moving lever. When the lever is activated, the
fully managed.
paddle flips over. This is designed to scare the cat
but the paddle prevents injury, because the cat can- Prognosis is good in young cats when signs constitute
not get its paw or face caught in the trap. normal investigative behavior.
RECOMMENDED READING
Beaver B. Feline Behavior: A Guide for Veterinarians. Philadelphia, PA, W.B. Saunders Company, 2003.
Houpt KA. Domestic Animal Behavior for Veterinarians and Animal Scientists. Ames, Iowa State University Press,
1998.
Landsberg G, Hunthausen W, Ackerman L. Handbook of Behaviour Problems of the Dog and Cat. Oxford,
Butterworth-Heineman, 2003.
Overall KL. Clinical Behavioral Medicine for Small Animals. St Louis, Missouri, Mosby, 1997.
Seksel K, Lindeman MJ. Use of clomipramine in the treatment of anxiety-related and obsessive-compulsive disor-
ders in cats. Aust Vet J 1998; 76: 317–321.
Simpson BS, Simpson DM. Behavioral pharmacotherapy. In: Voith VL, Burchelt PL (eds) Readings in Companion
Animal Behaviour. Trenton, NJ, Veterinary Learning Systems, 1996, pp. 100–115.
PART 13
Cat with skin problems
48. The cat with miliary dermatitis

Ruadhri Michael Seosaimh Breathnach and Mike
Shipstone
KEY SIGNS
● Multiple papulocrustous skin lesions.
MECHANISM?
● Miliary dermatitis is a distinct clinical entity, consisting of the presence of multiple papu-
locrustous lesions affecting the skin. Pruritus contributes to lesion development. Alopecia and
secondary infection are common sequelae.
WHERE?
● Skin – widespread papulocrustous lesions can develop in many sites of the body. The precise
location of lesions will vary with the specific condition.
WHAT?
● Most cases of miliary dermatitis are due to hypersensitive reactions, with flea allergy being the
most common. Other causes include ectoparasitism, microbial infections, neoplasia and various
miscellaneous factors such as dietary imbalances, etc.
1022
48 – THE CAT WITH MILIARY DERMATITIS 1023

Diseases causing miliary dermatitis
NUTRITIONAL
● Essential fatty acid or biotin deficiency (p 1041)
Widespread papulocrustous dermatitis. Dry, brittle coat in growing cats. Excess scale formation.
Uncommon in cats on well-formulated diets. History of a poorly formulated diet, or poor storage
conditions leading to rancidity, or prolonged antibiotic therapy.
INFECTIOUS:
Bacterial:
● Staphylococcal dermatitis (p 1041)
Erythema, scale and crustiness. Hair follicles are commonly involved. Papules are common, but
not pus. Primary staphylococcal dermatitis is uncommon in cats.
Fungal:
● Dermatophytes** (p 1032)
More common in young kittens. Erythematous plaques, alopecia and scale. Lesions may
progress to larger gray areas of alopecia and hyper-keratosis.
Parasitic:
● Flea dermatitis*** (p 1025)
Extremely common problem. Pruritus, alopecia and crustiness occur commonly on the dorsal spine
and abdomen. Fleas and/or flea feces may be evident in the coat, but may require careful combing
to find.
● Otodectes cynotis (p 1037)
Papulocrustous dermatitis, often associated with otitis externa. Pruritus, alopecia and secondary
infection. Miliary dermatitis is less common than otic signs.
● Notoedres cati (notoedric mange) (p 1039)
Severe pruritus. Only common in certain geographical areas. Alopecia, hyperkeratosis and gray,
crusty exudate. Secondary infection common.
● Cheyletiella species (cheyletiellosis) (p 1036)
Seborrhea and papules, most marked on dorsum. Mild to moderate pruritus. Movement of mites in
heavy infestations resembles walking dandruff.
● Neotrombicula autumnalis (neotrombiculosis) (p 1038)
Erythema, papules and alopecia. Moderate to marked pruritus. Any contact surface on the body
can be involved. Feet, head and limbs most common sites. Larval stages appear as red-orange dots
to the naked eye.
● Felicola subrostratus (p 1035)
Pruritus, alopecia and occasional secondary infection. Lice and lice eggs may be visible. Often
associated with neglect, malnutrition, matted coats, etc.
continued
1024 PART 13 CAT WITH SKIN PROBLEMS
continued
● Cat fur mite (Lynxacarus radovsky) (p 1040)

Dry, dull coat with scale and scurf. Hairs are easily epilated leading to patchy alopecia. Variable
pruritus. Common sites include tail-head, perineum and thighs. Only common in limited geo-
graphic locations.
IMMUNE-MEDIATED
● Flea allergic dermatitis (FAD)*** (p 1025)
Extremely common cause of miliary dermatitis. Lesions most prevalent along dorsal spine,
caudo-medial thighs and ventral abdomen. Signs may be seasonal or perennial. Pruritis is a clas-
sical feature.
● Adverse food reaction (food hypersensitivity)** (p 1029)
Probably the second most common allergic cause of miliary dermatitis. Results in moderate to
marked pruritus, often involving the head and ears, which is often poorly responsive to corti-
costeroids. Non-seasonal and may mimic many other cutaneous disorders. Concurrent signs of
gastrointestinal or respiratory involvement are usually absent. An affected cat may have been
on diet for some time.
● Atopic dermatitis** (p 1030)
Variably pruritic condition which may present as miliary dermatitis, symmetrical alopecia or
eosinophilic granuloma complex. Secondary infection may occur. Some animals have only alope-
cia, and no history of pruritus or skin lesions. Can be seasonal or perennial. Most common in
young to middle-aged cats.
● Mosquito bite hypersensitivity** (p 1031)
Variable pruritus with lesions most commonly affecting hairless areas of head, nose, ears and pads.
Lesions include papules, crusted papules, plaques, nodules and alopecia. Common in certain geo-
graphical locations.
● Drug reaction/hypersensitivity (p 1034)
Uncommon cause of miliary dermatitis, but can occur in any age group. Signs vary from mild ery-
thema to urticaria to necrosis/sloughing. Variably pruritic. Often mimics many other dermatoses.
Most common signs are erythema, pruritus and self-induced trauma in areas where topical medica-
tions are being applied.
● Intestinal parasite hypersensitivity (p 1035)
Multifocal or generalized papulocrustous reaction pattern. Seborrhea and pruritus. Gastrointestinal
signs occasionally present. Pruritic.
● Auto-immune dermatoses (p 1042)
Primarily a pustular or erosive group of conditions resulting in scale, erosions and alopecia. Face,
ears and feet are common sites. Pruritus and pain are variable.
IDIOPATHIC
● Idiopathic (p 1043)
Papulocrustous dermatitis. Pruritic. Diagnosis of exclusion when all other etiologies ruled-out.
● Other causes include ectoparasitism and microbial

INTRODUCTION infections.
● Neoplasia and various miscellaneous factors such
MECHANISM? as dietary imbalances are possible causes in a small
minority of cats.
Miliary dermatitis is a term used to describe a cuta- ● Diseases covered in The Cat With Pruritus Without
neous reaction pattern in cats consisting of multiple
Miliary Dermatitis may also present with military
papulocrustous lesions. It is important to emphasize
dermatitis and should be considered.
that it is a clinical, not an etiological, diagnosis. Miliary ● Many factors including the history, age of cat,
dermatitis should be suspected when a cat shows evi-
lesion distribution and even geographical location
dence of:
should help to limit the list of differentials in certain
● Multiple papulocrustous lesions on the skin surface.
cases.
● Lesions which typically appear in clusters.
● Alopecia.
● Secondary bacterial infection is sometimes present. DISEASES CAUSING MILIARY
The skin/coat may feel hot and sticky. DERMATITIS
● The mechanism of lesion development is often
inflammatory or immune-mediated in nature, FLEA ALLERGIC DERMATITIS (FAD)***
but can vary with the underlying etiology.
● Pruritus is a significant feature, which contributes
Classical signs
to lesion development. The typical response of cats
to pruritus is to lick or over-groom rather than ● Moderate to severe pruritus, seasonal or
scratch, and it is believed that the barbs on the all year round.
tongue may contribute to lesion development. ● Numerous papules mainly on the dorsum
● Controversy exists as to whether the term miliary and ventral abdomen.
dermatitis should be limited to a few distinct causes, ● Self-trauma leads to alopecia, crustiness,
rather than an exhaustive list of differentials. erosions and secondary infection.
● A definitive etiology is not always apparent, and in ● Because cats are very efficient at
such cases the cat is usually treated symptomatically. grooming the fleas from the coat, fleas or
flea dirt may or may not be seen.
WHERE?
Pathogenesis
Skin: Widespread papulocrustous lesions can develop
in many sites of the body. Ctenocephalides felis is the species most frequently
● The precise location of lesions will vary with the involved in flea allergic dermatitis on a worldwide basis.
specific condition. Other species of flea, including hedgehog and rabbit
● The most common sites affected include the dorsal fleas may be involved.
trunk, flanks, caudo-medial thighs and ventral Flea allergic dermatitis is the most common hyper-
abdomen. sensitive skin disease reported in cats, and has been
associated with many cutaneous reaction patterns,
such as miliary dermatitis, symmetrical alopecia and
WHAT?
feline eosinophilic granuloma complex.
Most cases of miliary dermatitis are due to hyper-
The hypersensitive response develops following bind-
sensitivity reactions.
ing of haptens in flea saliva to dermal collagen.
● Flea allergic dermatitis is by far the most com-
mon underlying etiology of this syndrome. Whilst flea allergic dermatitis can represent both
● Food allergy, atopic dermatitis and other hyper- a type I and type IV hypersensitive reaction in dogs,
sensitive disorders are less common. only the immediate type reaction is currently recog-
nized in cats.
The development of hypersensitivity is not dependent chin. The collected debris should be examined on a
on the number of fleas infesting or biting the host. white piece of paper. The flea feces appear as fine black
fragments, but can be present as fine coils. This will
It is postulated that the presence of atopy may predis-
turn a red/brown (rust) color if water is dropped onto it,
pose to the development of flea allergic dermatitis.
because the major component of the feces is dried
The clinical condition may be seasonal or perennial in blood.
individual animals, depending on geography and other
An intradermal challenge with commercially avail-
environmental conditions.
able flea saliva antigen may be used, with the reaction
being read at 15–20 minutes. The reaction is compared
Clinical signs to a positive and negative control (histamine and phos-
phate-buffered saline). In practice, however, this test
Numerous papules are principally seen on the dorsum,
may be difficult or even impossible to interpret in cats.
caudo-medial thighs, flanks and ventral abdomen,
The presence of a positive test does not confirm flea
though individual lesions can occur in other sites.
allergic dermatitis nor does a negative test rule it out. It
Pruritus is a classical feature. The manifestation merely shows sensitization to the allergen, NOT
of which may be biting, licking, rubbing, chewing, whether or not this sensitization is significant.
scratching or any combination of these. This may be
Blood eosinophilia and skin biopsy may be sugges-
done out of the owner’s view, so tufts of hair in the
tive of flea allergic dermatitis, but are not in themselves
environment, hair caught in the teeth or within the feces
diagnostic.
are clues to pruritus. Self-trauma leads to alopecia,
crustiness, erosions and secondary infection. Serological tests based on such techniques as ELISA
are available, although their sensitivity and specificity
There may be evidence of fleas, or flea feces may be
are still under some investigation. The problem is that
present within the coat.
the incidence of sensitization in normal cats is so high,
Lesions present as a papulocrustous dermatitis with that the positive predictive value of the test is low.
alopecia, and rarely, secondary infection characterized
Response to a strict insect elimination trial may
by pyotraumatic dermatitis.
prove a more reliable means of establishing a retro-
Severely affected animals may be depressed and spective diagnosis. One method is to apply Fipronil
inappetent, with occasional cases showing peripheral spray to the whole body at 0, 2 and 4 weeks and assess
lymphadenopathy. the reduction in pruritus. Greater than 80% improve-
ment confirms the diagnosis. An approximately
Other cutaneous reaction patterns may be evident.
50% improvement shows that insects are a compo-
Some affected cats may also be infested with Dipylidium nent of the problem, and < 30% rules the diagnosis out.
caninum. However, in practice, the percentage improvement may
be difficult to gauge.
Diagnosis
A tentative diagnosis is based on the history and
All of the conditions included in this chapter should be
physical examination. Finding fleas on the cat is not
considered as differential diagnoses. However, flea
essential, although fleas and/or flea feces will be pres-
allergic dermatitis is by far the single most common
ent in some cats. Cats are very efficient at grooming the
cause of this syndrome.
fleas from the coat, and fleas or flea dirt may or may
not be seen. Other differentials which warrant consideration include
atopic dermatitis, food allergy and various ectopar-
Using a fine flea comb is essential in cases of low lev-
asitic and microbial skin infections.
els of infestation, particularly when the coat color is
dark. The comb should be brushed through the entire Response to a strict insect elimination trial as out-
coat including the perineal, inguinal and ventral lined is the first step in the investigative process.
Treatment Depot corticosteroid preparations and megoestrol

acetate are sometimes used when oral therapy is unable
Flea control is vitally important. A wide variety of to be given, but are more likely to be associated with
anti-flea preparations are available, for example, topi- side effects.
cal powders, sprays, spot-on formulations and collars.
Active ingredients that act as adulticides include: Antihistamines may be useful, although they gener-
pyrethrins, organophosphates, fipronil, imidaclo- ally have a slow onset of action and so may need to be
prid, nitenpyram and selamectin. Insect growth combined with prednisolone for the first week or two of
regulators (lufenuron, methoprene, pyriproxyfen) therapy. Chlorpheniramine (2–4 mg q 12 h PO) or
may also be used as part of a complete control program hydroxyzine (2 mg/kg q 12 h PO) are the most com-
to reduce environmental stages of the lifecycle. It is monly used.
essential to treat in-contact dogs and cats because they Topical or systemic antimicrobial therapy may be
may act as reservoirs that will contaminate an environ- used if secondary bacterial infections are present.
ment.
Hyposensitization has been attempted, but to date
The ideal flea control program should include the most reported results have been disappointing. However,
concurrent use of an adulticide to eliminate adult work is continuing with different vaccine antigens and
fleas on the pet, and an insect growth regulator to future results may be more encouraging.
control immature flea stages.
● The easiest adulticide to apply is a monthly “spot
on” application of either fipronil, imidacloprid Prognosis
or selamectin (all have similar therapeutic claims), The prognosis is good but strict flea control must be
together with an insect growth regulator, which maintained life-long or relapses will occur. To date,
may be administered topically (methoprene, hyposensitization results have been disappointing.
fenoxycarb, pyriproxyfen), orally (lufenuron) or as
a depot injection (lufenuron).
● This integrated approach is essential because no
Transmission
adulticide has 100% consistent activity for the Fleas are transmitted principally by contact with an
registered duration of action. This means that infested environment, although some direct animal-to-
viable egg production may begin from day 22 animal transfer is possible. The hypersensitive compo-
after application, although the application interval nent is not contagious.
is 30 days. The modern adulticides (fipronil, imida-
cloprid and selamectin) are only available as prod- Prevention
ucts with a recommended dosing interval of 30
days. Thus, the integrated approach ensures that Adoption of strict flea control measures (see flea
any eggs laid are non-viable, and also delays dermatitis).
development of resistance to both the adulticides Intermittent or long-term alternate day use of pred-
and the insect growth regulators. It also means that nisolone may be required to control clinical signs if the
any infestation picked up through contact with flea control is inadequate.
untreated animals or their environment does not
become established on the treated animal, or con-
tinue to contaminate its environment. FLEA DERMATITIS***
In sick or neonatal animals, simple combing of the Classical signs

coat with a flea comb may be sufficient to remove fleas.
● Lesions on dorsum and ventral abdomen.
Systemic corticosteroids are indicated initially, for ● Pruritus, alopecia, crust formation and
example, prednisolone (1–2 mg/ kg q 24 h for 7–10 secondary bacterial infection.
days), tapering over 7–14 days to 0.25–0.5 mg/kg q 48 h ● Fleas and/or flea feces may be seen but
as required. If good flea control can be achieved, long- may be difficult to find.
term cortisone use is unnecessary.
The movement and blood-sucking activities of fleas Diagnosis is based on clinical signs and finding evi-
leads to irritation, pruritus and self-trauma. dence of fleas. The absence of fleas on examination does
not rule out a diagnosis, because cats are very efficient
Many species can parasitize the cat. Ctenocephalides
at grooming the fleas and flea dirt from the coat.
felis is the dominant species involved.
Fleas may be detected by a methodical examination of
The rabbit flea, Spilopsyllus cuniculi, may cause pinnal
the skin and coat, and with the use of a flea comb. Flea
dermatitis.
feces can be identified by its red-brown color when
Adult C. felis begin feeding immediately on the host. If suspect material is placed onto damp white paper.
reproduction is not disturbed, the female may produce
Evidence of infestation on in-contact animals or in the
up to 50 eggs a day (average 25) and lay for up to 100
environment may be relevant.
days, so the potential for environmental contamination
is large, although the normal grooming habits will sig- Response to a strict insect elimination trial is a reli-
nificantly reduce this. able means of diagnosis.
The lifecycle is typical for insects with an egg, larvae, Flea dermatitis is the result of flea infestation. It does
pupa, and adult stage, and under conditions of ideal not imply or require a hypersensitivity or allergic
temperature and humidity, may occur in as little as 21 response to be developed in the affected animal for lesions
days. However, the duration of the pupal stage is very to occur. The pruritus and self-trauma are related to the
variable and if conditions are not ideal, the flea may irritation of the flea feeding and moving through
rest in the pupae in a dormant state for up to 180 days, the coat.
extending the overall lifecycle to around 200 days.
C. felis acts as the intermediate host for Dipylidium Differential diagnosis
caninum, so the cat may also be infected with tape- Other ectoparasitic, hypersensitive and psychogenic
worms. skin conditions. Response to a strict insect elimination
Many cases of infestation are sub-clinical, but these trial (outlined under flea allergic dermatitis) is the first
animals may act as the reservoir contaminating the step in investigation.
environment for other co-habiting clinically affected
animals. Treatment and prevention
Transmission is via direct contact with an infested A wide variety of anti-flea preparations are avail-
environment, although some direct transfer from an able. See section on flea allergic dermatitis. It is essen-
infested animal may occur. tial to treat in-contact dogs and cats, because they may
act as reservoirs that will contaminate an environment.
Clinical signs In sick or neonatal animals, simple combing of the coat
may be sufficient.
Pruritus and self-trauma occur, and are expressed as
licking or over-grooming rather than scratching. Antibiotics and glucocorticoids may be indicated.
This results in alopecia, crust formation, miliary der-
matitis and secondary infection. Prognosis
Lesions occur mainly along the dorsal, inguinal and Prognosis is excellent with diligent flea control.
ventral abdominal areas. However, re-infestation is common.
Severe infestation may lead to anemia, especially in
young kittens. Transmission
Occasionally, D. caninum segments are identified in Transmission is by direct or indirect contact, but occurs
feces. largely from a contaminated environment.
Peripheral lymphadenopathy is rarely present.

FOOD ADVERSE REACTION (FOOD
HYPERSENSITIVITY)** Signs of adverse food reaction may mimic many other
cutaneous disorders.
Classical signs
● Moderate to marked pruritus, often
involving the head and ears. Diagnosis
● Often poorly responsive to corticosteroids.
Intradermal and scratch testing are of no practical
● Non-seasonal.
benefit in establishing a diagnosis.
● May mimic many other cutaneous
disorders. Serological testing is available, but has a very low pre-
● Concurrent signs of gastrointestinal or dictive index and is not recommended.
respiratory involvement are usually
Feeding a true elimination diet for a period of 6–13
absent.
weeks, and demonstrating recovery, and then relapse
on challenge with the original diet, is the only accurate
Pathogenesis method of making a diagnosis. An accurate dietary
history is essential so that the protein selected for the
Adverse food reaction or food hypersensitivity
diet is one that the cat has never been exposed to.
accounts for 1–2% of feline dermatoses seen in prac-
Depending on the local feeding history this could be
tice, and is probably the second most common allergic
goat, horse, rabbit, kangaroo, duck or venison. This diet
cause of miliary dermatitis.
is fed exclusively for the period of the feeding trial.
Adverse food reactions have been reported to be asso- ● If the condition then markedly improves, the diag-
ciated with both immediate and delayed hypersensi- nosis is confirmed by provocative exposure to the
tive reactions. previously incriminated diet. If the cat is food aller-
gic, a flare in pruritus is expected within 7–10
Ingestion of the offending allergen may occur for
days, although most will flare within 24–48 hours
months to years before there is sensitization and subse-
of exposure.
quent clinical reaction.
● In practice, however, many owners are content to
No sex, age or breed predisposition. simply let their cat remain on the new diet. If this is
done, then they must be warned that the diagnosis
Cats may become sensitized to whatever is being
has not been confirmed, and that any return in the
fed, and so the common allergens will vary with local
clinical signs warrants further investigation for
feeding habits of the country. However, beef, lamb,
other allergic diseases that may have been out of
fish, milk and chicken are most often implicated.
season at the conclusion of the food trial (e.g. atopy,
flea allergic dermatitis).
Clinical signs ● Once the diagnosis has been confirmed by
provocative exposure, the cat can be left on the
The dominant clinical sign is pruritus, the manifesta-
new diet, provided it is complete and balanced.
tion of which may vary from licking, rubbing, biting,
Alternatively, a sequential rechallenge with indi-
scratching through to severe excoriation. Pruritis is
vidual food allergens can be done to try and iden-
often poorly responsive to corticosteroids.
tify the specific food that is causing the problem,
Lesions include erythema, papules, pustules, crusts because in over 90% of cases only 1 or 2 aller-
and ulcers. gens are involved. All the previous diet compo-
nents should be fed sequentially over a short
Whilst any part of the body can be involved, the head
period so that it minimizes the chance of a sea-
and ears are common sites.
sonal change occurring, causing a flare in atopic
Gastrointestinal tract and respiratory signs are dermatitis, which may then erroneously be attrib-
occasionally present. uted to a specific food.
Differential diagnosis Classical signs—Cont’d

All of the conditions included in this section can ● Self-trauma, alopecia and secondary
be considered as differential diagnoses. However, flea infection.
allergic dermatitis is the single most common differen- ● Some animals have only alopecia and no
tial for this syndrome. history of pruritus or skin lesions.
Other differentials which warrant consideration, include ● Seasonal or year round.
atopic dermatitis and various ectoparasitic and
microbial skin infections.
Pathogenesis
The investigation must follow a step-wise process to
eliminate other diseases and confirm the diagnosis. That The precise pathogenesis of atopic dermatitis is not
is, if signs still persist after a strict insect elimination well understood in cats. A genetic predisposition is
trial with control of any secondary infection, a food trial suspected but has not been proven.
is performed. If the clinical signs still persist, then other
Clinical signs may be seasonal or non-seasonal
differentials including atopy must be considered.
depending on the allergen(s) involved.
Most cats first develop clinical signs before 3 years of
Treatment
age.
A nutritionally balanced elimination diet will need
There are no known breed or sex predilections.
to be fed long-term.
● If home-produced diets are to be fed for mainte- The route of entry of the offending allergen(s) is not
nance, they must be properly balanced to meet the well understood, but may include both inhalation and
animal’s long-term nutritional requirements. A home- cutaneous absorption.
prepared diet can be balanced using a meat protein,
A range of allergens including dust mites, grass, weed
combined with a carbohydrate (potato, sweet
and tree pollens and mold spores have been identified
potato, tomato, lentils) supplemented with a bal-
as causing disease. The clinical signs are not related to
anced calcium source (with correct calcium:phos-
the specific allergen sensitivity identified.
phorus ratio), safflower, flax seed oils and a
multivitamin additive.
Alternatively, commercial hypoallergenic diets are Clinical signs
more convenient and provide a nutritionally balanced
diet designed for long-term maintenance. A variety of Some cats with atopic dermatitis have pruritus, papu-
hypoallergenic diets is available including diets using locrustous lesions and/or alopecia.
hydrolyzed protein (e.g. Hills z/d). Other cats are not seen to be pruritic by the owner,
and may have no lesions on the skin but present with a
Prognosis non-inflammatory alopecia. In these cats examination
of the hairs in the affected area will show that they have
The prognosis is excellent. However, some cats may been cropped and have broken ends.
later become hypersensitive to the new diet.
Distribution of lesions is not as well defined as in dogs,
although the face and ears are frequently involved.
ATOPIC DERMATITIS**
Cats may present with a particular cutaneous reaction
Classical signs pattern, such as eosinophilic granuloma complex,
symmetrical alopecia or miliary dermatitis.
● Pruritic dermatosis presenting as miliary
dermatitis, symmetrical alopecia or Occasionally peripheral lymphadenopathy may be
eosinophilic granuloma complex. seen, particularly in cats with miliary dermatitis or
eosinophilic plaques.
Some cats may present with respiratory signs includ- Treatment

ing rhinitis, chronic cough or asthmatic wheeze.
Prednisolone (initial dose 1–2 mg/kg/day for 7–10
days) should be used to control the clinical signs. The
Diagnosis dose may be gradually tapered over 2–3 weeks to
In cats with no history of pruritus, a trichogram and 0.5–1.0 mg/kg q 48 h as required to control clinical
possible trial therapy with an Elizabethan collar signs.
should be considered to ensure the lesions (particularly Antihistamines such as chlorpheniramine (2–4 mg/cat
alopecia and miliary dermatitis) are not self-induced. twice daily) may be effective.
When questioning the owner, all manifestations of pru-
ritus should be described including biting, rubbing, Essential fatty acid supplements of the omega 3 and
licking, biting scratching, as some owners only recog- omega 6 series may help in treatment regimes, particu-
nize or equate scratching with itch. larly if combined with prednisolone or chlorpheniramine.
● A trichogram is collected by plucking hairs using Hyposensitization is often the treatment of choice,
mosquito forceps, padded with tape, from the affected and can be expected to give some control in 60–70% of
area. The ends of the hairs are examined micro- cases. An accurate diagnosis of the offending aller-
scopically for signs of trauma including splitting, gen(s) is essential.
fractures, cropped, squared off ends, rather than a
smoothly tapered end of the undamaged hair. In severe, refractory cases immunosuppressive therapy
using chlorambucil (0.1–0.2 mg/kg q 24 h) has been
Histopathology is not diagnostic. reported, but should only be used where high-dose pred-
Intradermal skin testing is potentially useful using a nisolone (2–3 mg/kg q 24 h) has been unsuccessful.
panel of allergens based on geographical location. All Cyclosporin (5 mg/kg q 24 h for 2–3 weeks and then
tests should include dust mites, but the grass, weed reducing to 5 mg/kg q 48–72 hours) has been effective, but
and pollen selection will depend on the specific loca- large-scale controlled studies have yet to be published.
tion. Allergen manufacturers generally have well-estab-
lished recommendations for specific antigen selection Prognosis
in the USA and Europe. However, it should be empha-
sized that the results of intradermal testing can be diffi- The prognosis is good, although on-going medication
cult to interpret in some cats. or hyposensitization, will be required.
Serological tests (ELISA, etc.) for the detection of If the allergen(s) can be successfully avoided, e.g.
allergen-specific IgE are commercially available, tobacco smoke, then the prognosis is excellent.
although data to confirm the sensitivity and specificity
of many of these tests are often lacking. Prevention
Future episodes may be ameliorated by appropriate
Differential diagnosis medication or hyposensitization.
All conditions included in this section can be consid- Whilst a specific inherited predisposition has not yet
ered as differential diagnoses. been proven in cats, judicious breeding programs may
● Flea allergic dermatitis is the single most common be appropriate.
differential for this syndrome, and should be first
ruled out by a thorough insect elimination trial.
● Adverse food reaction is the next most common
MOSQUITO BITE HYPERSENSITIVITY**
condition, and can be eliminated on the basis of a
strict food trial. Classical signs
● Other differentials which warrant consideration, ● Papules, erosions, crusting and
include various ectoparasitic and microbial skin depigmentation of the nose and pinnae
infections.
Classical signs—Cont’d In mosquito bite hypersensitivity, the presenting lesions

and restriction to the hairless areas of the head and
principally, although the preauricular skin feet are quite characteristic.
may also be affected.
● The footpads may become swollen and Flea allergic dermatitis is the most common differential
develop fissures and scale. for this syndrome. Other differentials, which warrant
● Pruritus is variable. consideration include food hypersensitivity, atopic
dermatitis and various ectoparasitic and microbial
skin infections.
Pathogenesis
Disease is restricted geographically to areas where Treatment and prevention
mosquitoes are endemic, and is more common in
spring and summer in association with an increase in Maintain the cat indoors during the mosquito season
mosquito breeding, and regresses through winter. or at times of potential mosquito feeding.
The condition is seasonal, and involves cats with out- Use suitable mosquito repellents containing dimethyl
door access. metatolilimide (DEET) or put butoxypolyporpon on
areas of the cat likely to be bitten.
Some components appear to involve a type I hyper-
sensitive response. Glucocorticoids can be used judiciously to ameliorate
clinical signs.
Lesions resolve spontaneously when the cat is moved
to a mosquito-free environment.
DERMATOPHYTES**
Clinical signs
Classical signs
All ages and breeds of cat are affected.
● More common in young kittens.
Pruritus is variable, and is not a constant feature. ● Erythematous plaques and scale.
Initial papules and plaques commonly ulcerate and ● Lesions progress and expand to form
crust over. larger grayish areas of alopecia and
hyperkeratosis.
Later lesions include nodules, alopecia, excess scale ● Infection may be sub-clinical.
and depigmentation.
Sites include the bridge of the nose, ears and preau-
Pathogenesis
ricular areas. Other sites include the chin, lips and feet.
The pads are swollen with cracking and scale formation. Dermatophyte species parasitize the superficial kera-
tinized layers of the skin, hair follicles and nails.
Pyrexia, peripheral blood eosinophilia and peripheral
lymphadenopathy may be seen. Microsporum can is is frequently involved in the cat.
Younger or immunosuppressed cats are at particular
Diagnosis
risk.
Diagnosis is based on the response to therapy, or by
Dermatophytes can induce a localized inflammatory or
maintaining the animal indoors. There is no specific
even a hypersensitive response.
laboratory test.
Infection may lead to hyperkeratosis, epithelial
Differential diagnosis hyperplasia and folliculitis. This can result in hair
shaft breakage and alopecia.
All conditions included in this section can be potentially
considered as differential diagnosis. Secondary bacterial infection may occur.
Viable dermatophyte organisms can still be isolated Skin scrapings and hair plucks may allow identifica-
from lesions after clinical resolution. In the case of tion of the spores and fungal hyphae on the outside of
M. canis, viable fungal elements can survive up to 18 the hair shaft. Rarely, fungal hyphae can be identified
months in the environment. on stained acetate preparations of the epidermis overly-
ing lesional skin.
A genetic predisposition is possible in certain breeds
(e.g. Persians). Fungal culture of scrapings, hair plucks and nail sam-
ples can identify the species of dermatophyte involved.
M. canis has a high zoonotic potential, and it has been
reported in 30–70% of cases, that at least one in-contact Biopsies of affected tissue can be collected to allow
human becomes infected in households with infected visualization of dermatophyte hyphae in the follicles or
cats. stratum corneum. This may require special stains to
highlight the fungal elements.
Transmission is via direct contact with infected animals
or indirect contact of contaminated environment or
fomites (bedding, grooming equipment, etc.). Spores Differential diagnosis
have survived in the environment for over a year.
Dermatophytosis is a follicular infection and as such
the major differentials also affect the follicles and
Clinical signs include demodicosis and staphylococcal folliculitis.
The face, head and feet are common initial sites. Differentials for circular areas of alopecia with crust
Raised, erythematous plaques and scale may be seen and inflammation include pemphigus, flea bite hyper-
clinically. sensitivity, food allergy and atopy.
Alopecia develops and lesions expand to form larger

plaques, which appear grayish and hyperkeratotic. Treatment
Initial hair loss occurs in the center of the lesion. Hairs A variety of agents are available for both topical and
on the periphery appear discolored and brittle. systemic treatment of dermatophytosis.
Upon regression, initial hair re-growth appears in the Topical agents include clotrimazole, ketoconazole,
center of the alopecic areas. enilconazole and miconazole.
Secondary bacterial infection is common. Systemic agents include griseofulvin (from 10–50 mg/
kg/day for 4–8 weeks). As this is potentially terato-
Infection that involves the whiskers or nail beds may
genic, it should not be administered to pregnant cats.
lead to deformities of these structures on resolution of
Anemia, leucopenia, vomiting, diarrhea, depression,
the infection.
pruritus, fever and ataxia have been described. This
Infection of deeper tissues may result in nodular skin reaction is thought to be idiosyncratic but may be more
lesions. common and more severe in Persian, Himalayan,
Siamese and Abysinnians and FIV-positive cats. Thus, if
it is used, bone marrow monitoring via complete blood
Diagnosis
tests must be done.
Fluorescence under ultraviolet light (Wood’s lamp),
Ketoconazole (10 mg/kg bid PO) for 4 weeks is also
may detect approximately 30–80% of cases of
effective. Hepatic dysfunction and pregnancy are con-
M. canis infections. The Wood’s lamp must be turned
traindications. Although more expensive, itraconazole
on and warmed up for 5–10 minutes prior to use to
(2.5–5.0 mg/kg bid PO) and fluconazole (10–20 mg/kg
allow the wavelength of light produced to stabilize. The
bid PO) are highly effective and generally less toxic.
affected area is exposed to the light in a dark room for
3–5 minutes. A positive result is a bright apple green Terbinafine (30–40 mg/kg PO sid) is a newer systemic
fluorescence of individual hair shafts, not the scale agent with relatively high efficacy, although treatment
and sebum. may need to be administered for up to 4 months or more.
Although fungal vaccines have not been effective as Classical signs—Cont’d

prophylactic agents in challenge exposure experiments,
data are available to indicate they may be beneficial as ● A wide range of skin reactions is possible,
an adjunct to conventional therapies once clinical dis- varying from urticaria, to erythema
ease has occurred. multiforme to auto-immune skin disease.
● Often mimics many other dermatoses.
Anecdotal reports on the efficacy of lufenuron have not ● Most common signs are erythema, pruritus
been supported by corroborative data. and self-induced trauma in areas where
The hair coat should be clipped in affected cats. In topical medications are being applied.
short-coated cats, clip a 6 cm margin around all
lesions. In long-haired cats, the body should be com-
pletely clipped including the whiskers. The rationale is
Pathogenesis
to remove infective material that would otherwise be Virtually all drugs are capable of inducing an
shed into the environment, and make topical treat- adverse reaction. Reactions to drugs are predictable or
ment easier for the owner. unpredictable. Unpredictable reactions may have an
immunological or genetic basis.
Secondary bacterial infections should be treated with
● Predictable reactions occur when the adverse
appropriate antibacterial therapy.
effects are related to the drug’s mode of action,
and are normally dose-dependent.
Prognosis
● Unpredictable or idiosyncratic reactions are nor-
Prognosis is generally good, but if lesions persist after mally not dose-dependent, and are related to the cat’s
8 weeks of treatment, suspect either a resistant strain, immunological response to the drug, or are the
an underlying systemic disorder that is interfering result of differences in the individual’s suscepti-
with a normal immune response, or that the genetic bility to the drug, commonly because of a metabolic
background of the cat (e.g. Persians) is such that pro- variation, for example an enzyme deficiency.
longed treatment may be necessary.
Predictable reactions include signs such as alopecia
due to corticosteroids or anti-neoplastic drugs.
Prevention
Immunological reactions can be types I, II, III or IV
New animals in catteries should be isolated until con-
hypersensitivity responses.
firmed free of infection.
Some cases of toxic epidermal necrolysis (TEN), ery-
Isolate infected animals. All in-contacts should be
thema multiforme (EM) and systemic lupus erythe-
examined and treated prophylactically with a systemic
matosus (SLE) may have an underlying drug etiology,
medication until all cats are culture negative. This is
but these presentations are rare in cats.
especially important in large pure-bred catteries.
Certain drugs are over-represented in many surveys,
Disinfect premises and potential fomites with undi-
including sulfonamides, penicillins and cephalosporins.
luted bleach (5.25% sodium hypochlorite) or 1% forma-
lin, or dispose of bedding, clothing, grooming combs, etc. Generally, drug reactions occur in the first few
weeks of therapy, and while the drug is still in the
Immunity to dermatophyte infection is not complete at
body. However, exposure and sensitization to the drug
the time of clinical resolution.
could have been in the preceding weeks or months. Re-
exposure in these circumstances can lead to the very
DRUG REACTION/HYPERSENSITIVITY rapid (within hours) development of new lesions.
Classical signs
Clinical signs
● Variably pruritic affecting skin or mucous
membranes. The clinical signs can mimic most, if not all, other
types of skin diseases.
Erythema, papules, plaques, vesicles/bullae and Prognosis

urticaria may be seen initially, and may become annu-
lar or ulcerate. Generally good, unless lesions affect a significant area
of skin, e.g. necrosis.
Necrosis and sloughing of affected skin is possible,
particularly in more severe cases. The prognosis is more guarded for serious systemic
involvement.
The most common morphologic patterns in cats are
contact dermatitis to topical agents, and pruritus
with self-induced traumatic lesions. INTESTINAL PARASITE
HYPERSENSITIVITY
Common sites include the mouth, face, ears, mucocu-
taneous junctions, groin and feet. Classical signs
Pruritus is variable, but can be severe.
● Multifocal or generalized papulocrustous
The extremities may exhibit lesions, including annular reaction pattern.
areas of necrosis and ulceration, particularly if a vas- ● Pruritus.
culitis reaction is involved. ● Seborrhea and urticaria.
Systemic signs including inappetance and pyrexia may
● GI tract signs sometimes exhibited.
be present.
A definitive diagnosis is often difficult to make, and No age, breed or sex predilection is reported.
may only be confirmed retrospectively. Suggestive fac- Pruritus and a papulocrustous reaction pattern,
tors include: either multifocal or generalized is reported.
● Prior history of drug administration.
● The reaction pattern resembles one of hypersensitivity.
Seborrheic dermatitis with erythema, grease and scale
● The clinical signs resolve following withdrawal of
may be present. Urticarial lesions may be present.
the drug. Provocative exposure is theoretically pos- Gastrointestinal tract signs may be present.
sible, but not recommended.
● Histopathology is suspicious, but not diagnostic.
Diagnosis
Differential diagnosis Confirm the presence of intestinal parasites with fecal

tests. Ascarids, hookworms, tapeworms and coc-
All conditions included in this section can be consid- cidia have all been reported causing the disease.
ered as differential diagnoses.
A tentative diagnosis is possible based on resolution
The most common presenting pattern for a drug reac- of skin signs with appropriate anthelminthic therapy.
tion in cats is contact dermatitis, so the index of suspi-
cion should be increased if an animal suddenly
deteriorates, and develops erythema, pruritus and FELICOLA SUBROSTRATUS
self-induced trauma in areas where topical medica-
tions are being applied. Classical signs
● Pruritus, alopecia and occasional
Treatment and prevention secondary infection.
Withdraw the suspect medication. ● Lice and lice eggs may be evident on visual
inspection.
Symptomatic therapy to alleviate signs. ● Cat may be immunosuppressed or have
Do not use the offending drug or any cross-reacting intercurrent disease.
drug in the future in that patient.
Pathogenesis Treatment and prevention

Felicola subrostratus is a biting louse. The adults feed Pyrethrins are commonly used. Ivermectin and
on epithelial debris and hair. fipronil are not licensed for this particular indication, yet
appear to have good efficacy. Organophosphates are less
Pruritus develops as a result of the movement and
popular and have a much lower safety index. Selemectin
feeding behavior of the louse.
is registered for use on cats and should be effective.
Infestation is commonly a disease of poor hygiene,
Repeat treatment is indicated to kill newly hatched
immunosuppression or over-crowding.
eggs.
Cats with matted coats are more at risk.
Grooming equipment and in-contact animals should
Disease is more common in colder months of the year. be treated also.
Transmission is via direct contact with an infested animal Predisposing factors should be addressed. Grooming
or with contaminated bedding or grooming equipment. of the coat is important.
They do not survive for more than a few days off the host.
Prognosis
Clinical signs
Excellent, if predisposing factors are addressed.
Infestation may be sub-clinical, but in most cases pru-
ritus is reported. Alopecia, seborrhea and secondary
infection can develop subsequent to the lice infestation.
CHEYLETIELLA SPECIES
Common sites include body apertures (mouth, anus, (CHEYLETIELLOSIS)
vulva) and under long, matted hair.
Classical signs
The cat may exhibit signs of intercurrent disease.
● Pruritus.
● Seborrhea and papules. Often referred to
Diagnosis
as “walking dandruff”.
Diagnosis is based on finding lice by gross visual ● Most common in young animals.
inspection. Both the adults and eggs are visible.
A hand-held magnifying lens may aid this exercise.
Clear acetate tape can be used to trap and immobilize Pathogenesis
adults for identification microscopically. The lice are
Cheyletiella mites are superficial, surface dwellers
stuck to the acetate tape, which is then adhered to a
that feed on skin debris and are quite mobile.
glass microscope slide for examination.
Cheyletiella blakei is the most common species in cats.
Differential diagnosis The entire life cycle is completed on the host in as lit-
tle as 21–35 days.
All conditions included in this section can be consid-
ered as differential diagnoses. The feeding behavior leads to pruritus and self-trauma.
Flea allergic dermatitis is the single most common A hypersensitive response may develop.
differential for miliary dermatitis and should be ruled
Most common in young animals.
out with a strict insect elimination trial.
Mites are contagious.
Other differentials which warrant consideration include
food hypersensitivity, atopic dermatitis and various These mites are zoonotic and may cause a pruritic,
ectoparasitic and microbial skin infections. papular rash on in-contact people.

