ANHE 426/427 Introduction to Animal Diseases

Lecture Notes by Dr. Dominic Mureithi

Sep/Dec Semester 2019
Course Content
Good health status, Disease status, Etiology of disease, Disease transmission, Definition, Etiology,
Distribution and transmission, Clinical signs, Diagnosis, Treatment and control: East coast fever,
Babesiosis, Trypanasomiasis, Coccidiosis, Trichomoniasis, Anaplasmosis, heart water, Bovine petechial
fever, Parasitic gastroenteritis, fascioliasis, Cystcercosis, Hydatidosis, Anthrax, Clostridial diseases (BQ,
Tetenus, Enterotoxemia, Botulism), Salmonellosis, fowl typhoid, Brucellosis, Leptospirosis,
Paratuberculosis, Mastitis, Actinobacillosis, Actinomycosis, Foot rot, Pink eye, Foot and mouth,
Rinderpest, Rabies, Lumpy skin disease, Rift valley fever, Nairobi sheep disease, Sheep and goat pox,
Newcastle disease, Mareks disease, Avian leucosis, Contagious bovine pleuropneumonia and contagious
caprine pleuropneumonia, Dermatomycosis and streptothricosis, Hypocalcaemia, Ketosis and
Hypomagnesaemia
*Quizzes and Final Exam will be off of Notes Handed Out in Class*

Introduction to Animal Diseases

Diseases and Disease Agents
Disease: the term disease broadly refers to any condition that impairs the normal functioning of the
animal.
Per acute Disease: disease of immediate-term nature
Acute Disease: disease of a short-term nature
Sub chronic Disease: disease of a moderate-term nature
Chronic Disease: disease of a long-term nature
Not Disease: Trauma, Injury, Wounds.
Congenital Disease: present at birth
Genetic Disease: caused by genetic mutation
Hereditary Disease: caused by genetic mutation and passed to offspring
Idiopathic Disease: cause of the disease is unknown
Iatrogenic Disease: disease caused by medical intervention
Primary Disease: disease that is not the root cause
Secondary Disease: disease that is a sequela of another primary disease, kidney failure would be
an example of this
Progressive Disease: a disease whose course worsens until death, serious debility, or organ failure
occurs. Slowly progressive diseases are also chronic or degenerative diseases.
Stable or Static Disease: a disease condition that exists, but does not get better or worse over time
Refractory Disease: disease that resists treatment
Subclinical Disease: prior to showing clinical signs, or no clinical signs associated with the disease
Signs vs. Symptoms
Signs: observations made by secondary observer that are either normal or, more importantly, abnormal
Symptoms: medical conditions self-reported by the patient to the secondary observer
For example, by definition, animals cannot have symptoms.
Examples: Symptom: “My head hurts”
Sign: “The abdomen is tense and guarded”
Types of Diseases
Infectious Disease: Bacteria, Virus, Parasite, Prion
Deficiency Diseases: Nutritional, Vitamin, Mineral
Genetic Diseases: Hereditary, Non-Hereditary, Lethal, Congenital
Physiological Diseases: Endocrine, Immune
Neoplastic Diseases: Cancer
Disease vs. Syndrome
Syndrome refers to a set of signs and symptoms that are associated with an illness or disease

• Down’s Syndrome (trisomy21)