Initially, a fine dry scale with minimal pruritus may Prognosis is excellent with appropriate treatment.
be seen along the backline, but with time the pruritus
may become extreme along with an increase in the
Transmission
severity of the scale formation.
Transmission is via direct contact with an infested ani-
Some cats will develop a widespread papulocrustous
mal or with contaminated bedding or grooming
reaction.
equipment. The immature stages do not survive for
The mites are large (~400 μm) and visible to the naked more than a few days off the host, but the adult female
eye. In heavy infection, movement of mites through may survive up to 10 days.
the coat may resemble the appearance of “walking
dandruff ”.
OTODECTES CYNOTIS
Diagnosis
Classical signs
Diagnosis is based on clinical signs and finding the
● Signs of miliary dermatitis may be
mites. Mites and mite eggs may be visible on the skin
accompanied by an exudative otitis
or hair coat with a magnifying glass.
externa.
If mite numbers are low, the chance of success is ● Pruritus, alopecia and secondary infection.
increased by combing the coat with a fine comb. The ● Lesions around head and neck.
collected debris is then examined microscopically for
the presence of mites.
Occasionally, mites have been detected via fecal floata- Pathogenesis
tion techniques as a result of grooming.
Otodectes mites cause irritation because of their
movement and feeding habits. They feed on the
epithelium and tissue fluid from the superficial epi-
dermis. The resultant inflammation leads to pruritus
The differential diagnoses for the early lesions of mild and self-trauma.
scale include ectoparasitism, poor nutrition, dia-
The primary site of infestation is the external ear canal,
betes or hepatic disease.
although ectopic infestations may also be found on other
With more severe pruritus and a papulocrustous erup- areas including the abdomen, neck, rump and tail.
tion, all the differentials for miliary dermatitis need to
Papules and secondary staphylococcal dermatitis
be considered. Combing with a fine comb and exami-
develop on the skin.
nation of the debris microscopically will facilitate a
diagnosis. The life cycle typically takes 3 weeks. Eggs are laid,
and after 4 days hatch to produce a larva which feeds
for 3–10 days. The larva then molts to form a
Treatment and prevention protonymph, and after a short resting phase, the
protonymph molts to form a deutonymph. Adults are
Pyrethrins are effective. Other effective agents include
produced once the deutonymph molts and can survive
sulfur preparations and ivermectin (not licensed).
for approximately 2 months.
Selamectin is registered for cats and should be effec-
tive. Organophosphates are more toxic and should be Sub-clinical infection is common.
used with great care, if at all.
Most cats acquire the infestation as kittens from a car-
In-contact animals should also be treated. rier queen. An entire litter may be affected.
Clinical signs not licensed for this purpose. The systemic medication
is essential in cases (or suspected cases) of ectopic
Many cases present with a waxy otitis externa and infestation, and because of the highly contagious nature
head-shaking due to irritation generated by the mites of mites, all in-contact animals should also be treated.
feeding. Classically the debris has a brown “coffee
ground” appearance. However, the amount of debris Antibacterial treatment, with or without corticos-
can range from minimal to near complete obstruction of teroids, may be indicated to alliviate severe self-trauma.
the canal.
The ectopic infestations can cause pruritus, alopecia, Prognosis
miliary dermatitis and secondary infection which Prognosis is excellent with appropriate treatment.
resembles other allergic disease, but is less common
than otic signs.
Prevention
Diagnosis Repeat treatment of the affected cat and all in-contact
animals is required to prevent reinfection.
Diagnosis is based on clinical signs and finding
the mites. Mites are often visible on otoscopic exami-
nation. Transmission
● Samples of exudate can be examined using magni-
Transmission occurs via direct spread from one cat to
fying glasses, or microscopically on slides to iden- another in most cases, but mites may survive off host
tify mites. for a short period.
Ectopic infestations may not be identified on cytology,
rather a presumptive diagnosis is made on response to NEOTROMBICULA AUTUMNALIS
systemic miticide therapy. (NEOTROMBICULOSIS)
Differential diagnosis Classical signs
The aural manifestation of mites is quite distinct, but

● Pruritus.
other infectious causes of otitis (including bacteria
● Erythema, papules and alopecia.
and malassezia) need to be ruled out.
● Feet, head and limbs commonly involved.
● Larval stages appear as orange-red dots
The ectopic infestation may cause a pruritic dermatitis with the naked eye.
that can resemble flea allergic dermatitis, food hyper-
sensitivity, atopic dermatitis and various ectopara-
sitic and microbial skin infections. Pathogenesis
There are over 700 species of harvest mites, although
only approximately 20 have been identified as causing
Treatment animal disease.
Otitis externa may be treated with drops containing
The adult stages are not parasitic and are free living,
agents such as milbemycin, pyrethrins/piperonyl
feeding on decaying vegetable matter. The six-legged
butoxide, thiabendazole or lindane. Fipronil and imi-
larval stages of the mites are parasitic of animals and
dacloprid have also been reported as effective topical
feed on surface debris.
therapies. If the discharge is marked, the ears may need
to be cleaned with a ceruminolytic first to allow ade- The resultant reaction may give rise to significant self-
quate penetration and dispersion of the miticide. trauma and in some cases a hypersensitivity response
may develop.
Systemic medications that are effective include sele-
mectin and ivermectin (200 μg/kg subcutaneously or More common in summer and autumn, particularly in
orally, repeated 2 weeks later). However, ivermectin is grassy areas or hedgerows.
Larval stages are contracted from gardens, hedges, Prognosis

etc, and are not normally spread from cat to cat.
Prognosis is excellent with appropriate treatment.
However, re-infestation is common if the cat has con-
Clinical signs tinued access to the infested vegetation.
Pruritus occurs, and in some cases is extreme, and
self-trauma. Prevention
Papules, crusted papules, alopecia are common and Repeat courses of treatment are required to combat
secondary infections of the affected areas may also re-infestion.
develop.
Keep cats away from contaminated grass and hedge-
The most common areas affected are in contact with the rows during summer and autumn.
vegetation, so feet, lower limbs, ventrum and the
head are common sites.
NOTOEDRES CATI (NOTOEDRIC MANGE)
Infestation seems to be more common around the head
and ears of cats, but this can be differentiated from Classical signs
Otodectes by the bright red/orange color of the larvae.
● Severe pruritus, with marked secondary
changes.
Diagnosis ● Ears, neck, face and occasionally paws.
● Alopecia, hyperkeratosis and gray, crusty
mite. Larval stages are the size of a pin-head, and are exudate.
a characteristic bright orange-red color, tightly adhered
● Secondary bacterial infection.
to the skin.
The mites may be collected via mild superficial Pathogenesis
scrapes or adhering the mites to acetate tape and trans-
ferring this to a glass microscope slide for examination. The burrowing activity of Notoedres cati produces
mechanical irritation, with resultant inflammation.
Differential diagnosis A hypersensitive response may develop.
All conditions included in this section can be consid- The mites feed on skin debris.
ered as differential diagnoses. N. cati has been reported virtually worldwide in the
Allergies (flea, food and atopy) are the most common, past. However, its occurrence today seems to be very
and can be differentiated by identification of the char- localized or sporadic.
acteristic mites on the skin and at the sites of the papu- Infestation is generally spread via direct contact, and is
locrustous eruptions. highly contagious, so that entire litters may be affected.

Sulfur-containing products are effective. Non-licensed Initial lesions usually appear on the tips and edge of
agents include fipronil and ivermectin. Selemectin is the ears, and then spread over the face and neck.
registered for use on cats, has a similar mode of action
The mites burrow through the superficial epidermis
as ivermectin and should be effective, although no
and this leads initially to the production of very small
efficacy data have been published for this indication.
papules. With time the skin thickens and marked
Organophosphates are less popular because of their tox-
hyperkeratosis develops, which is seen grossly as
icity and low safety index, and should be used with care.
thick scale and crust formation. This may develop a
Corticosteroids may be indicated to relieve pruritus. yellow to gray color.
Pruritus is marked which may lead to self-inflicted

CAT FUR MITE (LYNXACARUS RADOVSKY)
trauma and quite severe excoriation which may then
become secondarily infected.
Classical signs
Less commonly the feet may also be involved.
● Dry, dull coat with hairs easily epilated.
● Excess scale and scurf.
● Tail-head, perineum and thighs affected.
Diagnosis
● Variable pruritus.
mites. The mites are found in burrows in the superficial
Pathogenesis
epidermis. Superficial skin scrapes should be col-
lected: use a blunt scapel blade to remove the surface Lynxacarus radovsky is reported in northern Australia,
scale and crust. This material is transferred to a micro- USA and certain other tropical regions.
scope slide for examination.
All stages of the life cycle are found on the cat.
Biopsy of affected skin may reveal mites or eggs along
Adult and larval stages feed on skin debris and secre-
with non-specific superficial perivascular inflammation.
tions.
The mites generally do not burrow. Hence, lesions are
Differential diagnosis mainly found on the coat.
All conditions included in this section can be consid- Immunosuppression may be a factor.
ered as differential diagnoses.
Transmission is via direct contact, but the contagious
Flea allergic dermatitis is the single most common dif- nature of the mite is variable.
ferential for miliary dermatitis.
Clinical signs
Other differentials which warrant consideration include
food hypersensitivity, atopic dermatitis and various Typically there is scurfiness of the coat. The mites
ectoparasitic and microbial skin infections. appear as white flecks on the hairs, towards the tips
and are best visualized on cats with dark coat colors.
Treatment and prevention The coat is dull and dirty, and the hairs are frail and
easily epilated leading to patchy alopecia. In more
Lime-sulfur dips or shampoos (2.5%) are highly severe cases, a generalized maculopapular to exfolia-
effective. Treatment should be repeated every 10–20 tive dermatitis may develop.
days. Malathion dips (0.25–1.25%) and amitraz
washes (0.025%) are also effective. Lesions common along the lower back and per-
ineal/thigh areas.
Ivermectin (usually at dose levels of 200–300 μg/kg
SC although occasionally at dose levels as high as Pruritus is mild to absent, unless lesions develop on the
1000 μg/kg SC for 2–3 treatments) has been success- skin.
fully used, but is not licensed.
Antibacterial cover and corticosteroids may be indicated. Diagnosis
In-contact animals should be treated if appropriate. Diagnosis is based on clinical signs and finding the
mites. Examination of affected hairs under the micro-
scope reveals adult mites attached to the hair.
Prognosis
Prognosis is excellent with appropriate treatment. In
some cases, an immune response may develop leading All conditions included in this section can be consid-
to resolution of infection, even without treatment. ered as differential diagnoses.
Flea allergic dermatitis is the single most common Diagnosis

differential for this syndrome.
Cytological examination of either acetate prepara-
Other differentials, which warrant consideration, tions or impression smears of the lesions (papules)
include food hypersensitivity, atopic dermatitis and may show the presence of activated (multi-nucleated)
various ectoparasitic and microbial skin infections. neutrophils, along with cocci either extra- or intra-
cellularly. This is the fastest method and may easily
Treatment and prevention be performed in the consultation room.
Lime-sulfur dips are effective, although several dips Culture from infected lesions may be helpful. Care is
may be required. Other routine agents are also effective. required, as most normal cats possess coagulase-posi-
tive staphylococci on their skin.
Selemectin may be effective and ivermectin, whilst not
registered for this use, has been reported as effective. Biopsy may show evidence of bacterial folliculitis,
pyoderma or deeper infection.
In-contact animals may require treatment. Not all in-
contact animals will be infested.
ESSENTIAL FATTY ACID OR BIOTIN
Assess for underlying immunosuppressive diseases. DEFICIENCY
Classical signs
Prognosis
● Widespread papulocrustous dermatitis.
Prognosis is excellent, provided there is no underlying
● Dry, brittle coat, with excess scale.
immunosuppressive disorder.
Pathogenesis
STAPHYLOCOCCAL DERMATITIS
Deficiencies of essential fatty acids (EFA) are uncom-
Classical signs mon. They are reported in animals fed dry diets that
are poorly formulated or inappropriately stored, home-
● Erythema and scale/crustiness.
made recipes, and diets that are poorly preserved. Cats
● Hair follicles often involved.
require arachidonic acid and linoleic acid in the diet.
● Lesions may progress to papules, but pus
is rare. Rancidity may lead to a deficiency of essential fatty
acids, as can a deficiency of antioxidants.
Clinical signs Essential fatty acid deficiency leads to abnormal ker-
atinization, hyperplasia and hyperkeratosis. Clinical
Primary staphylococcal dermatitis is rare in cats.
signs only develop after several months.
Consequently, there may be signs of an underlying
immunosuppressive disease which allows the infection Biotin deficiency can arise from diets rich in uncooked
to develop. eggs or prolonged antibiotic therapy.
There may be erythema and scale/crustiness.
Clinical signs
The hair follicles are usually involved, which com-
Papulocrustous lesions can be seen particularly with
monly leads to papule formation centered on the fol-
biotin deficiency.
licle, so a miliary dermatitis pattern may develop.
Excess scaling, alopecia and a poor hair coat occur
Frank purulent material or pustules are rarely present.
in cats with essential fatty acid deficiency.
Staphylococcal infection may present as abscesses
The skin becomes thick and greasy. Affected sites
or infections of the ears or conjunctiva. Generally the
include the ears, feet and various skin folds.
infections are superficial, involving the epidermis to
superficial dermis, and deeper infections are infrequent. Pruritus and secondary infection occur.
Diagnosis Classical signs—Cont’d

Diagnosis is based on clinical signs and a detailed ● In SLE and discoid lupus erythematosus,
dietary history or food analysis demonstrating defi- lesions consist of exfoliative erythroderma,
ciency of the appropriate dietary component. seborrhea, scale, crusts and alopecia. The
Biopsy is non-specific. face and ears are commonly involved.
All conditions included in this section can be consid- The pathogenesis varies dependent on the form of
ered as differential diagnoses. autoimmune disease present. Many accepted theories
may not be relevant to cats.
Flea allergic dermatitis is the single most common
differential for this syndrome. Pemphigus foliaceus is the most common clinical
form of autoimmune disease in cats.
Other differentials which warrant consideration include ● Tissue is damaged from a type II hypersensitivity
food hypersensitivity, atopic dermatitis and various reaction where IgG or IgM antibody binds to cel-
ectoparasitic and microbial skin infections. lular antigens, resulting in destruction of the cells.
In pemphigus, antibodies are directed against
Treatment intercellular space substances and parts of the
epidermal cell wall. This leads to release of
Rectify the dietary imbalances present, using commer- enzymes causing degeneration of intercellular
cial diets where appropriate. space substances and destruction of the intercellular
Change any feeding practices which predispose to biotin bridges. The result is loss of intercellular adhesion,
or essential fatty acid deficiencies. and break down of the cohesion between neighbor-
ing cells, called acantholysis. Separation of epithe-
Prognosis lial cells occurs causing bullae, erythema, scaling,
crusting, ulceration and tissue proliferation.
Prognosis is excellent with correction of the diet.
In systemic lupus erythematosus (SLE), tissue is
Prevention damaged by a type III hypersensitivity reaction.
Circulating immune complexes composed of IgG or
Feed a well-balanced diet that meets current interna- IgM antibodies bound to antigens diffuse through the
tional standards for feline diets. Store food at appro- vascular endothelium into the tissues and activate the
priate temperatures and use before expiry date. complement cascade. This stimulates migration of
Anticipate possible biotin deficiency if the cat requires mononuclear cells and neutrophils into the area, pro-
prolonged antibiotic therapy and prevent by supple- ducing vasculitis and tissue destruction.
● In SLE, damage to keratinocytes by ultraviolet
menting with a B-group multivitamin including biotin.
light is thought to predispose to antibody formation.
● Damaged keratinocytes release various mediators,
AUTOIMMUNE DERMATOSES which potentiate the inflammatory response.

● Vesico-bullous, pustular or erosive lesions. Pruritus and pain are variable. Many cats with pemphi-
● Erythema, pustules, scale, erosions and gus or discoid lupus erythematosus (DLE) are other-
alopecia in pemphigus foliaceus. wise healthy.
● Common sites include the face, ears, feet,
footpads, groin and nipples. Pemphigus foliaceus presents as erythematous
macules or pustules. The pustules are quite fragile and
may be quite transient and develop to form scale, Differential diagnosis

crusts, erosions, epidermal collarettes and later
alopecia. Occasionally a positive Nikolsky sign may be Differentials for pemphigus include bacterial folliculi-
present. This is considered positive if, when the edge of tis, dermatophytosis, demodicosis which are common,
the lesion is rubbed, the skin is easily peeled/pushed off and discoid lupus and SLE which are much rarer.
the underlying dermis.
Lesions are common on the face, ears, feet, groin Treatment and management
and nipples, but may become generalized. Often the Immunosuppressive doses of prednisolone (2.2–4.4
feet lesions present as a characteristic, thick creamy/ mg/kg orally per day) until complete resolution is
cheesy exudate around the nail beds. achieved. The dose may then be gradually tapered,
Mucocutaneous and oral involvement are rare. reducing the dose by 25% per fortnight in a step-wise
process. Cats that fail to respond to prednisolone may
In SLE, lesions are extremely variable but may include respond to dexamethasone (0.2–0.4 mg/kg q 24 h).
exfoliative erythroderma (generalized erythematous
hue to the skin along with generalized scale), crusts Chlorambucil (0.1–0.2 mg/kg q 24–48 h) has been
and alopecia. The face, pinnae and feet are com- additionally employed in difficult cases.
monly involved. Gold therapy may be useful for refractory cases of
Lesions in discoid lupus erythematosus are similar pemphigus (aurothioglucose 1 mg/kg IM weekly until
to SLE, with the face and pinnae most commonly remission). After remission, the dose is reduced to q 14
affected. Pedal involvement is uncommon. days for 28 days and then to q 28 days for 3 months.
Both chlorambucil and aurothioglucose may cause bone
marrow suppression, and so complete blood counts
should be performed weekly during the induction,
Diagnosis then monthly whilst on therapy.
Cytology of pustular lesions of pemphigus may show Insufficient data are currently available to make any
non-degenerate neutrophils along with rafts of acan- recommendation on the use of cyclosporin in the man-
tholytic keratinocytes (rounded up with a viable agement of feline pemphigus complex.
nucleus).
Cats with discoid lupus erythematosus may respond
Histopathology is the procedure of choice for the to avoiding sunlight, and application of sun-screens
diagnosis of pemphigus, however, it is not always diag- or topical glucocorticoids. If this is unsuccessful, sys-
nostic. Classically, lesions of pemphigus foliaceus will temic medication may be required. Niacinamide
show subcorneal pustules with large numbers of (nicotinamide or vitamin B3) in combination with
acantholytic keratinocytes, and may be associated doxycycline has been used in dogs (but not cats) with
with non-degenerate neutrophils. Discoid lupus ery- variable efficacy. Other alternatives are prednisolone,
thematosus classically shows a superficial lichenoid chlorambucil or aurothioglucose.
inflammatory infiltrate (lymphocytes, plasma cells),
along with hydropic degeneration of the basal epithelial Cats with SLE require systemic immunosuppressive
layer. SLE has a similar histopathologic picture as dis- therapy (prednisolone, chlorambucil).
coid lupus, except that the predominate inflammatory
cell are lymphocytes, there may be thickening of the
Prognosis
basement membrane and vasculitis may be associ-
ated with the inflammation. The long-term prognosis for pemphigus complex and
discoid lupus is generally good.
Tests for antinuclear antibody titers in serum are rec-
ommended for diagnosing SLE. However, most pub- The prognosis for SLE depends on the extent of other
lished data relates to the dog and man. organ system involvement.
results in alopecia, crust formation, miliary dermatitis

IDIOPATHIC MILIARY DERMATITIS
and secondary infection.
Classical signs Lesions occur mainly along the dorsal, inguinal and
ventral abdominal areas.
● Papulocrustous dermatitis.
● Pruritus.
Diagnosis
Clinical signs
Pruritus and self-trauma occur, and are expressed as Diagnosis is based on clinical signs and exclusion of all
licking or over-grooming rather than scratching. This other etiologies after extensive diagnostic work-up.
RECOMMENDED READING
Baker KP, Thomsett LR. Disorders associated with pathogens. In: Canine and Feline Dermatology. Oxford, UK,
Blackwell Scientific Publications, 1990, pp. 95–171.
Foil CS. Dermatophytosis. In: Griffen CE, Kwochka KW, McDonald JM (eds) Current Veterinary Dermatology.
Missouri, Mosby, 1993, pp. 22–33.
Gauguere E, Prelaud P. A Practical Guide to Feline Dermatology. Paris, Merial, 2001.
Moriello K, Mason I. Pruritus in cats. In: Handbook of Small Animal Dermatology. Oxford, Pergamon, 1995,
pp. 153–162.
Pedersen NC. Viral diseases. Parasitic diseases. In: Feline Infectious Diseases. Goleta, CA., American Veterinary
Publications Inc., 1988, pp. 11–15, 347–366.
Quinn PJ, Donnelly W, Carter ME, et al. Diseases of the skin. In: Microbial and Parasitic Diseases of the Dog and
Cat. Philadelphia, PA, W.B. Saunders, 1997, pp. 292–340.
Rosenkrantz WS. Immune-mediated dermatoses. In: Griffen CE, Kwochka KW, McDonald JM (eds) Current
Veterinary Dermatology. Missouri, Mosby, 1993, pp. 141–166.
Scott DW, Miller WH, Griffen CE. Immunologic skin diseases. In: Muller and Kirk’s Small Animal Dermatology,
6th edn. Philadelphia, PA, W.B. Saunders, 2001.
49. The cat with pruritus without miliary
dermatitis
Ruadhri Michael Seosaimh Breathnach
and Mike Shipstone
KEY SIGNS
● Licking or over-grooming.
● Alopecia, erythema.
● + Papules, plaques.
MECHANISM?
● Pruritus in cats usually manifests as licking or over-grooming, rather than scratching or self-
trauma obvious to the owner. In many instances, owners are not aware that the cat is pruritic.
WHERE?
● Skin.
WHAT?
● Diseases presenting with pruritus without miliary dermatitis are most commonly eosinophilic
plaques, poxvirus and neoplasia. However, all the differentials covered in Chapter 48
(The Cat With Miliary Dermatitis) should be considered for a cat that presents with pruritus,
even if no miliary dermatitis pattern is evident.

Diseases causing pruritus without miliary dermatitis
INFECTIOUS
Viral:
● Feline orthopoxvirus infection** (p 1047)
Initial solitary lesion is commonly present on the head or neck. Numerous papules develop later.
Ulceration and scab formation occurs. Alopecia and scarring are evident when the scabs fall off.
Pruritic.
Parasitic:
● Demodicosis (p 1047)
Localized or generalized alopecia of the face and trunk. Erythema and scale. Periocular and nasal
involvement is common. Most cases are non-pruritic.
continued
1045
continued
Neoplastic:
● Cutaneous lymphoma (p 1049)
Presentation varies. Multiple erythematous nodules, ulcers or proliferative lesions. Exfoliative ery-
throderma with general flushing and scaling of skin. Lymphadenopathy and systemic illness may
be present. Uncommon.
● Mast cell tumor (p 1050)
Single or multiple lesions which are usually benign. Papules and plaques are common. Poorly cir-
cumscribed dermal masses are possible. Head and neck are common sites. A papular form occurs
in young Siamese on the head and ears and may spontaneously regress.
Miscellaneous:
● Contact dermatitis (p 1048)
Erythema and papules on affected surfaces. Pruritus leads to skin thickening and hyper-
pigmentation.
● Eosinophilic plaques** (p 1046)
Well-circumscribed plaques, which often ulcerate. Common on the abdomen and medial thighs.
Very pruritic.
animal that presents with pruritus, even if no miliary der-

INTRODUCTION matitis pattern is clinically evident. This chapter lists
some additional conditions, which may also present with
MECHANISM? pruritus and are less likely to have miliary dermatitis.
Pruritus is not as common a presentation in feline prac- DISEASES CAUSING PRURITUS

tice as compared to the situation in the dog. That is not WITHOUT MILIARY DERMATITIS
to say that the problem is unusual, rather it points to
the fact that feline pruritus may manifest in ways other
than scratching, or self-trauma, which is immediately EOSINOPHILIC PLAQUES**
obvious to the owner. In many instances, owners are not
aware that the cat is pruritic. The cat may be presented Classical signs
with a complaint of excessive licking, alopecia or mil- ● Raised “glistening” plaques, well
iary dermatitis. circumscribed and often ulcerative.
● Pruritus.
WHERE? ● Regional lymphadenopathy possible.
Skin.
Clinical signs
WHAT? Eosinophilic plaques are usually multiple, raised,
round to oval lesions, often several centimeters in
The list of differential diagnoses for pruritus in cats is
diameter. Common sites include the abdomen, medial
long. Most cases are due to infectious agents such as
thighs and mucocutaneous junctions.
microbes and ectoparasites, or hypersensitivities. As
miliary dermatitis is frequently associated with pruritis, Frequently there is ulceration and serum oozing from
all of the differentials covered in Chapter 48 (The Cat the lesion, which may give the classic “glistening”
With Miliary Dermatitis) should be considered for the appearance to the lesion.
49 – THE CAT WITH PRURITUS WITHOUT MILIARY DERMATITIS 1047
The lesions are generally markedly pruritic, evidenced Secondary infection, abscesses or cellulitis are
by licking and trauma to the area. possible.
Regional lymphadenopathy and secondary infection Vesicular to ulceroproliferative lesions may develop in
are sometimes present. the mouth, pharynx, conjunctiva and on the muzzle.
Affected cats may also exhibit indolent ulcers, Many cats are systemically ill with mild pyrexia, inap-
eosinophilic granulomas or ocular lesions. petence and depression, particularly during the viremic
stage.
Diagnosis
Diagnosis is via biopsy and demonstration of the Diagnosis
characteristic histopathology consisting of markedly
thickened epidermis with spongiosis and eosinophil Diagnosis is based on biopsy demonstrating intracy-
infiltration, which may also extend to affect the fol- toplasmic inclusion bodies (types A or B). Healing
licular epithelium. Erosions may be present. lesions may be negative for inclusion bodies.
Peripheral blood eosinophilia may be present. Electron microscopic examination of an unfixed scab
or biopsy material can identify orthopoxvirus particles.
Intercellular immunoglobulin is frequently found Immunohistochemical techniques can also be per-
within the epidermis; however, this should not be mis- formed on skin biopsies.
taken for an autoimmune skin disease.
Viral isolation techniques are available in specialist
laboratories.
FELINE ORTHOPOXVIRUS INFECTION**
Serological tests are available at certain laboratories.
Classical signs
● Initial single lesion around head or neck.
DEMODICOSIS
● Numerous papules develop later, and
frequently erode or ulcerate.
Classical signs
● Scab formation. When scabs fall off,
alopecia and scarring evident. ● Localized/generalized alopecia of face and
● Pruritus and secondary infection. body trunk.
● Erythema and scaliness. Secondary
Clinical signs infection.
● Periocular and nasal involvement is
Orthopox virus is more common in young to middle- particularly common.
aged cats.
The initial lesion is a macular eruption (5 mm diam-
eter), which rapidly progresses to a non-healing ulcer
Pathogenesis
with a raised indurated border on the head, neck or
forelimbs. Whilst most normal animals have a low mite bur-
den probably derived from maternal transmission,
Eroded or ulcerated papules, which scab over,
cats with clinical demodicosis have a proliferation in
appear in several sites.
mite numbers.
When the scabs fall off, areas of alopecia and scarring
Immunosuppression appears to be an important fac-
are evident. These lesions gradually heal. As some
tor, and has been associated with diabetes mellitus,
lesions heal, new lesions may also develop.
FeLV and FIV infections, hyperadrenocorticism and
Pruritus is variable, but may be present at all stages. systemic lupus erythematosus.
New hair growth takes 6–8 weeks. A genetic predisposition has not been reported in cats.
In cats, there are two species of democid mites that are Treatment
recognized to cause disease.
Lime-sulfur baths (once/week for 4–8 weeks) are safe
Demodex cati inhabits hair follicles and sebaceous and effective. This agent has sometimes been combined
glands. Demodex gatoi appears to replicate within pits with phosmet.
of the stratum corneum. The clinical significance of a
third, as yet unnamed species, is currently unknown. Amitraz (0.0125–0.0250%) applied topically once a
week for 6–8 weeks is effective, although clinicians
The proliferation of mites leads to damage to hair should beware of toxicity.
shafts, folliculitis and follicular disruption.
Efficacy of ivermectin in feline demodicosis is unclear.
D. gatoi is contagious, so all in-contact cats should
Clinical signs be treated simultaneously.
D. cati causes disease which is variably pruritic, con- Address any underlying immunosuppressive disease.
sisting of patchy erythema, scale, crust and alopecia,
more commonly seen affecting the eyelids, periocular
area, head and neck although generalized disease may Prognosis
also develop. Spontaneous remission is possible in some younger
Pruritus is not a dominant feature in most cases. animals after weeks to months.
Secondary infection is possible, particularly if there is However, in many cats signs persist and may worsen
significant self-trauma. over time. The prognosis is affected by underlying dis-
ease conditions that cannot be rectified, e.g. FIV or
D. gatoi causes signs that are more consistent with FeLV infection.
allergic skin disease, including severe pruritus, alope-
cia, scale, crust and excoriation, particularly on the
head, neck and elbows. Some cats may develop more Prevention
generalized disease. Avoid stress and treat potentially immunosuppressive
diseases (diabetes mellitus, hyperadrenocortism).
Diagnosis There is no evidence to currently support the exclusion

of clinically affected animals from a breeding program,
Diagnosis is based on clinical signs and demonstra- although such an approach may be judicious.
tion of the mites via skin scrapes. Superficial scrapes
are sufficient for D. gatoi; however D. cati requires
deeper scrapings. Squeeze the affected area, apply a CONTACT DERMATITIS
small amount of mineral oil to the skin and scrape using
a blunt scalpel blade until capillary oozing is present. Classical signs
Biopsy may also be used to demonstrate mites. ● Erythema and papules on contact surfaces.
● Pruritus and secondary infection.
● Skin thickening and hyperpigmentation.
Differential diagnosis ● Severe cases may develop ulceration.
Differential diagnoses which should be considered for
D. gatoi include hypersensitivities (atopy, food, flea), Pathogenesis
contact dermatitis and psychogenic causes. Careful
Irritant contact dermatitis is more common than
skin scrapings should be performed, followed by thera-
contact allergic dermatitis.
peutic trial (e.g. lime-sulfur weekly for 4–8 weeks). If
there is no response to a treatment trial, then a food Primary irritant contact dermatitis causes an inflam-
elimination trial and other diagnostic tests should be matory response in the majority of exposed cats. No
performed. prior sensitization is required.
Allergic contact dermatitis is an immunologic Differential diagnosis

response to a hapten. Haptens are small chemically
reactive compounds that must bind to a protein before Other hypersensitive, ectoparasitic and psychogenic
becoming a complete antigen. The initial phase of the skin conditions should be considered.
hypersensitivity is the afferent phase during which time Whilst the lesions and clinical signs may be similar,
the immune system is sensitized. Experimentally this generally it is possible to differentiate on the basis of
may be as little as 3–5 weeks, although it is much longer the lesion distribution limited to hairless areas, history
in naturally occurring cases (> 2 years in > 70% of of exposure and response to provocative exposure
cases). Subsequent exposure in a sensitized animal leads and patch testing.
to the development of the efferent (or elicitation) phase,
during which time a gross clinical lesion develops.
Treatment
Whilst a delayed-type hypersensitive reaction has tradi-
tionally been suspected, recent studies have shown this Treatment involves avoiding the suspect irritant or
may not be the case. allergen. If this is not possible, some form of sympto-
matic therapy will be required as long as exposure to
the irritant/ allergen continues.
Clinical signs
Glucocorticoids (topical or systemic). In some
Initial lesions may present as erythema, macules and instances topical cortisone creams may be sufficient. If
papules. Chronically, alopecia, hyperpigmentation, not, then oral prednisolone may be used (2 mg/kg q 24
lichenification, excoriation may develop. h for 5 days, then 1 mg/kg q 48 h as required).
Lesions are initially confined to the hairless (or sparsely Symptomatic therapy, if appropriate.
haired) contact areas including ventral abdomen, tho-
rax, scrotum, lips, point of chin, concave aspect of pin- Mild, non-medicated cleansing shampoos may be
nae. However, the lesions may be widespread for an used to remove irritant chemicals.
agent applied over most of the body, e.g. shampoo.
Irritant contact dermatitis may occur as a single Prognosis
episode, whereas contact allergic dermatitis often has Prognosis is excellent, if avoidance possible.
repeat episodes.
If not, then judicious glucocorticoid medication is
indicated.
Diagnosis
Irritant contact dermatitis is often initially suspected Prevention
on the basis of clinical signs and history of acute
exposure to an irritant compound. Try to avoid any offending irritants or allergens.
Response to symptomatic therapy and avoidance is

helpful in supporting the diagnosis. CUTANEOUS LYMPHOMA
Provocative exposure is possible, but often unnecessary. Classical signs

In the case of contact allergic dermatitis, the diagnosis ● Presentation varies with tumor type.
may be confirmed by provocative exposure or patch ● Non-epitheliotropic forms exhibit multiple
testing. erythematous nodules, with occasional
Close patch testing may be performed by applying the exfoliative erythroderma.
suspected allergen(s) to the skin, and then applying a
● Epitheliotropic forms exhibit exfoliative
body bandage to secure the site. This is removed after erythroderma, plaques/nodules, ulcers or
48 hours and the site examined for the presence of ery- proliferative lesions.
thema and edema at 72 and 96 hours.
● Lymphadenopathy occurs in epitheliotropic
cases.
Biopsy is non-specific.

Clinical signs vary markedly. Lesions are most commonly reported around the head
and neck.
Non-epitheliotropic forms commonly present as
multiple, solid erythematous nodules, dermal or Four different presentations are recognized:
subcutaneous in position. ● Multiple poorly demarcated masses (up to 5 cm
in diameter), which are often edematous and fixed
Exfoliative erythroderma seen as generalized flush-
to the skin.
ing of the skin with excess scale formation. Arciform
● Smaller (2–10 mm) multiple, well-circumscribed
(semicircular) or solitary lesions are less common.
papules which are solid and light in color.
Epitheliotropic forms commonly present in the later ● A plaque-type form (1–7 cm), which is erythema-
stages as one or a combination of the following: tous, firm, raised and well circumscribed. These
exfoliative erythroderma, ulcers and depigmentation at plaques are generally pruritic and may ulcerate.
mucocutaneous sites, multiple plaques or nodules. ● Solitary, often alopecic, well-circumscribed, vari-
ably sized (3–30 mm), dermal nodules are occa-
Ulcerative or proliferative oral lesions are possible.
sionally seen.
Generalized lymphadenopathy may be present in many – A papular form on the head and ears of young
epitheliotropic cases. Siamese cats (6 weeks to 4 years) which may
spontaneously regress.
Earlier lesions include focal alopecia, erythroderma
and scale.
Diagnosis
Signs of systemic illness may be present, and include
inappetence, lethargy and depression. Diagnosis is based on characteristic histopathology.
Stained impression smears and tissue aspirates are
Diagnosis often diagnostic.
Diagnosis is based on characteristic histopathology. Electron microscopy is often required for rarer forms.
Direct immunofluorescence testing may reveal deposi-
tion of immunoglobulin in the affected cells. This should Treatment
not be mistaken for a diagnosis of pemphigus complex. Surgical excision is the treatment of choice for soli-
tary lesions that cause difficulties.
MAST CELL TUMOR In disseminated forms, prednisolone (0.5 mg/kg sid)
may be used.
Classical signs
The majority of these tumors in the cat are not malig-
● Lesions are very variable from single or nant, and so chemotherapeutic and radiotherapeutic
multiple lesions, well-circumscribed measures are often unnecessary. However, a metastatic
papules and plaques to poorly rate of up to 22% has been reported in one study.
circumscribed multiple dermal masses.
● Head and neck common sites. The rare papular form in Siamese cats often sponta-
neously regresses.
RECOMMENDED READING
Baker KP, Thomsett LR. Disorders associated with pathogens. In: Canine and Feline Dermatology. Oxford, GB,
Blackwell Scientific Publications, 1990, pp. 95–171.
Moriello K, Mason I. Pruritus in cats. In: Handbook of Small Animal Dermatology: Oxford, GB, Pergamon, 1995,
pp. 153–162.
Pedersen NC. Viral diseases. Parasitic diseases. In: Feline Infectious Diseases. Goleta, CA., American Veterinary
Publications Inc., 1988, pp. 11–15, 347–366.
Quinn PJ, Donnelly W, Carter ME, et al. Diseases of the skin. In: Microbial and Parasitic Diseases of the Dog and
Cat. Philadelphia, PA, W.B. Saunders, 1997, pp. 292–340.
Scott DW, Miller WH, Griffen CE. Immunologic skin diseases. In: Muller and Kirk’s Small Animal Dermatology,
6th edn. Philadelphia, PA, W.B. Saunders, 2001.
50. The cat with alopecia
Ruadhri Michael Seosaimh Breathnach and Mike
Shipstone
KEY SIGNS
● Partial or complete loss of hair.
MECHANISM?
● Alopecia is the loss or absence of hairs from areas of the body that would normally possess
hairs.
● The most common mechanism is the excessive loss from over-grooming because of pruritus.
The characteristic feature of this mechanism is the presence of damaged/fractured ends to the
remaining hair shafts in the area of alopecia.
WHERE?
● Skin.
WHAT?
● Numerous pruritic conditions, most commonly allergic in origin, lead to alopecia from self-
trauma. Occasionally self-trauma can also arise for psychogenic reasons. Non-pruritic causes
may be congenital or hormonal in etiology, with hyperthyroidism and diabetes mellitus most
common. Folliculitis is seen with microbial or ectoparasitic infections, leading to non-pruritic
loss of hair.

Diseases causing alopecia
PRURITIC CAUSES OF ALOPECIA
INFLAMMATORY
● Allergic (p 1030)
If fractured or cropped hairs are present in the affected areas, pruritus is the most likely cause. See
Chapter 48 (The Cat With Miliary Dermatitis or Pruritus).
1052
50 – THE CAT WITH ALOPECIA 1053
NON-PRURITIC CAUSES OF ALOPECIA

FAILURE OF NORMAL HAIR PRODUCTION
ANOMALY
● Congenital/genetic alopecia** (p 1055)
Focal or generalized alopecia seen at birth or in first months of life. Alopecia may be pathologic,
or result from an intentional breeding program where it is not viewed as abnormal, for example
perauricular alopecia in some Siamese cats and generalized alopecia of Sphinx cats.
● Pili torti (p 1062)
Generalized alopecia which can also involve the feet and eye regions resulting in pedal dermatitis
and paronychia. Many affected kittens die.
LOSS OF EXISTING HAIRS
METABOLIC
Alopecia and an unkempt coat. Thin and fragile skin. Secondary infection and comedones possi-
ble. Systemic signs often present.
Systemic signs are present in most cats and include polyphagia, weight loss, restlessness, tachycar-
dia and/or intermittent vomiting or diarrhea. Cutaneous signs occur in 30% of cats and include dry
or greasy seborrhea, matting of the coat, focal or regional alopecia and thinning of the skin.
Symmetrical alopecia is occasionally seen.
● Diabetes mellitus** (p 1059)
Polydipsia, polyuria, weight loss and polyphagia or inappetence are typically present. A poorly
groomed seborrheic coat is common with generalized fine dry scale, and thinning of the skin.
Symmetrical alopecia on abdomen, perineum or groin regions may be present. Secondary bacterial
or fungal infections are sometimes present.
● Telogen defluxion (p 1062)
Gradual alopecia affecting part or all of the body several months after a stressful event. Rest of
skin appears normal.
NUTRITION
● Dietary alopecia (p 1065)
Patchy or generalized alopecia. Seborrhea and poor coat quality. Secondary infections are possible.
NEOPLASTIC
● Alopecia mucinosa (p 1065)
Alopecia and excess scale of the head, neck and ears. Plaque-type lesions may develop later and
have histological findings consistent with lymphoma or mycosis fungoides. Very rare disease.
PSYCHOLOGIC
● Psychogenic** (p 1056)
Loss of hair from excessive grooming commonly affects the abdomen, thighs, inguinal region,
forelegs or dorsal spinal region. Hairs appear broken and uneven, and the coat can feel rough.
continued
contined
Affected skin may become thickened and hyperpigmented. An environmental stressor may be
identified in the history.
INFLAMMATION/INFECTION:
Bacterial:
● Staphylococcal dermatitis* (p 1064)
Primary staphylococcal dermatitis is uncommon in cats, and an underlying disease process should
be suspected. Typically there is erythema, scale and crustiness. Hair follicles are commonly
involved. Papules are common, but rarely is pus present.
Fungal:
● Dermatophytosis** (p 1060)
More common in young kittens. Erythematous plaques, alopecia and scale. Lesions may progress
to larger gray areas of alopecia and hyperkeratosis.
Parasitic:
● Demodicosis* (p 1061)
Localized or generalized alopecia of face and trunk. Periocular and nasal involvement are most
common. Lesions have erythema and scale. Most cases are non-pruritic.
Immune:
● Alopecia areata (p 1066)
Focal or multi-focal alopecia which is gradual in onset, and not symmetrical. The skin is not
inflamed and there is no pruritus. Hyperpigmentation may occur chronically. Rare.
Toxic/drug
● Drug reaction* (p 1061)
Usually associated with immunosuppressive or anti-neoplastic agents. Alopecia is most common
on the body trunk, but can affect other sites. Secondary infection is often present. Glucocorticoids
may produce cutaneous signs of hyperadrenocorticism.
Some causes of alopecia are genetically programmed.

INTRODUCTION Acquired cases may arise because of hormonal influ-
ences that interfere with hair growth, or as a result
of folliculitis. Hairs may also be lost as a direct result
MECHANISM?
of self-trauma for a variety of reasons.
● Failure to grow hair may be a life-long problem,
Alopecia is the loss or absence of hairs from areas of
as occurs in congenital or genetically programmed
the cat’s body that would normally possess hairs.
alopecias.
● This phenomenon can result either from a failure to
grow hair or as a consequence of the abnormal Abnormal hair loss has a wide variety of causes, and is
loss of hairs. normally divided clinically into those cases which are
accompanied by pruritus and those which are not.

WHERE?
The majority of cases seen in feline practice are due to
self-trauma as a consequence of pruritus. The abnormal organ is skin, but it may be affected sec-
ondarily by disease of other body systems.
The breakage of hair shafts may occur in dermato-
phytosis and psychogenic dermatoses. Alopecia can affect any part of the body, although certain
conditions tend to cause hair loss in characteristic areas.
Cessation of hair growth may arise due to endo-
crinopathies, telogen defluxion and drug reactions. The hair loss may be partial or complete, focal or
generalized.
Hairs may also be shed following an episode of folli-
culitis.
Rare causes of feline alopecia include pancreatic neo-
WHAT?
plasia.
Numerous pruritic conditions lead to alopecia from
Some conditions give rise to specific focal alopecia,
self-trauma. Allergic diseases are the most common
often in association with underlying skin pathology,
and are covered in the chapters on Miliary dermatitis
such as injection reactions, solar dermatitis or squa-
and Pruritus.
mous cell carcinoma.
● Self-trauma can also arise for psychogenic reasons.
The term feline symmetrical alopecia (FSA) repre- ● Folliculitis is seen with microbial or ectoparasitic
sents a cutaneous reaction pattern, rather than a distinct infections.
syndrome.
Non-pruritic alopecia can be congenital or acquired.
● It is characterized by a seemingly non-pruritic,
● Congenital alopecia often arises because of inten-
symmetrical alopecia affecting the abdomen,
tional breeding programs and is considered normal
caudo-medial thighs, proximal tail and perineum.
for the breed.
Affected hairs are easily epilated and no inflamma-
● Hormonal causes of acquired alopecia include
tory changes are usually present in the skin.
diabetes mellitus, hyperthyroidism and hyper-
● Most, if not all, such cases are the result of pruritus
adrenocorticism.
or self-trauma due to an underlying problem,
and are not related to sex steroids or other hor-
mones.
● Feline symmetrical alopecia is not included as a
distinct condition in this chapter. Rather the clini-
DISEASES CAUSING NON-PRURITIC
cian is encouraged to investigate such cases to see
ALOPECIA
if an underlying etiology such as flea allergic der-
matitis or psychogenic factors can be identified. CONGENITAL/GENETIC ALOPECIA**
● If no such cause can be found, then the term idio-
pathic feline symmetrical alopecia may be used. Classical signs
The histologic appearance of the hair follicle varies ● Focal or generalized alopecia or thin hair
with the stage of the follicle’s growth cycle. Anagen is coat present at birth.
the active growth phase and is characterized by a well- ● Further hair loss may occur in the first few
developed hair follicle bulb. Catagen is a transition months of life.
period between the active growth and resting stage. ● Excessive sebum or wrinkling of the skin.
Telogen is the resting stage, characterized by a small ● Often breed specific and considered
dermal papilla, separate from the bulb, absence of an normal.
inner root sheath and a club or brush-like hair.
Pathogenesis appears to be quite sparse so that the underlying skin

is more visible. This is the result of selective breeding.
Congenital alopecia has been reported in Sphinx cats Many kittens in a litter can be involved.
with affected individuals being the result of an inten- ● The hair coat can be deficient or totally absent at
tional breeding program involving cats with a sponta- birth. Any hair initially present can be lost in the
neous mutation. first months of life.
Animals born with congenital alopecias may possess ● Excessive wrinkling of the skin occurs in these
additional ectodermal defects. kittens.

● Affected Burmese kittens also lack whiskers and
The mode of inheritance involves a monogenic reces- claws.
sive trait. However, in Russian hairless cats, the alope-
cia is determined by a semi-dominant gene with the
participation of other genes. Diagnosis
Congenital hypotrichosis has been reported in several Diagnosis is often possible on the basis of the breeding
breeds including Burmese, Devon Rex, Cornish Rex, history and clinical signs.
Siamese and Birman cats. The condition is inherited as Histopathology of affected skin can provide additional
an autosomal recessive trait in Birman and Siamese cats. diagnostic information.
Although several kittens in the one litter may be
affected, no sex predisposition has been reported. Treatment
Skin pathology can vary from hypoplasia to complete Mild anti-seborrheic shampoos (containing sulfur, sali-
absence of hair follicles and related adnexal structures. cylic acid) may be required intermittently in Sphinx
cats to remove the excess sebum accumulation.
Clinical signs Owners should also be warned to minimize UV exposure
Clinical signs vary with the specific condition and the in cats with non-pigmented skin, so that cumulative
breed involved. Alopecia or thin hair coat is present at actinic damage is avoided later in life.
birth. Further hair loss may occur in the first few
months of life.
Depending on the syndrome, there may be an absence PSYCHOGENIC**
of primary hairs.
Classical signs
Congenital alopecia may be pathologic, but is more
often the result of an intentional breeding program, ● Loss of hair commonly affecting the
and is not viewed as abnormal by the owner. abdomen, thighs, inguinal region, forelegs
or dorsal spinal region.
Alopecia may be regional or focal, for example preau- ● Hairs appear broken and uneven and the
ricular alopecia seen in some Siamese cats. coat can feel rough.
A more generalized alopecia known as feline alopecia ● Affected skin may become thickened and
universalis is seen in Sphinx cats. These cats have no hyperpigmented.
primary hairs and no whiskers.
● Excess sebum is commonly present on the skin due
to an abnormal opening of the sebaceous glands
Pathogenesis
onto the skin surface.
● Poor grooming habits frequently lead to poor skin The main reason for the alopecia is excessive or inap-
hygiene. propriate grooming behavior.
Devon and Cornish Rex cats, Siamese, Burmese and Most cases are presumed to have an underlying psy-
Birmans can exhibit hypotrichosis. The hair coat chological component.
Various stressful factors can be involved including Even if the owner has not noticed excessive grooming
a new pet, change of home or routine, or competition behaviour, facts such as tufts of hair in the animal’s
from a dominant animal. bed or the vomiting up of hairballs are suspicious.
Videotaping of cats in the cattery may reveal evidence
The action of licking/chewing is postulated to stimu-
of self-grooming.
late release of ACTH and MSH. This in turn can lead
to an increase in endorphin production. Clinical examination reveals short, broken hairs,
● Endorphins help to reduce stress, but may rein- often with roughened ends. The hairs are not easily
force the behavior pattern. epilated.
● A trichogram reveals broken tips to the hairs and
Some cats concentrate on a particular area, and lick or
may also demonstrate that some of the hairs were in
chew incessantly at that site. This can lead to signifi-
anagen.
cant lesion development.
All the other differentials for alopecia need to
Other cats may have milder signs or the excessive lick-
be ruled out. Thus a basic work-up consisting of skin
ing/chewing may be concentrated over a much wider
scrapings, fungal culture etc. is normally warranted.
area.
Flea dermatitis and flea allergic dermatitis are particu-
Excessive grooming, etc. may not actually be noticed larly important differentials.
by the owner, as many cats are secret groomers.
Biopsy is non-diagnostic, but may help to rule-out
many other differentials.
Clinical signs Placing an Elizabethan collar on the cat for a period of
weeks will often lead to a significant re-growth of hair
Hair loss is typically concentrated on the areas of the
in affected areas.
body where the cat can access to lick or chew.
The ventral abdomen, inguinal region, inner thighs Differential diagnosis
and inner aspects of the forelegs are common sites.
Alopecia can be caused by all the conditions listed in
Some cats concentrate on the dorsal spinal region, this chapter. Exogenous administration of progesto-
particularly in the lumbar and sacral/tail areas. gens or glucocorticoids should also be excluded, as
should dietary causes. Ectoparasites also need to be
The licking/chewing behavior leads to fracture of the
excluded, particularly fleas. Diabetes mellitus, hyper-
hair shafts, roughening of the coat and alopecia.
adrenocorticism and hyperthyroidism can produce sim-
Some cats develop an inflammatory pattern, character- ilar alopecia but systemic signs are present.
ized by red plaques.
Treatment
The alopecia may be symmetrical in some cases.
Try to remove or ameliorate any stressful factors that
Long-standing cases develop thickening and hyperpig-
may be acting as the underlying cause.
mentation of the affected sites.
An Elizabethan collar will often give a clinical
improvement. However, it does not properly address
Diagnosis the issue and is resented by many cats.
A tentative diagnosis is based on clinical signs and In cases that warrant such an approach, medical therapy
excluding other causes of alopecia. A definitive diag- may be attempted. Phenobarbitone (2–6 mg/kg orally
nosis is rarely possible. bid) and diazepam (1–2 mg/cat orally sid or bid) have
both been employed.
A detailed history should be taken to try and elucidate
any cause of stress or anxiety. If one cannot be identi- Naloxone, an endorphin blocker, has been used suc-
fied, it does not rule out a diagnosis of psychogenic cessfully at a dosage rate of 1 mg/kg subcutaneously
alopecia. every few weeks.
Clomipramine and various progestogens have also Excessive rates of nail growth may give rise to over-
been reported to be somewhat effective. grown claws.
Some of the above medications are not licensed for use
in cats in many countries. Diagnosis
A tentative diagnosis is based on age, history and clin-
Prognosis
ical signs.
The prognosis depends totally on whether the inciting
An enlarged gland or thyroid nodule may be palpable.
cause can be identified and resolved.
Various abnormalities may be encountered on routine
If not, then long-term management, sometimes involv-
hematological and biochemical analysis.
ing drug therapy is generally required.
● These commonly include increases in serum ALP,
AST, LDH and blood urea concentrations.
● Changes on hematology are variable and unreliable.
HYPERTHYROIDISM**
● A mature neutrophilia, or an eosinophilia, are
sometimes present.
Classical signs
Cardiac abnormalities may be detected on ECG and
● Systemic signs including polyphagia,
echocardiography.
weight loss, restlessness, tachycardia.
● Dry, greasy, seborrheic or matted coat. A definitive diagnosis is based on finding an increased
● Focal or regional alopecia or shedding of basal thyroxine (TT4) concentration in blood.
the coat.
As not all hyperthyroid cats will exhibit elevated values
● Overgrown nails.
for basal thyroxine, measurement of free thyroxine,
a triiodothyronine (T3) suppression test or TRH stimu-
See main reference on page 304 (The Cat With Weight
lation test may be necessary. Further testing should
Loss and a Good Appetite).
only be performed if signs are consistent with hyper-
thyroidism, and thyroxine concentration is in the top
half of the reference range.
Clinical signs
● Free thyroxine must be measured with a validated
Hyperthyroidism occurs mainly in older cats (> 8 years feline assay using equilibrium dialysis, and if avail-
of age). able, is the easiest test to use in cats with clinical
signs consistent with hyperthyroidism but thyroxine
The majority of cats have systemic signs including
concentration does not exceed the upper limit of the
polyphagia, weight loss, restlessness, tachycardia
reference range.
and/or intermittent vomiting or diarrhea.
● In the T3 suppression test, thyroxine and T3 con-
Approximately 30% of cats with hyperthyroidism centration are measured before and 3 hours after the
exhibit cutaneous manifestations. administration of seven doses of 20 μg of liothyro-
nine sodium (T3) at intervals of 8 hours. Euthyroid
Often there is excessive matting of the hair coat, and
cats will exhibit a significant drop in thyroxine
the cat may groom excessively.
concentration (approximately 50%) after T3 admin-
A dry coat, or dry or greasy seborrhea may be present. istration, and a significant rise in total T3 concen-
tration. Hyperthyroid cats will have no significant
Alopecia, when present, may be patchy, regional or
inhibition.
generalized, and in some cases may appear symmetrical.
● In the TRH stimulation test, thyroxine concen-
● The major site affected by alopecia is the body
tration is measured before and approximately
trunk.
4 hours after the intravenous administration of
Thinning of the skin (or loss of skin elasticity) is a 0.1 mg/kg of TRH. Hyperthyroid cats exhibit no
common finding. significant stimulation of thyroxine concentration
(< 50% increase in concentration) following TRH

DIABETES MELLITUS**
administration, whereas euthyroid cats or cats
with non-thyroidal illness show a more signifi-
Classical signs
cant increase (>60%).
● Polydipsia, polyuria, weight loss and
Radionuclide thyroid scanning is available in certain
polyphagia or inappetence.
specialist referral centers.
● Plantigrade stance.
● Scurfy seborrheic haircoat.
● Symmetrical alopecia of the groin,
Differential diagnosis perineum, abdomen and hindlimbs.
Alopecia can be caused by all the conditions listed
in this chapter. However, as most cats presenting with
Clinical signs
this complaint will have a combination of systemic
and cutaneous signs, the major differentials would be Polydipsia, polyuria, weight loss and polyphagia or
hyperadrenocorticism and diabetes mellitus. Exo- inappetence are typically present. Cutaneous mani-
genous administration of progestogens or glucocorti- festations are less obvious.
coids should also be excluded.
A poorly groomed seborrheic coat is commonly pres-
ent. It is most commonly a dry scurfy seborrhea.
Alopecia involving the groin, perineum, lateral
Treatment
abdomen and hindlimbs is occasionally present, and
Medical treatment may be attempted using either car- may or may not be symmetrical.
bimazole or its metabolite, methimazole. Carbimazole
A few cats with diabetes mellitus also have underlying
is generally given at a dosage rate of 5 mg/cat q 8 h
hyperadrenocorticism, which may be responsible for
until the cat is euthyroid. Once euthyroid, the frequency
some of the cutaneous signs.
of administration may be reduced to twice daily.
Carbimazole has also been used prior to surgery. The skin appears thin and hypotonic, which may be
from hyperadrenocorticism or protein catabolism as
Surgery can be performed in many cases to remove
a result of the failure to properly utilize glucose.
the hyperplastic or neoplastic tissue. The effects of
hyperthyroidism on other tissues increase the anes- Secondary bacterial and fungal skin infections may
thetic risk. occur because the immune system is compromised.
● If a nodule can be felt on one side of the gland ● Staphylococcal dermatitis, Candida spp. infections
only, some veterinarians prefer to remove just that and dermatophytosis have all been reported.
one lobe. Others choose to remove the gland in its
A rare skin manifestation is the presence of xan-
entirety and may supplement the cat with exo-
thomas. These are benign, granulomatous lesions asso-
genous thyroid hormones. If all four parathyroid
ciated with abnormal lipid metabolism.
glands are also removed, supplementation with
calcium and vitamin D is required. Severe life-
threatening hypocalcemia can occur rapidly after Diagnosis
surgery and needs intensive monitoring and
A tentative diagnosis is based on history, clinical signs
treatment.
and glycosuria, with or without ketonuria.
Radioactive iodine therapy can be employed in
Definitive diagnosis is confirmed by documenting
certain referral establishments. The hyperfunctional
persistent fasting hyperglycemia (blood glucose >
thyroid cells concentrate the radioactive iodine, whilst
12 mmo1/L).
surrounding normal tissue receives a much smaller
dose. This technique is simple and effective in many Routine biochemical analysis may demonstrate
cats. increased hepatic enzymes, cholesterol and triglyceride
concentrations. Electrolyte abnormalities (sodium and Recovery from infection requires a strong cell-mediated
potassium) may also be present. immune response. Anti-dermatophyte antibodies do not
provide protection, and a failure to form a strong cel-
Radiology and ultrasonography usually reveal
lular response may be the cause of chronic infection or
hepatomegaly.
tolerance in some cats. Concurrent immunosup-
Demonstrating increased fructosamine concentration pressive drug therapy, compromised immune status,
is useful to confirm that hyperglycemia is persistent poor nutrition, stress and the presence of intercurrent
and not transient. The normal fructosamine concentra- disease, e.g. multiple-cat environment with poor health
tion in the cat is 175–400 μmol/L. care (strays) with endemic infections (FIV/FeLV) may
facilitate transmission.
DERMATOPHYTOSIS**
Clinical signs
Classical signs
Skin fungal infections are more commonly seen in
● More often in young kittens, rather than young kittens, rather than adults.
adults.
Initial lesions are commonly present on the face, head
● Erythematous plaques, alopecia and scale.
and feet. Large areas of the body can be involved.
● Lesions progress to larger grayish areas of
alopecia and hyperkeratosis. Raised, erythematous plaques may develop, and are
accompanied by scaling.
Pathogenesis Alopecia develops and lesions expand to form larger
plaques, which appear grayish and hyperkeratotic.
In cats, 94–98% of cases are caused by Microsporum
Erythema may still be a feature.
canis. Occasionally lesions are caused by Trichophyton
mentagrophytes or Trichophyton terrestre, but Micro- Initial hair loss tends to be in the center of the lesion.
sporum gypseum is rare. Hairs on the periphery appear discolored and brittle. As
lesions regress, initial hair re-growth appears in the
The prevalence of dermatophytosis varies with the
center of the alopecic areas.
climate and the natural reservoirs. In a hot, humid
climate, a higher incidence is observed than in a cold, Secondary bacterial infection is commonly seen.
dry climate. The mere presence of a dermatophyte Infection may involve the whiskers or nail beds, with
spore is generally insufficient to cause infection and resultant deformities.
clinical disease. Transmission occurs via contact with
Infection of deeper tissues may result in nodular skin
an infected particle. In the case of M. canis, this occurs
lesions.
via contact with an infected animal or environment.
Infection with M. gypseum is via exposure to spores Infection may be sub-clinical or mild, and easily over-
in soil, and Trichophyton infection occurs via contact looked.
with rodents (usually asymptomatic carriers), horses,
cattle or a contaminated environment.
Diagnosis
A minimum number of spores is required for infec-
A tentative diagnosis is based on clinical signs.
tion along with other factors that allow an infection to
Definitive diagnosis is based on skin scrapings, hair
develop.
plucks and fungal culture.
These factors include: grooming behavior (provides
Fluorescence under ultraviolet light (Wood’s lamp),
mechanical removal of the spores), presence of micro-
may detect approximately half the cases of M. canis
trauma on the skin which allows invasion, increased
infections in cats.
hydration and maceration of the skin also increases
probability of infection establishing. The immune Skin scrapings and hair plucks may be examined
competence of the host is extremely important. microscopically for the presence of spores or hyphae.
Fungal culture of scrapings, hair plucks and nail sam- Classical signs—Cont’d
ples can identify the precise species of dermatophyte
involved, but is time-consuming. ● Ulceration or necrosis on trunk, limbs or
mucocutaneous junctions may be evident.
Biopsy of affected tissue may confirm a diagnosis. ● History of treatment with
Special stains may be required. immunosuppressive or anti-neoplastic
drugs.
DEMODICOSIS*
Pathogenesis
Classical signs
Most of the drugs implicated in cutaneous drug reactions
● Non-pruritic alopecia typically periocular are immunosuppressive or anti-neoplastic agents. The
and nasal. reaction pattern varies with the specific drug.
● Erythema and scaliness are often present.
Drugs such as glucocorticoids and anti-neoplastic
agents can often interfere with hair follicle activity,
Clinical signs resulting in alopecia.
Most cases exhibit focal, partial alopecia particularly
in the region of the eyes, nose and ears. Lesions may Clinical signs
also develop on the chin, thorax, abdomen, inner thighs,
flanks and perineum. Drugs such as glucocorticoids and anti-neoplastic
agents may produce alopecia, primarily affecting the
Mild erythema, scale and occasional papules. body trunk.
The alopecia may become more generalized in some cases. ● The skin may become thin and hypotonic, partic-
ularly with glucocorticoid medication.
Hyperpigmentation and bilaterally symmetrical alope- ● The classical cutaneous changes of hyperadreno-
cia may develop. corticism may develop.
Secondary infection and a crusting dermatitis may be ● Secondary bacterial or fungal infection is not
seen. Pruritus is not a dominant feature in the majority uncommon.

of cases. When the reaction mimics a hypersensitive response,
the signs may be more severe and involve ulceration or
Diagnosis necrosis. The extremities and mucocutaneous junc-
A definitive diagnosis is based on identifying tions or trunk may be affected (see page 1034, The
Demodex species mites in skin scrapings. Superficial Cat With Miliary Dermatitis).
scrapes are normally sufficient for detecting D. gatoi
and the other unnamed species in the epidermis. Diagnosis
D. cati, on the other hand, requires deeper scrapings.
Diagnosis can be difficult in some cases, because the
Mites may also be detected on biopsy. drug reaction may cause cutaneous or systemic signs
Attention should be paid to identifying any underlying similar to the disease for which the cat was initially
cause of immunosuppression. placed on that medication.
A tentative diagnosis is based on history and clinical
DRUG REACTION* signs. As alopecia is well recognized as a complication
of treatment with glucocorticoids and anti-neoplastic
Classical signs agents, use of these drugs should always be ascertained
from the history.
● Alopecia primarily of the body trunk.
● Bacterial, and less commonly, fungal skin Withdrawal of the drug usually leads to a gradual
infections. resolution of the alopecia, although this is not true in
all cats. If the cutaneous changes are not interfering
with the quality of life, drug withdrawal may not be Both autosomal dominant and recessive inheritance
appropriate, depending on the underlying condition for patterns have been reported in human patients with a
which the drug was prescribed. combination of pili torti and varying degrees of hearing
loss. Other ectodermal defects are also documented in
If drug hypersensitivity is suspected, see page 1034, The
affected individuals.
Cat With Miliary Dermatitis, for details of diagnosis.
A localized form of disease may occur secondary to
follicular inflammation.
Clinical signs
Alopecia can be caused by all the conditions listed in
this chapter. However, the major differentials would be Appears as generalized alopecia in young kittens
diabetes mellitus, hyperadrenocorticism and hyper- affecting secondary but not primary hairs. Most affected
thyroidism. Dietary causes should also be excluded. kittens have marked alopecia by 10 days of age.
Periocular and pedal involvement are commonly pres-
ent. Affected kittens thus commonly present with pedal
Treatment
dermatitis and paronychia.
If appropriate, the offending medication should be
Affected kittens usually die or are euthanized.
withdrawn.
Treat any secondary infection, and crusted or ulcerated Diagnosis
areas with appropriate antimicrobial agents and symp-
A tentative diagnosis is based on the history and clin-
tomatic therapy as indicated.
ical signs.
A definitive diagnosis is possible with skin biopsy of
PILI TORTI
affected areas and examination of affected secondary
hairs.
Classical signs
Electron microscopy of these secondary hairs can pro-
● Generalized alopecia by 10 days of age.
vide additional diagnostic information.
● Pedal dermatitis and nail-bed infections.
● Affected kittens normally die or require
Treatment
euthanasia.
No treatment is available.
Pathogenesis
TELOGEN DEFLUXION
The pathogenesis is unknown.
Curvature of the hair follicle results in flattening and Classical signs
rotation of hair shafts.
● Alopecia affecting any or most parts of the
This leads to a generalized alopecia in young kittens, body.
with virtually all secondary hairs becoming involved. ● Gradual shedding of telogen hairs, usually
Primary hairs are not usually affected. 1–3 months after a stressful event.
● Skin is clinically normal.
Pili torti is usually an inherited disorder in man, with
affected individuals having additional systemic and
skin abnormalities. Clinical signs
Acquired syndromes similar to pili torti are addition- Telogen defluxion normally results from the premature
ally reported following various physical and chemical cessation of hair growth in anagen follicles because of
insults in man. a stressful factor, e.g. pregnancy, internal disease, etc.
Signs compatible with the underlying problem Clinical signs

may be present or have been present in the past.
The majority of cats with hyperadrenocorticism have
Telogen defluxion results in widespread loss of hairs systemic signs including polyuria, polydipsia and
from many or most parts of the body. polyphagia. Intermittent inappetence or anorexia may
The hair loss normally occurs 1–3 months following be present.
the stressful event. Many cases have concomitant diabetes mellitus.
The skin is clinically normal. Abdominal distention, giving a pot-bellied appear-
The hairs themselves often appear normal. They are not ance is commonly seen.
fractured or broken. Muscle wastage is a prominent feature.
Affected cats exhibit alopecia and an unkempt hair
Diagnosis coat. Hair loss is commonly seen on the trunk, flanks
A tentative diagnosis is based on the combination of and ventrum.
history and clinical signs. Often, the history or signs Hyperpigmentation occurs in a small number of
would indicate a stressful event such as pregnancy or cases. Secondary bacterial dermatitis may be a feature.
internal disease within the last 1–3 months. Abscessation is occasionally present.
Examination of hair samples microscopically reveals The skin is thin and very fragile in many cases. This
the typical features of telogen hairs. These include uni- leads to bruising and tearing with mild trauma.
form shaft diameter, as well as slightly clubbed and
non-pigmented roots. Affected cats have poor wound healing ability.
● There is no evidence of dysplastic changes or frac-
Comedone formation is also present in some cases.
turing of the hair shaft. In many cases, the disease is iatrogenic and there is a
Skin biopsy is of little additional benefit, because it long history of depot glucocorticoid or progestagen use.
simply reveals that all the hair follicles are in telogen.
Diagnosis
Re-growth of the coat within a few months if the
stress factor is removed or managed successfully can be Routine hematology and biochemistry values are not
used to confirm the diagnosis retrospectively. as markedly affected by hyperadrenocorticism in cats
as they are in the dog. Consequently, many of the
changes seen in the dog are inconsistently found in
HYPERADRENOCORTICISM the cat.
● When present, such changes are frequently attribut-
Classical signs able to secondary diabetes mellitus, e.g. hyper-

glycaemia, hypercholesterolaemia.
● Polyuria, polydipsia and polyphagia.
● Abdominal distention and pot-bellied The cat does not have a glucocorticoid-induced isoen-
appearance. zyme of alkaline phosphatase.
● Alopecia of the trunk, lateral thighs and Urine specific gravity may on occasions be reduced to
ventrum, and unkempt hair coat. isosthenuric levels, except in cats with secondary dia-
● Thin, fragile skin. betes mellitus, where glycosuria will affect the specific
● Bruising and tearing of the skin with mild gravity value.
trauma.
● Secondary bacterial skin infections and Adrenal function tests are not as well established in cats
poor wound healing. compared to dogs.
A normal urine cortisol:creatinine ratio is useful for
See main reference on page 251 (The Cat With excluding hyperadrenocorticism, but lacks specificity
Polyuria and Polydipsia). for diagnosis.
The low-dose dexamethasone suppression (LDDS) ● Metyrapone has been used successfully prior to
test using 0.1 mg/kg is the screening test of choice for adrenalectomy in some cats.
feline hyperadrenocorticism. Cats with pituitary-
Adrenalectomy is favored by many authors as the cur-
dependent hyperadrenocorticism may fail to suppress,
rent treatment of choice. This procedure can result in
or exhibit suppression at 3 or 4 hours followed by
a significant survival time and a reduced insulin
“escape” of suppression at 8 hours. The latter pattern
requirement.
is diagnostic for pituitary-dependent disease, and makes
● Unilateral adrenalectomy is performed in cases
further testing unnecessary.
of an adrenal tumor. Bilateral removal is per-
The corticotropin (ACTH) stimulation test is best formed for pituitary-dependent hyperadreno-
used to differentiate endogenous from iatrogenic hyper- corticism.
adrenocorticism, rather than as a diagnostic test for ● Mortality rates higher than 25% have been
hyperadrenocorticism, because 15–30% of cats with reported post-operatively, especially where diabetes
hyperadrenocorticism have a normal response. mellitus is present.
● Post-operative complications include electrolyte
The combined dexamethasone suppression/ACTH
imbalances, pancreatitis, thrombosis and sepsis.
stimulation test has been used successfully to diag-
Glucocorticoids and mineralocorticoids are required
nose hyperadrenocorticism in cats. The combined test
peri- and post-operatively. Following successful con-
does not appear to be more advantageous than either
trol of the hyperadrenocorticism, the requirement for
the ACTH stimulation or dexamethasone suppression
insulin therapy in diabetic cats may be reduced or
test evaluated separately.
abolished altogether.
Measurement of endogenous ACTH concentrations
is useful in differentiating pituitary-dependent from
adrenal hyperadrenocorticism. Normal to increased
STAPHYLOCOCCAL DERMATITIS*
ACTH concentrations support a diagnosis of pitu-
itary-dependent disease. Low concentrations support
Classical signs
adrenal disease. This test must only be used after
hyperadrenocorticism is confirmed by other tests. ● Erythema and scale/crustiness.
● Hair follicles are often involved.
Abdominal ultrasonography may provide evidence of
● Lesions may progress to papules, but pus
unilateral or bilateral adrenal enlargement.
is rare.
Exogenous administration of progestogens or glucocor-
ticoids should also be excluded.
Clinical signs
Differential diagnosis Primary staphylococcal dermatitis is rare in cats.
Consequently, there may be signs evident which relate
Hyperthyroidism and diabetes mellitus are the major to an underlying disease condition e.g. diabetes
differential diagnoses as most cats presenting with hyper- mellitus or FeLV/FIV.
adrenocorticism will have a combination of systemic
and cutaneous signs. Erythema and scale/crustiness are seen clinically.
The hair follicles are usually involved. Lesions may
progress to appear as papules, and thus take on a
Treatment
miliary pattern.
The success rates reported with drugs including
Affected cats may exhibit alopecia over the head and
mitotane, ketoconazole and metyrapone have been
neck. Other common sites affected include the feet,
poor to moderate.
ears and dorsum.
● Whilst successful management is possible in indi-
vidual cases, the overall results are not as encour- It is rare for purulent material to be present in or on the
aging as in the dog. lesions.
Staphylococcal infection in the cat is more commonly diabetes mellitus, hyperadrenocorticism and hyper-
seen as abscesses or infections of the ears and conjunc- thyroidism. Exogenous administration of progesta-
tiva. Deeper infections, such as granulomas with fistu- gens or glucocorticoids should also be excluded.
lation, are infrequent.
Treatment
Diagnosis Correct the underlying dietary imbalance.
A tentative diagnosis is based on clinical signs. Often, simply feeding a well-balanced commercial for-
mulation appropriate to the cat’s requirements, will be
Staphylococci can be readily cultured from infected
sufficient to give an overall improvement within weeks
lesions. Care must be exercised in interpretation of
to months.
culture results, however, as most normal cats possess
coagulase-positive staphylococci on their skin.
ALOPECIA MUCINOSA
Biopsy of affected tissue may show evidence of bacte-
rial folliculitis, pyoderma or deeper infection.
Classical signs
● Alopecia and scaling of affected skin on the
DIETARY ALOPECIA
ears, head and neck.
● Plaque-type lesions may develop at lesion
Classical signs
site at a later date.
● Patchy or generalized alopecia.
● Seborrhea and poor coat quality.
● +/- Secondary skin infection. Clinical signs
Alopecia mucinosa is a very rare syndrome in cats,
Clinical signs which is suspected of being a precursor lesion for
cutaneous lymphoma.
This syndrome is not commonly seen in practice,
except where economic conditions are poor or cats are Typically there is alopecia, which affects the head,
fed on improperly balanced diets, for example, vege- ears and neck, and fine scaling of the affected skin.
tarian diets, or diets low in vitamin A. Pruritus is not a feature initially.
Alopecia may be patchy or generalized. Within months, plaques may develop at the lesion
site. Biopsy of these plaques has yielded results com-
Seborrhea and poor coat quality are sometimes seen.
patible with cutaneous lymphoma or mycosis fun-
Hairs may be brittle and easily broken. goides in the two cats reported in the literature.
Poor skin hygiene and immune function may predis-
Diagnosis
pose to secondary skin infections.
Diagnosis is based on biopsy of the affected skin.
Initial histopathology reveals mucinosis of the epider-
Diagnosis
mis and of the outer root sheath of the hair follicles.
A tentative diagnosis is based on clinical signs and a
Later, biopsy specimens of plaque-type lesions may
detailed dietary history.
reveal findings consistent with cutaneous lymphoma or
Other causes of alopecia need to be ruled out. mycosis fungoides.
Differential diagnosis Treatment

Alopecia can be caused by all the conditions listed in No effective treatment is currently available. Treatment
this chapter. However, the major differentials would be as for cutaneous lymphoma could be attempted if the
biopsy results were suggestive of this. There are too The most common locations affected include the head,
few case reports to make any prescriptive treatment neck and trunk.
recommendations.
The affected skin appears otherwise normal. There is
The prognosis is therefore poor. no inflammation evident grossly and pruritus is not a
feature.
ALOPECIA AREATA Chronic lesions may develop hyperpigmentation.
Classical signs
Diagnosis
● Gradual onset of focal or multi-focal areas
of alopecia. A tentative diagnosis is based on the history of grad-
● Non-pruritic. ual hair loss, and the clinical signs of well-demarcated
● The skin is non-inflamed and appears alopecia, without any significant inflammation.
otherwise normal. Biopsy of early skin lesions reveals a mononuclear
● Long-standing lesions may become inflammatory cell infiltrate both surrounding and
hyperpigmented. within the hair follicles.
At later stages, the inflammation is largely absent.
Pathogenesis Catagen and telogen hair follicles predominate at this time-
In humans, an immune-mediated basis is suggested point. Follicular atrophy is also evident. In some biopsy
by: specimens, there is complete absence of follicles.
● Accumulations of lymphoid cells around hair bulbs
during the active phase of the disease.
Treatment
● Occasional association of alopecia areata with other
immune-mediated diseases. There may be spontaneous re-growth of hair in some
● Increased incidence of various autoantibodies in cats after a variable period of time.
alopecia areata.
Glucocorticoids have been employed by a variety of
● Decreased numbers of circulating T-cells.
routes. However, no data are available to support the
● Deposition of C3 or IgG or IgM at the basement
use of glucocorticoid medication in the treatment of
membrane zone of hair follicles.
this disease.
Clinical signs
Rare condition in cats.
Typically there are single or multiple sites of alopecia,
which are generally well-demarcated and usually non-
symmetrical. Hair loss is gradual.
RECOMMENDED READING
Baker KP, Thomsett LR. Heritable defects. In: Canine and Feline Dermatology. Blackwell Scientific Publications,
1990, pp. 63–75.
Mooney CT. Unusual endocrine disorders in the cat. In Practice 1998; 20(7): 345–349.
Moriello K, Mason I. Alopecia in cats. In: Handbook of Small Animal Dermatology. Pergamon, 1995, pp. 163–168.
Scott DW, Miller WH, Griffen CE. Acquired alopecias. Congenital and hereditary defects. Psychogenic skin dis-
eases. In: Muller and Kirk’s Small Animal Dermatology, 5th edn. Philadelphia, PA, W.B. Saunders, 1995,
pp. 720–735, 736–805, 845–858.
51. The cat with skin lumps and bumps
Rodney Clement Straw
KEY SIGNS
● Soft or firm masses on the skin or under the skin.
MECHANISM?
● Masses are usually inflammatory and infectious in nature.
● Neoplasia is less common and may be caused by cumulative solar irradiation (SCC), viruses
(fibrosarcoma), as a sequel to vaccination (sarcoma) or have an unknown etiology.
WHERE?
● Skin, subcutaneous tissue and superficial, palpable anatomical structures.
WHAT?
● Most cats with skin lumps and bumps have inflammatory lesions such as abscesses; neoplasia
is less common.

Diseases causing skin lumps and bumps
ANOMALY
● Multiple cartilaginous exostosis (p 1079)
Young cat (less than 2 years old) with hard masses fixed to underlying bone on extremities or
skull, scapula, ribs, pelvis or multiple sites. These are progressive and painful swellings.
MECHANICAL
● Foreign body* (p 1073)
Typically vegetable material such as a grass seed or awn is involved. Relatively acute onset of
swelling, often with draining tracts. Can become chronic discharging sinus and location of
swelling may move in position on the body.
continued
1067
continued
NEOPLASTIC
● Squamous cell carcinoma** (p 1069)
Usually occurs in older cats and appears as a crusty or ulcerated lesion in poorly pigmented and
sparsely haired regions of skin.
● Basal cell tumor* (p 1070)
Solitary cutaneous lesion in an older cat usually on the dorsum.
● Fibrosarcoma* (p 1071)
Soft, subcutaneous mass with poorly defined margins; 50% occur on the limbs and 25% on the
head and neck.
● Fibroma (p 1077)
Small, solitary, non-invasive mass in the skin or subcutaneous tissue.
● Mast cell tumor* (p 1074)
Solitary or multiple cutaneous masses especially on the head and neck of oriental breeds. Usually
firm, raised, well-circumscribed, hairless dermal nodules between 0.5–3 cm in diameter.
Intermittently pruritic and occasionally ulcerated (especially histiocytic form). If disseminated,
there may be signs of systemic illness including weight loss, anemia, vomiting and anorexia.
● Sweat gland neoplasia (p 1077)
Subcutaneous masses often around the base of the ear and ear canal.
● Hemangioma and hemangiosarcoma* (p 1075)
Appear as dark-red, cutaneous nodule or nodules. In the subcutaneous and muscular tissue appear
as a soft mass, and there may be a zone of echymosis surrounding the mass. May also appear as an
ulcerated lesion on the nose.
● Cutaneous lymphosarcoma (p 1078)
Very rare tumors in cats. Appear as solitary or multiple skin or subcutaneous masses varying from
a few millimeters to over a centimeter in diameter. Can be moist and erythematous or dry and flaky.
Mucocutaneous junctions may be involved with areas of superficial ulceration. Lesions may consist
of plaques, papules, nodules and areas of erythema, focal alopecia with crusting and ulceration.
● Melanoma (p 1079)
The majority appears as dark-pigmented nodules in the skin of the head, and very rarely on the
extremities. Ocular melanomas may occur and very rarely melanoma involves the oral cavity.
● Mammary gland tumors* (p 1076)
Nodule or nodules in the mammary chain, on average 3 cm in diameter. Often multiple, and
may involve both mammary chains. May be ulcerated.
INFECTION
● Catfight abscess*** (p 1079)
Painful subcutaneous mass, usually febrile.
● Fungal (p 1080)
Variably ulcerated, cutaneous or subcutaneous mass. (e.g. Cryptococcus sp.)
TRAUMA
● Hematoma (p 1080)
Subcutaneous mass, acute onset, painful.
51 – THE CAT WITH SKIN LUMPS AND BUMPS 1069
INTRODUCTION Diagnosis
Purulent exudate or sheets of neutrophils with intra-
and extracellular bacteria are evident on cytology.
MECHANISM?
Masses seen on the skin, or palpable masses on or SQUAMOUS CELL CARCINOMA**

under the skin are usually inflammatory, or less com-
monly neoplastic in origin. Classical signs
Neoplasia may be caused by cumulative solar irradia- ● Reddened flaky skin on sparsely haired,
tion (SCC), viruses (fibrosarcoma), as a sequel to vac- non-pigmented skin.
cination (sarcoma) or have an unknown etiology. ● Non-healing ulcer on predisposed areas of
head.
Multiple cartilaginous exostosis is probably of viral eti-
ology.
Pathogenesis
WHERE?
Chronic exposure to UV light may lead to the devel-
Skin, subcutaneous tissue and superficial, palpable opment of dysplasia of epithelial cells in poorly pig-
anatomical structures. mented and sparsely haired skin. The effect of UV
irradiation is cumulative, and the dysplastic cells may
undergo neoplastic change, with development of carci-
WHAT?
noma in situ. This lesion will progress to invasive
Most cats with skin lumps and bumps have inflamma- squamous cell carcinoma.
tory lesions such as abscesses; neoplasia is less com-
mon and often more serious, requiring early diagnosis Clinical signs
and prompt appropriate treatment.
Most squamous cell carcinomas occur on the head of
older cats.
DISEASES CAUSING LUMPS AND ● Predisposed sites include non-pigmented areas of
BUMPS ON THE SKIN the nasal planum, eyelids (including the third eyelid)
and periorbital skin, infra-auricular skin and pinnae.
CATFIGHT ABSCESS*** Lesions vary from small areas of reddened and flaky
skin, to deep ulcers with peripheral zones of swelling
Classical signs and proliferation.
● Characteristically cats are presented because of
● Painful subcutaneous mass, usually febrile.
chronic non-healing ulcers. There can be consid-
erable necrosis and odor with advanced lesions.
See main references on page 390 (The Pyrexic Cat) and
page 401 (The Cat With Enlarged Lymph Nodes). Squamous cell carcinoma occasionally involves the ear
canal.
● In advanced lesions there can be extension to the
Clinical signs osseous bullae, and vestibular signs may be present.
There is a sudden onset of swelling under the skin often
Bone lysis accompanies advanced-stage lesions, partic-
with a discharging sinus.
ularly those located in the periorbital area or ear
Many cats are depressed, febrile and/or anorexic. canal.
Diagnosis – Soft external beam therapy delivered by ortho-

voltage machines.
A tentative diagnosis is based on the history and typi- – Electron beam treatment from a linear accelerator.
cal lesions located on poorly pigmented and sparsely – Brachytherapy using radioactive implants.
haired regions.
Definitive diagnosis depends on histopathological Prognosis
evaluation of a biopsy specimen.
Prognosis varies with the stage of disease, but is usu-
Radiological studies are rarely useful unless there is ally good.
considerable extension to underlying bone.
Squamous cell carcinomas of the skin are generally
Cytology may be helpful. very slow to develop and progress.
Cytological evaluation of any enlarged regional lymph ● However, cats with late stages of disease seem to
node can be very useful for staging. deteriorate quickly.

Metastasis to regional lymph nodes occurs late in the
Differential diagnosis course of the disease.
The main differential diagnosis is eosinophilic granu- The major debilitating signs are associated with the
lomas of the lips, which can appear similar to squa- local tumor.
mous cell carcinoma lesions on the nasal planum. ● Pulmonary metastases are rare for solar-induced
● Eosinophilic granuloma lesions are usually con-
cutaneous squamous cell carcinoma.
fined to the lips and are often quite symmetrical.
● Diagnosis is based on histopathology or perhaps With complete surgical excision, the prognosis is very
cytology. Classical cytological appearance is of good, and 80–100% control rates can be achieved.
sheets of well-differentiated eosinophils. New lesions can develop as a consequence of continued
exposure to the sun.
Treatment
The treatment of choice is ablative surgery with wide Prevention
margins.
● This may involve such procedures as removal of Prevent exposure of high-risk cats to UV irradiation by
pinnae, nasal planectomy, full-thickness eyelid keeping them indoors during high-risk times of the
resection, enucleation with partial orbitectomy and day.
reconstructive procedures such as caudal auricular ● It is very difficult to prevent sun exposure in cli-
artery axial pattern flap. mates where UV irradiation is high.
Resected specimens should be evaluated histopatholog- In geographic regions where there is a high risk of UV
ically for completeness of resection. Incomplete resection irradiation, breeding cats with pigmented skin would
is associated with very high rates of tumor recurrence. decrease the incidence of tumors.
Cryosurgery may be useful for carcinoma in situ, or Tattooing non-pigmented skin does not prevent the
early stages of invasive squamous cell carcinoma, and development of squamous cell carcinoma.
is particularly useful for small lesions of the eyelids.
● At least two freeze–thaw cycles (rapid freeze and
slow thaw) should be used. BASAL CELL TUMORS*
● The lesion and a cuff of normal-appearing sur-
rounding tissue should be frozen to –25˚C or colder. Classical signs
● Unfortunately recurrence rates are high. ● Skin nodule often on the dorsum.
● Radiation therapy can be used, and generally is ● May have intact epithelium or variably
most effective for carcinoma in situ or early stages ulcerated.
of invasive squamous cell carcinoma. Radiation ● Often chronic history.
therapy includes:
Pathogenesis FIBROSARCOMA*
Basal cell tumors result from malignant transforma-
tion of the basal cells of the skin. Classical signs
The etiology of these tumors is unknown, but they tend ● Soft, subcutaneous mass with poorly
to affect older cats. defined margins.
● Slowly growing.
● Not painful.
Clinical signs
Basal cell tumors are a common skin tumor in older cats.
These tumors develop in the basal epithelium of the Pathogenesis
skin. Fibrosarcomas are non-encapsulated tumors of malig-
The tumors are usually solitary. nant mesenchymal cells with potential for local tissue
● They usually occur on the skin on the dorsum of the invasion.
head, neck, thorax and lumbar area. Feline sarcoma virus, which is a retrovirus that
depends on feline leukemia virus for replication, causes
Diagnosis multicentric fibrosarcomas in young cats.
Cytological examination of a fine-needle aspirate may The cause of solitary fibrosarcomas in older cats is usu-
be suggestive, but definitive diagnosis requires ally unknown.
histopathological evaluation of a biopsy specimen. There is a form of fibrosarcoma that grows in vaccina-
tion sites that is thought to be associated with post-vac-
Differential diagnosis cination inflammation (vaccine-associated sarcoma,
VAS).
Diagnosis cannot be necessarily made by the gross ● Killed vaccines with aluminum salt adjuvant have
appearance, and basal cell tumors need to be differenti- been implicated as causative agents, but the true eti-
ated from other skin neoplasms such as squamous cell ology, pathogenesis and epidemiology are still
carcinoma and mast cell tumors by histopathology. unknown.
● Rabies vaccines have been implicated, but other
Treatment vaccines may also play a role.