• Dry Eye Syndrome
• Chronic Fatigue Syndrome
• Chronic Fatigue Syndrome
• Cushing’s Disease
• Procine Disease
• Sudden Death Syndrome
Disease Agents
-Infections
-Bacteria (gram-negative enteric, gram-positive skin and respiratory, gram-indeterminate
causing inflammatory diseases)
-Virus (respiratory, enteric, systemic)
-Parasite (roundworms, flatworms, tapeworms, single-celled)
-Prions (protein-based infectious agents)
Spread of Disease
-Communicable vs. Non-Communicable : able to spread to another animal
-Zoonotic: able to spread from animal to human
-Direct contact to skin and mucus membranes
-Vectors vs. Fomites (example: doorknob, indirect contact)
-Through the air by aerosols and droplets
-By fecal-oral route
Pathology: the study of disease
By system: circulatory, nervous, digestive, musculoskeletal, respiratory, immune, cardiovascular,
skeletal, reproductive, integumentary, special senses (eye, ear)
How to Study Diseases
-Memorization of facts
-Associate common facts that leads to recall of additional facts
-Visualize
-Study pictures/photos
-Study lesions
-Go into field and see as many cases as possible
- Accumulate experience with normal vs. diseased so both are easily recognized
Disease Prevention
Risk Management
-Hierarchy of controls for managing risk
-elimination: removal of the infectious agent from the environment
-substitution: use of a non-infectious agent in place of pathogen
-engineering controls: use of physical barriers, bio-safety cabinets, building systems, etc. to provide a
barrier to infection
-administrative controls: risk assessments, written safety policies-SOP’s (example: showering before
entering farm, spraying down trucks before entering the farm to prevent disease), rules-institutional and
lab policies, safe work practices, supervision, scheduling and training
-personal protective equipment (PPE): task specific, choices based on risk assessment
-hand washing- after animal contact, in the field (use of wipes or purell), before eating/drinking/applying
contact lenses
-limit contact with animals - wear gloves, no sandals or open-toed shoes
-no food or drink in animal areas
-cover cuts/wounds with a waterproof bandage to prevent contamination
-gloves - create a physical barrier especially for hands with cuts, abrasions, chapped (change often)
-coveralls, tyveks, boots, goggles, masks, protective sleeves
Biosecurity
-Biosecurity: a series of management practices that are employed to prevent the importation of
infectious agents from entering a farm
-Bio-containment: strategies reduce the consequence of disease challenge by limiting the opportunity
for challenge (bio-exclusion), enhancing resistance (immunization), and preventing spread (quarantine).
-Isolation: the single biggest biosecurity risk is posed by the addition of animals to a herd or flock;
establish a perimeter of containment
Resistance: the second important aspect of a biosecurity program
-includes nutritional, environmental, pharmacological and immunological practices
Sanitization: key factor in minimizing spread and limiting the course of infectious disease
Zoonotic Diseases
Definition: contagious diseases spread between animals and humans
-zoonoses (plural)
-zoonotic (adjective)

Mode of transmission
Contact direct Direct physical contact between infected animal and susceptible host
(mucous membranes, open cuts)
indirect Infectious agent deposited onto an object or surface (fomite) and
survives long enough to transfer to the next person who touches
object
droplet Coughing or sneezing (droplets > 5um)
Non-Contact Air-borne Transmission via aerosols (airborne particles < 5um) that contain
organisms
vehicle A single contaminated source spreads the infection..can be a common
source or point source..Common source: Listeria outbreak from
contaminated cantaloupes..Point Source: food- borne outbreak from
infected batch of food
Vector- Transmission by insect or arthropod vectors
borne
Transmission
Fomites -contaminated inanimate objects -buckets, shovels, vehicles, clothing
-Vector -living organism transfers disease between animals -mosquitos, ticks, biting midges, fleas
-Environment -contaminated soil- spores that persist and are ingested while animal is grazing
Signs of Disease in Animals
Sick animals show certain signs when they are diseased. Some of these signs are not specific to a
particular disease but a general sign of ill-health. Some of these unspecific signs of disease are;
Isolation. A sick animal tends to isolate itself from the rest of the group. When they are moving in a herd
it would be found lagging behind or show exercise intolerance.
Dullnes. The normal instinct of a health animal is to move away when being approached, but a sick
animal will not move away or do so sluggishly.
Inappetence. A healthy animal will rush to food when it is provided. Therefore, indifference to food or
refusal to eat is a sure sign of ill-health.
Fall in egg and milk production.
This is a sign that the animal may be sick and should be investigated.
Ceasation of rumination. Ruminants in some cases stop ruminating when they are sick.
Poor hair coat. The hair coat of a healthy animal should be smooth and shiny. Therefore, rough and poor
hair coat may be a sign of a disease.
Unthriftiness. Poor growth or animal inability to reach market size or come into production at the
normal time may indicate sickness.

ANIMAL DISEASES

EAST COAST FEVER

Definition-East Coast fever (ECF) is a tick-transmitted protozoan disease of cattle characterized by high
fever, dyspnea, lymphadenopathy and high mortalities. It is confined to eastern, central, and parts of
southern Africa.

Etiology The causative agent of classical ECF is the protozoan Theileria parva parva

Geographic Distribution- distribution of ECF is associated with the distribution of the vector tick species
Rhipicephalus appendiculatus. This affects cattle in East and Central Africa, particularly in Kenya,
Uganda, Tanzania, Rwanda, Burundi and Malawi. The disease has also been found in DRC, Zambia and
Mozambique. It extends into South Sudan and perhaps West to Angola and South Zimbabwe

Transmission.