● Frequency of occurrence varies worldwide.
Nearly all basal cell tumors can be permanently con- ● There is a low incidence in some countries such as
trolled by complete surgical excision, although the Australia, perhaps because rabies vaccine is not
histological appearance of these tumors would tend to used.
imply an aggressive natural behavior.
● Margins of about 5–10 mm are appropriate. Solitary fibrosarcomas in adult, FeLV-negative cats are
locally invasive and have a low metastatic rate (approxi-
mately 10% of cats will develop distant metastasis).
Prognosis
The prognosis is very good if these tumors are
Clinical signs
removed completely.
● Only rarely have metastases been reported. Typical signs are a solitary, soft, subcutaneous mass
growing larger and firmer over a period of months.
With increasing size, the mass may ulcerate and
Prevention become secondarily infected.
Since the etiology is unknown, preventative measures The multicentric form occurs in cats generally less
cannot be recommended. than 5 years of age.
Vaccine-associated sarcoma arises in the area of vac- ● Adjuvant chemotherapy has been recommended
cination, usually in the interscapular space in the dor- but has not been shown to be beneficial.
sal subcutaneous tissue.
Cats with multicentric fibrosarcomas can only expe-
Fibrosarcomas are usually not painful. rience temporary palliation.
● Surgery cannot be expected to cure these cats.
Tumors may occur anywhere on the body, with 50%
occurring on limbs and 25% on the head and neck. Cats with vaccine-associated sarcoma are also more
difficult to treat.
● Recurrence and metastasis has been reported after
Diagnosis
surgery.
Cytological examination of fine-needle aspirates ● Combinations of surgery, external beam radia-
demonstrates mesenchymal cells with malignant char- tion and chemotherapy show promise in control-
acteristics. This suggests fibrosarcoma. ling these very aggressive tumors.
Definitive diagnosis requires histopathological evalu-
ation of properly acquired biopsy material.
● Care must be taken to perform the biopsy, so the Prognosis
entire biopsy site may be removed with the tumor at The prognosis is good for solitary fibrosarcomas in
the time of resection. adult cats where complete surgical excision has been
There is usually an inflammatory component to the performed.
● The ability to completely excise the mass depends
histology of vaccine-associated sarcoma, with pre-
dominantly lymphocyte and macrophage populations. on the tumor location, tumor size and expertise of
the surgeon.
Histological grading including determining the
mitotic index, derived from evaluating ten high-power Histological grade including mitotic index may help
fields, may add prognostic information. predict survival following surgery, and cats with high-
grade tumors should be followed more closely or may
Regional radiography may help determine the local be given adjuvant therapy.
tumor stage and direct surgical planning.
The prognosis is poor with multicentric fibrosarcomas.
Thoracic radiography and regional lymph node
cytology are required for staging although metastasis is Vaccine-associated sarcoma is associated with a
rare for cats with solitary fibrosarcoma. variable prognosis with often disappointing out-
comes even with wide excision.
Cats with viral multicentric fibrosarcoma will be FeLV
positive.
Prevention
Differential diagnosis The Vaccine-Associated Feline Sarcoma Task Force
Fibromas and old wounds with abundant fibroplasia (VAFSTF) was formed to address this evolving and
can have similar cytological appearance on fine-needle important issue and can be found at http://www.
aspirates. avma.org/vafstf/default.htm on the Internet.
Other names are given to these soft tissue sarcomas The VAFSTF has made a number of recommendations:
such as spindle cell tumors, neurofibrosarcomas or ● Cats should not be vaccinated unnecessarily.
nerve sheath tumors. – Rabies vaccines licensed for every 3 years

should not be given yearly and strictly indoor
cats should not be vaccinated for FeLV.
Treatment
● Vaccines should not be given in the interscapular space.
Wide surgical excision is the treatment of choice. – It is suggested that the rabies vaccines are given
● Tumor margins should be evaluated histologically on the right hindlimb and the FeLV be given on
for completeness of resection. the left hindlimb.
– It is recommended that these vaccines be given in ● If a sarcoma is identified, then wide or radical sur-
a distal location when possible, so that the limb gical excision should be performed.
may be amputated if a sarcoma develops, thus
Test for FeLV to reduce the suspicion of FeSV-related
sparing the cat’s life.
sarcoma.
– Other vaccines should be given over the lateral
shoulders away from the interscapular site. Although the rate of distant metastasis is low, it is rec-
● Single-dose vial usage is recommended. ommended that thoracic radiographs be performed
– Multi-vaccine products should be avoided. prior to excisional surgery.
● When giving booster vaccinations, previous vac-
Wide surgical excision with margins of up to 5 cm has
cine sites should be avoided.
been recommended. Margins should be evaluated via
● In the past, it has been suggested that IM adminis-
histology.
tration be performed instead of SQ injection. This
may only result in more difficult detection, reduc- Wide surgical excision with less than 5 cm performed at
ing the chance of early detection and surgical cure. the first occurrence with adjuvant external beam radia-
● Monitoring for masses occurring in common vacci- tion therapy has a good chance of long term control of
nation sites should be performed by owners and this cancer.
reported to the veterinarian.
Recurrent tumors are always more difficult to manage
– Vaccine-associated granulomas are common.
than the initial tumor with adjustments external been
A recent study evaluated cats receiving rabies
radiation thoraphy.
vaccines from four different manufacturers, and
found that 100% of the cats developed local
reactions. Reactions often occurred within a few FOREIGN BODY*
weeks, and resolved by 1–2 months later.
● Do not vaccinate cats that have had a prior history Classical signs
of a vaccine-associated sarcoma.
● Mass under the skin, often with a
discharging sinus.
GUIDELINES FOR RECORDING ● Swelling may “come and go” and may be
SUSPECTED CASES OF VACCINE- chronic.
ASSOCIATED SARCOMA
The location, vaccine type, manufacturer, serial numbers Pathogenesis
of the vaccine should be recorded in each patient’s record.
Any foreign body under the skin may result in an abscess
All other medications administered subcutaneously or or chronically draining lesion. The foreign body is usu-
intramuscularly should be recorded as well. ally of plant origin such as a grass seed or awn, but may
Any vaccine response, whether inflammatory or neo- even be a tooth broken off during a cat fight.
plastic, should be reported to the vaccine manufacturer.
● Also report outcome of the case as it becomes known.
Clinical signs
Typically there is an acute onset of a soft tissue
MANAGEMENT OF VACCINE-ASSOCIATED swelling under the skin, which can occur anywhere on
SARCOMA IN CATS the body.
If a mass in a vaccine site persists for longer than The swelling may be acute or chronic.
1 month, or if it exhibits rapid growth, a Tru-cut®,
Purulent material sometimes drains from a sinus in
wedge or excisional biopsy should be performed.
the mass.
● If a granuloma is identified, a conservative resec-
tion may be planned, if excision was not already The swelling is variably painful, and is often less
performed. painful if chronic.
The owner may describe the lesion as “moving”, because Pathogenesis

it may appear in slightly different locations if the foreign
body is migrating. Alternatively it may appear to “come Mast cell tumors are comprised of anaplastic mast
and go”. cells and histiocytic cells.
The mass is persistent, and wound drainage is only par- There is no known etiology for feline mast cell tumors.
tially responsive to antibiotics. Siamese cats appear to be predisposed.

Definitive diagnosis requires identification of the for- Mast cell tumors typically appear as firm, raised, well-
eign body. circumscribed, hairless dermal nodules varying in
size from 0.5 cm. They are often multiple; 20% were
Fine-needle aspirate cytology is consistent with gran-
multiple in one report and the majority in another.
ulomatous inflammation and contains neutrophils and
macrophages. The head and neck are more commonly affected than
the trunk or limbs.
The foreign body is usually discovered at surgery, and
rarely by radiography or ultrasonography. Tumors are usually not painful, but may be itchy.
Occasionally the tumors may become ulcerated, espe-
cially the histiocytic form.
Treatment
Mast cell tumors can have visceral involvement, but the
Treatment involves surgical removal of the foreign
visceral form usually occurs as a separate entity (see
body, and drainage or removal of the sinus tract.
systemic mastocytosis, page 689).
Perioperative antibiotics are indicated.
Lesions may become erythematous and edematous
after manipulation (Darier’s sign).
Prognosis
Cats with systemic involvement are usually sick, with
Prognosis is excellent with surgical removal of the for- weight loss, anorexia, vomiting, diarrhea (variably with
eign body, but the foreign body can be hard to find. bloody stools), anemia and even shock.
● Usually, however, cats with cutaneous mast cell
tumors are otherwise healthy.
MAST CELL TUMORS* There are two major forms of cutaneous mast cell
tumors in cats, mastocytic and histiocytic.
Classical signs ● Mastocytic mast cell tumors occur typically in
middle- to old-aged cats.
● Solitary or multiple cutaneous masses.
● Most mastocytic tumors are the compact form with
● Usually on the head and neck.
a fairly benign behavior.
● Usually firm, raised, well-circumscribed,
– A few are the diffuse form, which are more
hairless dermal nodules between 0.5–3 cm
anaplastic and malignant.
in diameter.
● Histiocytic mast cells tumors are uncommon,
● Intermittently pruritic and occasionally
occur in cats less than 4 years of age (mean age 2.4
ulcerated (especially histiocytic form).
years) and Siamese are predisposed.
● If disseminated, there may be signs of
● Histiocytic tumors usually occur as multiple cuta-
systemic illness.
neous nodules around the head.
● Weight loss, anemia, vomiting and
– These lesions are of low grade and may even
anorexia.
spontaneously regress.
Diagnosis The metastatic rate has been reported to be as high as

22%.
Fine-needle aspirate cytology is often diagnostic
showing round cells with metachromatic granules. Some cats do acquire new primaries.
Histopathology is usually necessary to diagnose the
histiocytic form where granules are not prominent. HEMANGIOMA AND HEMANGIOSARCOMA*
Extension to regional lymph nodes is not common,
but any enlarged node should be evaluated at least by Classical signs
fine-needle aspirate. ● Dark red cutaneous nodule.
In cats where disseminated disease (spleen or intes-
tinal forms) is suspected, tests such as hematology, Pathogenesis
serum biochemistry, buffy coat smear or bone marrow
aspirate, coagulation studies, thoracic and abdominal Hemangiomas are benign tumors of vascular
radiography and abdominal ultrasonography should be endothelium. The malignant, anaplastic counterpart is
considered. hemangiosarcoma.
Hemangiosarcomas of the nasal planum and eyelid may
Differential diagnosis be solar induced.
Other cutaneous neoplasms should be considered as Clinical signs

differential diagnoses. Differentiation is based on fine-
needle cytology or histological examination. Hemaniomas and hemangiosarcomas are very rare in
cats.
Treatment In the skin, they usually appear as red to dark-red

nodules of varying size.
For the mastocytic form, surgery is the preferred ● Spontaneous hemorrhage from the lesions may be
treatment. Surgical margins need not be as wide as for a feature.
canine mast cell tumors (3 cm), since most have a rela-
tively benign biological behavior. Wider margins are They may also appear as an ulcerated lesion on the nose.
necessary in the case of diffuse mastocytic forms. Hemangiosarcoma can occur in the subcutaneous and
Conservative resection is appropriate for the histiocytic muscular tissue as a soft mass, and there may be a
form. zone of echymosis surrounding the mass.
Cats with the splenic form benefit from splenectomy, Hemangiosarcoma can also occur in visceral organs,
even though tumor cells may be disseminated. and rarely the skin lesions may be secondaries to pri-
Little is know of the efficacy of adjuvant therapy for mary disease in the viscera.
mast cell tumors in cats.
Diagnosis
Cytological examination may be unrewarding because
Prognosis
the cells do not exfoliate well.
In general, the prognosis for most cats with mast cell ● Malignant mesenchymal cells may be found at the
tumors is very good. feathered edge of cytology slides.
Most cats experience long-term control after complete Definitive diagnosis requires histological examination.
surgical excision.
Treatment
Local recurrence rates for the mastocytic form fol-
lowing surgery vary up to 24%. Surgical resection is the treatment of choice, and for
● If the tumor recurs, it usually does so within 6 hemangiosarcomas, as wide a margin as possible
months of surgery. should be taken, preferably greater than 10 mm.
Prognosis ● Adenocarcinomas may further be divided into tubu-

lar, papillary and solid carcinomas.
Hemangiomas are benign.
Cutaneous and subcutaneous hemangiosarcomas Clinical signs
appear to be locally invasive only, and metastases are The tumors usually lie in the subcutaneous tissue adja-
not common. cent to the nipple, and adhere to the overlying skin.
Hemangiosarcomas have a high metastatic potential ● The size of tumor is variable, with a mean size of
when intra-abdominal or intrathoracic organs are 3 cm and rarely exceeding 9 cm in diameter.

involved. About 15–25% are ulcerated at the time of diagnosis.
However, hemangiosarcomas involving muscles also Local invasion into underlying musculature and cuta-
appear to have a high incidence of metastasis. neous ulceration is common.
Feline mammary tumors grow rapidly.
● The average duration of the history at the time of
MAMMARY GLAND TUMORS*
diagnosis is 5 months.
Classical signs About 66% of feline mammary tumors will be multi-
ple, and about 35% involve both chains of mammae.
● Nodule or nodules in the mammary chain,
on average 3 cm in diameter. Regional lymph nodes are involved early.
● Often multiple, and may involve both
Some cats with tumors that have been present for a long
mammary chains.
time may present with signs referable to metastasis,
including weight loss, dyspnea and coughing.
Pathogenesis
There is a seven-fold greater risk of mammary carci-
Benign lesions such as adenomas, focal mammary
noma in intact cats compared to spayed cats.
dysplasia and fibromas can mimic the gross appear-
● Unlike in dogs, ovariohysterectomy before the first
ance of mammary gland tumors, and can be differenti-
estrus does not eliminate the possibility of mammary
ated on histopathology.
tumor, but appears to have some sparing effect.
It has been observed that long-term progesterone Diagnosis
therapy in cats is associated with an increased inci-
dence of mammary tumors and dysplasias. Presumptive diagnosis of a mammary gland tumor can
be made on the presence of a mass in the breast tissue.
Mammary tumors are the third most common tumor
in cats. Cytological examination of a fine-needle aspirate may
● The overall risk is 25.4/100 000 female cats. reveal malignant cells, but false-negative cytology is
● Age range is 2.5–19 years with 70% between 9–13 possible.
years, and an average of 10.8 years. Definitive diagnosis can only be made by a surgical
● There is no breed predilection.
biopsy and histological examination.
The majority of mammary gland tumors are malignant Due to the high metastatic potential of female mam-
(86%). mary gland tumors, chest radiography should be per-
● Of the malignant tumors, adenocarcinoma is the
formed before any surgical procedure.
predominant type.
● Mammary neoplasia can further be evaluated based
Treatment
on (l) cellular differentiation and the degree of tubule
formation, (2) nuclear pleomorphism, and (3) the fre- The treatment of choice is radical mastectomy of all
quency of mitosis. glands on the affected side, because of the high local
recurrence rate, high rate of malignancy and the fre- Clinical signs
quent multicentric origin of feline mammary gland
tumors. Fibromas are either slow growing or have a long his-
● The opposite side should be removed in 2–4
tory of stable size.
weeks, or a bilateral mastectomy performed if pos- Typically they appear as a non-painful small cuta-
sible. neous or subcutaneous mass, usually less than 10 mm
● All regional lymph nodes should be palpated and diameter, which is generally not ulcerated.
removed if enlarged.
● In cases of local recurrence, a second surgery is
Tumors are mobile, and not invasive to adjacent struc-
often possible and may be indicated to prolong sur- tures.
vival.
Doxorubicin alone (1 mg/kg IV every 21 days for 4–5 Diagnosis
treatments), or doxorubicin and cyclophosphamide On fine-needle aspirate, not many cells exfoliate and
(200 mg/m2 IV or orally) combination chemotherapy the cells do not have characteristics of malignancy. The
may help as adjuvant therapy to prolong the disease- cells are elongated with small nuclei.
free survival.
A fibrous and tough texture is often noticed when per-
forming needle aspirates.
Prognosis
No bone lysis is evident in adjacent skeletal structures.
The prognosis in general is poor.
● The median survival time of cats treated with sur-
Definitive diagnosis requires histopathological exam-
gery alone is 10–14 months. ination of an excised specimen.
Tumor volume has a significant effect on postoperative

survival time. Treatment
● Cats with a total tumor volume of < 9 cm3 can be Excisional biopsy is diagnostic and curative.
expected to survive greater than 18 months, cats
with a total tumor volume of 10–27 cm3 can be
expected to survive 12 months, and cats with a Prognosis
tumor volume greater than 27 cm can be expected Prognosis is excellent.
to survive 7 months.
Cats with well-differentiated tumors appear to sur-
vive longer than those with poorly differentiated SWEAT GLAND NEOPLASIA
tumors.
Classical signs
● Masses of the head and neck, especially
FIBROMA around the external and middle ear canal.
Classical signs
Pathogenesis
● Solitary cutaneous or subcutaneous mass
usually not greater than 10 mm in Sweat gland tumors arise from apocrine or cerumi-
diameter. nous gland cells. Most commonly they arise around
the external and middle ear canal.
The etiology of sweat gland tumors is unknown.
Pathogenesis
Most of these adnexal tumors are malignant (carcino-
Fibroma is caused by benign hyperplasia of fibromas), and are locally invasive with a variable
cytes. The cause not known. metastatic potential.
Extension to regional lymph nodes and later to the

CUTANEOUS LYMPHOSARCOMA
lung can be seen.
Classical signs
Clinical signs ● Solitary or multiple skin or subcutaneous
masses varying from a few millimeters to
Ceruminous and apocrine gland neoplasms are rela-
over a centimeter in diameter.
tively common in cats, however perianal tumors are
● Can be moist and erythematous or dry and
rare.
flaky.
Cats usually present because of a mass often around the ● Mucocutaneous junctions may be involved
base of the ear and ear canal, or for signs of otitis with areas of superficial ulceration.
externa.
Regional lymph nodes may be enlarged. Pathogenesis
Cutaneous lymphosarcoma lesions are comprised of
diffuse infiltrates of malignant, poorly differenti-
Diagnosis
ated lymphoid cells (B-lymphocytes). A T-cell form
Cytological examination and demonstration of typical (mycosis fungoides) has been described.
polyhedral cells in rafts with nuclear pleomorphism
Since affected cats are usually older and FeLV nega-
and other malignant characteristics may be helpful as a
tive, the cause of this disease is not well understood.
screening test, but definitive diagnosis requires histo-
logical evaluation of a biopsy.
Clinical signs
Regional lymph nodes, particularly cranial cervical
nodes, need to be evaluated by cytology, histology or These tumors are very rare in cats.
both, and pulmonary radiography should be per- Appear as solitary or multiple skin or subcutaneous
formed for staging. masses varying from a few millimeters to over a cen-
● Palpate the neck carefully and perform fine-needle
timeter in diameter.
aspirate cytology on any enlarged nodes, or ● Can be moist and erythematous or dry and flaky.
remove or perform Trucut needle biopsy on such ● Mucocutaneous junctions may be involved with
nodes for histopathology. areas of superficial ulceration.
● Take thoracic radiographs in both lateral projec-
tions and ventrodorsal or dorsoventral projections. Lesions may consist of plaques, papules, nodules,
and areas of erythema, focal alopecia with crusting
and ulceration.
Treatment Usually there is no systemic involvement, and there
Wide surgical excision including total ear ablation are minimal abnormalities on hematology or serum
for external ear canal ceruminous carcinomas is the biochemistry.
treatment of choice.
Diagnosis
Adjuvant radiation and chemotherapy have been
described, however many lesions will progress despite Cytological examination showing abundant malig-
extensive treatment. nant round cells is useful to establish a presumptive
diagnosis.
Prognosis Definitive diagnosis requires histopathology.
Long-term remission is possible where clean surgical

margins are attained in cats with no metastatic disease. Treatment
Overall a fair prognosis must be given. For solitary lesions, excisional surgery may be curative.
Small lesions may respond well to superficial radia- but a definitive diagnosis should be obtained by
tion therapy. histopathology.
Single or multimodal chemotherapy may be used, but
the response to therapy is often disappointing. Mycosis Treatment
fungoides may be treated with retinoides such as Treatment of choice is surgical excision, preferably
isotretinoin. with margins of 10 mm or greater. Cryosurgery is an
alternative for small lesions or eyelid tumors.
Prognosis
Prognosis
The prognosis for cats with widespread disease is
poor. The prognosis for non-ocular dermal melanomas is fair;
reported metastatic rates are 5–25%.
Cats with small solitary lesions may do well initially
with surgical excision, but generalized disease is
likely to occur within 12 months. MULTIPLE CARTILAGENOUS EXOSTOSIS
Classical signs
MELANOMA ● Multiple firm masses palpable mostly over
the ribs, scapulae, pelvis, the skull and
Classical signs possibly some long bones in a young,
skeletally mature cat.
● Black pigmented cutaneous lesion.
● Swellings are progressive and painful.
Pathogenesis Pathogenesis
● Melanoma can be induced experimentally with Multiple cartilaginous exostosis is thought to have a
feline sarcoma virus, but this is not thought to be viral etiology because virtually all cats are FeLV pos-
involved in the pathogenesis of the clinical disease. itive. It does not appear to have a familial basis as it
does in dogs.
There is continuous bone growth from ectopic carti-
Clinical signs
lage caps particularly on flat bones, and at sites such as
Melanoma is very rare in cats and can be benign or the scapulae, vertebrae, mandible and skull.
malignant.
Lesions progress after skeletal maturity, unlike the
The majority appears as dark-pigmented nodules in static character of solitary cartilaginous exostoses in
the skin of the head, and very rarely on the extremi- mature dogs.
ties.
Exostoses may undergo malignant transformation.
Very rarely melanoma involves the oral cavity.
Ocular melanomas usually affect the intraocular Clinical signs
structures or the eyelid, and may occur in the uveal Multiple firm masses occur which are palpable mostly
tract. over the ribs, scapulae, pelvis, the skull and possibly
some long bones in a young, skeletally mature cat.
Diagnosis Rapid progression may occur over just a few weeks to
months, resulting in prominent hard swellings causing
Cytological examination showing heavily pigmented
pain, lameness and loss of function.
large solitary cells or lightly grouped cells varying
from round to spindloid in shape is highly suggestive, Occur in young cats, less than 2 years old.
Differential diagnosis Numerous common and less common fungi are capable
of producing cutaneous masses in cats including
The main differential diagnosis is osteosarcoma which Cryptococcus, Sporothrix and Coccidiodides.
usually only affects one bone at presentation.
Systemic signs such as inappetence, weight loss and
Diagnosis fever may be present. Dyspnea or CNS signs may be
present in some cats.
Diagnosis is based on clinical signs, radiographic find-
ings and biopsy results.
Diagnosis
Radiographic appearance is of multiple, focal exos-
toses that blend with normal underlying bone. The diagnosis is made by demonstrating the organisms
on cytology, histology, fungal culture or serology.
Most cats are FeLV positive.
Definitive diagnosis relies on histopathology.
HEMATOMA
Treatment
Classical signs
Lesions can be excised for palliation, but there is no
effective cure.
● Subcutaneous mass, acute onset, painful.
Prognosis
Clinical signs
Prognosis is extremely poor, because the lesions are
usually progressive, and recurrence following surgery Hematomas may occur as solitary or multiple subcuta-
is common. The disease is painful and debilitating. neous swellings. Purple dicoloration of the overlying
non-pigmented skin may be evident. There may be a
Fungal history of trauma or coagulopathy.
Classical signs
Diagnosis
● Variably ulcerated, cutaneous or
subcutaneous mass. (e.g. Cryptococcus sp.). A presumptive diagnosis is based on ruling out other
disorders by fine-needle cytology (peripheral blood,
Clinical signs macrophages and other inflammatory cells may be
identified), combined with a history of trauma or iden-
There are often ulcerated skin lesions which do not tification of a coagulopathy.
respond to antibiotics.
RECOMMENDED READING
Withrow SJ, MacEwen EG (eds) Small Animal Clinical Oncology, 3rd edn. WB Saunders Co., Philadelphia, 2001.
52. The cat with non-healing wounds
Gregory Burton
KEY SIGNS
● Erosion, ulceration.
● Nodules or plaques with ulceration or fistulae.
● Serosanguineous to purulent exudate +/- tissue grains.
● Subcutaneous fibrosis.
● Extracutaneous symptoms may be present.
MECHANISM
● Non-healing wounds occur where there is a failure of re-epithelialization, dermal fibroplasia
and or angiogensis.
WHERE?
● Skin (diseases involving the epidermis, dermis, panniculus and cutaneous blood vessels)
and mucocutaneous junctions.
WHAT?
● Most cats with non-healing skin wounds have infections (mycobacteria, aerobic and/or anaerobic
bacteria, or fungi). Neoplasia, allergies, immune-mediated and metabolic diseases are less
common.

Diseases causing non-healing wounds
ANOMALY
● Cutaneous asthenia (p 1100 - 1101)
Congenital disease resulting in hyperextensibility and fragility of the skin. Kittens present with
spontaneous tears or necrotic, slow-healing crusted ulcerations.
● Epidermolysis bullosa (p 1101)
Congenital epidermal basement membrane disease with signs evident shortly after birth. Skin, foot
pad and mouth ulcers particularly at frictional areas. Nail shedding is common.
continued
1081
continued
METABOLIC
● Acquired cutaneous fragility syndrome (p 1098)
Thin, fragile skin which is not hyperextensibile, and which tears easily. Secondary to metabolic
conditions such as hyperadrenocorticoidism (endogenous or iatrogenic) or diabetes.
● Xanthoma (p 1099)
Plagues or nodules with a yellowish-white appearance which often ulcerate and occur mostly over
bony protuberances (areas of incidental trauma). Most common in cats associated with hyperlipi-
demia.
● Metabolic epidermal necrosis (MEN) (p 1099)
Crusting lesions at mucocutaneous junctions and pressure points in an unwell cat. Skin lesions are
secondary to pancreatic or hepatic disorders.
NEOPLASIA
● Squamous cell carcinoma** (p 1089)
Occurs in old cats (average age 9 years). Multiple or single lesions occur on the pinnae, philtrum,
nares, forehead and palpebrae, in non-pigmented, thinly haired areas. Lesions may be proliferative
or ulcerative, and are slow to metastasize.
● Multicentric squamous cell carcinoma in situ (p 1089)
Occurs in older cats (> 10 years). Multifocal lesions occur over the head, neck, shoulders and fore-
limbs on pigmented, thickly haired skin. Begin as hyperkeratotic macules and evolve to thick-
crusted, ulcerated plagues. Progress slowly, with waxing and waning signs.
● Melanoma (p 1097)
Occurs in older cats (average age 10 years) as solitary lesions on the head or neck. Size and shape are
variable ranging from a dome, to a plague or polypoid shape, and ulceration is frequent.
● Basal cell carcinoma (BCC) (p 1097)
Frequently pigmented and/or cystic tumors of the head, neck, thorax, nasal planum and eyelids of
older cats. Usually solitary and frequently ulcerated.
● Mast cell tumor* (p 1092)
Occur as single to multiple tumors on the head of older cats. Tumors may “enlarge” and become
erythematous after palpation or aspiration. Rarely young Siamese cats have multiple nodules
around the head.
● Cutaneous lymphoma (p 1097)
Very rare tumors in cats. Signs of T cell tumors (mycosis fungoides) include “non-inflammatory”
alopecia, scaling, erythroderma (diffuse reddening of the skin), hypopigmentation of hair or skin,
ulceration, plagues and nodules. B cell neoplasia produces dermal nodules with or without ulcera-
tion. Systemic signs of weight loss, diarrhea and respiratory distress may be present.
NUTRITIONAL
● Pansteatitis/vitamin E deficiency (p 1104)

Cats eating diets high in oils, especially fish oils may develop fever, lethargy, painful skin, general-
ized firm feel to the subcutaneous fat, and skin sinuses with gelatinous exudate.
52 – THE CAT WITH NON-HEALING WOUNDS 1083
INFLAMMATORY/INFECTIOUS
Viral:
● Pox virus (feline cowpox)* (p 1091)
Caused by orthopoxvirus, which is not uncommon in Western Europe. Transmission is via direct
contact with rodents, mostly in male free-roaming adult cats. Focal ulcer or abscess is followed 7–10
days later by generalized small (0.5–1 cm) crusted ulcers. Concurrent pneumonia is a poor prognos-
tic sign.
● Herpesvirus 1* (p 1092)
Cutaneous manifestation of feline rhinotracheitis infection produces ulcerative lesions seen mostly
on the nasal planum. There may or may not be concurrent ocular or respiratory disease.
Bacterial:
● Bacterial infections*** (p 1086)
Usually preceded by history of skin penetration, e.g. cat fight. Actinomycotic mycetoma are char-
acterized by the triad of tumefaction, sinus tract formation and tissue grains within the exudate.
Other bacterial infections include Nocardia, Staphylococcus, L forms, and Yersina pestis.
Staphylococcus produces a firm subcutaneous to dermal nodule, which may be alopecic, ulcerated,
abscessed with or without numerous draining tracts. Yersina pestis (plague) infection commonly
results in submandibular lymphadenopathy, fever and subcutaneous abcessation. L forms produce
cellulitis 4–5 days after injury. The cellulitis spreads rapidly with the development of multiple fis-
tulae and febrile response. Septic arthritis is a common sequel, and affected joints ulcerate produc-
ing a grayish mucinous exudate.
Mycobacterial:
● Atypical mycobacterial infections*** (p 1085)
Occur secondary to skin penetration, for example, the cat bite abscess that does not heal. Insidious pro-
gression from circumscribed plague or nodule to multiple sinuses with seropurulent exudate, board-like
fibrosis and pain on palpation. Occur mostly on the tail-base and ventral abdomen.
● Feline leprosy* (p 1090)
Mostly young cats (1–3 years). Non-painful, ulcerated nodules on the limbs and head.
● Cutaneous tuberculosis (p 1093)
Mostly caused by M. bovis from ingestion of unpasteurized milk. Abscesses, nodules, ulcers and
plaques develop with thick green or yellow exudates. Many cats have other organ involvement
including GIT, CNS or respiratory signs.
Fungal:
● Sporotrichosis (p 1095)
Traumatic implantation of fungi occur via vegetable foreign bodies, or secondary to a cat fight.
Sporotrichosis is an important zoonosis. The cutaneolymphatic form is most common. It appears
as a wound on a limb, with a tract of nodules which may ulcerate, extending along the local lym-
phatics.
● Eumycotic mycetoma (p 1093)
Occurs in geographic areas along the Tropic of Cancer. Infection occurs via wound contamination.
Ulcerated papules or nodules on the limbs or face, which develop draining sinus tracts. Black or
continued
continued
white grains are evident in the mycetoma from the fungal hyphae. Black-grained – Curvularia genic-
ulata and Madurella grisea. White-grained – Pseudoallescheria boydii and Acremonium hyalinum.
● Pseudomycetoma (p 1094)
Occurs exclusively in Persian cats. Subcutaneous nodules form mainly on the dorsum and may
ulcerate. They represent granulomas from Microsporum canis infection. More typical signs of
superficial dermatophytosis may be evident.
● Cryptococcosis* (p 1089)
Skin lesions occur as multiple or single papules and nodules, which often ulcerate. They may or
may not occur with CNS, respiratory or ophthalmic signs. Most common sign is a firm swelling
over the bridge of the nose or planum nasale, or a polyp-like mass in the nasal opening.
● Pheohypomycosis (p 1095)
Occurs as a solitary nodule, usually on the paw, nose, limb or trunk. The lesion may ulcerate with
sinus formation. Dissemination is rare.
● Histoplasmosis, blastomycosis and coccidiomycosis* (p 1090)
Chronically draining lesions together with dyspnea and weight loss. Blastomyces and coccid-
ioidomyces are very rare in cats. Histoplasmosis is most frequent along Ohio, Missouri and
Mississippi river valleys in the US.
Immune-mediated:
● Feline eosinophilic granuloma complex*** (p 1088)
Brightly erythemic plague associated with incessant grooming of the site, or appears as an indolent
ulceration of the upper lip adjacent the nasal philtrum. Oral ulcerations and nodules may be present.
● Vasculitis and miscellaneous ulcerative dermatoses (p 1103)
Ulcerations of extremities (nose, ear tips, tail tip and foot-pads). In some cats is associated with neopla-
sia or a drug reaction.
● Erythema multiforme/toxic epidermal necrolysis (p 1105)
Multifocal (erythema multiforme) or confluent (toxic epidermal necrolysis) ulceration and crusting
of skin and mucous membranes.
Idiopathic:
● Idiopathic feline ulcerative dermatosis (p 1103)
Sudden appearance then insidious course of ulceration and crusting of the dorsal cervical area.
Pruritus is variable but may be intense and not glucocorticoid responsive.
Toxic/drug:
● Chemical dermatitis (p 1102)
Hair loss, ulcers or crust-covered erosions on contact sites. Oral ulceration and ptylism may result
from ingestion of the chemical during grooming.
Trauma:
● Traumatic panniculitis (p 1104)
Non-antibiotic responsive, discharging wound in inguinal or dorsolumbar area which presents 2–3
weeks after blunt trauma at that site.
INTRODUCTION DISEASES CAUSING NON-HEALING

WOUNDS
MECHANISM?
Wound healing is characterized by chronologically over- ATYPICAL MYCOBACTERIAL
lapping phases of inflammation, proliferation (epithelial INFECTIONS***
regeneration and fibroplasia), angiogenesis and tissue
remodeling. Classical signs
Wound healing is prolonged or prevented if there is

● Alopecic plaques with multiple fistulae.
prolongation of inflammation (e.g. because of infec-
● Chronic serosanguineous exudate.
tious agents), or proliferation is inhibited (e.g. from
● Progressive subcutaneous fibrosis.
ischemia, ongoing cellular injury, anti-mitotic drugs),
● Discomfort on palpation of skin.
or there is inhibition of angiogenesis or altered tis-
sue remodeling (e.g. from increased tissue protease
activity). Pathogenesis
Each stage of wound healing is intrinsically interde- Mycobacteria organisms are ubiquitous within the
pendent. Interference at any stage can lead to a failure environment in soil and water. They enter the body via
of wound healing. penetrating wounds including cat fights, vegetable
foreign body and abrasions.
Wounds that have not resolved within 3 weeks should
be considered non-healing wounds. Organisms most frequently isolated include
Mycobacterium smegmatis, M. fortuitum, M. chelonae,
M. thermoresistible, M. xenopi, M. phlei. They are
selective for the panniculus because of their triglyceride
WHERE? requirement and the immunological advantage. The
Epidermis, dermis, panniculus and cutaneous blood complex cell wall structure allows mycobacteria to
vessels. survive intracellularly.
Clinical signs
WHAT?
Initially there is a circumscribed plaque or nodule that
Non-healing wounds involving the epidermis are progresses to alopecic areas with numerous fistulae.
most commonly: neoplasia, viral, chemical toxicity,
immune-mediated diseases and congenital abnormal- Serosanguineous exudates are typical.
ities. Board-like thickening of the skin and pain is evident
Non-healing wounds involving the dermis are most on palpation. Lesions occur most commonly on the
commonly: infectious agents, hypersensitivy diseases, ventral abdomen and lateral flanks.
neoplasia. There may be a history of trauma to skin.
Non-healing wounds involving the panniculus are
most commonly: infectious agents, traumatic ischemia. Diagnosis
Non-healing wounds involving blood vessels are most Diagnosis is based on demonstration of the organism
commonly: immune-mediated disease. in the exudate or in biopsied tissue.
Cytological examination of material obtained from Surgery requires a wide excision. Extensive recon-
the sinus tracts reveals pyogranulomatous inflamma- struction may be required following excision of
tion. Ziehl–Neelsen (ZN) stain may show acid-fast affected tissue.
bacilli.
Antimicrobial drugs should be continued for several
Histopathological examination requires deep biopsy months post-operatively.
to include subcutaneous fat. Take a wedge section
avoiding the sinuses. This is submitted in formalin for
Prognosis
routine H&E stains, Gram stain for bacteria, Gomori
methanine silver stain for fungi and ZN stain for Prognosis is guarded where extensive disease exists at
mycobacteria. Histopathology reveals pyogranuloma- the time of presentation. Early diagnosis, including
tous to granulomatous panniculitis with neutrophil- identification of the organism, and aggressive surgical
rimmed lipocysts. With ZN stain low numbers of and antimicrobial treatment offers a more favorable
acid-fast bacilli may be seen within the lipocysts outcome.
(extracellular).
Culture additional wedges biopsies collected. Sterilely BACTERIAL INFECTIONS***
trim off the epidermis, and submit the remaining tissue
in a sterile, saline-moistened guaze swab for culture. Classical signs
Specifically request mycobacterial culture if suspected.
● Nodules, plaques or abscesses.
Aspiration of wound fluid and rapid innoculation of a
● Fistula formation.
culture medium may be better than a deep tissue sample,
● Serosanguineous to purulent to “tomato
if you have ready access to a laboratory that specializes
soup” exudate +/- tissue grains.
in mycobacterial culture and identification.
PCR confirmation of mycobacteriosis and species
Pathogenesis
identification is available at some laboratories.
Infections usually involve commensal mouth organ-
isms or ubiquitous environmental organisms intro-
duced to the skin through traumatic implantation via
Differential diagnoses include bacterial mycetoma, claw wounds, bites, vegetable, foreign bodies, etc.
subcutaneous mycosis, sterile panniculitides.
Organisms include:
Clinical signs can be indistinguishable if tissue grains
● Actinomyces from oral and bowel flora.
are not evident. Special stains of histological sections
● Nocardia, a soil saprophyte.
and anaerobic, aerobic, fungal and mycobacterial cul-
● Staphylococcus from the oral cavity.
ture allow for differentiation.
● Yersinia pestis (plague) from a lagomorph or rodent
reservoir and transmission via inhalation, ingestion
or arthropod vector.
Treatment
● L forms which are mutated from the parent organism.
Treatment involves prolonged antibiotic therapy
(months) to reduce the size of the lesion combined
Clinical signs
with surgical excision.
Actinomyces and Nocardia have several different
Where possible, choice of antibiotic should be based on
presentations but dissemination is rare.
in-vitro sensitivities.
● Cutaneous form is associated with firm subcuta-
Commonly used drugs for atypical mycobacteria neous to dermal nodules which frequently are
include doxycycline 5 mg/kg/day, fluoroquinolones ulcerated, abscessed or contain numerous drainage
5 mg/kg/day, clofazamine 2–8 mg/kg/day and clar- tracts.
ithromycin 10 mg/kg bid. Combinations may be con- – Head, neck, flank, thoracic and abdominal wall
sidered where sensitivities are not known. are the most common sites.
– The exudate often appears as “tomato soup Culture of deep tissue is required for successful diag-
with sulfur granules”. nosis. A large tissue sample is best, for example,
– Regional lymph nodes are enlarged. a cubic centimeter of tissue. Prepare the biopsy site as
– Actinomycotic mycetoma are characterized by for sterile surgery, remove an elliptical biopsy which
the triad of tumefaction, sinus tract formation must include the subcutaneous fat, and avoid sampling
and tissue grains within the exudate. sinuses because of surface contamination. Trim the epi-
● Effusive form occurs in the chest or abdomen. dermis and submit the remaining tissue in a sterile
Signs include fever and depression as well as respi- moistened swab within an air-tight sterile specimen
ratory distress or abdominal enlargement. container for culture.
● Osteomyelitis form presents with lameness, fever ● Request aerobic, anaerobic, fungal and mycobacte-
and hyperesthesia. rial culture.
● If copious exudate is present, aspirate the exudate
Staphylococcus (botryomycosis) produces a firm subcu-
into a sterile syringe, cap the syringe and submit for
taneous to dermal nodule that may be alopecic, ulcerated,
culture.
abscessed, with or without numerous draining sinuses.
● Visceral forms have been reported with symptoms For plague, culture is a public health risk.
varying dependent on organ involved.
Indirect fluorescent antibody testing of a fine-needle
Yersina pestis (plague) infection commonly results in aspirate, or of tissue collected by biopsy gives the
submandibular lymphadenopathy, fever and subcuta- fastest diagnosis for plague. False negatives can occur.
neous abcessation.
Serology for plague requires two blood samples to
● Septicemia has also been reported and mortality
demonstrate an increasing titer. Maximum titer occurs
rates are up to 33%.
at day 12 after infection, therefore the first sample for
L forms produce cellulitis 4–5 days after injury. The serology must be collected early to be useful.
cellulitis spreads rapidly with the development of mul-
L forms are not visible in tissue samples even with
tiple fistulae and febrile response.
special stains, and do not grow on culture. On elec-
● Lameness from septic arthritis is a common sequel.
tromicroscopy, organisms are visible intracellularly
Joints are affected by hematogenous spread, and
within phagocytes. Diagnosis is often made by
may be distant to the initial site. Lower limbs, espe-
response to tetracyclines as a therapeutic trial.
cially the tarsus and carpus, are the most commonly
affected.
● Most affected joints ulcerate producing a grayish
mucinous exudate.
● There is no systemic spread of lesions throughout Differential diagnoses that should be considered
the body. include atypical mycobacteriosis, cutaneous tuberculo-
sis, dermatomycoses, foreign bodies, sterile and nutri-
tional paniculitides and neoplasia.
Diagnosis
Diagnosis is based on clinical signs and identification
Treatment
of the organism.
Treatment differs depending on the organism
Cytological examination of exudates or a squash
preparation of the “sulfur granules” may reveal the Nocardia: treatment involves lavage, drainage and
organism. debridement combined with long-term antimicrobial
therapy (enrofloxacin 5 mg/kg). Treatment should con-
Biopsy and histological examination is often required
tinue for several months after all lesions resolve.
to demonstrate organisms. Special stains should be
requested, for example, Gomorri Methanine Silver or Actinomyces: Penicillin is the drug of choice (e.g.
Ziehl-Neelson (ZN) stains because organisms such as amoxycillin 12 mg/kg twice daily). This should be
acid-fast bacilli, are not always visible on routine H&E. combined with en bloc excision of lesions, and careful
search for foreign bodies. Treatment course should be Indolent ulceration presents as a progressive erosion
prolonged for 3–4 months. on the upper lip and/or nasal philtrum region.
Botryomycosis: En bloc excision combined with long
duration anti-staphylococcal antimicrobials (e.g. Diagnosis
cephalexins 22 mg/kg twice daily).
Diagnosis is based on clinical and histological appear-
Plague: aminoglycosides, tetracyclines and trimetho- ance.
prim-sulfur are effective, but penicillins are not.
Histopathology of eosinophilic plaque shows severe
L forms: are exquisitely sensitive to tetracyclines (e.g. spongioisis, and intense neutrophilic and eosinophilic
doxycycline 5 mg/kg/day). dermal infiltration. Peripheral blood eosinophilia is
often present.
Prognosis
Indolent ulceration has a very characteristic clinical
Prognosis varies from fair to good depending on the appearance. Histopathology is non-specific but rules
practicality of surgical excision, and presence or out neoplasia. Blood eosinophilia is absent.
absence of dissemination.
It is important to note that indolent ulcer and
eosinophilic plaque are clinical symptoms, and are
Prevention
not a diagnosis. The underlying allergy needs to be
For plague, strict flea control in endemic areas is indi- determined.
cated. ● Allergy investigation involves a flea elimination
trial, a food allergy trial using a novel protein for
Zoonotic potential 6–12 weeks, and intradermal skin testing for atopy.
Plague (Yersinia pestis) is an important zoonotic
organism, and great care should be taken so that
human infection does not occur from suspect cats. The
relevant authorities should be notified. Differential diagnoses which should be considered for
eosinophilic plaque include pyoderma, lymphoma and
mast cell tumor.
FELINE EOSINOPHILIC GRANULOMA
COMPLEX *** The differential diagnosis to consider for indolent
ulcer is neoplasia.
Classical signs
● Glistening, erythemic plaque (eosinophilic Treatment
plaque).
Specific treatment involves treating the underlying
● Ulceration of the upper lip adjacent the
cause using flea control, dietary allergen avoidance or
philtrum (indolent ulcer).
hyposensitization for aeroallergies.
Non-specific treatment to reduce inflammation
Pathogenesis
involves use of corticosteroids (2–4 mg/kg daily) until
Eosinophilic plaque and indolent ulceration are cuta- signs are controlled, and then reducing dose to low-
neous reaction patterns in cats associated with allergic dose alternative day therapy.
skin disease. ● Chlorambucil, aurothioglucose and progesta-
gens may be indicated if specific therapy and corti-
costeroids are not effective. Use of progestagens is
Clinical signs
discouraged because of the high incidence of drug-
Eosinophilic plaque presents as variably sized, induced complications.
alopecic, glistening, red plaques most commonly found ● Cyclosporin 5 mg/kg/d (not registered for use in
on the ventral abdomen and medial thighs. cats).
Prognosis See main references on page 25 for details (The Cat

With Signs of Chronic Nasal Disease) and page 847
Prognosis is good if the allergy is identified, and signs (The Cat With a Head Tilt, Vestibular Ataxia or
can be controlled with specific therapy. Nystagmus).
SQUAMOUS CELL CARCINOMA (SCC)** Clinical signs

Typically there is a firm swelling over the bridge of
Classical signs the nose or planum nasale giving the appearance of a
● Proliferative and/or ulcerative lesions on Roman nose, or there is a polyp-like mass visible in
non-pigmented facial extremities. the nasal opening.
Cutaneous lesions occur in up to 40% of cases, and
See main references on page 1069 for details (The Cat consist of papules or nodules varying from 0.1–1 cm
With Skin Lumps and Bumps). in diameter.
Lesions may ulcerate and exude serous fluid, or remain
Clinical signs as intact nodules.
Squamous cell carcinoma affects any gender or breed Skin lesions may be single or multiple, and occur
of cat, and the average age of affected cats is 9 years. alone, or with involvement of other organs.
The pinnae, philtrum, nares, forehead and palpe- Lesions favor face, pinnae and paws, and can occur
brae are the most affected sites, especially in non- with or without co-existent respiratory, CNS or oph-
pigmented, thinly haired areas. thalmic signs.
Lesions are multiple in 45% of affected cats.
Diagnosis
Lesions may be proliferative or ulcerative, and occa-
Diagnosis is based on clinical signs and demonstra-
sionally cutaneous horns are seen.
tion of the organism in association with the lesion.
SCC tends to be locally invasive and slow to metasta-
Cytological examination of fluid draining from
size.
a skin lesion, nasal exudate, a fine-needle aspirate of
Nail-bed SCC behave more aggressively. a skin nodule, spinal fluid, vitreal or aqueous para-
centesis stained with new methylene blue (NMB)
and Gram stains usually demonstrates the organism.
Diagnosis
Organism is yeast-like (5–15 μm) and is surrounded
Diagnosis is based on histopathology of the lesion by a wide, clear capsule.
which shows irregular cords of keratinocytes which
breach the dermo–epidermal junction and invade the der-
blood, CSF or urine is useful if positive. Note that this
mis. Cellular atypia, dyskeratosis, loss of cellular orien-
test may be negative when the disease is localized to the
tation with or without solar elastosis may be evident.
skin.
Tissue biopsy can be used to identify the pleomorphic
CRYPTOCOCCOSIS*
yeast-like organisms with a refractile halo (mucinous
capsule). PAS and methanamine silver stains make the
Classical signs
organisms more readily detectable.
● Soft tissue swelling over the bridge of the
nose (Roman nose) or polyp in nasal
opening. Differential diagnosis
● Single or multiple papules or nodules in
Differential diagnoses that should be considered for
the skin which may ulcerate.
the cutaneous form of cryptococcosus include feline
leprosy, atypical mycobacteria, bacterial granuloma, Spontaneous remission has been reported.
other fungal granulomas, xanthoma and neoplasia.
The organism has been reported to respond to fluoro-
quinolones and clofazamine. Dose of clofazamine is
FELINE LEPROSY* 2–8 mg/kg daily then twice weekly for 1–2 months.
Reversible pinkish-orange discoloration of the skin and
Classical signs elevated liver enzyme (alanine transferase) have been
reported.
● Young cats in coastal locations.
● Painless, ulcerated nodules on head and/or
limbs. Zoonotic potential.
There is no zoonotic potential.
Pathogenesis
The causative agent of feline leprosy is thought to be
Mycobacterium lepraemurium. HISTOPLASMOSIS, BLASTOMYCOSIS AND
COCCIDIOMYCOSIS*
Infection is probably acquired from cats contacting
rodents. Cat-to-cat transmission has not been reported. Classical signs
The incubation period is 2–12 months. Immuno- ● Dyspnea.
deficiency is not needed for infection to occur. ● Weight loss.
● Chronically draining skin lesions.
Clinical signs
Typically occurs in young cats in coastal locations. See main references on pages 371, 387 for details (The
Pyrexic Cat) and page 755 details (The Cat With Signs
Multiple or single cutaneous nodules mostly on the of Chronic Small Bowel Diarrhea).
head and limbs.
Lesions are painless, and often ulcerated, but rarely
Clinical signs
fistulated or exudative.
Histoplasmosis is most frequent along Ohio, Missouri
Local lymphadenopathy may be seen but visceral dis-
and Mississippi river valleys in the US. Blastomyces
semination is rare.
and coccidiomyces are very rare in cats.
Diagnosis Clinical signs are often non-specific and include
fever, anorexia and weight loss.
Diagnosis is based on clinical signs and demonstration
of the organism. Dyspnea and harsh lung sounds without coughing is
common in histoplasmosis and bastomycosis, but
Cytological examination demonstrates pyogranuloma-
occurs in only 25% of cats with coccidiomycosis.
tous inflammation with intracellular acid-fast bacilli.
Solitary, regional or generalized peripheral and vis-
Histopathology shows tuberculoid or lepromatous
ceral lymphadenopathies are frequently present.
forms of the organism.
Pale mucous membranes, icterus, hepatomegaly or
Culture is rarely used in diagnosis because the organ-
splenomegaly may be evident, most often with histo-
ism has fastidious growth requirements.
plasmosis.
PCR where available.
Chronically draining skin lesions are the most fre-
quent sign of infection in cats with coccidiomycosis,
Treatment
and were reported in 56% of cats in one study.
Treatment is best accomplished via a wide surgical ● Lesions begin as small bumps and progress to
excision. abscesses, ulcers or draining tracts.
● Draining skin lesions may occur in blastomycosis Pathogenesis

and are usually a manifestation of systemic disease
rather than local disease. Orthopoxvirus infection causing feline cowpox is not
● Skin lesions may occur with histoplasmosis. uncommon in Western Europe.
Ocular signs are common with blastomycosis, but Transmission is via direct contact with rodents, usu-
infrequent with histoplasmosis and coccidiomycosis, ally through a bite or already broken skin. The oro-
and may include conjunctivitis, anterior uveitis, retinal nasal route of transmission may also be possible.
detachment or chorioretinitis. Disease occurs mostly in male free-roaming adult
Gastrointestinal signs may occur infrequently with cats.
histoplasmosis, and include chronic diarrhea and The viremic stage virus is transported via monocytes.
mesenteric lymphadenopathy.
Osseous lesions produce soft tissue swelling and lame- Clinical signs
ness.
Primary lesions vary from a small ulcer on the head
or limbs, to a large abscess with cellulitis. Secondary
Diagnosis lesions appear 7–10 days later as generalized small
Diagnosis is based on the history of travel to endemic (0.5–1 cm) crusted ulcers.
area, clinical signs and identification of the organism Mild lethargy, anorexia and coryza occur.
in cytological or histological samples.
With immunosuppression, for example with concomitant
Serology may be useful for diagnosis of blastomycosis FIV, pneumonia and non-healing wounds may occur.
and coccidiomycosis, but is unreliable for histoplas-
mosis. Pneumonia is a poor prognostic sign.
Culture for histoplasmosis is not recommended in a In immunocompetent cats, host healing occurs within
veterinary practice because the organism is a dangerous 4–6 weeks.
zoonotic.
Direct animal-to-animal, or animal-to-human transmis- Diagnosis
sion has not been reported, and infection occurs from a Diagnosis is based on finding characteristic
common environmental source. histopathological changes, consisting of typical bal-
looning degeneration and viral inclusion bodies within
Differential diagnoses the epidermis.
Differential diagnoses that should be considered Viral culture can be used for definitive diagnosis of the
include disseminated mycobacteriosis, feline plague virus.
and neoplasia.
POX VIRUS (FELINE COWPOX)* The differential diagnosis which should be considered
for the primary lesions is a cat bite abscess; for second-
Classical signs ary lesions, causes of miliary dermatitis should be con-
● Focal ulcer, or large abscess with cellitus. sidered. In immunocompromised cats, bacterial and
● Followed 7–10 days later by generalized fungal granulomas, systemic mycoses, tuberculosis and
small (0.5–1 cm) crusted ulcers. neoplasia are differentials.
● Occurs in roaming adult male cats.
Treatment
With Paw or Pad Problems). No specific treatment is available.
Antibiotics and symptomatic treatment should be used Diagnosis

where indicated.
Histopathological examination of a biopsy shows
Corticosteroids are contra-indicated. eosinophilic dermal inflammation. In acute lesions,
basophilic, intranuclear inclusion bodies may be evi-
dent within the epithelium at the margin of the ulcer.
Prognosis
Demonstration of feline herpevirus 1 in tissue from the
Prognosis is good in an immunocompetent cat and ulcer by PCR is available from some laboratories.
spontaneous resolution occurs in 4–6 weeks.
Virus culture is available from some laboratories.
Virus can be demonstrated in lesional tissue with elec-
Transmission
tromicroscopy, but this is not routinely available.
Scabs shed virus, which survives in cool dry environs
for months to years. Differential diagnosis
Cats represent a common zoonotic threat to people. Chronic non-healing erosions on the nasal planum or
Normal hygiene measures generally suffice for preven- bridge of the nose may occur with mosquito bite hyper-
tion. sensitivity, squamous cell carcinoma and eosinophilic
granuloma complex. Differentiation is based on
appearance of the lesion and any other associated
lesions, and biopsy with histopathology.
FELINE HERPES VIRUS*
Treatment
Classical signs
Lysine supplementation (250 mg PO daily).
● Non-healing ulceration of the dorsal nasal
bridge or nasal planum. Prognosis
See main references on page 7 (The Cat With Acute Based on reports in the literature, it suggests a guarded
Sneezing or Nasal Discharge) and page 1212 and page prognosis. However in the author’s experience, lysine
1208 (The Cat With Ocular Discharge or Changed therapy has resulted in resolution of the ulcer.
Conjunctival Appearance).
MAST CELL TUMOR*
Pathogenesis Classical signs

Feline rhinotracheitis is an α herpesvirus. ● Single to multiple tumors on the head of
Trauma may initiate nasal lesions. older cats.
● Tumors may “enlarge” after palpation or
aspiration.
● Rarely young Siamese cats have multiple
Clinical signs
nodules around the head.
Chronic non-healing ulceration or erosion on the
nasal planum or dorsal nasal bridge may occur with See main references on page 1074 for details (The Cat
herpesvirus infection. With Skin Lumps and Bumps).
Ulceration can also occur elsewhere, including on the
paws. Clinical signs
The cat may or may not have signs of concurrent ocu- The average age of cats with mast cell tumors is 10
lar or respiratory disease. years, and there is no sex or breed predisposition.
Tumors may occur at any site, but the head is most fre- M. tuberculosis is a reverse zoonosis.
quently affected.
The method of transmission with M. avium and
Appearance varies from a discrete solitary nodule to M. microti is unknown. It may involve the cat’s natural
multiple papulonodular tumors to a plaque-like predation of rodents and birds.
mass.
Incubation period in natural infections is months to
Skin tumors may “enlarge” and become erythematous greater than one year.
after palpation or aspiration.
A breed susceptibility for M. avium infections has been
Paraneoplastic syndromes may be evident including reported in the Siamese cat.
gastrointestinal tract ulceration, delayed wound heal-
ing, hypotension, cutaneous flushing, local ulceration Clinical signs
and swelling and coagulation abnormalities.
Skin lesions are usually part of a more generalized dis-
Histiocytic mast cells tumors are uncommon, occur as ease, evident in 56% of cases.
multiple skin nodules around the head of cats less than
4 years of age (mean age 2.4 years) and Siamese are Single or multiple ulcers, abscesses, plaques or nod-
predisposed. ules with thick green or yellow purulent exudate.
Additional signs vary with route of entry and degree of
Diagnosis dissemination of the organism, and may include GIT,
respiratory, CNS or ophthalmic signs.
Diagnosis is based on demonstration of characteristic
mast cells associated with a skin mass. Fine-needle
aspirate shows round cells with granules, which stain Diagnosis
well with Wright’s stain.
Diagnosis is based on clinical signs and identification
Histopathological examination shows a round cell of the organism.
tumor with variable pleomorphism and granule for-
mation, which is dependent on the grade of the tumor. History, physical examination, radiography, urinalysis
and blood testing (hematology and biochemistry) are
Abdominal radiology, ultrasound and laparotomy may important in the diagnostic work-up.
be useful for staging the tumor.
Cytological examination may reveal acid-fast bacilli
in skin aspirates or biopsies, or in urine.
CUTANEOUS TUBERCULOSIS
On microbiological culture the organisms are slow to
Classical signs grow, and require special media.
● Yellow/green thick purulent exudate from Intradermal skin testing with BCG or purified protein
skin lesions. derivative (PPD) is not reliable.
● Lymphadenopathy. Serological testing is unreliable in cats.
● GIT, respiratory, CNS or ophthalmic signs.
Pathogenesis EUMYCOTIC MYCETOMA

Mycobacterium bovis is the causative agent in 96% of
cases. M. tuberculosis, M. avium and M. microti have
Classical signs
also been reported. ● Papules or nodules on the limbs and face.
● Sinus formation.
The reservoir of M. bovis is infected cattle.
● White or black tissue grains in the
Cats are infected via ingestion of unpasteurized milk mycetoma.
or eating contaminated meat or offal.
Pathogenesis cotic mycetoma, pseudomycetoma, botryomycosis,

foreign bodies and chronic bacterial abscesses.
Eumycotic mycetomas are subcutaneous fungal infec-
tions.
Treatment
Organisms are ubiquitous in soil. Infection occurs via
wound contamination. Wide surgical excision is the treatment of choice,
which may require limb amputation to remove suffi-
Most frequently occurs in geographic areas along cient tissue.
the Tropic of Cancer.
Antifungal therapy is often ineffective. The imida-
Black-grained mycetomas are produced by Curvularia zoles are worth trying where in vitro sensitivites are
geniculata and Madurella grisea. not available, for example itraconazole (10 mg/kg
White-grained mycetomas are produced by Pseudo- twice daily). Anorexia and elevated liver enzymes are
allescheria boydii and Acremonium hyalinum. the most frequently encountered adverse effects.

Solitary papules occur on the limbs and face, and Cutaneous mycetomas are not life threatening, but can
evolve to painful nodules and fistulae, resulting in be difficult to resolve if wide surgical excision is not
sinus tracts. possible.
White or black tissue grains are evident in the myce-

toma, which represent the fungal hyphae. PSEUDOMYCETOMAS
Infection may involve the underlying deeper structures. Classical signs
● Exclusively Persian cats.
Diagnosis ● Subcutaneous nodules often together with
Diagnosis is based on clinical signs and demonstra- superficial dermatophytosis.
tion of the organism.
For cytological examination, make a squash prepara- Pathogenesis
tion of the tissue grains. Gritty grains may need 10%
Pseudomycetomas represent subcutaneous infection
KOH digestion first. Fungal hyphae are visible micro-
caused by the dermatophyte, Microsporum canis.
scopically.
They occur exclusively in Persian cats and immune
Histopathological examination reveals granulomatous
incompetence has been suggested.
to pyogranulomatous inflammation and tissue
grains of fungal hyphae.
Clinical signs
Culture requires special media using SDA.
Non-painful subcutaneous nodules that may ulcerate
Immunodiffusion is available in some laboratories. and drain.
Some fungi can be diagnosed by serum testing for spe-
cific antibodies with agar immunodiffusion. Tissue Most occur on the dorsum.
samples may also be stained with fluorescein conju- The nodules may or may not be associated with obvious
gated with specific antibodies. superficial dermatophyte infection.

Differential diagnoses that should be considered Diagnosis is based on signalment (Persian cats), signs
include mycobacterial infections, neoplasia, actinomy- and demonstration of organism.
On histopathological examination a Splendori- The cutaneolymphatic form has corded lymphatics

Hoeppli reaction is evident, which consists of fungal with secondary ulcerations occurring along the
hyphae surrounded by amorphous eosinophilic lymph pathway, extending away from the primary
material, which represent antibody–antigen com- wound.
plexes. PAS stains show up the fungal hyphae.
The disseminated form is rare.
Examine coat for signs of superficial infection using
a Wood’s lamp, and sterile coat collection using the
toothbrush technique and culture for M. canis. Diagnosis
Assess the immune status of the cat and determine if Diagnosis is based on identification of the organism.
intercurrent disease is present using hematological, bio-
chemistry, urinalysis, FeLV and FIV testing. Cytological examination shows numerous pleomor-
phic yeasts, which may be intra- or extracellular.
Differential diagnosis Histopathological examination reveals oval, round

or cigar-shaped organisms. PAS and GMS stains
Differential diagnoses that should be considered facilitate identification.
include bacterial, fungal and mycobacterial granulomas
and neoplasia. Immunoperoxidase or fluorescent antibody techniques
are useful if tissue numbers are low. This is usually not
required in cats.
Treatment
Culture from a deep sinus tract swab or tissue
If there is a single lesion, surgical excision is the treat-
biopsy for definitive identification of organism.
ment of choice.
Medical treatment using itraconazole (20 mg/kg
daily) for several months may be effective. Anorexia Differential diagnosis
may occur and reflect hepatopathy and require cessa-
tion of therapy. Differential diagnoses that should be considered
include bacterial, mycobacterial, fungal granulomas,
neoplasia, sterile panniculitis.
SPOROTRICHOSIS
Classical signs Treatment

● Chain of subcutaneous nodules following
Traditional therapy involved use of a saturated solution
the lymphatic tract, and extending away
of potassium iodide (SSKI; 20 mg/kg PO q 12–24 h)
from primary wound.
administered for 30 days beyond clinical cure. Cats are
susceptible to iodism, and many develop signs includ-
Pathogenesis ing anorexia, vomiting, depression, twitching, hypother-
mia and cardiovascular failure.
Sporothrix schenckii is the causative organism, and is
ubiquitous in soil and organic debris, especially in Ketaconazole (5–10 mg/kg twice daily) either singly
humid environs. or together with potassium iodide has been used suc-
cessfully. Gastrointestinal, neurological signs and
Infection occurs via traumatic inoculation via a veg- jaundice are reported associated with ketaconazole
etable foreign body, cat claw, or via wound contami- use.
nation.
Newer imidazoles may be useful, such as itraconazole
(10 mg/kg/day PO).
Clinical signs
Surgical excision is useful for the cutaneous form,
The cutaneous form looks similar to a cat bite abscess. where wide excision is possible.
Prognosis Cytological or histological examination can be used

to identify pigmented fungal elements.
Prognosis is guarded for all but the localized cuta-
neous forms. Definitive diagnosis is based on culture on SDA at
25–35˚C, and identification of the organism.
Sporothrix is a serious zoonosis. In households with
young children or immunosuppressed adults, it may be Assess for concurrent immunosuppressive disease by
unwise to treat the cat because of the risk of infection. testing for FIV and FeLV.
Prevention Differential diagnosis

To prevent zoonotic infections, all discharging non- Differential diagnoses that should be considered
healing wounds in cats, especially where lymphatic include bacterial, fungal and mycobacterial granulomas
cording is present, should be handled with great caution and neoplasia.
using gloves, careful cleaning after handling, etc.
Treatment
Treatment of choice for the cutaneous form is wide
PHEOHYPHOMYOCOSIS surgical excision. Where wide surgical excision is not
possible, amphotericin B combined with an imidazole
Classical signs such as itraconazole, and/or cryotherapy may be tried,
● Ulcerated nodule on the nose or limb. although relapse is common.
Fungi reported in cats associated with pheochromocy- Prognosis is good if surgical excision is possible,
tosis include Dresclera spicifera, Curvularia lunata although relapse may occur. The disseminated form has
and Exophiala jeanselmei. a grave prognosis.
These are saprophytic fungi that produce dermata-

ceous (dark) hyphal elements in tissues. They occur MULTICENTRIC SQUAMOUS CELL
most commonly in tropical or subtropical areas. CARCINOMA IN SITU
Infection is by traumatic implantation via cat claw Classical signs

wounds or a plant foreign body.
● Multifocal, hyperkeratotic or ulcerated
Immunosuppression increases susceptibility. plaques.
● Occur on pigmented, thickly haired skin of
older cats.
Clinical signs
Pheohypomycosis occurs as a solitary nodule, usually
Pathogenesis
on the paw, nose, limb or trunk.
Papilloma virus antigen has been detected in some
The lesion may ulcerate with sinus formation.
lesions.
Dissemination is rare.
Ultraviolet radiation and arsenicals are not thought to
play a role.
Diagnosis
Clinical signs
Diagnosis is based on identification of the organism
associated with the lesion. Lesions are found in older cats (> 10 years usually).
Multifocal lesions occur over the head, neck, shoul- Tumors usually occur as solitary lesions on the head
ders and forelimbs on pigmented, thickly haired or neck.
skin.
Size and shape are variable ranging from a dome, to a
Begin as hyperkeratotic macules and evolve to thick- plaque or polypoid shape, and ulceration is frequent.
crusted, ulcerated plaques.
The neoplasia often have a long course over a couple Diagnosis
of years, with waxing and waning signs.
Diagnosis is based on histopathological examination of
an excisional biopsy. Characteristic findings are atypi-
Diagnosis
cal melanocytes in nests, sheets and cords. Cells may
Diagnosis is based on histopathological findings. exhibit epithelioid or spindle morphology or a combin-
ation of both.
Excise the lesion and submit for histopathology.
Histologically, there is abrupt transition from normal to
atypical epithelium. The dermo–epidermal junction
BASAL CELL CARCINOMA (BCC)
is not breached.
Classical signs
● Pigmented, cystic tumor on head or neck of
Differential diagnoses which should be considered
older cats.
include mycobacterial, fungal and bacterial granulomas
and other neoplasia.
With Skin Lumps and Bumps).
Treatment
Treatment of choice for thin lesions is beta radiation.
Clinical signs
Treatment does not prevent new lesions.
Basal cell carcinoma occurs frequently as a pigmented
Etretinate and isoretinoin can be used in thicker
and/or cystic tumor of the head, neck, thorax, nasal
lesions, but the response is variable.
planum or eyelids in older cats.
Prognosis Usually occur as a solitary tumor and are frequently
ulcerated.
Cats are often euthanized for cosmetic reasons and
owner frustration at poor response to therapy.
Diagnosis
Metastases have not been reported.
Diagnosis is based on histopathology.
MELANOMA
CUTANEOUS LYMPHOMA
Classical signs
● Ulcerated, pigmented nodule on head or Classical signs
neck.
● Alopecia and scale.
● Erythroderma.
● Hypopigmentation of hair or skin and
With Skin Lumps and Bumps).
mucocutaneous junctions.
● Nodules or plaques which often ulcerate.
Clinical signs
Melanoma typically occurs in older cats of any breed See main references on page 1078 for details (The Cat
(average age is 10 years). With Skin Lumps and Bumps).
PATHOGENESIS Treatment
Cutaneous lymphoma is a very rare tumor in cats, and Retinoides (vitamin A analogs), such as isotretinoin
results when malignant T or B lymphocytes infiltrate (Accutane) or acitretin (Soriatane) can be used for pal-
the skin. liative treatment of the epitheliotropic form (mycosis
fungoides).
Most cases are FeLV negative.
B cell lymphoma is treated with excision of solitary
lesions and standard lymphoma protocols. Excisional
Clinical signs surgery may be curative for solitary lesions. Small
Signs of epitheliotropic T cell tumors (mycosis fun- lesions may respond well to superficial radiation ther-
goides) include “non-inflammatory” alopecia, scaling, apy. Results of chemotherapy for multiple lesions are
erythroderma (diffuse reddening of the skin), hypopig- often disappointing.
mentation of hair or skin, ulceration, plaques and nodules.
B cell neoplasia shows dermal nodules with or with- Prognosis
out ulceration, and with or without lymphadenopathy. Prognosis is poor.
Systemic signs of weight loss, diarrhea and respiratory Cats with small solitary lesions may do well initially
distress may be present. with surgical excision, but generalized disease is likely
to occur within 12 months.
The epidermotropic form often has an insidious pro-
Diagnosis gression.
Diagnosis is based on clinical signs and histological
examination of biopsied tissue. ACQUIRED CUTANEOUS FRAGILITY
Fine-needle aspirate and cytological identification of SYNDROME
abundant malignant round cells is useful to establish a
presumptive diagnosis. Classical signs
Histopathological examination is required for a defin- ● Large tears in paper-thin skin.
itive diagnosis to demonstrate diffuse infiltrates of ● Evidence of underlying disease, e.g.
malignant, poorly differentiated lymphoid cells. The hyperadrenocorticoidism.
epetheliotropic form has Pautrier’s microabscesses,
which are focal aggregates of neoplastic T cells in the Pathogenesis
epidermis.
Dermal and epithelial atrophy occurs secondary to
Blood evaluation, radiographs, ultrasound, lymph node hyperadrenocorticoidism, progestagen administra-
aspirates and bone marrow biopsy are important for tion or metabolic conditions and diseases such as star-
clinical staging. vation, neoplastic cachexia, diabetes, etc.
Clinical signs
Skin is thin (atrophic) and mechanically weak, and
Differential diagnoses for the epitheliotrophic may spontaneously tear.
form include systemic lupus erythematosus, der-
matophytosis, demodecosis, cutaneous flushing syn- Skin is fragile but not hyper-extensible.
dromes, drug eruption and hypersensitivities.
Diagnosis
Differential diagnoses for the nodular forms include
bacterial and fungal granulomas and other neoplasia. Cutaneous signs are very characteristic.
Histopathological examination reveals epidermal Diagnosis

and dermal atrophy.
Definitive diagnosis is based on histopathological evi-
Identification of the underlying pathology may require dence of Touton giant cells, which are considered
hematological and serum biochemistry examination, pathognomonic.
urinalysis, radiology, ultrasound and specific endocrine
testing. History taking including drug history, physical exami-
nation and blood testing is required to differentiate pri-
mary and secondary hyperlipidemia.
The main differential diagnosis is cutaneous asthenia.
Treatment Differential diagnoses which should be considered
include eosinophilic granuloma complex, bacterial and
Correct the underlying pathology.
fungal granulomas and neoplasia.
Avoid trauma to the skin, or exerting tension on the skin
while restraining the cat.
METABOLIC EPIDERMAL NECROSIS (MEN)
Prognosis
Prognosis is variable, and is dependent on the initiating Classical signs
cause. ● Crusting, erosions and erythema of
mucocutaneous junctions and bony
protuberances.
XANTHOMA ● Pad hyperkeratosis.
Classical signs
Pathogenesis
● Yellowish, ulcerated nodules or plaques
over bony points. Metabolic epidermal necrosis is the cutaneous mani-
● Associated with hyperlipidemia. festation of hepatic and occasionally pancreatic
disease.
See main references on page 570 for details (The Cat ● Other terms include superficial necrolytic dermati-
With Hyperlipidemia). tis, necrolytic migratory erythema (NME) and
hepatocutaneous syndrome.
Metabolic epidermal necrosis has been associated with
Clinical signs hepatic and pancreatic disease in cats, but is poorly
understood. It is possible that the pathological process
Xanthoma appear as alopecic nodules and plaques
causing the skin lesions is triggered by a variety of sys-
which are often ulcerated on foot pads, lateral hocks,
temic metabolic derangements.
elbows, oral cavity or at sites of injury.
● Deficiencies in certain nutrients such as amino
They often have a whitish or yellowish waxy appear- acids, zinc, essential fatty acids and biotin may
ance. cause keratinocyte degeneration.
● Because low plasma amino acid concentrations
Cutaneous xanthomatosis has been described in cats
were found in dogs and high-quality protein diets or
with diabetes mellitus and is associated with hyperlipi-
supplementation with egg leads to resolution of
demia.
signs in some animals, it has been postulated to be
Most common in cats associated with hyperlipidemia. associated with an amino acid deficiency.
In dogs and people it is associated with glucagon- recovery diet containing high-quality protein and
secreting tumors and a variety of other diseases not increased levels of amino acids.
associated with a hyperglucogonemia, especially ● A slow IV infusion of an amino acid formulation
hepatic disease. The role of glucagon is not understood, designed for parenteral administration has been
but it is postulated to affect catabolism of amino acids to used successfully in some patients.
glucose.
Supplementation with zinc and essential fatty acids
In cats it has been reported with pancreatic carcinoma, may help some patients.
chronic hepatopathy and thymic amyloidiosis.
Anti-malassezial shampoos (miconazole containing)
may help control the skin lesions.
Clinical signs
Surgical resection of glucogonoma is indicated if present.
Alopecia, erythema, crusts, erosions and ulceration
of the skin most frequently seen at mucocutaneous
Prognosis
junctions and frictional areas of the skin. The skin can
be thickened and may become fissured. Prognosis is poor for long-term survival.
● The skin lesions are often secondarily infected
with bacteria or yeast.
CUTANEOUS ASTHENIA
Footpads show marked hyperkeratosis and fissuring.
Classical signs
Diagnosis ● Fragile, hyperextensible skin which tears
easily.
Diagnosis is based on histopathological examination
● Focal necrosis and paperaceous scars.
of the skin lesions and demonstration of diffuse parak-
● Patchy alopecia.
eratosis, which includes follicles, epidermal pallor,
basal cell hyperplasia (red, white and blue effect).
Measurement of plasma glucagon concentration is Pathogenesis
indicated to rule out a glucagonoma. Cutaneous asthenia results from a congenital defect of
Diagnosis of the hepatic or pancreatic disease requires collagen I synthesis.
serum biochemistry analysis to demonstrate
increased liver enzymes, and ultrasound to demon- Clinical signs
strate liver or pancreas pathology. Cutaneous asthenia appears as hyperextensible skin
Hepatic or pancreatic biopsy via ultrasound guidance and/or “spontaneous” tearing of the skin.
or exploratory laparotomy is usually needed for defini- Focal necrosis of the skin (necrotic eschars), particu-
tive diagnosis of the underlying condition. larly involving the dorsal neck, may occur.
Numerous paperaceous scars and patchy alopecia
Differential diagnosis may be evident.
Differential diagnoses include bacterial and fungal Hematomas may occur.
infections, neoplasia and pemphigus foliaceous.
Occasionally joint laxity and/or ophthalmic opacities
are seen.
Treatment
Treatment should be directed at controlling the underly- Diagnosis
ing disease and nutritional support.
Diagnosis is based on clinical appearance and
Amino acid supplements can be given by feeding a increased extensibility index of the skin. An extensi-
cooked egg yolk daily, and/or feeding a commercial bility index of greater than 19% is considered abnormal.
● The extensibility index is measured by stretching The disease is classified as epidermolysis bullosa sim-
the skin dorsally within pain limits. The vertical plex, junctional epidermolysis bullosa and dystrophic
height of this skin fold is expressed as a percentage epidermolysis bullosa, depending on the ultrastructural
of the crown to rump length. defect.
Histopathological examination with routine H&E is
not diagnostic. Masson’s trichrome stain, which is
designed to stain dysplastic collagen red and normal Clinical signs
collagen blue, has been reported to be a sensitive indi-
Signs appear in kittens often by 5–12 weeks of age, at
cator of this disease. However, the author has not found
the time of increased activity and mechanical stress on
this stain to be helpful in Burmese cats.
the skin.
Electron microscopy is the definitive test and shows
Signs include nail shedding, foot pad ulceration,
irregular orientation of collagen fibrils.
hard palate ulceration or skin ulceration in frictional
sites.
The differential diagnosis which should be considered
is acquired cutaneous fragility secondary to hyper-
Diagnosis
adrenocorticoidism, progestagen administration, or Clinical signs in a young kitten are highly suggestive.
other metabolic conditions. Importantly, the skin is
Histopathological examination of skin shows
fragile but not hyperextensible in acquired cutaneous
dermo–epidermal separation (cleft formation) with-
fragility.
out inflammation.
Electro microscopy together with immunolabeling
Treatment is necessary to identify the ultrastructural level of the
Management involves avoiding injury by keeping the split, and the nature of the defect at that level, that is,
cat indoors, and taking care when handling the cat not the specific element that is missing.
to exert tension on the skin.
Suture tears rapidly to prevent further tearing.
Differential diagnoses that should be considered
Prognosis include thermal injuries, chemical burns and vasculitis.
Most cats can have a good-quality life if trauma is min-
imized.
Treatment
There is no specific treatment for epidermolysis bul-
EPIDEMOLYSIS BULLOSA losa.
Classical signs Avoid trauma and provide symptomatic wound care.
● Ulcerative lesions in young kittens. Onycectomy can be performed for pain relief, if the
● Nail shedding. major sign is nail shedding.
Epidermolysis bullosa results from a congenital Prognosis is guarded. Euthanasia is an option if the
defect of the dermo–epidermal junction of the skin. quality of life is not adequate.
CHEMICAL DERMATITIS Prognosis

Prognosis is good if there is not extensive skin involve-
Classical signs ment.
● Ulcers or crust-covered erosions at contact
sites. TRAUMATIC PANNICULITIS
● Ptalism.
Classical signs
Pathogenesis ● Multiple fistulae with serosanguineous to
Strong alkalis, acids or cationic detergents can cause gelatinous exudates.
a chemical dermatitis if they are in contact with the ● Inguinal or dorsolumbar area.
skin. ● History of prior blunt trauma to site.
Clinical signs
Pathogenesis
Ulceration or crust-covered erosions develop at con-
Ischemia of individual lipocytes may occur following
tact sites.
trauma, and the resultant release of triglycerides
Oral ulceration and ptalism may result from ingesting induces inflammation.
the chemicals while grooming.

Blunt trauma may cause panniculitis, which presents
A tentative diagnosis is based on clinical signs consis-
2–3 weeks later with signs.
tent with chemical dermatitis, together with a history
of possible exposure to irritant chemicals. Lesions are most common in the inguinal or dor-
solumbar areas. There is alopecia of the overlying
Differential diagnoses skin.
Differential diagnoses that should be considered include Sinus tracts or fistulae may form, with a resultant
thermal injuries, trauma and calicivirus infection. serosanguineous to gelatinous exudate.
Subcutaneous fibrosis occurs with healing.
Treatment
Remove chemical from skin using copious, gentle Diagnosis
irrigation with saline or 0.05% chlorhexidine.
A tentative diagnosis is based clinical signs and a his-
Use prophylactic antibiotic cover to minimize sec- tory of trauma.
ondary bacterial infection.
No organisms are detected on cytology, biopsy or culture.
Feed soft foods, or if oral ulceration is severe, use
nasogastric or esophageal tubes for feeding. There is no response to antimicrobial therapy.
Intravenous fluids may be required, so monitor care-

fully for dehydration and protein loss through the skin. Differential diagnoses
Wound care may require judicious debridement, and Differential diagnoses that should be considered
use of non-adherent bandages changed daily until the include infectious, immune-mediated and nutritional
lesions re-epithelialize. panniculitis.
Treatment Cold agglutinin disease is a rare disease where cold-

reacting IgM erythrocyte antibodies cause autoaggluti-
Treatment involves surgical excision of the involved nation in the cooler peripheral vasculature of the
fat pad. extremities resulting in ischemic necrosis of the ear and
Glucocorticoids (prednisolone at anti-inflammatory tail tips and foot pads.
doses of 0.5–1 mg/kg q 24–48 h for 4–6 weeks) help
reduce inflammation. Clinical signs
Vitamin E 200 IU/cat/day may help reduce inflamma- Typically there is cutaneous ulceration, which may be
tion. crust-covered.
Lesions often involve the muco-cutaneous junctions,
Prognosis foot pads, nail–skin junction, oral cavity, inguinal
and axillary areas and extremities (ear and tail tips).
Traumatic panniculitis is often frustrating to treat if sur-
gical excision is not possible. Vasculitis may be associated with necrosis particularly
of pinnae, foot pads and tip of the tail.
Prevention Systemic signs such as fever and lethargy are not
uncommon.
Oxypentoxifylline (10 mg/kg q 12 h) and vitamin E
(200 IU/cat q 24 h) immediately following trauma may
help to improve tissue perfusion and stabilise cell mem- Diagnosis
branes.
Diagnosis is based on clinical signs and histological
Early debridement of necrotic fat following trauma is findings.
indicated to reduce inflammation.
Early and late lesions should be examined
histopathologically. For small ulcers, excise the entire
ulcer together with the marginal skin. For large ulcers,
VASCULITITIS AND MISCELLANEOUS an elliptical biopsy should be collected extending from
ULCERATIVE DERMATOSES grossly normal skin through the edge of the ulcer to the
ulcerated skin.
Classical signs
An accurate drug history is important.
● Ulcers and crusts (skin and/or
Diagnostic tests should be performed to rule-out con-
mucocutaneous junctions).
comitant neoplasia.
Pathogenesis
Differential diagnoses which should be considered
Immune-mediated ulcerative dermatoses represent a
include bullous pemphigoid, systemic lupus erythe-
heterogeneous group of diseases in which the primary
matosus (SLE), discoid lupus erythematosus (DLE),
lesion is cutaneous ulceration.
vasculitis, cold agglutinin disease, erythema multi-
Vasculitis resulting in skin lesions is rare in cats. It may forme (EM), toxic epidermal necrolysis (TEN).
be associated with immune complexes secondary to
infectious or neoplastic disease, drugs and as part of
Treatment
autoimmune syndromes, such as SLE or be idiopathic.
● Predisposed sites have minimal collateral circula- Treat the underlying disease if possible, and stop drug
tion such as the pinnae, paws and tail tip. treatment or change to a different class of drug if signs
● Ulceration and necrosis are typical. appeared during drug treatment.
Where an underlying trigger (drug or neoplasia) cannot Diagnosis

be found, immunomodulation is recommended rather
than immunosuppression. Diagnosis is based on clinical signs and histological
examination of biopsied fat.
Drugs commonly used include pentoxifylline (10 mg/kg ● Grossly, affected fat may have a brownish discol-
q 12 h) which is a gastrointestinal tract irritant so orization.
should be given with food, prednisolone (2–4 mg/kg q ● Histopathological examination shows lobar and
24 h or divided into twice daily and taper to response), septal panniculitis with characteristic ceroid depo-
chlorambucil or aurothioglucose. sition.