Rhipicephalus appendiculatus is the main field vector of ECF, although in certain areas other field vectors
occur, such as R. zembeziensis in drier areas of southern Africa and R. duttoni in Angola

Incubation Period

The incubation period has a medium range of 8 to 12 days and may vary due to differences in challenges
experienced by the cattle and may extend to beyond 3 weeks after attachment of infected ticks.
Clinical Signs

• The first clinical sign of ECF in cattle appears 7 to 15 days after attachment of infected ticks.
• Swelling of the draining lymph node, usually the parotid, for the ear is the preferred feeding site
of the vector,
• Fever that may reach 42° C
• Lack of appetite and loss of body condition
• Lacrimation, corneal opacity, serous nasal discharge
• Petechiation on the gums, underside of the tongue and vulva mucosa,
• initial constipation and later diarrhea which may be bloody stained with bloody mucus
• Recumbency before death and death usually occurs 18 to 30 days after infestation of
susceptible cattle by infected ticks
• Mortality in fully susceptible cattle can be nearly 100 percent

Diagnosis

1. Presence of the tick vector Rhipicephalus appendiculatus

2. Clinical signs- Fever with signs of enlarged lymph nodes associated with infestation by tick
vectors is suggestive of ECF. An acute disease with high mortality on farms, where tick control is
not effectively applied, also is suggestive of ECF, Postmortem findings.
3. In the field, diagnosis is usually achieved by finding Theileria parasites(piroplasm) in Giemsa-
stained blood smears and Koch blue bodies in lymph node needle biopsy smears
4. Serological tests - Indirect fluorescent antibody test, Enzyme-linked immunosorbent assay,
capillary tube agglutination test, passive hemagglutination test, Compliment fixation test,
polymerase chain reaction

Differential Diagnosis Corridor disease , Mediterranean or tropical theileriosis, Heartwater,

Trypanosomiasis, Babesiosis, Anaplasmosis, Malignant catarrhal fever

Treatment: Consult the Veterinarian

Control

1. Vaccination- "infection and treatment method" initially using oxytetracycline

2. Vector control using acaricides-Organochlorides, organophosphorus, Synthetic pyrethroids are
applied in dips, spray races, or by hand spraying.

ANAPLASMOSIS
Definition. This is an infectious hemoparasitic, anaemic disease of cattle, sheep and goats caused by
Anaplasma Spp.

Etiology
Cattle and wild ruminants are infected by Anaplasma marginale while sheep and goats are infected by
Anaplasma ovis. Anaplasma centrale causes mild infection in cattle.

Epidemiology
Occurrence
Anaplasmosis is distributed throughout the tropics and subtropics in every continent.

Transmission
The source of infection is always blood of an infected animal. Spread from one animal to another is by
tick vector Boophilus spp. that also transmit babesosis, i.e. B. microplus, B. decolaratus and B. annulatus

Clinical findings
• In cattle, incubation period is 3-4 weeks with tick borne infection and 2-5 weeks with inoculation
of blood.
• The disease is asymptomatic, mild, acute, peracute or chronic.
• The temperature – 40 .5, may remain elevated or fluctuate with irregular periods of fever and
normal temperature for from several days up to 2 weeks.
• Anorexia is seldom complete, emaciation, anemia, impaired fertility, mucous membrane are pale
land later jaundiced.
• In per acute form there is sudden onset on high fever, anemia, icterus, severe dyspnea and death
often within 4 hours, hyperexcitability, attack attendants, just before death,
• Pregnant cows abort. Testicular function depression in bulls in convalescent bulls.
• There is also weakness staggering gait, ruminal stasis, constipation, depression, dehydration,
dyspnea, in acute cases.
• In sheep and goats the disease is subclinical, but severe anemia in goats may occur.

Necropsy findings
Emaciation, jaundice and pallor of tissues, thin, watery blood, enlarged liver with deep orange colour,
congested kidney, enlarged liver with soft pulp and hemorrhages in the myocardium.

Diagnosis
1. History – change of management, cattle movement, tick levels, introduction of new stock-
particularly exotic animals.
2. Clinical symptoms.
3. Pathological lesions.
4. Haematology – low pcv and demonstration of organism in blood films/Giemsa stains
5. Serological tests – CFT, Card and capillary agglutination tets

Differential diagnosis: babesiosis.

Treatment: Consult a Veterinarian

Control

a) Tick control and eradication using acaricides

b) Disinfection of instrument used for injections or surgical operations
c) Immunization
BABESIOSIS
Definition- This is a tick-borne protozoan disease of domestic animals transmitted by ticks and
characterized by anemia, occasionally hemoglobinuria and protozoan parasites in hosts erythrocyte.