Prognosis is guarded if the trigger cannot be found Differential diagnoses which should be considered
and resolved. include infectious panniculitides, traumatic panniculitis
and immune-mediated panniculitis.
PANSTEATITIS/VITAMIN E DEFICIENCY
Treatment
Classical signs Treatment involves dietary correction and use of anti-
● Fever, lethargy and pain on cutaneous inflammatory drugs such as prednisolone (1
palpation. mg/kg/day).
● Cutaneous ulcerations with gelatinous
exudate. Prognosis
Prognosis is guarded to poor.
Pathogenesis
Vitamin E is an important natural antioxidant. A rela-
tive or absolute deficiency of vitamin E can result in IDIOPATHIC FELINE ULCERATIVE
peroxidation of bonds in unsaturated fat. This may DERMATOSIS
occur with diets containing large amounts of unsatu-
rated fish oils. Classical signs
The unsaturated oils undergo oxidation, and release ● Dorsal neck ulceration.
reactive peroxides in the body fat of the cat, causing
painful inflammation of fat (pansteatitis).
Pathogenesis
Signs have been reported in cats that were fed mainly
Pathogenesis is unknown and may be multifactorial.
oily fish such as red tuna. Cats fed diets supplemented
with cod-liver oil deficient in vitamin E are also at risk. Ulceration has been associated with use of topical
spot-on insecticidal agents as an idiosyncratic reac-
tion.
Clinical signs
There is often a history of vaccination at the site
Classical signs are lethargy, inappetence, fever, reluc-
within the last 12 weeks. This is a common site for vac-
tance to move and pain on cutaneous palpation.
cination, therefore a positive history does not equal
Subcutaneous fat has a generalized firm feeling on pal- causative role.
pation.
It has been associated with a variety of allergies includ-
Cutaneous ulcerations may form with a gelatinous exu- ing food allergy, and especially flea allergy, ectoparasites
date. (demodex, notoedres, otodectes) and dermatophytosis.
Clinical signs In cats resistant to treatment or where there is reoc-

currence of the lesion after surgical excision, declaw-
Chronic ulceration is usually present on the dorsal ing of the hind feet has led to successful resolution of
neck area, but may involve the face and base of ears. the lesion. However, Soft Paws should be trialed first
Ulceration appears rapidly, and then follows a very and declawing used only as a last resort.
insidious course.
The lesion may spontaneously resolve over 8–12 ERYTHEMA MULTIFORME (EM) AND TOXIC
weeks or persist. EPIDERMAL NECROLYSIS (TEN)
Pruritus varies from intensely itchy to not at all.
Classical signs
● Multifocal to confluent cutaneous
Diagnosis
ulceration.
Clinical signs are classical. ● Muco-cutaneous junction ulceration.
Check history of injections or application of insectici-
dal agents at the site.
Pathogenesis
Histological examination of a deep elliptical biopsy
including the area affected with panniculus may show Erythema multiforme and toxic epidermal necrolysis
lymphocytic vasculitis/panniculitis, faded follicles and involve a cytotoxic CD8+ T-cell response against ker-
linear subepidermal fibrosis. atinocytes, which can be activated by drugs, viruses,
neoplasia and foods.
Erythema multiforme is an acute eruption of the
skin and mucous membranes and is most commonly
Differential diagnoses that should be considered associated with a drug sensitivity. Penicillin and
include trauma, cutaneous asthenia, necrotizing enven- aurothioglucose have been associated with erythema
omation and thermal injury. multiforme in cats.
Toxic epidermal necrolysis is an acute disseminated
Treatment disease involving the mucous membranes and skin, and
is associated with systemic signs.
Response to use of glucocorticoids is often disap- ● There is intracellular edema in the dermis and sep-
pointing because the pruritus is often steroid resistant. aration of the dermo–epidermal layers.
A small number of cases treated by the author have
responded (or spontaneously resolved) while on pen-
toxifylline (10 mg/kg twice daily). Clinical signs
Keeping the lesion wrapped until it is completely healed, Typically, onset of signs is acute.
and using Soft Paws (Soft Paws Inc., Lafayette, LA,
In both conditions, lesions consist of erythematous
USA) on the hind feet may be successful in some cats.
macules (flat circumscribed red areas of skin ≤ 1 cm)
Soft Paws are vinyl caps that glue to the cat’s claws and
and ulceration, which may be annular, arciform or ser-
protect against skin damage from scratching.
piginous (snake-like).
A hypoallergenic diet may help some cats and a lime-
Vesicules, blisters or bullae may be observed which
sulfur dip every 5 days for 5–7 treatments has been sug-
ulcerate, ooze and crust over.
gested to rule out Demodex gatoi.
The ventral abdomen, peri-mammary area, ear pinae,
Wide surgical excision of the lesion and the use of
perioral and perineal areas are often affected.
Soft Paws on the claws of the hind feet are curative in
some cats. Erosion or ulcers may be present on the oral mucosa.
Toxic epidermal necrolysis is associated with sys- Differential diagnosis

temic signs including pyrexia, depression, anorexia.
Other vesicular and pustular disorders, e.g. bacterial
infections, pemphigus foliaceous, burns, chemical der-
Diagnosis matitis need to be ruled out.
A presumptive diagnosis is based on the clinical Treatment

appearance of an acute ulcerative condition
involving the skin and mucous membranes, which Cyclosporin 5 mg/kg PO q 24 h. Not registered for use
is associated with a recent history of drug adminis- in cats.
tration. Other differential diagnoses need to be Remove drug or diet triggers if identified.
excluded.
Supportive treatment (intravenous fluids, warmth,
Histopathological examination of erythematous avoidance of sepsis) needed where large amounts of
macules or ulcer margins reveals epidermal changes epithelium are lost.
including hydropic degeneration, prominent single
cell to apoptosis, lymphocyte and macrophage satelli-
tosis and variable dermal edema (EM) to full thick- Prognosis
ness epidermal necrosis (TEN). Inflammatory Prognosis is good if the trigger can be removed and the
changes in the dermis are mild to marked in EM but area affected is small, but is poor where large areas of
often absent in TEN. epidermis have been lost.
RECOMMENDED READING
Baldwin CJ, Panciera RJ, Morton RJ, Cowell AK, Waurzyniak BJ. Acute tularaemia in three domestic cats. J Am Vet
Med Assoc 1991; 199: 1602–1605.
Dillberger JE, Homer B, Daubert D, Altman NH. Protothecosis in two cats. J Am Vet Med Assoc 1988; 192:
1557–1559.
Dunstan RW, Credille KV, Walder EJ. The light and the skin. Kwochka K, Willemse T, von Tscharner C (eds)
Advances in Veterinary Dermatology, Vol 3. Blackwell, Cornwall, UK. 1998, pp. 3–37.
Eidson M, Thilsted JP, Rollag OJ. Clinical, clinicopathological, and pathological features of plague in cats: 119 cases
(1977–1988). J Am Vet Med Assoc 1991; 99: 1191–1196.
Gunn-Moore D, Shaw S. Mycobacterial diseases in the cat. In Practice 1997; 493–500.
Jacobs GJ, Medleau L, Calvert C, Brown J. Cryptococcal infection in cats: Factors influencing treatment outcome,
and results of sequential serum antigen titers in 35 cats. J Vet Int Med 1997; 11: 1–4.
Lemarie RJ, Lemarie SL, Hedlund CS. Mast cell tumors: Clinical management. Compendium 1995; 17: 1085–1099.
Malik R, Martin P, Love DN. Localised Corynebacterium pseudotuberculosis infection in a cat. Aust Vet Pract 1996;
26: 27–31.
Ruslander D, Kaser-Hotz B, Sardinas JC. Cutaneous squamous cell carcinoma in cats. Compendium 1997; 19:
1119–1127.
Theon AP, VanVechten MK, Madewell BR. Intratumoral administration of carboplatin for treatment of squamous cell
carcinomas of the nasal plane of cats. Am J Vet Res 1996; 57: 205–209.
Werner AH, Werner BE. Feline sporotrichosis. Compendium 1993; 15: 1189–1197.
53. The cat with paw or pad problems
Isobel Phebe Johnstone
KEY SIGNS
● Erythema, scaling, crusting, and/or pruritic lesions.
● Nodules, draining tracts, ulcers and/or abscesses.
● Distortion of the nails or deformity of the foot.
MECHANISM?
● A wide variety of diseases can have paw or pad problems as part of more generalized signs, or
the lesions can be confined solely to the foot.
WHERE?
● Disease of the feet includes the paw, pads, digits and nails. Interdigital spaces are seldom affected
in cats.
● It is rare for the disease to be confined solely to the feet. Usually the feet are affected in
conjunction with other areas of the skin.
WHAT?
The most common problems seen in the paw are:
● Bacterial paronychia from a variety of causes.
● Immune-mediated diseases.
● Nodules or ulceration due to infections or neoplasia.

Diseases causing paw or pad problems
ANOMALY
● Variation in number of the digits* (p 1118)
Hereditary variations in the number of digits, generally six toes, occur most commonly on the
front feet.
● Hypomelanosis (vitiligo) (p 1122)
Loss of epidermal melanin is evidenced by non-pigmented patches in otherwise pigmented areas
such as the nose, lips, mouth and paw pads.
continued
1107
continued
● Hyperpigmentation (lentigo simplex)** (p 1113)

Dark pigmented patches (“freckles”) occur in the non-haired areas of orange cats older than
1 year of age.
● Epidermolysis bullosa (p 1123)
A hereditary claw-shedding disease seen in Siamese kittens causes the claws to shed easily with
minor trauma.
METABOLIC
● Hypothyroidism (p 1121)
Erythematous, scaling lesions of the footpads occasionally occur with hypothyroidism. Seborrhea
sicca and a dry lusterless hair coat, which is easily epilated, and has poor regrowth after clipping
may be evident. It is very rare in cats, and occurs most commonly after bilateral thyroidectomy.
Unkempt hair coat and overgrown claws are commonly seen. Systemic signs include weight loss,
polyphagia, polydypsia/polyuria and nervous/hyperactive temperament. Usually seen in cats older
than 8 years.
Rare condition in cats that results in very thin and easily torn skin, especially on the digits.
Other systemic signs include polyphagia, polydypsia/polyuria, abdominal enlargement and skin
infections.
Whitish, waxy nodules in the paws are a rare complication of diabetes mellitis. Other systemic
signs include polyuria/polydypsia, weight loss and polyphagia or anorexia.
● Calcinosis cutis (p 1123)
Metastatic calcification occasionally occurs in the pads of the feet secondary to renal failure.
Affected pads are enlarged, firm and painful. A chalky white-to-pink material may be visible
through the intact epidermis. Pads may ulcerate and exude a chalky, white, pasty material.
MECHANICAL
● Foreign bodies (p 1120)
Foreign bodies may result in nodules, abscesses or draining tracts in the interdigital web. Foreign
bodies are much rarer in cats than dogs.
NEOPLASTIC
● Primary and secondary neoplasia (p 1116)
Neoplasia may cause swollen painful pads or digits that become ulcerated. Various neoplasms
have been recorded as having a predilection for the feet; squamous cell carcinoma, metastatic
ungual carcinoma, fibrosarcoma and malignant fibrous histiocytoma have been more commonly
reported.
● Cutaneous horns (p 1122)
Cones of hard keratin growing out from the skin occasionally occur on the feet.
53 – THE CAT WITH PAW OR PAD PROBLEMS 1109
PHYSICAL
● Irritant contact dermatitis or chemical burns* (p 1119)
Erythema and ulceration of the footpads often occur together with salivation, mouth ulcers and
anorexia.
● Burns (thermal)* (p 1119)
Superficial to deep ulceration on the footpads occurs, depending on the severity of the burn.
● Frostbite (p 1120)
Frostbite may result in erythema, edema, necrosis and sloughing of extremities.
INFECTIOUS (VIRAL)
● Feline pox virus infection** (p 1113)
Multiple papules, vesicles, plaques or crusts and ulcers may occur on the face, ears, limbs and
paws associated with pox virus. Paronychia and sloughing of footpads may occur.
● Infectious pododermatitis*** (p 1111)
Viral, bacterial (most common), fungal and parasitic agents may cause pad and paw disease.
Bacterial: Paronychia involving one or more claws, and more rarely pyoderma or fistulated inter-
digital abscesses are usually caused by the more common opportunistic bacterial infections such
as S. intermedius and more rarely by the yeast M. pachydermatitis. Fungal: Single or multiple
ulcerated nodules, or draining fistulated areas are usually associated with the rare opportunistic
bacterial and fungal infections. Pheomycotic lesions are very darkly (black) pigmented. Non-
pruritic, erythematous scaling, alopecic lesions are associated with dermatophytes and usually
there are lesions elsewhere on the body as well. Kerion (nodular furunculosis) formation and
onychomycosis (fungal claw infection) are rare. Malassezia causes brown staining at the base of
the nails only, or a more generalized scaly erythematous dermatitis. Viral: Calici virus may pro-
duce footpad ulceration in association with oral ulceration, usually without the more classical
respiratory signs of sneezing and nasal discharge. Parasitic: Erythematous, alopecic lesions may
occur with Demodex cati infections, or pruritic crusting lesions with Notoedres cati. Usually
there are lesions on other parts of the body.
INFLAMMATION (IMMUNE-MEDIATED)
● Pemphigus* (p 1117)
Pemphigus foliaceus is most common. A symmetrical pattern of lesions occurs on the face, ears,
trunk, feet and mucocutaneous junctions consisting of erythema, oozing, crust, scales and alope-
cia. Some cats may present with only foot lesions.
● Systemic lupus erythematosus (p 1121)
SLE is a multi-systemic disease, which may involve the skin with ulcerative lesions of the feet and
paronychia.
● Plasma cell pododermatitis* (p 1115)
Plasma cell pododermatitis results in swollen and very soft (“mushy”) footpads with normal pad
symmetry. Normally it is non-painful, but the pads may become ulcerated.
● Insect bite hypersensitivity** (p 1114)
Symmetrical pattern of erythematous papules, ulcers and crusts occur on thinly haired areas,
especially the bridge of the nose and/or ear tips. Sometimes the footpads are also affected.
Lesions have a seasonal occurrence.
continued
continued
ALLERGY
● Atopy and adverse food reaction* (p 1116)
Atopy or adverse food reaction may just involve the feet with nail biting and chewing. More typi-
cally it manifests as skin lesions affecting the head, face, ears and inner thigh. These include non-
inflammatory alopecia, miliary dermatitis and granulomatous ulcerated skin from licking and
scratching, particularly of the face and neck.
TOXIC
● Thallium poisoning (p 1124)
Thallium-containing rodenticide toxicity results in hyperkeratosis and scaling of the footpads,
as well as similar lesions elsewhere on the body.
TRAUMA
● Shredded nail tips or avulsed nails (trauma)*** (p 1111)
Shredded nail tips or avulsed nails are typically evident in cats involved in road accidents.
● Declawing complications (p 1120)
Deformed claws, keratinaceous foreign bodies at the ends of the digits or draining tracts may
result from imperfectly completed declawing procedures.
● Arteriovenous fistulae (p 1124)
An arteriovenous fistula is a very rare condition resulting in local edema and distinct, tortu-
ous, pulsating blood vessels near the area.
● Disorders of the claws and paronychia, which

INTRODUCTION usually result from trauma, bacterial paronychia or
neoplasia.
MECHANISM?
Foot problems are less commonly seen in cats as a pre- WHERE?

senting complaint than in dogs. Disorders of the feet including paws, pads, claws and
The feet of cats can be affected, along with other areas ungual folds.
of the body, in numerous feline dermatoses and sys- Careful history taking and a thorough physical exami-
temic diseases. nation are very important in establishing a list of dif-
Lesions confined primarily to the paw or pads are ferential diagnoses and for selection of appropriate
rarely seen. laboratory tests.
Three categories of lesions are seen: For many of the diseases, definitive diagnosis is by his-
● Scaling, crusting and pruritic lesions, which usu- tological evaluation of biopsy specimens.
ally result from immune-mediated and allergic dis-
eases or infectious causes such as viral, fungal and
WHAT?
parasitic.
● Nodules, draining tracts, ulcers and abscesses, The most common causes of foot problems are infec-
which usually result from the more unusual bacterial tious agents, especially bacterial and fungal, and
and fungal infections or neoplasia. trauma.
Less common causes are tumors, immune-mediated medius, Escherichia coli, Pseudomonas sp.,
diseases and endocrinopathies. Proteus sp. or Pasteurella sp.
● More rarely other bacteria reported are Myco-
DISEASES CAUSING PAD OR PAW bacterium sp., Listeria monocytogenes, Dermato-
PROBLEMS philus congolensis, Nocardia asteroides.
Fungal.
● Dermatophytes, primarily Microsporum canis,
SHREDDED NAIL TIPS OR AVULSED
NAILS (TRAUMA)*** M. gypseum and Trichophyton mentagrophytes, can
be found on the paws but would rarely be found
Classical signs there as the only site on the body.
● Rare cases of opportunistic saprophytic fungal
● Broken or torn claws. infections have been reported including:
● Feathered ends to claws. – Pheohyphomycosis caused by Exophiala jean-
selmei, Moniliella sauveolens, Cladosporium sp.,
Clinical signs Stemphyllium sp. and Scolecobasidium humicola.
– Paecilomyces fumosoroseus and Sporothrix
Broken or torn claws. schenckii.
● Yeast infections with Cryptococcus neoformans,
Feathered ends to claws are classically seen in cats
involved in a road accident, and result from dragging Rhodotorula mucilaginosa and Malassezia pachy-
of the claws on the rough road surface. dermatis usually also involve other areas of the
● If the history of an injured cat is unknown, then
body.
feathered claw tips can be a clue to road trauma. Viral.
● Pox virus causes foot lesions and is covered sepa-
Diagnosis rately (see page 1113).

● Occasionally Calici virus may cause footpad ulcer-
Diagnosis is based on history and physical examination. ation, in addition to the more common clinical signs
in other organs.
Parasitic.
INFECTIOUS PODODERMATITIS***
● Demodicosis is reported to be a rare cause of claw
disease.
Classical signs
● An opportunistic infection with Leishmania brazilien-
● Paronychia involving one or more claws. sis has been reported causing a large vegetative
● Ulcerated nodules or fistulated areas. lesion in the interdigital area.
● Non-pruritic, erythematous, scaling,
alopecic lesions.
Clinical signs
Bacterial.
Pathogenesis
● Paronychia involving one or more claws, and more
Common cause of foot problems in cats and is often rarely pyoderma or fistulated interdigital abscesses
secondary to factors such as trauma or immune sup- are usually caused by the more common oppor-
pression (FeLV, FIV, systemic disease). tunistic bacterial infections such as S. intermedius.
● Single or multiple ulcerated nodules, or draining
Infectious agents can be bacterial, fungal or viral.
fistulated areas are usually associated with the rare
Bacterial. opportunistic bacterial (including Nocardia,
● Various opportunistic bacteria have been Listeria monocytogenes Dermatophilus congolen-
reported, most commonly Staphylococcus inter- sis) and fungal infections.
Fungal. Serology to detect cryptococcal antibody is usually

● A variety of saprophytic fungi produce draining positive in cats with cryptococcosis.
tracts, ulcerated nodules and chronic non-healing
Hair pluck/skin scrape to detect Demodex.
wounds. Pheomycotic lesions are very darkly (black)
pigmented.
● Kerion (nodular furunculosis) formation and ony- Differential diagnosis
chomycosis (fungal claw infection) are rare.
● Malassezia pachydermatitis is a yeast which is a Symmetrical bacterial paronychia can appear similar to
secondary infectious agent, causing brown stain- immune-mediated disease such as pemphigus foli-
ing at the base of the nails only, or a more gener- aceus.
alized scaly erythematous dermatitis. Rarely it
Nodules and ulcerated areas can appear similar to neo-
causes paronychia involving one or more claws.
plastic lesions.
● Infection by dermatophytes causes hair loss and
rarely infection of the nails (onychomycosis). Other
areas of the body are usually also involved with Treatment
irregular or circular alopecic patches, with or with-
out scale, that are non-pruritic and may be ery- Bacterial infections.
thematous. ● Use appropriate antibiotics selected based on cul-
ture and sensitivity.
Viral.
● Treatment for several weeks may be necessary for
● Pox virus produces multiple papules, vesicles,
deep infections.
plaques or crusts and ulcers, which may occur on
● If lesion recurs, check immune status (FeLV, FIV,
the face, ears, limbs and paws. Paronychia and
systemic disease).
sloughing of footpads may occur.
● Calici virus infection may produce footpad ulcera- Fungal infections.
tion in association with oral ulceration, usually with- ● Griseofulvin (50–100 mg/kg PO q 24 h, preferably
out the more classical respiratory signs of sneezing with a fatty meal) is effective only for dermato-
and nasal discharge. phytes. Beware of adverse drug reactions including
teratogenicity, gastrointestinal upsets and bone
Parasitic.
marrow suppression.
● Erythematous, alopecic lesions may occur with
● Ketoconazole (5–10 mg/kg PO q 24 h) has been
Demodex cati infections, or pruritic crusting lesions
effective for most fungal and yeast infections but
with Notoedres cati. Usually there are lesions on
has more side effects than itraconazole. Adverse
other parts of the body.
reactions include anorexia, fever, depression, vom-
iting, diarrhea and neurologic abnormalities. Lower
Diagnosis doses or alternate day therapy may be necessary if
reactions occur.
Wood’s lamp examination or direct examination of
● Itraconazole (5–10 mg/kg PO q 24 h) may work
hair and scales mounted in paraffin oil or KOH may
better than ketoconazole, and has fewer side effects,
detect dermatophytes.
but is more expensive.
Cytological examination of smears of the exudate
Parasitic infections.
from moist lesions, stained with Diff-Qik may reveal
the primary organism present including Malassezia, Demodex.
Cryptococcus or bacteria. ● Feline demodicosis has responded to simple treat-
ments such as three dips of malathion or lime-
Culture exudate to identify the organism, and obtain
sulfur at weekly intervals.
sensitivity for antibiotic treatment if bacterial.
● Ivermectin is very effective against mites, although
Biopsy nodular or fistulous areas for histopathology, and its use in cats is off-label. For demodectic mange
culture tissue to identify the rarer opportunistic infections. the dose rate is 0.6 mg/kg daily orally continued
for up to 30 days after negative skin scrapings.

HYPERTHYROIDISM**
Stopping too early results in relapses.
● Similarly Doramectin at 0.6 mg/kg sc weekly can
Classical signs
be used.
● Weight loss with polyphagia.
Leishmania.
● Unkempt hair coat.
● Successful treatment in cats has not been reported.
● Nervous, hyperactive.

Prognosis With Weight Loss and a Good Appetitie).
Prognosis varies depending on the type of infection and
the underlying cause. The recurrence rate is high for Clinical signs
bacterial paronychia if there is an underlying immune
Most commonly there is weight loss despite a raven-
deficiency.
ous appetite. More rarely is appetite depressed.
The prognosis is more guarded for the rarer opportunis-
Other signs may include tachycardia, polydipsia/
tic bacterial and fungal infections. Cures are reported
polyuria, vomiting or diarrhea, and a heart murmur.
with the use of the imidazole drugs (ketoconazole and
itraconazole). A palpable thyroid nodule in the neck is present in the
majority of cats.
Restlessness and hyperexcitability are often evident.
HYPERPIGMENTATION (LENTIGO
An unkempt haircoat and overgrown claws are typical.
SIMPLEX)**
● The overlong claws catch in floor coverings or click
on bare floors as the cat walks.
Classical signs
Usually occurs in cats older than 8 years of age.
● Black asymptomatic spots that gradually
enlarge and become more numerous.
Diagnosis
● Occur in cats with orange coat color.
A tentative diagnosis is based on history and physical
examination.
Clinical signs Increased total thyroxine (T4) levels confirm the diag-
nosis. Cats with a high normal T4 concentration and
Hyperpigmented areas (“freckles”) in orange (gin-
signs consistent with hyperthyroidism should either be
ger) cats are termed lentigo simplex.
retested several weeks later, or free T4 concentration be
Freckles usually appear before 1 year of age and measured by equilibrium dialysis, or a T3 suppression
increase in number with age. test performed. Concurrent disease can decrease a high
T4 into the normal range.
There are multiple hypermelanotic macular lesions on
the nose, lips, eyelids and footpads.
FELINE POX VIRUS INFECTION**
Lesions are asymptomatic and do not develop into
melanomas.
Classical signs
● Multiple nodules, papules, crusts, and
ulcerative plaques.
Diagnosis
● Commonly on the face, limbs and paws.
Diagnosis is based on the history of asymptomatic ● Pruritis, pain, fever, conjunctivitis and
black spots developing in the poorly haired areas of dyspnea may be present.
cats with a ginger coat color.
Pathogenesis Transmission
Infection is caused by a virus from the orthopoxvirus The natural reservoir for infection is not known, but is
genus. The origin of the virus is unclear. It was attrib- thought to be small wild animals and the cat is infected
uted to the cow-pox virus, but now it is thought there whilst hunting them.
could be a feline pox virus.
Transmission of cow pox virus from infected milk has
Reported infections are from England and Europe. also been blamed.
The pox virus can be transmitted to in-contact cats,
Clinical signs dogs and humans; immunocompromised individuals
Skin lesions occur on the face, ears, limbs and paws are more at risk. Warn in-contact people of the zoonotic
with multiple papules, vesicles, plaques or crusts potential.
and ulcers. The virus is killed by most disinfectants, particularly
On the feet there can be paronychia and sloughing of chlorine-based ones.
the footpads.
Prevention
Diagnosis Prevent the cat from hunting or contact with an infected
Biopsy and histologic examination of the crust or cat.
affected skin demonstrates eosinophilic intracytoplas-
mic inclusion bodies within keratinocytes.
Specialist tests that may be available also include a INSECT BITE HYPERSENSITIVITY**
serologic test for virus-neutralizing antibodies, electron
microscopy of crusts or affected skin to detect the virus, Classical signs
and virus isolation. Virus isolation is currently the only ● Erythematous, crusted, pruritic lesions.
method for making a precise diagnosis. ● Symmetric lesions on ear tips, face, nose
and footpads.
Bacterial and fungal infections, eosinophilic granu- Pathogenesis
loma and neoplasia may all cause similar lesions but
Hypersensitivity resulting in skin lesions is associated
can be differentiated on biopsy and histological exami-
with flying and biting insects.
nation.
It is most often seen in cats that go outdoors when
mosquitoes or midges (Lasiohelia townsvillensis) are
Treatment present.
Treatment is not thought to affect the outcome of the
disease, and is not regarded as necessary as most cats
Clinical signs
recover spontaneously within 1–2 months.
Thinly haired areas are most commonly affected, espe-
Secondary bacterial infection should be treated with
cially the bridge of the nose, ear tips and the junc-
antibiotics.
tion of haired skin and the footpad (“ears, nose and
Glucocorticoids are contraindicated. toes syndrome”).
Lesions have a symmetrical pattern, and begin with
Prognosis erythematous papules to plaques.
Prognosis is good as cats recover spontaneously, however, Lesions are pruritic, and the cat traumatizes itself, so
there may be permanent scarring. that the affected areas become ulcerated and crusted.
Chronic lesions develop nodules, pigment changes Prognosis and prevention

(dark or pale patches), and alopecia.
Good control of the problem is possible if the cat can
Footpads may be affected with swelling, scales or be kept away from biting insects, or will tolerate insect
crusts, hyperkeratosis, fissures and pigment changes. repellent.
However, lesions may increase with severity over the
Diagnosis years if exposure cannot be controlled.
Seasonal occurrence is evident coinciding with mos-
PLASMA CELL PODODERMATITIS*
quito or midge season in cats allowed outdoors.
Tentative diagnosis can be confirmed by keeping the Classical signs
cat indoors or hospitalized for 5 days and demon-
● Swollen, very soft footpads, generally non-
strating great improvement of lesions.
painful.
Biopsy and obtain small specimens (4-mm biopsy punch) ● Normal pad symmetry.
carefully, as the ears and nose bleed easily and readily
show scars. Histopathological changes are similar to those
of cats with atopy, food and flea bite hypersensitivity. Pathogenesis
Plasma cell pododermatitis is a rare skin disease
affecting the footpads.
The cause is unknown, but is thought to be immune-
Food allergy commonly results in pruritis of the face,
mediated or allergic.
head, pinnae and neck, in contrast to just the nose
and/or ears affected with insect hypersensitivity. One study found 50% of cases to be feline immuno-
Lesions are usually asymmetrical and very excoriated. deficiency virus-positive.
Non-seasonal occurrence, and does not respond to the
indoor confinement trial, but responds to an elimination Clinical signs
dietary trial.
Typically, the footpads are swollen, very soft and
Autoimmune diseases such as pemphigus foliaceus/ fluctuant (mushy). Usually the larger metacarpal and
erythematosus and discoid lupus erythematosus typi- metatarsal pads are the ones affected.
cally also have a symmetric pattern, but usually there is
Normal pad symmetry is not disturbed by the swelling,
extensive crusting and exudation of head and body.
but the stretching of the skin over the swollen pad
Depression and anorexia are often present. Pruritis is
results in a white, silvery, cross-hatched appearance.
variable.
Lesions involve one or more feet.
Normally, the lesions are non-painful and the cat is
Treatment
not lame, although cases of cats limping on the affected
Keep the cat indoors at the times of greatest insect feet have been reported.
activity, usually early morning and dusk.
The pad may become ulcerated, and drain hemor-
Topical insect repellents applied to the affected area. rhagic fluid.
Try a variety, as not many are well tolerated by cats;
Some cats also have plasma cell stomatitis, immune-
ointments or creams are best tolerated.
mediated glomerulonephritis or renal amyloidosis.
Petroleum jelly smeared on the ear tips and nose has
also been used successfully. Diagnosis
Oral prednisolone (0.5–2 mg/kg on alternate days) or Fine-needle aspirate of the lesion contains large num-
injectable glucocorticoids (repositol methyl pred- bers of uniform plasma cells with a few neutrophils and
nisolone acetate, 20–40 mg/cat subcutaneously). lymphocytes.
Deep wedge biopsy from a footpad near the pad mar- Pruritis is present but may not be obvious to the owner.
gin is diagnostic. A punch biopsy may not go deep ● Over-grooming results in non-inflammatory alope-
enough to be diagnostic. cia (“fur mowing”).
● If a number of pads are affected choose a more
Foot or claw chewing may initially be the only pre-
mildly affected one to biopsy as a severely affected
senting clinical sign.
one may not heal well.
● The cat drags the claws through the teeth with loud
clicking noises, which brings the problem to the
attention of the owner.
Differential diagnosis ● One or more ulcerated areas of the paws (digits,
Undifferentiated sarcoma may appear very similar and periungual areas or interdigital spaces) may be
needs a biopsy to differentiate. present.
● Histologically these lesions are typical of eosino-
philic granuloma complex.
Treatment
Diagnosis
This is not necessary if the cat is asymptomatic, as the
disease may spontaneously regress. Rule out other causes of claw problems, especially
infectious pododermatitis and neoplasia.
Immunosuppressive doses of prednisolone (up to
4 mg/kg/day) have been recommended, but may not be Control external parasites. A good choice is fipronil as
effective. this controls fleas, and anecdotally mites (Cheyletiella,
Sarcoptes, Otodectes and Notoedres) and provides partial
Chrysotherapy (aurothioglucose; Solganol; 1–2 mg/kg control of ticks.
IM weekly) may be effective.
Try a dietary trial using a food source that the cat has
Surgical excision of the footpad. A new footpad not been exposed to before. It may take ingenuity to
grows back. Reported to be the best therapy at present. find a new food that the cat is willing to eat. Duck,
venison or rabbit (2/3 cup) with cooked rice or pasta
(1/3 cup) are often tolerated. A trial period of a mini-
Prognosis mum of 9 weeks has been advocated for cats and up to
Prognosis is guarded as the recurrence rate is high, 16 weeks preferably. Re-challenge the cat with the old
usually within 4–6 months. diet to confirm the diagnosis, although owners may be
unwilling to risk signs recurring.
Intradermal skin testing to test for atopy. This is tech-
ATOPY AND ADVERSE FOOD REACTION*
nically more difficult in cats than dogs, as reactions are
less intense and more transient.
Classical signs
● Pruritis, which is manifested as scratching,
licking or chewing. PRIMARY AND SECONDARY NEOPLASIA*
● Skin lesions varying in severity from
alopecia to miliary dermatitis to ulcerated Classical signs
plaques or granulomas. ● Swollen, painful digit(s) and/or paronychia.
● Ulcerative destructive lesion of the paw
and digits.
Clinical signs
Atopy and adverse food reactions result in various
other dermatological manifestations such as ulcer-
Pathogenesis
ated plaques, miliary dermatitis, symmetrical alopecia Neoplasia involving the foot is rare in cats and is usu-
and pruritis of the face and neck. ally seen in older cats. The neoplasia may be primary
or secondary. Secondary neoplasia results from metas- Bacterial or fungal infections, especially the rarer
tasis of primary neoplasia in other organs. opportunistic ones, can look very similar. Biopsy for
histopathology and culture will distinguish between
Squamous cell carcinoma.
these.
● Rare primary tumor arising from the nail bed
epithelium.
● Appears to be more aggressive than squamous cell Treatment
carcinomas in other parts of the body.
Radical surgical excision is the treatment of choice for
● On clinical examination it may be mistaken for
tumors without evidence of metastasis.
paronychia or pyoderma.
Mean survival for metastatic digital carcinoma was 67
Metastatic digital (ungual) carcinoma.
days.
● Usually presents as lameness associated with multi-
centric digital carcinoma.
● Seen in aged cats (average age 13 years) with
asymptomatic bronchogenic carcinoma or squa- PEMPHIGUS*
mous cell carcinoma of the lung.
● Lesions can involve a number of digits and more Classical signs
than one paw. Typically there is swelling of the
● Crust, scales, alopecia in a symmetrical
digit, ulceration of the skin or purulent discharge,
pattern.
and either fixed exsheathment, deviation or loss of
● Areas usually involved are face, ears,
the nail.
trunk, feet and mucocutaneous junctions.
Fibrosarcoma. ● Occasionally have only foot lesions.
● Seen in older cats and is not associated with feline
sarcoma virus.
Pathogenesis
● Lesions are usually solitary and can involve the digits.
● The area is alopecic, ulcerated and the tumor has Pemphigus is an immune-mediated disease, with
rapid infiltrative growth. auto-antibodies directed against intercellular cement in
the epidermis causing loss of cohesion between ker-
Undifferentiated sarcoma.
atinocytes and resulting in the formation of bullae.
● Seen in older cats and involves the footpads of one
● Bullae are very transient in cat skin due to the thin
or more feet.
epidermis, and may not be observed.
● Affected pads are soft, mushy, painful and maybe
ulcerated. What initiates the auto-antibodies is unknown, but
drugs and chronic skin disease have been implicated
Malignant fibrous histiocytoma.
in some cases.
● Seen in older cats.
● The lesions are solitary, firm, poorly circumscribed, Different types of autoimmune dermatitis may involve
variable in size and shape and locally invasive. cats’ paws but the most common is Pemphigus foli-
● Legs, especially the paw, and shoulders are the aceus.
most common sites.
Clinical signs
Diagnosis Erythema, oozing, crusts, scales and alopecia occur
Biopsy of representative areas and histopathology. with a symmetrical pattern on the face, ears, trunk,
feet and mucocutaneous junctions.
Lesions commonly involve the feet and footpads, caus-
ing hyperkeratosis and ulceration. Some cats are pre-
Plasma cell pododermatitis also has swollen mushy sented with only footpad lesions and sometimes
pads, which may be ulcerated. lameness.
Paronychia and involvement of the nipples are com- Prognosis

monly seen in cats.
Prognosis is guarded, because the inciting cause is
usually unknown, and the side effects of the therapy are
Diagnosis often severe.
Direct smears from intact vesicles or pustules may
show numerous acantholytic keratinocytes; these are
strongly suggestive of pemphigus.
Biopsy of primary lesions or at the periphery of the VARIATION IN NUMBER OF DIGITS*
most recent lesions shows subcorneal pustules con-
sisting of acantholytic keratinocytes and neutrophils. Classical signs
Direct immunofluorescence of biopsies shows diffuse

● Abnormal number of toes (six most
intercellular fluorescence. common).
● Agenesis or fusion of digits.
Systemic lupus erythematosus is rare and usually also
has systemic signs. Clinical signs
Insect hypersensitivity is common, but lesions are Variation in the normal number of digits is present
usually confined to the bridge of the nose, tips of the ears, from birth.
and occasionally footpads. Seasonal occurrence and
Ectrodactyly is agenesis of all or part of a digit and is
history of biting insects being observed around the cat
an inherited defect involving the fore-paws.
helps differentiate this from pemphigus.
Polydactyly refers to extra toes.
● The mode of inheritance is dominant.
Treatment ● There is considerable variation from animal to ani-
Therapy is often difficult as side effects from the drugs mal with the number of extra toes and how perfectly
are common. formed they are.
● Usually there are six toes on each front foot, but
High doses of glucocorticoids (4–8 mg/kg daily) will
sometimes there can be seven toes on the front feet
induce remission in most cases (about 2 weeks). Once
and six on the hind feet. The hind feet are not
in remission, reduce to alternate day therapy and to the
affected unless the front feet are involved.
minimum dose which maintains remission.
● The incidence varies with it being common in some
Chlorambucil (0.1–0.2 mg/kg every 24–48 hours) can countries and not seen in others.
be added if glucocorticoids are insufficiently effective.
Syndactyly refers to fusion of the digits. It is also
Chrysotherapy (gold salts; aurothioglucose: Solganal; called “split-foot” or “lobster-claw”.
Schering) has been useful in cats when other treatments ● Typically it manifests as a central cleft of either
have failed. Begin with 1 mg/kg IM weekly until remis- one or both front feet. However, there may be
sion, which may take up to 12 weeks to occur. If no fusion of the bones of the foot to produce double
response is evident after 12 weeks of therapy, increase claws.
dose to 1.5–2 mg/kg. Once the cat responds, give the ● The evidence is for dominant heredity, possibly
dose every 2 weeks and then monthly for several with variable expression, as the number of affected
months. Alternatively the dose can be started at 0.25 mg/kg animals is less than expected, with some geneti-
IM for the first week, 0.5 mg/kg the second week, then cally affected animals appearing normal. The right
1 mg/kg weekly until remission and then a gradually side tends to be more severely affected than the
decreasing dosage. left.
IRRITANT CONTACT DERMATITIS Diagnosis

OR CHEMICAL BURNS* Diagnosis is based on history and physical examina-
tion.
Classical signs
● Variable erythema, ulceration, necrosis of Treatment
the contact areas. Bathe to remove traces of offending chemical.
● Hyperkeratosis and scaling.
● Salivation and saliva staining around the Corticosteroids (prednisolone, 0.5–1 mg/kg PO q 24
mouth and paws with chemical burns. h) to reduce inflammation.
Non-steroidal antiinflammatory drugs can be given for
pain relief and to reduce inflammation. Ketoprofen is reg-
Pathogenesis istered for use in cats (2 mg/kg SC or PO initially then
1 mg/kg PO daily). Meloxicam (0.2 mg/kg SC or PO ini-
Irritant contact dermatitis or chemical burns are com- tially then 0.025 mg/kg PO 2–3 times/week.
monly caused by chemicals used in the environment
such as herbicides, garden fertilizers, fuel oil and Antibiotics, if there is secondary infection.
other common household or cattery cleaning products Protective dressings may be necessary if ulceration is
and disinfectants including chlorine bleach (sodium severe to promote healing.
hyperchlorite), strong alkalis, strong acids, pine oils,
phenolic compounds and quaternary ammonium com-
pounds. BURNS (THERMAL)*
Chemical burns with ulceration may occur if the prod- Classical signs
uct is incorrectly diluted.
● Typically this occurs if the product is applied undi- ● Initially the skin may be dry and hard.
luted and then water is used to dilute and wash the ● Necrotic skin sloughs leaving large raw
chemical away. Highly concentrated product may areas.
remain in less accessible areas, causing chemical ● Purulent discharge when secondarily
burns to the feet and mouth. infected.
● Signs develop when the cat inadvertently walks on
them.
Pathogenesis
Most common in cats living outdoors.
Burns occur when cats walk or jump onto hot surfaces
such as barbecues or stove hot plates, usually with the
Clinical signs intent of stealing food.
Typically, there is erythema and ulceration of the More generalized burns occur in cats trapped in house
footpads, interdigital spaces and around the nails. fires.
Usually more than one paw is affected.
Pain and pruritis are sometimes evident.
Clinical signs
Oral ulcers and salivation are often present, and result
from the cat licking its feet. Regurgitation may result Signs depend on the severity of the burn, and include
from chemical esophagitis. superficial to deep ulceration and sloughing of the
burnt area.
Less toxic chemicals or concentrations may cause ery-
thema, and excessive licking of the feet rather than Initially the skin may be dry and hard. Necrotic skin
ulceration. sloughs leaving large raw areas.
Purulent discharge occurs when the burnt area Clinical signs

becomes secondarily infected.
Frostbite typically affects the tips of the ears and the
digits, areas that are not well insulated.
Treatment
Whilst frozen, the skin appears pale and cool to touch,
Silver sulfadiazine cream or aloe vera gel applied and has decreased sensation.
under a non-adherent dressing are excellent topical
treatments for burns. After thawing, there may be mild erythema, edema
and pain.
Burn healing is slow, taking weeks to months of treat-
ment. In severe cases, the skin becomes necrotic and sloughs.
Very extensive or deep burns may heal with scarring

that interferes with function, necessitating reconstruc- Treatment
tive surgical procedures.
Rapidly thaw frozen area by the gentle application of
warm (42–44˚C) water.
DECLAWING COMPLICATIONS
Handle tissues gently to prevent further damage and
Classical signs pain.
● Claw deformity or keratinaceous growths Aloe vera gel applied topically helps to prevent vaso-
at the end of the digits. constriction and tissue hypoxia.
● Swollen ends of digits and draining tracts. Any resulting necrotic areas may need surgical debrid-
ing.
Clinical signs Antibiotics may be needed to control secondary infec-
Regrowth of claws may result from persistent germi- tion, in cases where there is extensive tissue damage.
native epithelium after incomplete removal during
declawing.
Regrowth can vary from deformed claws to keratina- FOREIGN BODIES
ceous foreign bodies at the ends of the digits.
Swollen ends of digits and draining tracts may develop. Classical signs
● Nodules, abscess and draining tracts.
Diagnosis
A history of a declawing procedure having been per-
formed.
Clinical signs
Excisional biopsy of deformed ends of the digits is
diagnostic and curative. Objects such as plant awns, thorns can become
embedded in the interdigital space. This is much rarer
in cats than in dogs.
FROSTBITE
Nodules, abscesses and draining tracts result.
Classical signs
● Frozen skin is pale and cool to the touch.
● Mild erythema, edema and pain after Treatment
thawing. Surgical debridement and removal of foreign body.
● Necrosis and sloughing in severe cases.
Use antibiotics if secondary infection develops.
Often there is seborrhea sicca and a dry, lusterless hair

SYSTEMIC LUPUS ERYTHEMATOSUS
coat, which is easily epilated, and has poor regrowth
after clipping. The skin may be myxoedematous and
Classical signs
thickened.
● Multi-systemic disease including the skin.
Other signs of hypothyroidism may be present
● Generaliszd or localized erythematous,
including lethargy, inappetence, obesity, hypothermia
scaly or crusted skin lesions.
and bradycardia.
Most commonly occurs after bilateral thyroidectomy
Clinical signs for hyperthyroidism. Spontaneous hypothyroidism is
very rare.
Dermatological signs occur in 20–30% of cases.
● Typically, there are generalized or localized scaly
or crusted lesions on the face, ears and eyelids.
Alternatively, ulcerative lesions may be present on Diagnosis
the face, trunk and feet. Periocular leukotrichia may
If available, the thyroid stimulation test shows mini-
be evident.
mal to no stimulation.
● Paronychia and oily seborrhea may occur.
Free T4 or free T4 by equilibrium dialysis are below the
Systemic signs include intermittent pyrexia, anorexia,
normal values for the laboratory.
depression and weight loss.
Response to trial therapy with thyroxine (0.05–0.1
Involvement of other organs may result in immune-
mg once daily) for 4 weeks results in improved clinical
mediated anemia, thrombocytopenia, glomeru-
signs.
lonephritis and polyarthritis.
Diagnosis HYPERADRENOCORTICISM
Definitive diagnosis is very challenging, as the dis-
Classical signs
ease is so variable in its clinical presentation.
● Pot-bellied appearance and muscle
Skin biopsies show hydropic interface dermatitis.
wasting.
A high positive ANA titer may occur in some cats. ● Unkempt hair coat with thin, easily torn
skin.
Laboratory results demonstrating multi-systemic dis-
● Polydypsia/polyuria and often associated
ease suggest a tentative diagnosis of SLE.
diabetes mellitus (80% of cases).
HYPOTHYROIDISM See main reference on page 251 for details (The Cat
With Polyuria and Polydipsia).
Classical signs
● Lethargy, inappetence, obesity.
● Seborrhea sicca and a dry, lusterless hair Clinical signs
coat, easily epilated with poor regrowth.
Bilaterally symmetrical alopecia involving the face,
flanks and limbs.
Clinical signs The skin is often very thin and easily torn especially
on the digits.
Hypothyroidism may result in erythematous, scaling
and papular lesions, which affect the forehead, Systemic signs of polydypsia, polyuria and weight
abdomen, tail and footpads. loss are usually associated with diabetes mellitus.
Diagnosis Vitiligo is a hereditary lack of pigment in the skin,

and may have an autoimmune pathogenesis.
Low-dose dexamethasone test (0.1 mg/kg) or ACTH ● Three affected Siamese cats had antimelanocyte
stimulation test is used for diagnosis. antibodies, whereas four normal Siamese cats did
Imaging the adrenals by abdominal ultrasound not.
helps differentiate pituitary from adrenal-dependent ● There can be symmetric macular depigmenta-
hyperadrenocorticism. tion, especially of the nose, lips, buccal mucosa and

facial skin, also footpads and claws.
● Lesions are most noticeable in the dark coat colors
DIABETES MELLITUS where the normally dark footpads have pink
patches.
Classical signs ● Onset of the condition is usually in young adult-
● Polydypsia, polyuria, polyphagia and hood.
weight loss.
See main reference on page 236 for details (The Cat With Diagnosis
Polyuria and Polydipsia).
Diagnosis is based on the history of a young age with
patches of unpigmented skin in normally dark-
Clinical signs pigmented areas.
Cutaneous xanthomatosis has been described in cats In vitiligo there is no history of trauma or inflammation
with diabetes mellitus. that could have damaged melanocytes.
This may present as whitish, waxy nodules in the
paws.
CUTANEOUS HORNS
Typical signs include polydypsia, polyuria, polyphagia
and weight loss.
Classical signs
● Firm, horn-like protuberance on the skin.
Diagnosis
A tentative diagnosis is based on a history of poly-
dypsia and polyuria with weight loss. Pathogenesis
A definitive diagnosis is based on demonstrating per- The term cutaneous horn is used to describe a keratotic
sistent hyperglycemia > 12 mmol/L (> 216 mg/dl). mass that is generally higher than it is wide, usually
several millimeters in diameter and 1–2 cm high.
HYPOMELANOSIS (VITILIGO) Cutaneous horn of the footpads in cats is a rare disor-

der. Affected cats have been positive for FeLV and the
Classical signs virus has been isolated from the horn material.
● Patches of complete lack of pigment. The viral-affected horns occur on the footpads only.

Loss of epidermal pigmentation (hypomelanosis) can Single or multiple firm horn-like formations arising
be primary as with vitiligo, or secondary as in post- from any area of skin. Footpads seem to be predis-
inflammatory change. posed sites.
Diagnosis EPIDERMOLYSIS BULLOSA

Diagnosis is based on the typical clinical appearance
and histopathology of dense laminated hyperkeratosis. Classical signs
Biopsy may be necessary to check for squamous cell ● Uncommon congenital disorder.
carcinoma at the base. ● Avulsion of the claws with minor trauma.
● Erosive lesions on the hard palate.
Check FeLV status.
Treatment
Pathogenesis
Surgical excision is the treatment of choice.
Recurrences are frequent. Separation of epidermal tissues from the dermis
occurs after minor trauma because of defective adher-
ence of the dermo–epidermal junction.
CALCINOSIS CUTIS Epidermolysis bullosa is an uncommon congenital

disorder, that has been reported in a line of Siamese
Classical signs cats.
● Enlarged, painful and firm pads.

● The pads may be ulcerated and exuding
Clinical signs
a white paste of gritty material.
● Signs of chronic renal disease. Nails are shed after minor trauma. The entire claw is
avulsed, leaving the corium quick exposed. Regrown
See main reference on page 245 (The Cat With Polyuria claws may be deformed.
and Polydipsia).
There may also be ulcers on the footpads and hard
palate.
Clinical signs
The onset is noticed when kittens become ambulatory
Calcinosis cutis is a rare complication of chronic renal and start climbing.
disease.
Lesions may have secondary bacterial infection.
Affected pads are enlarged, firm and painful.
A chalky white-to-pink material with feathery mar-
gins may be seen through the intact epidermis of non- Diagnosis
ulcerated lesions.
A definitive diagnosis is based on histopathology
Older lesions may ulcerate and extrude a chalky, of an amputated P3 which demonstrates dermo–
white, pasty to gritty material. epidermal separation without inflammation or basal
Other signs associated with chronic renal disease such cell injury.
as polyuria/polydypsia, and weight loss.

A definitive diagnosis is based on biopsy of the lesion Bacterial paronychia can be very similar, but the his-
that demonstrates metastatic calcium deposition in the tory and histopathology will differentiate.
tissues.
Immune-mediated disease affecting the claws, but
Clinical and laboratory findings are consistent with generally there are severe dermatological signs else-
chronic renal failure. where on the body.
Treatment THALLIUM POISONING

Curative treatment is not available, but amputation of
P3 of affected digits will prevent recurrent claw loss Classical signs
with associated pain and infection. ● Easily epilated hair.
Secondary infection should be managed with suitable ● Cutaneous erythema, erosions, crusts,
antibiotics. necrosis and alopecia.
● Lesions on ears, nose, abdomen.
Avoid trauma. ● Marked redness of mucous membranes.
ARTERIOVENOUS FISTULAE Pathogenesis

Thallium is a cumulative rodenticide rapidly absorbed
Classical signs through the mucosae and skin. Its use is now banned in
● Localized persistent or recurrent edema. many countries.
● Distinct and tortuous blood vessels near
the area.
Clinical signs
Skin lesions are seen in association with chronic toxi-
Pathogenesis city, and are characterized by chronic dermatitis. There
is severe redness of mucous membranes, cutaneous
Arteriovenous fistulae are traumatically induced from erythema, erosions, crusts, necrosis and alopecia.
penetrating wounds, blunt trauma or post-surgical com-
plications of onychectomy. Lesions are usually present around body orifices and
on the nose, ears, abdomen and feet. The footpads
become hyperkeratotic and ulcerated.
Clinical signs Hair is easily epilated.
Arteriovenous fistulae may be associated with persist-

ent or recurrent edema and bacterial paronychia of Diagnosis
one paw.
Diagnosis is based on a history of exposure to thallium
Pulsating blood vessels, palpable thrills and contin- and positive test for thallium in the urine.
uous machinery murmurs are present in the area of
the fistula. Skin biopsies demonstrate dermatitis consistent with
thallium poisoning.

A tentative diagnosis is based on the clinical signs. A number of diseases can have a similar crusted and
Definitive diagnosis is by demonstration of the fistula ulcerated appearance, and distribution to thallium toxi-
by contrast radiography. cosis, and skin biopsies are needed to differentiate.
These include:
● Autoimmune disorders.
● Drug eruptions.
Treatment ● Erythema multiforme and toxic epidermal
Surgical removal of the fistula or amputation of the necrolysis.

affected part. ● Lymphoreticular neoplasia.
Treatment (1–2 g q 8–12 h) to promote renal excretion of thal-

lium.
Prussian blue (100 mg/kg IV) given daily until urinary
tests for thallium are negative has been used to treat Supportive care such as intravenous fluids and anti-
thallium toxicosis, but is relatively ineffective when biotics for secondary infection.
clinical signs are already present.
The recommendation at present is combination treat-
Prognosis
ment with charcoal for gastrointestinal trapping of
thallium and potassium chloride supplementation Prognosis is very guarded, and most cases die.
RECOMMENDED READING
Bertazzolo W, Toscani L, Calcaterra S, Crippa L, Caniatti M, Bonfanti U. Clinicopathological findings in five cats
with paw calcification J Feline Med Surg 2003; 5: 11–17.
Dias-Pereira P; Faustino A. Feline plasma cell pododermatitis: a study of 8 cases. Vet Dermatol 2003; 14: 333–337.
Foil CS. Facial, pedal, and other regional dermatoses. Vet Clin North Am Small Anim Pract 1995; 25: 923–944.
Guaguere E, Hubert B, DeLabre C. Feline dermatoses. Vet Derm 1992; 3: 1–12.
Scott DW, Miller WH Jr, Disorders of the claw and clawbeds in cats. Comp Cont Educ 1992; 14: 449–455.
Scott DW, Miller WH Jr, Griffin CE. Muller and Kirk’s Small Animal Dermatology, 5th edn. 1995.
PART 14
Queen and kitten with problems
54. The fading kitten

Julie Levy
KEY SIGNS
● Crying.
● Ineffective nursing.
● Weakness and inactivity.
● Hypothermia.
MECHANISM?
● Kittens appear healthy and vigorous at birth. The fading syndrome develops when an under-
lying medical problem results in poor nursing, hypoglycemia and hypothermia.
Signs of the fading syndrome include:
● Loss of suckling reflex.
● Weight loss.
● Weakness and inactivity.
● Bloated abdomen.
● Hypothermia.
● Crying.
WHERE?
● Polysystemic effects lead to generalized weakness, ineffective nursing and inactivity.
WHAT?
● Fading and death may result from the primary condition or from the debilitation that follows.
1126
54 – THE FADING KITTEN 1127

Diseases causing a fading kitten and neonate
ANOMALY
● Congenital defects* (p 1138)
Most common life-threatening congenital anomalies are cleft palate (nasal reflux, sneezing and
dyspnea), portosystemic vascular shunt (stunted growth, neurological signs), cardiac (heart murmur,
cyanosis, dyspnea, palpable thrill and stunted growth), gastrointestinal defects including mega-
esophagus (regurgitation), blind intestinal loops (vomiting) and atresia ani (abdominal distention).
METABOLIC
● Neonatal isoerythrolysis (NI)** (p 1134)
Acute hemolytic anemia in the first 2 days of life in kittens with blood type A who nurse on
type B queens. Signs range from acute death on the first day of life to a fading syndrome over
several days. Hemoglobinuria and anemia are highly suggestive.
● Hypoglycemia*** (p 1133)
Life-threatening complication of other conditions, including sepsis, malnutrition, hypothermia,
parasitism. Signs usually occur in kittens up to 6 weeks of age, and include weakness and cessa-
tion of nursing or eating, ataxia, disorientation, agitation and in severe cases seizures, blindness,
coma and death.
● Prematurity* (p 1141)
Respiratory distress due to immature pulmonary development is life threatening. Kittens also have
no hair on ventrum or paws, ineffective sucking and MCV > 90 fl.
NUTRITIONAL
● Nursing failure** (p 1135)
May result from inadequate maternal milk supply due to agalactia or mastitis. Also ineffective
nursing occurs due to weakness, competition or congenital anomaly. Occasionally, inappropriate
milk replacer or feeding techniques are the problem. Signs usually occur in the first week of life
and include weight loss, weakness and ineffective nursing.
● Weaning stress* (p 1127)
Transition to solid food may be affected by delayed physical development of unthrifty kittens or
attachment to bottle feeding in hand-reared kittens. Kittens (6–8 weeks old) are reluctant to accept
solid food but suckle well.
PSYCHOLOGICAL
● Maternal neglect* (p 1135)
Inexperienced queens, maternal illness or a distracting environment may cause queens to neglect
their kittens. Queens may actively reject or attack sick kittens. Kittens may be agitated and crying
or be small, weak and have little suckling activity. Usually occurs in the first week of life.
continued
1128 PART 14 QUEEN AND KITTEN WITH PROBLEMS
continued
PHYSICAL
● Hypothermia*** (p 1131)
Hypothermia develops rapidly in neonatal kittens deprived of an external heat source or second-
ary to many other diseases. Hypothermia leads to gastrointestinal stasis, bradycardia, hypo-
glycemia and dehydration. Usually occurs in kittens <3 weeks of age but occurs as a secondary
problem up to 6 weeks of age. Signs include cessation of nursing, inactivity and the kittens are
cold to touch.
INFLAMMATION/INFECTIOUS
Viral:
● Feline leukemia virus infection (FeLV) (p 1142)
Systemic viral infections such as FeLV may cause fetal losses, fading neonates or illness of
weanling kittens, but disease is most common in kittens 8 weeks and older. Likely to affect most
or all of the litter.
● Feline infectious peritonitis infection (FIP) (p 1143)
FIP may cause fetal losses, fading neonates, or illness of weanling kittens, but disease is most
common in kittens 8 weeks and older. Weight loss, ascites and cycles of unexplained fever may
occur in kittens older than 8 weeks.
● Panleukopenia virus infection (p 1142)
Typically causes severe vomiting, diarrhea, dehydration and panleukopenia, most commonly in kit-
tens older than 6 weeks of age. May cause peracute deaths without typical signs. Intrauterine
infection may cause an intention tremor apparent when the kittens begin to walk.
● Upper respiratory infection (herpes virus**, calcivirus**) (p 1137)
Herpes and calicivirus typically cause upper respiratory infections from 2 weeks and older.
Infected kittens are inactive, crying and have a poor appetite, lose weight and may be hypothermic
or pyrexic. Sneezing, nasal discharge, oral ulcers, corneal ulcers, conjunctivitis are common.
BACTERIAL
● Bacterial sepsis*** (p 1128)
This is the most common cause of death in 1–6-week-old kittens. Pathogens are most likely to be
acquired from the normal flora of the queen and the environment. Signs range from sudden death
to a fading syndrome lasting a few hours to a few days. Signs include inactivity, weakness, crying
and ineffective nursing. Abdominal bloating and dyspnea may also occur.
PARASITIC
● Intestinal parasitic infection (ascarids*, coccidia*, giardia, toxoplasmosis) (p 1141)
Diarrhea, dehydration and cachexia due to coccidia (common) and giardia (uncommon) occurs in
kittens 5 weeks and older. Ascaridiasis (very common) causes weight loss, diarrhea, and intestinal
obstruction in 8-week and older kittens if severe. Toxoplasmosis (uncommon) causes systemic ill-
ness in kittens of all ages.
● Flea anemia* (p 1140)
Severe anemia due to heavy flea infestation is common in all ages of kittens.
INTRODUCTION Classical signs—Cont’d

● Crying.
MECHANISM? ● Gastrointestinal stasis and bloating.
● Inactivity.
Kittens appear healthy and vigorous at birth. ● Dyspnea.
Infectious diseases, inadequate nutrition, congenital ● Kittens 1–6 weeks of age.
conditions or environmental extremes debilitate kittens.
The fading syndrome develops when the primary con-
dition leads to poor nursing, hypoglycemia and Pathogenesis
hypothermia. Sepsis is the leading cause of death in neonatal
kittens in the 1–6-week age range.
WHERE?
In most cases, septic kittens have become systemically
Regardless of the cause of illness, fading kittens infected with organisms that are found among the nor-
frequently have a similar appearance: generalized weak- mal cutaneous and intestinal flora of cats and not from
ness, ineffective nursing, hypothermia and inactivity. exotic pathogens.
The primary condition produces adverse effects on Kittens are born with an immature immune system
multiple organs, resulting in fading kitten syndrome. and are largely dependent on passive immunity
acquired from maternal colostrum to prevent bacter-
WHAT? ial infection.
● Failure of passive transfer is an important cause
The cause of fading kitten syndrome is frequently of sepsis in kittens.
related to the age of the kitten. ● Other contributing factors are poor nutrition, envi-
Neonates succumb to congenital defects, maternal ronmental stress and concurrent debilitating illness.
neglect, nursing failure, neonatal isoerythrolysis Bacterial sepsis frequently affects entire litters, with
and environmental stresses. kittens falling ill and perishing within a few hours or
Bacterial sepsis is the biggest threat to 1–6-week-old days of each other.
kittens.
Viruses, parasites, and weaning stress are more com- Clinical signs
mon in 4–8-week-old kittens.
Clinical signs range from sudden death to a fading
Hypoglycemia occurs most commonly up to 6 weeks syndrome that lasts a few hours to a few days.
of age.
Neonatal sepsis is characterized by rapid deteriora-
Hypothermia occurs most commonly up to 6 weeks of tion and lack of response to therapy in kittens that
age. appeared to be healthy a few hours earlier.
Dyspnea may develop in the presence of bronchopneu-
DISEASES CAUSING THE FADING monia.
KITTEN OR NEONATE
External abscessation, particularly of the umbilical
stump, may be present.
BACTERIAL SEPSIS***
Hypothermia is common. Young kittens are unable to
Classical signs mount a febrile response to infection, so fevers are not
present even in severe systemic infections.
● Loss of suckling reflex.
● Hypothermia. Abdominal distension due to gastrointestinal stasis
leading to gas accumulation is common.
Diagnosis needle is inserted in the proximal humerus or femur

and can be bandaged in place for repeated or long-
Sepsis is difficult to differentiate from other causes of term use. Most fluids, medications and transfusions
fading kitten syndrome because there are rarely specific administered IV can also be given IO.
findings such as external abscesses. ● The peritoneum provides a large surface area for
Hypoglycemia is common. absorption of fluids, blood products and drugs, but
systemic blood levels following intraperitoneal (IP)
Complete blood count often reveals leukocytosis administration may be delayed compared to IV and
with left shift and toxic changes. Leukopenia is a par- IO routes.
ticularly grave finding. ● The small muscle mass of neonatal kittens makes
Bacterial culture and sensitivity may be performed repeated intramuscular (IM) administration of med-
on blood, urine and exudates. ications impractical.
● Fluids and medications can also be administered
Complete necropsies with microbial culture and subcutaneously (SC), although absorption may be
sensitivity of kittens that succumb to fading kitten syn- poor if peripheral vasoconstriction is present.
drome are essential to prevent deaths of remaining lit-
termates and to resolve recurrent problems in breeding Antibiotic therapy should cover the spectrum of the
programs and facilities that house kittens. most commonly isolated agents of neonatal sepsis.
These include Streptococcus, Staphylococcus, and
Necropsies often reveal widespread visceral abscessa- Gram-negative enteropathogens. Bordetella bron-
tion in kittens that appeared to be thriving only hours chiseptica may cause life-threatening bronchopneumo-
before death. nia. Dose adjustments of antibiotics may be appropriate
in neonatal kittens, but guidelines are largely empirical
Differential diagnosis and based on other species.
● Enrofloxacin (5 mg/kg once daily, SC; current data
Hypoglycemia, hypothermia, and most causes of fad- suggest that absorption of enrofloxacin following
ing kitten syndrome mimic the clinical signs of bacte- oral dosing may be poor in neonatal kittens). Dose
rial sepsis. reduction of enrofloxacin is not required in kittens.
Inflammatory leukogram changes in combination It is effective against many agents of neonatal sep-
with clinical signs are highly suggestive of sepsis. ticemia, but has poor activity against streptococcal
species and anaerobes.
Because sepsis is so common in kittens aged 1–6 – SC administration of enrofloxacin may result in
weeks, it should be the leading differential for fading permanent alopecia at the site of injection.
kittens in this age group. – Cartilage erosions have not been reported in kit-
tens treated with clinically relevant dosages.
Treatment – Blindness due to retinal degeneration has been
Treatment for sepsis should begin as soon as the reported in adult cats, especially at higher doses.
● Broad-spectrum parentally administered anti-
condition is suspected and should not be delayed for
confirmation of the diagnosis. biotics (e.g. enrofloxacin 5 mg/kg IV or SC q 24 h
plus ampicillin 22 mg/kg IV or SC tid).
Parenteral administration of fluids, medications and ● Amoxicillin-clavulanate (22 mg/kg PO bid) pro-
blood products can be challenging in neonatal kittens vides extended coverage for kittens that do not
due to their small size. require parenteral administration.
● Intravenous (IV) access can be achieved via the ● Initially, antibiotics are administered parenterally
jugular vein with a short 24- or 22-gauge catheter, to assure reliable absorption and adequate blood lev-
even in very young kittens. els. As the kitten returns to health, oral administration
● If venous catheterization is not feasible, the may replace injection, although disruption of the nor-
intraosseous (IO) route may be used. After prepar- mal intestinal flora and diarrhea may result.
ing the site aseptically, a 22-gauge hypodermic or spinal ● Treatment duration should be a minimum of 2 weeks.
Because passive immunity is believed to be critical colonization of the gastrointestinal, respiratory or uri-
for protecting the neonate against bacterial nary tracts.
pathogens, it is essential to assure that affected kittens
S. canis is acquired from the vaginal mucosa of car-
have adequate levels of immunoglobulin. This may be
rier queens during birth. The organism is believed to
confirmed by measuring serum IgG levels. The delay
invade via the umbilicus and the oronasal passages.
in waiting for test results may put at-risk kittens in dan-
ger of illness however, so it may be warranted to
administer serum empirically to provide protection
for kittens at risk for septicemia. See page 1137 (mater- Prevention
nal neglect and nursing failure) for details of serum S. canis transmission from carrier queens can be
administration. prevented by routine use of penicillin at the time of
Nutritional support is usually required because sep- birth. The queen is given a 1-ml SC injection of a prod-
tic kittens fail to nurse. Even brief lapses in food intake uct containing 150 000 IU benzathine penicillin and
can lead to hypoglycemia, immunosuppression and vil- 150 000 IU procaine penicillin per ml. At birth, each
lus atrophy of the intestines, resulting in decreased newborn kitten receives 0.25 ml SC of a 1:6 dilution of
defenses against pathogens. Some form of assistedfee- the same product, and their navels are dipped in a 2%
ding is usually required. Nasogastric intubation (in- solution of tincture of iodine.
dwelling 3.5 or 5 French catheter) is a convenient route Passive transfer of maternal antibodies represents
for feeding without the stress of forced hand-feeding or the strongest protection against bacterial sepsis. If
repeated orogastric intubation. Use a formula suitable there is any question about adequate colostrum intake
for orphan kittens such as KMR (Kitten Milk by kittens, a serum IgG level can be determined.
Replacer). The recommended volume is 25 ml/100 g Alternatively, serum may be administered empirically
BW per day. Newborn kittens do not tolerate more than as a source of immunoglobulin to kittens at risk for
2 ml at a feeding for the first 1–2 days, and should be failure of passive transfer.
fed every 2–4 hours. Thereafter, feeding volumes can
be gradually increased to 5 ml/feed the first week, Because entire litters frequently succumb to bacterial
10 ml/feed the second week, and 15 ml/feed the third infections, littermates of kittens that have died of
week. After the first few days the kitten can be fed 4–6 sepsis should be treated with antibiotics.
times per 24 h. Weak kittens may not tolerate volumes If sepsis or failure of passive transfer is documented in
this large without regurgitating and need to be fed one kitten of a litter, it is wise to prophylactically pro-
smaller volumes more frequently. vide serum for the remaining kittens.
Prognosis
HYPOTHERMIA***
Survival is low in kittens that are showing clinical signs
of sepsis, particularly if dyspnea is present.
Classical signs
Prognosis for littermates that appear healthy at the time
● Inactivity.
therapy is initiated is good.
● Bradycardia.
Kittens from Streptococcus canis-infected queens that ● Respiratory depression.
are treated empirically at birth have an excellent prog- ● Intestinal gas accumulation.
nosis. ● Kittens less than 6 weeks of age, but
mostly less than 3 weeks.
Transmission
Pathogenesis
Most bloodstream infections are acquired from the
normal flora of the queen or from the environment. During the first two weeks of life, normal body tem-
They invade the bloodstream via the umbilicus or from perature is 35˚C.
Neonatal kittens lack a shiver reflex and are unable to ● Care should be taken to assure that recumbent kit-
raise their body temperature more than 7˚C above tens are not over-warmed or burned if they are too
ambient temperature. weak to move away from the heat source.
● Separation from the queen or littermates may
Severely hypothermic kittens (< 32.5˚C) should by
result in rapid loss of body heat.
warmed at the core before surface warming is
If the core temperature drops below 32˚C, the digestive attempted. Heating the skin first causes peripheral
tract becomes non-functional and nursing ceases. vasodilation before the cardiopulmonary system is
capable of supporting non-critical tissues.
Severe hypothermia depresses heart rate, respiration
● Core warming can be accomplished by administer-
and metabolic functions.
ing fluids warmed to 37˚C (IV, IO or IP), warm
Although kittens living outdoors may develop primary water enemas, and heated inspired air.
hypothermia from environmental exposure, most ● Care should be taken not to warm the kitten too fast
hypothermic kittens presented for veterinary care to avoid overtaxing the depressed cardiopulmonary
have a predisposing medical condition. system.
Hypothermia is an almost universal sequella of all Simultaneously, blood glucose should be measured. If
causes of fading kitten syndrome. Concurrent hypo- measurement is not available, the kitten should be pre-
glycemia is very common. sumed to be hypoglycemic and treated empirically
with dextrose (see Hypoglycemia for details).
Primary hypothermia due solely to exposure is most
● If the body temperature is below 32˚C, dextrose
common up to 3 weeks of age, whereas hypothermia
must be administered parentally since gastrointesti-
secondary to other stressors such as cachexia, systemic
nal dysfunction may prevent absorption of oral
illness and hypoglycemia may be seen in kittens as
sugar solutions.
old as 6 weeks or more.
Once body temperature and blood glucose have been
Clinical signs corrected, a search for a predisposing cause should be
initiated if environmental conditions do not explain the
Cessation of nursing.
hypothermia.
Inactivity.
Debilitated kittens frequently relapse with
Cold to touch. hypothermia and hypoglycemia, so careful monitor-
ing and preventive measures are important.
Diagnosis
Subnormal rectal body temperature. Prognosis
● < 35˚C in kittens under 2 weeks of age.
● < 37˚C in kittens greater than 2 weeks of age. Prognosis for a full recovery is good if hypothermia
and hypoglycemia were not too prolonged and if pri-
Differential diagnosis mary predisposing causes are correctable.
Any cause of fading kitten syndrome may result in

hypothermia. Prevention
Healthy kittens should thrive if they have access to the
Treatment
queen and littermates for warmth.
First efforts should be directed at correcting
Neonatal kittens without a queen should be kept in
hypothermia and hypoglycemia, if present.
warm quarters (≥ 27˚C) or have access to a heat
Mildly hypothermic kittens can be rewarmed by exter- source such as a lamp or heating pad. To avoid over-
nal heat sources such as heating blankets, warm water heating, kittens should be able to move to an unheated
bottles and heat lamps. area of the nest.
Neonatal kittens become inactive, whereas kittens

HYPOGLYCEMIA***
older than 3 weeks may be ataxic and appear disori-
ented or agitated.
Classical signs
Severe hypoglycemia may result in seizures, blind-
● Weakness.
ness, coma and death.
● Seizures.
● Blindness.
● Coma. Diagnosis
● Kittens up to 6 weeks of age, occasionally Hypoglycemia should be suspected in all fading kit-
older. tens.
Home glucometers can be used to measure glucose
Pathogenesis quickly with a drop of blood.
Regardless of the cause of illness, sick neonates fre- Laboratory glucose results are the most accurate, but
quently stop nursing, dehydrate and become hypother- may take longer.
mic, all of which contribute to hypoglycemia.
Blood glucose < 3.3 mmol/L (60 mg/dl) is consistent
Neonates are especially susceptible to hypoglycemia with clinical hypoglycemia.
because energy requirements of neonates are 2–3
times higher than adults. Limited fat and glycogen If blood glucose measurement is not available, response
stores further predispose neonates to hypoglycemia if to treatment with IV dextrose or oral sugar solutions
nutrition is inadequate. supports a diagnosis of hypoglycemia.
Hypothermia is a common sequella to many dis- Since hypoglycemia is frequently secondary to another
eases in neonates and contributes to hypoglycemia medical condition, a thorough evaluation for a predis-
by several mechanisms: posing problem should be performed.
● Mild to moderate hypothermia (< 34.5˚C) sup-
presses nursing behavior. Differential diagnosis
● Severe hypothermia (< 32˚C) results in gastro-
Any cause of fading kitten syndrome may resemble
intestinal stasis and prevents absorption of glucose hypoglycemia. Although a low blood glucose level
and other nutrients. confirms hypoglycemia, concurrent conditions are
● Hypothermia reduces metabolic activity, including
also common.
gluconeogenesis.
A normal blood glucose test differentiates hypo-
Parasitism and other intestinal diseases may disrupt glycemia from other causes of neurologic signs such
nutrient absorption, leading to malnutrition and hypo- as head trauma, encephalitis, primary seizure disorder,
glycemia. portosystemic vascular shunt and inborn errors of
Infection, inflammatory processes and stress metabolism.
increase utilization of glucose that may exceed the
neonate’s ability to replace it. Treatment
Hypoglycemia results in decreased metabolic func- Emergency treatment for life-threatening hypo-
tions, especially in the central nervous system. glycemia is 25% dextrose (1–2 ml/kg slowly IV). If
● Neurologic signs of hypoglycemia progress from venous access is not available, 10% dextrose may be
weakness, lethargy and mental dullness to administered IP or IO. Oral sugar solutions (e.g. 50%
seizures, coma and death if not corrected in time. dextrose, corn syrup) can be given if body temperature
is normal, but effect is slower and less predictable.
Clinical signs
Clinical response to glucose replacement should be
Early signs of hypoglycemia are weakness and cessa- rapid. Delayed or partial response may occur if pro-
tion of nursing or eating. longed, severe hypoglycemia is present.
Continuous infusion of 5–10% dextrose or repeated pass these antibodies to the newborn kittens in the
bolus q 2–6 h may be required to maintain eug- colostrum.
lycemia until the underlying cause can be eliminated.
When type A kittens (blood type inherited from type A
Hypothermia must be corrected before feeding is stud) absorb the anti-A antibodies from the type B
attempted. queen, the kittens’ own red blood cells are lysed
(neonatal isoerythrolysis), leading to acute anemia,
Frequent small meals of high-protein diet supple-
hemoglobinuria and organ failure.
mented with dextrose are given until euglycemia is
maintained. Because most mixed breed cats are type A, neonatal
● Nasogastric or orogastric tube feeding may be isoerythrolysis is uncommon.
required for neonatal or weak kittens with hypo- ● In the US, more than 95% of mixed breed cats are
glycemia. type A, < 5% are B, and AB is very rare.
● In other continents, B is more common in domestic
shorthair cats. For example, in Australia 73% are
Prognosis
type A, 26% are type B and AB < 1%.
If the underlying condition can be corrected, prognosis
Some breeds have up to 50% type B cats and are at
for full recovery is excellent.
high risk for neonatal isoerythrolysis. The breeds
In some cases, neurologic damage such as blindness with the highest percentage of type B cats are Devon
from hypoglyemia may be irreversible. Rex, British shorthair, Cornish Rex, exotic shorthair,
Sphinx, Scottish fold, Somali, Persian, Japanese bob-
Prevention tail, Birman and Abyssinian.
Good husbandry should assure against most causes of

hypoglycemia. Clinical signs
● Neonates should be kept warm and be evaluated for
Kittens are born healthy and nurse vigorously.
nursing effectiveness.
● Older kittens should receive adequate high-quality Dark red-brown urine (hemoglobinuria) appears
nutrition and be free of parasites and gastrointesti- soon after colostrum is ingested.
nal diseases. A fading syndrome develops in first few days of life.
Kittens should be evaluated daily for adequate food Death may also occur acutely without any prodromal
intake, weight gain and body composition. signs.
Tail tip necrosis may occur in milder cases.
NEONATAL ISOERYTHROLYSIS (NI)**

● Hemoglobinuria. The clinical history suggests kittens were healthy until
● Anemia. colostrum was ingested.
● Acute death on first day of life or gradual Urinalysis and PCV reveal hemoglobinuria and
decline over several days. hemolytic anemia.
Blood typing confirms incompatible parental blood
Pathogenesis types (type A stud, type B queen).
At this time, the blood group system in cats is known
to include: type A, type B and type AB, but additional
blood groups may emerge as more cats studied.
Type B cats produce natural anti-A antibodies, even Hemoglobinuria differentiates neonatal isoerythroly-
prior to first transfusion or pregnancy. Type B queens sis from other causes of early fading kitten syndrome.
Treatment Prevention
Remove kittens from queen during first day of life to Avoid incompatible breedings (type A stud, type B
prevent further colostrum ingestion. queen).
If a transfusion is required in the first days of life, Breeders may choose to eliminate type B cats from the
administer washed type B red blood cells (available breeding pool entirely.
from the queen) to the kitten.
If incompatible breeding is unavoidable, prevent nurs-
● 3–5 ml donor blood is collected in CPD-A (citrate-
ing on maternal queen for the first 2 days of life.
phosphate-dextrose-adenine). A heparinized syringe
Foster the litter on a type A queen or bottle feed during
can be used to collect donor blood in emergencies
this time. Administer serum from type A donor for
if CPD-A is not available.
passive immunity in place of colostrum. Kittens can
● The blood is centrifuged for 10 minutes at 1500
be returned to queen on day 3 because antibody absorp-
rpm. The plasma (containing anti-A alloantibodies)
tion is complete by that time.
is discarded. The red blood cells are reconstituted
with saline (volume equal to discarded plasma), Rapid in-clinic blood typing of kittens by card test
recentrifuged, and the saline discarded. A second can be used to identify and segregate kittens at risk for
saline wash is performed, and then the saline is dis- neonatal isoerythrolysis.
carded. A volume equal to half of the discarded
plasma is added, yielding washed packed red blood
NURSING FAILURE** AND MATERNAL
cells ready for transfusion.
NEGLECT*
● Administer the packed red blood cells IV, IO
or IP.
Classical signs
– Avoid volume overload when using IV or IO
routes. ● Ineffective nursing efforts.
– Approximately 70% of RBCs administered IP ● Crying.
reach the circulation by 72 h. ● Loss of suckling reflex.
● Weight loss.
If transfusions are required after 2 weeks of age, red
● Weakness.
blood cells of the kitten’s own type A can be trans-
● Usually present in first week of life.
fused. However, a major cross match (donor cells +
recipient plasma) should be performed to assure the
period of incompatibility has passed).
Pathogenesis
Routine supportive care is essential during the hemolytic
Inadequate milk supply.
phase of neonatal isoerythrolysis.
● Absent or inadequate milk production may be caused
by premature delivery, delayed milk letdown, or
maternal illness or malnutrition. Primiparous queens
Prognosis are more likely to have poor milk production.
● Mastitis may result in milk that is toxic or con-
Acute death without prodromal signs occurs in some
tains microbial pathogens. Uncomfortable queens
severe cases.
may reject nursing attempts.
Early recognition and treatment is expected to save ● Large litters may overwhelm the queen’s ability
many kittens with neonatal isoerythrolysis. to produce enough milk. Less-vigorous kittens
may not compete well for access to nipples.
Some mildly affected kittens have only laboratory evi-
● Poor maternal behavior may result from difficult
dence of disease without clinical signs.
delivery that causes illness or exhaustion in the
Kittens that survive the acute crisis generally recover to queen. Some queens simply fail to bond to their kit-
full health. tens and make no attempt to care for them.
Ineffective suckling. Examine the kittens for congenital anomaly, general

● Premature kittens commonly lack a suckle reflex. vigor, stomach fullness and suckling responses.
● Hypothermia, hypoglycemia and weakness due
Failure of passive transfer is diagnosed by serum
to other illnesses may abolish the suckle reflex.
IgG concentration (normal >1000 mg/dl the day after
● Congenital anomalies (e.g. cleft palate, mega-
colostrum ingestion).
esophagus) may prevent effective suckling.
Healthy kittens weigh approximately 100 g at birth and
Failure of passive transfer.
should gain 10% body weight daily during the first
● Colostrum is produced during the first 1–5 days of
week of life. Daily weight checks provide early detec-
lactation. Colostrum has increased IgG, IgM and
tion of kittens that fail to thrive.
IgA compared to milk.
● Kittens absorb virtually all of their maternal
antibody from colostral milk in first day of life. Differential diagnosis
Less than 10% of antibodies are acquired before birth.
● Failure to absorb adequate immunoglobulin Any cause of fading kitten syndrome may lead to weak-
leaves kittens susceptible to infection. Kittens at ness and failure to nurse.
the highest risk of failure of passive transfer are Queens that appear to be displaying poor or aggressive
orphans, those with delayed nursing after birth (e.g. maternal behavior may be culling kittens with subclin-
cesarean section delivery), and kittens nursing ical illnesses.
queens with poor colostrum quality.

Inadequate milk supply. Correct primary medical conditions of the queen or
● Kittens are vigorous and show strong interest in kittens that prevent effective nursing if possible.
suckling. Hungry kittens are agitated and cry
Poor maternal behavior can often be corrected by
continuously. Eventually, kittens may become
reducing stress and distraction in a quiet, safe envi-
weak from dehydration and malnutrition.
ronment free of human interference.
Ineffective suckling. ● If the queen still neglects the litter, she should be
● Kittens may be small, weak, inactive and show lit- confined to a small space with kittens. Resting
tle suckling activity in response to oral stimulation. benches and other alternatives to the nest box
● Milk may leak from the nostrils (cleft palate, regur- should be removed.
gitation). ● If necessary, the queen may be restrained to
allow the kittens to nurse. Queens often accept
Maternal neglect.
their litter after several nursing sessions.
● Queen is distracted and inattentive to kittens.
● If the queen is highly distracted or agitated, mild
Overt aggression toward kittens is sometimes
sedation may encourage maternal behavior.
observed.
Sedated queens should be monitored continuously
● Kittens are alert and agitated, crying and attempting
for aberrant behavior.
to nurse.
● Hand-rearing or transfer to a foster queen may
● Some queens may not care for any kittens until the
be required if bonding is unsuccessful.
entire litter is delivered. First-born kittens may suf-
fer from neglect during this time. Maternal neglect Because inanition occurs quickly in undernourished
is most common with inexperienced queens. kittens, prompt nutritional intervention is indicated
for kittens with nursing failure.
Diagnosis ● Feed kitten milk replacer by bottle or syringe if kit-
ten will nurse.
Examine the queen for general condition, mammary
● Transient forced feeding may be achieved by
gland health and milk supply.
repeated orogastric intubation. Prolonged feeding
Observe maternal behavior. is less stressful if an indwelling nasogastric (3.5
French catheter) tube is placed. See page 1131 ● Once signs of sepsis appear, prognosis for survival
(Bacterial sepis) for details. is poor. Administration of serum after clinical signs
● If the queen or a foster cat has good maternal appear is less likely to affect outcome.
behavior, she can be allowed to care for the kit- ● Serum administered prior to the development of
tens even if she is not lactating or if milk quality disease offers protection against sepsis.
is poor, as long as nutritional supplementation is
provided. Kittens raised by queens frequently have Prevention
better social development than hand-reared kittens. Breeding queens should be well-nourished and free
● If kittens are to be reared completely by hand, uri- of infectious disease. Vaccinations should be com-
nation and defecation must be stimulated by rub- plete prior to breeding. Queens with poor maternal
bing the perineum with a damp cotton ball. Kittens behavior should be eliminated from breeding pro-
develop the ability to urinate and defecate on grams.
their own by 3–4 weeks of age.
Kittens should be kept warm and well-nourished.
Documented or suspected hypoglobulinemia due to
failure of passive transfer can be corrected by Maternal behavior should be observed to ensure ade-
administration of donor serum. quate access to milk by the kittens.
● The best donor is a healthy, blood type A, vacci-
Queens and their litters should be kept in private,
nated cat free of FeLV, FIV and other infections. quiet quarters to avoid distracting or stressing the
Cats that share the same environment as the kittens queen.
are most likely to have antibodies against pathogens
the kittens may encounter. However, since most If ingestion of colostrum is uncertain, serum should be
infections in kittens are due to ubiquitous normal provided. Serum IgG can be measured in the kittens,
flora and common feline viral pathogens, serum from but it is often more practical to administer serum
any healthy, vaccinated cat is likely to be protective. empirically.
● Serum is administered at a dose of 15 ml/100 g
If sepsis or failure of passive transfer is documented
body weight SC or IP to achieve normal IgG con- in one kitten of a litter, it is wise to prophylactically
centration. provide serum and antibiotics for the remaining
– The serum administration is divided into 3 doses kittens.
of 5 ml each administered every 12 h to avoid
volume overload.
UPPER RESPIRATORY INFECTION
– Catteries and facilities caring for large num-
(HERPES VIRUS**, CALICIVIRUS*)
bers of young kittens can prepare single-dose
aliquots of donor serum for future use. Serum
stored at –20˚C remains adequate for immuno- Classical signs
globulin supplementation for more than a year ● Nasal discharge.
after collection. ● Sneezing.
● Conjunctivitis.
Prognosis ● Oral ulceration.
● Corneal ulceration.
Prognosis is excellent when the underlying cause of ● Dyspnea.
nursing failure can be corrected. ● Kittens 2 weeks and older.
Foster-rearing is time consuming, but can be performed See main reference on page 7 for details (The Cat With
by most pet owners. Healthy kittens that are free of Acute Sneezing).
underlying disease have an excellent prognosis if hand-
reared. Clinical signs
Septicemia due to failure of passive transfer is one of There is much overlap between the clinical signs
the leading causes of death in neonatal kittens. caused by herpes- and calicivirus, so it is impossible to
definitively distinguish between the two viruses based Differential diagnosis

on clinical signs alone. Mixed infections are common.
Bronchopneumonia, heart failure and oral ulceration
Neonatal kittens may develop severe viral respira- due to caustic substances or electric shock can be dif-
tory disease as early as 2 weeks of age. ferentiated from upper respiratory infection by careful
● At this age, kittens have nasal and ocular discharge physical examination ± thoracic radiography.
and may become severely dyspneic.
● Conjunctivitis neonatorum may accompany upper Treatment
respiratory infections in neonatal kittens that have
Safe and effective systemic antiviral agents for herpes-
not yet opened their eyes.
and caliciviruses are not available.
– The eyelids are greatly distended by accumula-
tion of fluid and purulent material in the con- Therapy is limited to supportive care including fluid
junctival space behind the sealed lids. (See page replacement, nutritional support and prevention of
1212, The Cat With Ocular Discharge or Changed secondary bacterial infection (amoxicillin/clavu-
Conjunctival apperance). lanate 10–20 mg/kg PO bid, doxycycline 10 mg/kg
PO q 24 h, or azithromycin 5–10 mg/kg PO q 24 h for
Kittens (> 6 weeks) are less likely to become severely 5–7 days).
dyspneic.
● Kittens with calicivirus or herpes virus may have oral
Conjunctivitis and corneal ulceration are treated with
ulcerations that lead to salivation and refusal to eat. topical antibiotic ointment (without corticosteroids).
● Severe ocular herpes infection may benefit from
● Older kittens with herpes virus may develop
corneal ulcers. topical antiviral compounds.
● Lysine has been shown to inhibit herpes virus in cats
● Some older kittens develop “febrile limping kitten
syndrome” following natural exposure or vaccina- at 100 mg/kg orally once daily.
tion with calicivirus. Although B. bronchiseptica may be susceptible to amox-
– High fevers (> 40˚C) and severe joint pain are icillin/clavulanate, some strains are resistant to penicil-
present. lins and cephalosporins. Fluoroquinolones, doxycycline,
– Classical signs of upper respiratory infection and azithromycin are effective against most isolates.
may be absent. In kittens with conjunctivitis neonatorum, the eyelids
– The syndrome spontaneously resolves within a should be gently separated and the purulent mate-
week with or without treatment. rial flushed out, followed by topical antibiotics and
frequent cleansing of the eyes.
Upper respiratory infection with Bordetella bron-
● Despite a dramatic clinical appearance at the time
chiseptica may be complicated by dyspnea due to bron-
of diagnosis, most kittens fully recover with normal
chopneumonia.
vision.
Intranasal vaccination against viral upper respiratory
Diagnosis infection (not panleukopenia virus) beginning as early
as 3–4 weeks of age has ameliorated upper respira-
Clinical signs are classical. In addition, there may be a tory outbreaks in some catteries with endemic infec-
history of upper respiratory infections in other house- tions.
hold cats.
Viral culture of pharyngeal swabs can be used to dif- CONGENITAL DEFECTS*
ferentiate herpes and calicivirus.
B. bronchiseptica is diagnosed by bacterial culture of Classical signs
pharyngeal swabs or tracheal wash specimens. ● Cleft palate: milk from nostrils during
Bulging eyelids (conjunctivitis neonatorum) may occur nursing.
in kittens prior to natural separation of the lids.
● Cardiac defect: heart murmur, dyspnea,
cyanosis.
Thoracic radiography may reveal pneumonia.
Classical signs—Cont’d Diagnosis

● Gastrointestinal defect: vomiting, Thorough physical examination (cleft palate, cardiac
regurgitation, constipation. defect, atresia ani) is essential.
● Portosystemic vascular shunt: salivation, Radiography ± contrast and ultrasonography (cardiac
neurologic signs. defect, megaesophagus, intestinal defect, PSS) may
characterize the specific anatomic defect.
Pathogenesis Post-prandial bile acids or plasma ammonia are ele-

vated in kittens with PSS.
Drug administration (e.g. cleft palate from griseoful-
vin), vaccination (e.g. cerebellar hypoplasia from mod- Nuclear scintigraphy is helpful for confirming diagno-
ified live virus panleukopenia), and infection (e.g. sis of PSS.
thymic atrophy from FeLV) during pregnancy may
cause congenital defects.
Genetic predisposition for specific deformities occurs Differential diagnosis
in some breeds (e.g. cleft palate in Siamese, craniofa- Transient innocent murmurs are common during the
cial deformity in Burmese). first weeks of life but usually cease by 8 weeks of age.
Spontaneous defects are the most common. A patent ductus arteriosus (PDA) may close sponta-
neously during the perinatal period.
Clinical signs Anemic kittens may develop a flow murmur that
resolves with correction of the anemia.
Signs are dependent on type of defect.
● In cleft palate, milk leaks from nostrils during
nursing. Rhinitis, sneezing and dyspnea may be
present. Treatment
● Cardiac defects may be accompanied by heart Surgical correction is often the ideal treatment (cleft
murmur, cyanosis, dyspnea, palpable thrill and palate, vascular ring anomaly, patent ductus arterio-
stunted growth. Many kittens may be asymptomatic sis, PSS).
until they are older.
● Kittens with megaesophagus (primary or second- Affected neonates may require aggressive nutritional
ary to vascular ring anomaly) have regurgitation support via nasogastric or esophagostomy tube feeding
from the time of birth. Other gastrointestinal until they are large enough for surgical correction.
defects such as blind intestinal loops, motility dis-
orders and atresia ani also have signs from the time
of birth including vomiting, abdominal distension, Prognosis
crying and constipation.
Prognosis is good to excellent for surgically correctable
● Signs in kittens with portosystemic vascular
defects (e.g. PDA, PSS).
shunt (PSS) are usually delayed until weaning or
later. Cleft palate repair is often complicated by post-
– Intermittent salivation and neurologic signs operative healing problems and may require multi-
(ataxia, seizures, disorientation, blindness) are ple surgeries.
common and may be associated with meals.
Early correction of vascular ring anomalies usually
– Signs of cystitis may occur if urate calculi form
improves regurgitation, but not all cases return to normal.
in bladder.
● Cerebellar hypoplasia is accompanied by intention Megaesophagus may occasionally resolve sponta-
tremor and ataxia, which is observed when kittens neously. Aspiration pneumonia is a common complica-
begin to walk. tion of megaesophagus and may lead to euthanasia.
Cardiac defects in some cats may remain asymptomatic Treatment

for years without treatment (e.g. ventricular septal
defect, tetrology of Fallot). Extend nursing or hand-rearing of kittens with
delayed maturation.
Congenital gastrointestinal defects carry a poor
prognosis for normal function following surgery. Hand-feed gruel (food–milk mixture) to assist transi-
tion to solid food.
House with other kittens of similar maturity.
Prevention
Hand-reared kittens with “bottle addiction” may require
Avoid drug administration, especially known terato- increasing time intervals between feedings and for-
gens, during pregnancy. mula offered in a dish before they will accept solid food.
Avoid modified live virus vaccination during preg-
nancy. FLEA ANEMIA*
Select breeding stock that is free of inherited diseases.
Classical signs
● Inactivity.
WEANING STRESS* ● Inappetence.
Classical signs ● Heavy flea infestation.
● Reluctance to accept solid food in kittens ● Kittens 2–8 weeks old.
6–8 weeks old.
● Crying, agitation.
Clinical signs
Progressive weakness and inactivity.
Clinical signs
Pale or white mucous membranes.
Reluctance to accept solid food in kittens 6–8 weeks
old. Kittens suckle well on queen or bottle. Heavy flea infestation or marked accumulation of flea
feces in hair-coat.
Inability to compete with larger littermates around the
food bowl. May develop systolic heart murmur secondary to
anemia.
Kittens may have a withdrawn or anxious personality.
Affects entire groups of cats with young kittens devel-
Crying, agitation. oping the most severe anemia.
Diagnosis Diagnosis
Good suckle reflex. Clinical signs are classic.
Thrives with queen or littermates of similar size and CBC reveals anemia and hypoproteinemia due to blood
maturity. loss. The anemia is usually regenerative unless concur-
rent iron deficiency develops.
Medical causes of failure to thrive can appear similiar.
Anemia secondary to hookworm infection is differenti-
Excessive competition from littermates. ated by fecal examination.
Severe anemia secondary to FeLV infection is uncom- Differential diagnosis

mon in young kittens and is excluded by testing for the
virus. Bacterial or viral gastroenteritis and malnutrition cause
similar signs and may occur concurrently with intes-
Severe anemia in mixed breed, Burmese and tinal parasitism.
Siamese kittens associated with transient hyperlipid-
emia at 4–5 weeks of age is eliminated based on lack
of severely lipemic plasma found in hyperlipidemia. Treatment
Supportive care (e.g. fluid replacement, nutritional
Treatment supplementation) as needed.
Remove fleas with a kitten-safe flea adulticide (imi- Coccidia: sulfadimethoxine (50 mg/kg PO first day,
dacloprid, fipronil). Treat the other household pets then 25 mg/kg PO q day for 10–20 days until asympto-
and the environment to prevent reinfestation. matic and fecal flotation negative). All exposed kittens
Selamectin can be used from 6 weeks of age, but debil- should be treated, and environmental contamination
itated kittens may have adverse reactions. should be controlled. Some kittens may have persistent
or recurrent infections.
If anemia is severe, whole blood or packed red blood
cell transfusion may be required. If intravenous Ascaridiasis: pyrantel pamoate (10 mg/kg PO, repeat
catheterization is not possible, blood may be adminis- in 2–4 weeks) or selemectin (administered topically to
tered IO or IP. Approximately 70% of red blood cells the skin can be used monthly for fleas and ascarids
administered IP reach the circulation within from 6 weeks of age). Because ascaridiasis is very
72 hours. common, all kittens should be routinely treated regard-
less of fecal test results.
INTESTINAL PARASITIC INFECTION Giardia: fenbendazole (50 mg/kg PO q day for 5 days).
(ASCARIDS*, COCCIDIA*, GIARDIA,
TOXOPLASMOSIS) PREMATURITY*

● Weight loss. ● Incomplete hair-coat.
● Diarrhea. ● Low birth weight.
● Dehydration. ● Ineffective suckling reflex.
● Abdominal distention. ● Dyspnea.
● Kittens 4 weeks and older. ● Kittens in first days of life.

Diarrhea, weight loss and abdominal distention are Lack of hair on ventrum and paws.
common findings of intestinal parasitism.
Low birth weight (< 80 g).
Severe coccidial diarrhea may cause dehydration and
hypoglycemia. Absent or ineffective suckling efforts.
Vomiting occurs uncommonly. Dyspnea if pulmonary development is inadequate.
Diagnosis Diagnosis
Fecal flotation and direct smear. Physical examination.
Response to treatment. Breeding date known.

Immature fetal hematology (mean corpuscular vol- months, leading to false-negative tests in litters of
ume > 90 fl, increased nucleated red blood cells). fading kittens at the time of initial testing.
Delayed seroconversion and inconsistent infection
within litters makes it inappropriate to test only repre-
None. sentative littermates.
● All kittens should be tested, and serial testing
Treatment may be required to confirm infection status.
● The probability that an infected queen will trans-
Tube feeding.
mit FeLV to her kittens is high.
Oxygen supplementation.
Some individuals in an affected litter may escape infection.
If dyspneic or more than a few days premature, prog-
nosis for survival is poor.
DIFFERENTIAL DIAGNOSIS
FELINE LEUKEMIA VIRUS (FELV) Any cause of fading kitten syndrome may mimic FeLV
INFECTION infection. Losses from FeLV occur more commonly in
older kittens (> 4 weeks) than in neonates.
Classical signs
Treatment
● Loss of suckling reflex or appetite.
● Weight loss. Treatment is largely supportive, although specific
● Hypothermia. antiviral therapy may have added benefit by reducing
● Inactivity. viral burden. Claims for clinical benefits of immune
● Crying. modulator therapy have not yet been substantiated
● Kittens 4 weeks and older. in controlled clinical trials.
Recombinant feline interferon omega (antiviral dose:
1 MU/kg SC × 5 days at day 0, day 14, day 60).
Clinical signs
AZT (antiviral dose: 5–15 mg/kg PO or SC bid).
Perinatal infection may result in abortions, stillbirths, Treated cats had improved one-year survival compared
and fading kittens, although most clinical illness is to cats receiving placebo.
seen in weaned kittens and adolescents.
Recombinant human interferon alpha (antiviral dose:
Poor appetite. 100 000–1000 000 IU/kg SC q day).
Weight loss. Recombinant human interferon alpha (immune modu-
lator dose: 30 IU/cat PO q 24 h alternate weeks).
Hypothermia if kittens are less than 6 weeks old.
Staphylococcus protein A (immune modulator dose: 10
Crying and inactivity. μg/kg IP twice weekly).
Perinatal FeLV is likely to affect most or all of the litter. Provide supportive care with fluid replacement, antibi-
otics and blood products if indicated.
Abortions and stillbirths.
Although aggressive therapy may improve the condi-
Kittens in apparently healthy litters individually tion of clinically ill kittens, seroconversion to negative
fade and die over several weeks to months. status is uncommon.
Some infected kittens are long-term survivors.
PANLEUKOPENIA VIRUS INFECTION
Diagnosis
Classical signs
Test queen and each kitten for FeLV antigen.
● Intention tremor (evident about 5 weeks of
It is common for infected kittens to have delayed age).
seroconversion for FeLV antigen for several weeks to
Classical signs—Cont’d usually much more severe in panleukopenia virus

infection.
● Severe vomiting and diarrhea (usually ≥ 7
weeks old).
● Hypothermia or fever. Treatment
● Severe dehydration. Aggressive intravenous fluid replacement is essential.
IO fluid administration may substitute if venous access is
Clinical signs limited. IP SC or oral fluid administration is less likely to
provide adequate fluid support for the duration of illness
Intrauterine infection may result in intention (5–10 days). Fluids should be supplemented with potas-
tremor (cerebellar hypoplasia), which becomes appar- sium, dextrose and water-soluble vitamins as needed.
ent when kittens begin to walk. This condition is non-
progressive and does not affect health unless tremor Parenteral broad spectrum antibiotics (e.g.
severity prevents adequate food intake or leads to injury. enrofloxacin 5 mg/kg IV or SC q 24 h plus ampicillin
22 mg/kg IV or SC tid) are administered due to the
Postnatal infection causes necrosis of intestinal mucosa severity of the leukopenia. Anti-emetics may be
and hematopoietic progenitor cells resulting in severe required if nausea is severe.
vomiting, diarrhea, dehydration and panleukopenia.
● Most common in kittens ≥ 7 weeks old when protec-
Blood transfusions may be required to treat anemia,
tion from maternal antibodies is lost. hypoproteinemia and to provide passive humoral
immunity.
Hypothermia occurs in kittens < 6 weeks old or older
kittens in endotoxic shock. Fever is common in kittens Nothing is offered orally until vomiting has ceased.
> 7 weeks old. Mortality is high in untreated kittens, but most
Panleukopenia commonly affects entire litters, but aggressively treated patients should survive.
some kittens may escape infection if passive immunity
is protective. FELINE INFECTIOUS PERITINITIS VIRUS
Peracute deaths may occur without typical signs in (FIP) INFECTION
some kittens.
Classical signs
Diagnosis
● Abortions, stillbirths, fading kittens.
Clinical signs of gastroenteritis in the presence of ● Recurrent fever.
severe panleukopenia are classical findings. ● Weight loss.
● Ascites.
Non-regenerative anemia and hypoproteinemia are
● Kittens 4 weeks and older.
common.
Detection of parvovirus antigen in feces by point-
of-care tests for canine parvovirus appears to be Clinical signs
useful, although the test accuracy of these tests in
Perinatal infection may result in abortions, stillbirths
cats is unknown. Cats recently vaccinated against
and fading kittens, although most clinical illness is
panleukopenia may also shed virus and test positive.
seen in weaned kittens and young adults.
Necropsy and histopathology findings are diagnostic.
Cycles of unexplained fever and weight loss are com-
mon in older kittens (> 8 weeks).
Ascites, pleural effusion or uveitis may be present in
Panleukopenia virus can be differentiated from other
older kittens (> 8 weeks).
causes of gastroenteritis such as sepsis, FeLV and
enteric bacterial infections by identifying parvovirus in FIP is more likely to affect individual kittens or lit-
the feces. In addition, the degree of leukopenia is ters than to cause widespread outbreaks of disease.

Biopsy and necropsy tissues contain pyogranuloma-
FIP can be difficult to differentiate from other causes of
tous inflammation and vasculitis.
fading kitten syndrome. Cyclic fevers and modified
Serum coronavirus antibody titers are unreliable transudates are strong evidence for FIP.
for diagnosis of FIP, but very high titers tend to corre-
late with clinical FIP.
Treatment
● Although a high percentage of kittens within the
household are likely to have positive coronavirus
Medical treatment is usually ineffective for FIP,
titers, only a few are expected to develop the disease.
especially for fading kittens. Transient palliation of
Coronavirus PCR is unreliable for confirmation of FIP. clinical signs may sometimes be possible with corti-
costeroid treatment.
Hyperproteinemia (polyclonal gammopathy), often
accompanied by non-regenerative anemia and lym-
phopenia, is consistent with FIP.
High-protein, pyogranulomatous effusion in the
peritoneal, thoracic or pericardial cavity is highly sug-
gestive of FIP.
The Rivalta test on serum or effusions may be the most
reliable diagnostic test for FIP.
RECOMMENDED READING
Hoskins JD (ed). Veterinary Pediatrics: Dogs and Cats from Birth to Six Months, 2nd edn. WB Saunders Co.,
Philadelphia, 1995.
Lawler DF. Causes and management of wasting syndromes in kittens. In: August JR (ed) Consultations in Feline
Medicine 2. WB Saunders Co., Philadelphia, 1994, pp. 645–652.
Murtaugh RJ. Pediatrics: the kitten from birth to eight weeks. In: Scherding RG (ed) The Cat: Diseases and Clinical
Management, 2nd edn. Churchill Livingstone, New York, 1994, pp. 1877–1891.
55. The infertile queen
Isobel Phebe Johnstone
KEY SIGNS
● Normal estrus cycles and failure to produce a litter.
● Failure to cycle.
● Prolonged interestrous intervals.
MECHANISM?
● Infertility is the failure of a queen to produce a litter. It is the result of abnormalities in the
female (e.g. infection, congenital abnormalities) or male or environmental management
practices which prevent successful mating and pregnancy.
Signs of infertility include:
● Normal estrus cycles and failure to produce a litter.
● Failure to cycle.
WHERE?
● Reproductive tract (ovaries, uterus, vagina and vulva).
WHAT?
● The most common problems associated with infertility are:
● Environmental and management practices.
● Viral or bacterial infections.

Diseases causing an infertile queen
ANOMALY
● Congenital abnormalities (p 1156)
The queen appears physically normal but there is a structural abnormality in the reproductive tract
that is a barrier to intromission or to the movement of sperm. Chromosomal abnormalities can
present as phenotypically normal females that do not exhibit estrus.
continued
1145
continued
METABOLIC
● Ovarian cysts (cystic follicles)** (p 1151)
Either prolonged anestrus or persistent estrus if the cysts are hormonally active. A possible prob-
lem in queens held back from breeding or the use of progestogen contraception products.
● Cystic endometrial hyperplasia** (p 1152)
Failure to produce kittens despite normal mating. Usually seen when queens have many estrus
cycles without being mated or after the use of progestogen contraception products.
NUTRITIONAL
● Hypovitaminosis A (p 1158)
Anorexia, weight loss, hyperkeratosis, corneal infections, night blindness and reproductive prob-
lems of anestrus, fetal resorption, abortion or kittens with birth defects. Can be a problem in
queens fed poor-quality food.
● Taurine deficiency (p 1159)
Retinal degeneration, cardiomyopathy and reproductive problems such as fetal resorption, stillborn
kittens or live kittens of low birth weight with brain and limb deformities. Rare now that the prob-
lem has been recognized and commercial diets are appropriately supplemented.
NEOPLASTIC
Maybe a palpable abdominal mass (unusual) or ascites from metastases. Irregular estrus cycles
occur with hormonally active ovarian tumors. Usually seen in older queens (9 years and over).
PHYSICAL/ENVIRONMENTAL
● Physical and environmental factors (female/queen)*** (p 1148)
A diverse range of causes producing signs ranging from anestrus, to prolonged interestrous inter-
vals to normal estrus but refusal to mate to normal mating but no pregnancy.
● Physical and environmental factors (male/tom)** (p 1150)
A variety of problems that can prevent successful mating or male infertility which will present as
normal mating but no ensuing pregnancy.
● Inadequate photoperiod* (p 1153)
The queen fails to exhibit estrus behavior and is housed in an area with inadequate lighting.
INFLAMMATION/INFECTIOUS
Viral:
● Feline panleukopenia (p 1154)
Fetal death, mummified fetuses or kittens born with neurological signs. The natural infection is
now rare, but vaccination of a pregnant queen with live virus vaccines can produce the same
problems.
● Feline leukemia virus* (p 1153)
Reproductive failure due to resorption or abortion. A common cause of reproductive failure in some
countries unless vaccination programs are in place.
55 – THE INFERTILE QUEEN 1147
● Feline herpes virus (p 1154)

Pregnant queens may abort after a severe bout of respiratory disease. Now a much rarer cause
of reproductive failure due to effective vaccines.
BACTERIAL/RICKETTSIAL
● Bartonella henselae (p 1155)
Infection has resulted in reproductive failure in experimentally infected cats.
● Chlamydophila felis (p 1155)
Causes acute respiratory disease and sometimes fatal pneumonia in 6–12-week-old kittens. It is
poorly documented whether it is a cause of poor reproductive performance, especially abortion
in cats.
– She should be housed with the male for as long

INTRODUCTION as she is in estrus as the queen is an induced ovu-
lator and needs a number of matings to stimulate
MECHANISM? a sufficient hormonal surge for ovulation.
– The stud cat owner should observe matings to
Infertility can be defined as the failure from any
ensure that normal matings and mating behavior
cause, of a female cat (queen) to produce a litter. It
are happening.
is not a specific diagnosis but a sign of a problem.
The problems encountered that can result in infertility Failure to cycle.
can be subdivided into three categories. ● Previous ovariohysterectomy should be ruled out.
● The general health of the queen may be compro-
Normal estrus cycle but failure to produce a litter.
mised to such an extent that her estrus cycles cease.
● Evaluate the general health of the queen.
– Factors such as poor nutrition, overcrowding,
– A queen may be infertile due to dysfunction of
stress of cat shows and debilitating illness can
other organ systems such as the kidneys or liver.
suppress estrus cycles.
– Ensure the queen is vaccinated and free of ● Inadequate photoperiod.
diseases known to affect fertility, such as feline
– Adequate light exposure is essential for normal
leukemia virus and Chlamydophila felis.
polyestrus cycles.
● Problems within the reproductive tract can cause
– Cats are seasonally polyestrus, commencing estrus
infertility.
cycles with increasing day length.
– Developmental defects or neoplastic masses can
– At least 12–14 hours of light per day are neces-
block the passage of sperm.
sary for normal estrus cycles.
– There can be implantation failure or abortion ● Disorders of sexual development.
of fetuses due to problems with the uterine
– Chromosomal abnormalities can result in a lack
wall such as cystic endometrial hyperplasia or
of fully functional ovaries and/or interfere with
neoplasia.
the normal development of the reproductive
● Evaluate the fertility of the male cat (tom).
tract.
– Review the breeding history of the male, parti-
cularly his ability to sire litters in the previous Prolonged interestrous intervals.
6–12 months. ● Pseudopregnancy produced by spontaneous ovu-
– Use a proven sire who works well with any queen. lation will produce a prolonged interestrous interval.
● Review breeding management practices. ● Hormonal dysfunction of the ovaries.
– Ensure the queen is allowed adequate time with the – Polycystic ovaries or ovarian neoplasia can
male for sufficient matings to stimulate ovulation. halt the normal functioning of the ovaries.
Spontaneous ovulation.
WHERE?
● Cats are normally induced ovulators but it is
Ovaries, uterus, vagina and vulva. now known that spontaneous ovulation in cats is
more frequent than once thought.
● If the queen has already ovulated then she may not
WHAT? permit mating.
● Pseudopregnancies from serial spontaneous ovula-
Environmental and management practices are a com-
tions, especially if the queen is a quiet caller, may
mon cause of infertility in the cat.
be interpreted as pathological prolonged intere-
In the cat there are many infectious diseases that can strous intervals.
cause infertility.
Insufficient matings to induce ovulation. A certain
level of luteinizing hormone is required to trigger
DISEASES CAUSING SIGNS ovulation. Normally this is only attained after several
OF INFERTILITY IN THE QUEEN matings over a number of days.
PHYSICAL AND ENVIRONMENTAL Clinical signs

FACTORS (FEMALE/QUEEN)*** An apparently normal, healthy cat with a history of fail-
ing to show estrus.
Classical signs
An underweight cat.
● Failure to exhibit estrus behavior.
● Failure to permit breeding. A nervous, highly strung cat.
● Normal mating but no pregnancy. Normal matings but failure to become pregnant.
Diagnosis
Pathogenesis
History, especially of the cattery environment and man-
Age of puberty varies markedly between breeds. agement practices such as:
● It may be as early as 4.5 months of age in Burmese ● Cattery mating practices and observations of mat-
and Siamese to as long as 18 months of age in ing behavior.
Persians. – Inexperienced queens and studs should be paired
● Failure to exhibit estrus can be as simple as insuffi- with experienced ones.
cient time to reach puberty. – The stud owner should remain in attendance
during mating as foreplay, mating and separation
Cats need to reach a body weight of 2.3–2.5 kg
can be quite violent. Some studs can become very
before normal estrus cycling commences. Although a
rough and frighten a queen, especially an in-
cat may be of a sufficiently mature age it may be
experienced one, and she may refuse to mate.
underweight.
Conversely a queen can be too aggressive for the
Previous ovariohysterectomy. A new owner may be stud and mating may be unsuccessful.
unaware of the previous history of the queen. – The stud owner needs to watch closely to ensure
that successful mating has actually taken place.
Environmental stress such as the show circuit, over-
– A queen should be allowed at least three ob-
crowding, travel or unfamiliar locations can suppress
served matings and the queen and stud should run
estrus cycles or estrus behavior (silent heat).
together for at least 2 days, mating at will.
Male preference; the queen may aggressively reject a – A queen usually needs 4–12 matings before
certain male. there is a sufficient luteinizing hormone (LH)
surge for ovulation. The more matings the higher Treatment

the LH surge.
– Quality and quantity of the food being fed. Correct housing conditions and management prob-
Poor-quality, incomplete diets or insufficient lems such that the queen is living in the least stressful
food can cause reproductive failure. environment that can be devised.
– The housing with respect to the amount of Ensure good nutrition and that the cat is actually eat-
light, overcrowding and other possible “stresses”. ing the food.
– The show history of the queen, for example, if
she was held back from breeding for a show For a queen that is aggressive towards a male:
● Try a more gentle introduction such as removing
career.
● Physical examination, noting weight and condi- the male from his pen and housing the queen there
tion of the cat as well as general health, especially for a few days to get used to the smell and new sur-
the condition of the teeth is important for detecting roundings and then reintroduce the male.
● Select a different, experienced male and see if the
physical causes of infertility.
● Severe dental disease is debilitating to general queen will accept him, if not try another.
health. – Some queens are aggressive to all males despite
– The cat may be reluctant to eat and be below being on full call, this is very unusual and it is
minimum weight for estrus cycles. possible that these have a subtle hormonal prob-
– Circulating bacteria and toxins can damage other lem affecting their mating behavior.
organs such as the heart, liver and kidneys, which For a queen that spontaneously ovulates, house her
in turn affect the health of the cat. long-term with a male so that he can mate her imme-
Vaginal smears obtained once or twice per week for diately he detects she is in estrus so that sperm are there
1–2 months during the breeding season can reveal if ready to fertilize the eggs.
the queen is silently calling. For queens that appear healthy and no problem can
● Cornified epithelial cells (superficial and anuclear) be found to account for the lack of estrus, try housing
predominate during the follicular phase and estrus these with calling queens and/or close to a tom cat,
coincides with the end of the follicular phase. so that pheromones may stimulate ovarian activity.
Progesterone levels measured 1–2 weeks after sus- Anestrus queens with normal ovaries can be induced to
pected estrus, detected either by vaginal cytology cycle by exogenous hormones.
or behavior, will diagnose pseudopregnancy. A level ● 2 mg follicle-stimulating hormone (FSH) IM once
> 6.36 nmol/L (2 ng/ml) indicates ovulation has daily until onset of estrus (3–7 days).
occurred and by 1–2 weeks the level has risen to ● Then follow with either natural mating or 250 IU of
between 31.8–63.6 nmol/L (10–20 ng/ml) whether human chorionic gonadotropin (hCG) to induce
pregnant or pseudopregnant. ovulation.

If mating occurred but there is failure to produce a lit- The prognosis is good for problems that can be solved
ter, or there is failure to cycle, or prolonged interestrus by adjusting cattery conditions and practices.
intervals are occurring, see other causes of female
infertility in this chapter.
Prevention
Chromosomal abnormalities can produce a small, non-
Ensure cattery conditions and management are always
cycling queen. Karyotyping is necessary to definitively
of the highest standard.
distinguish this from a problem due to poor nutrition.
However, ensuring proper feeding practices will solve Do not breed from a line of cats if breeding problems
the latter problem in time. are encountered in more than one female from that line.
● Normally the tom is housed in a stud cage, around

PHYSICAL AND ENVIRONMENTAL
which he sprays frequently to make it his territory,
FACTORS (MALE/TOM)**
and the queens are brought to him.
● New housing or too vigorous cleaning of his
Classical signs
cage will interfere with his familiarity with his
● No mating behavior. territory.
● Inability to mate.
Male infertility. Lack of sperm, abnormal sperm or
● Unsuccessful mating (copulation failure).
retrograde ejaculation into the bladder cause male
infertility.
Pathogenesis
Physical problems with the male such as:
Clinical signs
● Congenital or acquired phimosis or bands of tissue
connecting the penis to the prepuce. Disinclination to mate or aggressive behavior towards
– There will be an inability to extrude the penis the queen.
properly.
Attempts to mate are unsuccessful.
● Preputial hair ring.
– A matte of hair becomes wrapped around the Normal mating but the queen does not become pregnant.
shaft of the penis, particularly long-haired cats,
interfering with penile penetration.
● Dental disease. Diagnosis
– Tooth pain or lack of teeth can prevent the male
Ask questions regarding the housing of the tom and
from making the important neck grip during
mating practices at the stud cat’s establishment.
mating, and he cannot keep the female still and
● Are the stud quarters adequate for introducing the
remain mounted for intromission.
queen, and for mating behavior?
Behavioral and psychological problems with the male. ● Are the stud and queen allowed to live together for
● He may be timid and submissive. unlimited matings?
– This could be a basic genetic behavioral trait or
Ask questions regarding the mating behavior and
be due to insufficient testosterone.
ability of the tom.
● The male has not reached puberty yet.
● Are normal matings observed?
– Age at which males show mating behavior varies
● Are the tom and queen evenly matched in size?
markedly. Some have been known to sire litters
at 7 months of age, others do not start working Physical examination of the tom for general health
until about 2 years of age. and especially:
– Spraying behavior can start months before mat- ● The presence of two apparently normal testes.
ing behavior. ● Check teeth for dental problems.
● The male may have started working but is still very ● Extrude penis and examine for problems that would
inexperienced and may not be able to manage cer- prevent intromission.
tain queens. ● Measure serum testosterone to check for inade-
quate production. Normal levels range from non-
Mismatched body size.
detectable to 17.3 nmol/L (5 ng/ml) or more and so
● The male and female must be of similar body
a stimulation test is necessary to document ade-
size/length as the male has to have a firm neck grip
quate testosterone production.
at the front and yet be able to reach the vulva with
– Give 25 μg GnRH IM and measure serum testo-
his penis at the rear.
sterone 1 h later; normal range 17.3–41.6 nmol/L
Changes to the male’s territory may interrupt his (5–12 ng/ml).
mating behavior. – Or give 250 IU hCG and measure serum testos-
● Tom cats are very territorial and usually will only terone 4 h later; normal range 10.4–31.2 nmol/L
mate successfully in their own familiar territory. (3–9 ng/ml).
● Assess if the tom is fertile. ● If a pregnancy is desired from this particular stud
– Find out the reproductive success of queens then artificial insemination (AI) is successful in cats.
mated at around the same time as the queen in – Either train the male to use an artificial vagina or
question. find a specialist center with electro-ejaculation
– Swab the vagina of the mated queen to look for facilities.
sperm. – Allow the queen to come into a natural estrus
– Check the urine of the tom after mating for preferably, or estrus can be induced as per above
evidence of sperm. Their presence will at least (page 1149), then give 500 IU of hCG IM at the
confirm production of sperm, however, the infer- time of AI to induce ovulation.
tility problem may be retrograde ejaculation into
the bladder. OVARIAN CYSTS (CYSTIC FOLLICLES)**
– Electro-ejaculation of the tom to assess sperm
quality. This technique is likely to be only avail- Classical signs
able in specialist practices.
● Prolonged estrus behavior.
– Tom cats can be trained to an artificial vagina but
● Alternatively, prolonged interestrous
this takes time and patience.
interval or anestrus.
Treatment
Pathogenesis
Ensure adequate tom cat housing and allow the tom
to mark his territory adequately so that he is happy Cystic follicles may be hormonally active producing
to work there. estrogen and hence persistent estrus.
● The stud quarters should be of a sufficient size to
Non-functional follicles can interfere with normal ovar-
allow free movement for mating, at least 2.5 × 1.8 m
ian function and produce prolonged interestrous inter-
(8 × 6 ft), with sleeping quarters and shelves for
vals or anestrus.
observation, exercise and escape from the queen.
Ensure the health of the tom including provision of
Clinical signs
adequate nutrition, especially vitamin A for function-
ing testes and maintenance of dental health. Prolonged estrus behavior.
Remove physical obstructions to normal penile Alternatively, prolonged interestrous intervals or
function. anestrus.
Allow adequate time for puberty, and match an
inexperienced tom with an experienced queen. Diagnosis
Timid or submissive males could be given testosterone Abdominal ultrasonography is a reliable means of
(50–150 mg SC or IM monthly) to see if this improves identifying cystic structures.
their performance, however, it may be inadvisable to
Persistently increased plasma estrogen levels
persevere with them in case there is a hereditary basis
(> 20 pg/ml; 73 pmol/L) supports a diagnosis of cystic
to their inadequacy.
ovaries.
Prognosis Exploratory laparotomy and visualizing the ovaries.
This allows surgical treatment if the diagnosis is
Problems that can be solved by adjusting management
confirmed.
practices or attending to physical problems such as den-
tal disease or preputial hair rings hold a good prognosis
for future successful matings. Differential diagnosis
However, if there is male infertility, insurmountable Ovarian granulosa cell tumors can be hormonally
psychological problems or other unsolvable problems, active and also result in persistent estrus. These are
then it is best to choose a new stud. usually seen in cats older than 5 years and are rare.
Treatment Cystic endometrial hyperplasia is associated with

infertility from implantation failure or early embry-
Mate the queen to see if breeding can ovulate the onic death.
cysts.
The incidence of cystic endometrial hyperplasia
Try to induce follicular rupture with hCG (predomin- increases with age. It can be seen as early as 5–6 years
antly LH); 250 IU IM daily for 2 days. but is more likely from 10 years of age. It is more
Surgical removal of the cyst(s). Cysts can be ruptured common in nulliparous queens than in multiparous
mechanically, or if only one ovary is involved then queens.
remove the ovary if the cyst is large.
Clinical signs
Prognosis The queen is apparently healthy, with normal estrus
Prognosis is good for future pregnancies if the cysts can cycles. Mating behavior is normal but no litter eventu-
be ruptured by one of the methods above. ates.
Prevention Diagnosis
Do not allow a young queen frequent estrus cycles Abdominal ultrasound may be able to visualize the
without mating. Breed queens frequently, long periods cysts in the uterine wall and is a non-invasive way of
of estrus without mating are conducive to the formation detecting the condition.
of cystic ovaries. The statement “Queens should be Exploratory laparotomy and biopsy of the uterus pro-
pregnant, lactating or both” is often quoted as being the vide a definitive diagnosis.
ideal for good reproductive health.
CYSTIC ENDOMETRIAL HYPERPLASIA**
Other causes of normal mating but failure to produce a
Classical signs litter.
● Poor general health of the queen. A history and
● Normal estrus cycles and mating but physical examination should detect any problems.
failure to produce a litter. ● Fertility and mating problems of the male cat. A his-
tory of recently siring litters and observations of
Pathogenesis normal mating are reassuring of fertility of the stud.
● Management practices should be checked to ensure
Cystic endometrial hyperplasia involves chronic that they allow an adequate number of matings to
hyperplasia and cystic glandular development of the produce ovulation.
endometrium. ● Reproductive tract abnormalities. Ultrasonography
In the dog, these changes have been produced by pro- may reveal neoplasia. An exploratory laparotomy will
longed exposure to progesterone. be necessary to detect developmental abnormalities,
and biopsy of the uterus to detect abnormal conditions
This mechanism may be possible in those cats that such as cystic endometrial hyperplasia or neoplasia.
undergo serial spontaneous ovulations and hence pro- Cystic endometrial hyperplasia is a relatively com-
longed exposure of the uterus to progesterone. However, mon cause of the problem.
spontaneous ovulation is an uncommon occurrence in
cats.
Treatment
Usually intact non-pregnant females undergo waves of
follicular development and then atresia. Therefore, in Once the endometrium has undergone cystic change,
cats the changes in the endometrium are likely caused there does not seem to be a treatment that reverses the
by estrogens. changes.

Problem-Based Feline Medicine

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© 2006, Elsevier Limited. All rights reserved.

No part of this publication may be reproduced, stored in a retrieval system, or

First published 2006

ISBN - 10 0 7020 2488 0

British Library Cataloguing in Publication Data

Library of Congress Cataloging in Publication Data

● Competence at making a diagnosis is the most important part of being a

* infarct sider whether the typical signalment, history and

2. The cat with acute sneezing or nasal

QUICK REFERENCE SUMMARY

Necrosis of epithelium occurs within 24–48 h of viral

Signs in newborn kittens include continuous crying, Differential diagnoses

Avoid overcrowding and other causes of stress. mm in diameter) or as a large ulcer.

FELINE CALICIVIRUS (FCV)*** “paw and mouth disease”.

Acetaminophen (paracetamol) toxicity produces simi- most susceptible.

● Fomite transmission occurs, e.g. food and water Clinical signs

Treatment Clinical signs

Infection appears widespread in the feline popula- Differential diagnosis

Typically there is an acute onset of pyrexia, and Prevention

Bacteria can be isolated from the nasal discharge,

Diagnosis ● Radiography demonstrates increased opacity of

Classical signs ALLERGIC RHINITIS

QUICK REFERENCE SUMMARY

Careful history taking and physical examination help

Diagnosis dence of the organism on cytology, histology or

– Commonly used antibiotics include doxycy- ● Leukotriene antagonists like zafirlukast

Pathogenesis ● Occasionally, central nervous system signs occur,

Depression, anorexia or inappetence and weight loss are Differential diagnosis

● Fluconazole is better for CNS infection, but is Clinical signs

Clinical signs return if treatment is stopped too early. Diagnosis

Classical signs SECONDARY RHINITIS ASSOCIATED WITH

● Often, the tooth is still present, and a deep peri-

Differential diagnosis mal, and then becomes chronic.

Differential diagnosis Clinical signs

ORONASAL FISTULA OR NASAL Treatment

● Chronic snuffling, sneezing and nasal

Clinical signs Stertorous respiration (snoring) or stridor (whistling

See main reference on page 38 for details (The Cat

Radiography reveals a rounded density in the Diagnosis

Clinical signs Treatment

STRIDOR FROM PHARYNGEAL, LARYNGEAL OR TRACHEAL AREA

INTRODUCTION DISEASES CAUSING NASAL STRIDOR

MECHANISM? SECONDARY BACTERIAL RHINITIS***

Pathogenesis The discharge may initially be unilateral and

Narrow external nares in a brachycephalic cat. Diagnosis

Clinical signs Classical signs—Cont’d

Serology to detect cryptococcal capsular antigen in

● Nasal discharge and congestion. Laryngeal paralysis or edema, tracheal foreign

Examine a stained (e.g. Diff-Quick) preparation of a

Pathogenesis palatal resection, and resection of the everted lateral

Stenotic nares, hypoplastic trachea, etc., create a non-

Treatment Stertor occurs, which is worsened with excitement or

Nasal lymphoma responds well to standard chemother- Differential diagnosis

Clinical signs ● Dyspnea and stridor on inspiration.

Pathogenesis lateralization) may be required (see Laryngeal

Clinical signs Prevention

Diagnosis ● Inspiratory dyspnea and increased airway

5. The dyspneic or tachypneic cat

QUICK REFERENCE SUMMARY

● Weakness of ventilatory, muscles or diseases