Etiology
• In cattle there is B. bigemina found in Africa, S. America, Australia ; B. bovis is found in Africa,
Europe and Asia; B. divergens is found in N. Europe,U.K.; B. major is found in US and Canada.
• In sheep and goats- B. ovis and B. motasi found in Africa, S. America and S.E. Asia.
• In porcine- B. trautmani- Africa; B. perroncitoi- S.E. Europe
• In Equine- B. equi and B. caballi - Africa, South and North America and Europe.

Bovine Babesiosis
This is a major problem in the tropics where conditions favor large tick populations.

Etiology and transmission

It caused by B. bigemina and B. bovis both of which are transmitted trans-ovarially by one host
Boophilus ticks which are distributed worldwide.

Clinical signs

• There is fever of 410c and above, anorexia, depression, visible mucosa initially very pale but
soon turns yellowish due to jaundice.
• weakness, cessation of rumination and fall of milk yield,
• increased respiration and heart rate,
• terminal stages there is severe jaundice and urine is dark red to brown and produces stable
froth.
• Pregnant animals usually abort,
• loud heartbeat,
• Severely affected animals die after 24 hours.
• Those that survive, fever lasts for another week and the course may be three weeks.
• Animals affected by B. bigemina shows show nervous signs (cerebral form), incoordination,
posterior paralysis or mania, convulsions and coma.

Diagnosis
1. History and clinical signs- fever, anemia, presence of vectors -Boophilus ticks.
2. Confirmation by demonstrating the parasites in peripheral blood smears.
3. Serological tests- compliment fixation tests, indirect fluorescent antibody test(IFAT), Indirect
hemagglutination test, ELISA, Passive agglutination test, microplate enzyme immunoassay, latex
agglutination test, capillary agglutination and a slide and card agglutination test.
Control

a) Vector control-This involves tick control with appropriate acaricide- controlling one host tick
Boophilus ticks by dipping or spraying with acaricide should be designed to prevent adult
female ticks completing engorgement and detaching.
 b) Use of tick resistant cattle- Crossbreeding of cattle with zebu blood to increase tick resistance is
being practiced especially in Australia.
c) Stock movement control between enzootic and tick free regions.
d) Immunization
• Inactivated vaccine- Antigens produced from RBC of infected spleenectomised calves
• Live vaccines from the blood of carrier animals and treated or irradiated blood from
carriers. Not done in Kenya.

TRYPANOSOMOSIS
Definition- A collective term applying to a number of acute and chronic diseases of human and animals
caused by one or many protozoan parasites of the family trypanosomidae most of which are transmitted
by tsetse fly.
Synonym; Nagana, Surra, Mal-de caderas, Dourine, Sleeping sickness, Chagga
Geographical distribution- The disease is found in Africa and S. America and to an extent Southern USA
and Southern Asia.
Etiology
T. congolense – smallest monomorphic and non flagellated
T. brucei – larget, polymorphic with fair sized flagella
T. vivax – medium sized, monomorphic and excessively long flagella
T. simiae – medium sized, polymorphic with fair sized flagella
T. equiperdum – same size as brucei
T. equinum – like vivax
Transmission- the disease is transmitted by tsetse fly
Clinical signs

• There is per acute, acute or chronic disease with an incubation period of 8-20 days.
• Per acute and acute cases: Fluctuating temperature, tachycardia, anemia, jaundice, edema
mainly in the neck region, lacrimation and photophobia, salivation, anorexia, tachypnea,
nervous signs, dullness, arched back and tucked up abdomen, ocular discharge, swollen lymph
nodes, pale mucus membrane, occasional diarrhea
• Chronic form: Emaciation and anemia without jaundice.
Post mortem findings:

• Carcass is emaciated, anasarca, anemia, enlarged and congested liver, spleen and lymph node,
petechiation of body tissues, atrophy around heart and bone marrow, corneal opacity, testicular
degeneration, general congestion of the viscera and extensive hemorrhages in all tissues.
• Pathological specimen – smears from tissues, cut surface of lymph node or heart muscle for
trypanosomes.
Diagnosis
a) Clinical signs, presence of contact tsetse flies
b) Demonstrate organism in blood smear – microscopic examination of blood smear blood from
suspected cases taken differently.
c) Serological tests – Card agglutination test (TESTRYP), Complement fixation test on T. equinum
and T. equiperdum.
Control
1.General preventive measures
a. Avoid contact with tsetse flies. Tsetse flies have diurnal variation in their feeding times. The
most dangerous if just before sunset
b. House valuable stock in screened quarters
c. Demarcate fly free grazing areas
d. Plan stock routes to avoid tsetse infected areas. Trade cattle and trek routes present problems
in West and East Africa Cattle may trek from tsetse free areas to markets through infested
areas. This situation may be alleviated by wise demarcation of stock routes and use of
prophylactic drugs and motorized transport.
2.Tsetse fly control
a. Application of insecticides and insect repellant. Use pump, hand spray or aerial
b. Fly traps. May be of value in cleaning up small foci. often impregnated with oduor attractants
(e.g. acetone, octenol)
c. Bush clearing. Expensive. (l) Discriminate, only acacia (2) Indiscriminate; all vegetation. May
develop a barrier. Half a mile wide especially along rivers.
Problem G. palpalis feed on crocodile and still perpetuate the disease.
d. Agricultural settlement particularly effective against savannah flies. A population of 40 people
per square kilometer excludes tsetse fly.
e. Destruction of wild-animal hosts. Unacceptable
f. Biological method – cross breeding G morsitans with other tsetse fly produce sterile offsprings.
Irradiation produce sterile males which mate once in their life time. Females are not fertilized.
g. Use of synthetic pyrethroids applied as pour ons.
3. Use of trypanotolerant livestock
Ndama and the West African short horn (Muturo). They have hereditary ability to develop immunity
against trypanosomosis. Boran Zebu of the Orma tribe in East Africa also have a degree of
trypanotolerance.
Economic importance of trypanosomiasis
a) Constraint to livestock development and expansion particularly cattle production in Africa. Total
30 million square kilometers, Half is unsuitable (12 million – desert and semi-desert, 3 million –
 dense rain forest regions). Remaining 15 million of wooded steppe or savannah with large
suitable grazing, 7 million tsetse infested leaving approximately 7 million square kilometer with
tsetse free grazing suitable for livestock raising.
b) Direct cost of treatment and prevention
c) Control cost is a continuous strain to national finances through maintenance of tsetse and
trypanosomiasis control departments, purchase of insecticides, spraying equipment,
trypanocidal drugs etc.
d) Problem of desertification in semi-arid areas due to overstocking
e) Economic losses per square kilometer estimated to be Kshs.8,900.00 by Wilson et al, 1986 for
Boran cattle in the Galana ranch.
f) Draught animal power loss in tropical Africa because of trypanosomiasis.

COCCIDIOSIS
Definition-This is a contagious enteric disease of various domestic animals and poultry caused by invasion
and destruction of the intestinal mucosa by various species of the coccidia parasite of the two important
genera, Eimeria and Isospora.
Etiology
Cattle: Eimeria zuernii, E. bovis( smithii) and E. ellipsoidalis
Sheep: E. arlongi A( ovina),E. weybridgens ( E. arlongi B),E. crandalis(1), E. ahsata and E. ovinoidalis and
E. gilruthi
Goats: E. arlongi,E. faurei and E. gilruthi,E. caprivona, E. ninakohylakimovae and E. christenseni
Pigs: Isospsora suis, E. debliecki,E. scabra and E. perminuta
Horses and donkeys: E. leuckarti
Epidemiology
✓ Coccidiosis occurs universally but it is most important where animals are housed or confined in
small areas which are contaminated with oocysts.
✓ In lambs, infection occur soon after birth (before 4 weeks of age) and the sources of infection are,
oocysts surviving in old fecal contamination of the lambing area form previous occupation, fresh
oocysts from ewes, fresh oocysts passed out by other lambs.
✓ In goats, coccidiosis is very important in goats under intensive management systems and has a
high mortality.
✓ Piglets; the disease occurs at 5-15days of age and peaks up 7-10 days.
✓ Foals-The incidence of clinical disease is low in foals than other species but clinical cases and
deaths occurs in recently weaned foals.
Clinical findings
Cattle

• In cattle, a mild fever may occur in early stages but in most cases the temperature is subnormal
or normal in clinical disease.
• There is sudden onset of severe diarrhea with foul smelling, fluid feces containing mucus and
blood.
• The blood may appear as a dark tarry staining of the faeces or as streaks or clots or large clot of
fresh, red blood.
 • Acute outbreaks result in death.
• The course of the disease is 5-6 days but some animals undergo long convalescent period with
subnormal feed consumption and weight gain.
• Nervous signs include, muscular tremors,hyperesthesia, clonic-tonic convulsions with
ventroflexion of head and neck and nystgmus and high mortality rate.
Lamb

• Infection in lambs is similar to that in cattle but with less dysentery.

• There is inferior growth rate, gradual onset of weakness, inappetence, recumbency, emaciation
and death with a course of 1/3 weeks.
foal

• In foals, there is diarrhea of several days and acute massive intestinal hemorrhage leading to
death.
Piglets

• In piglets, severe outbreaks of coccidiosis occur between 5 and 15 days of age. There is anorexia,
depression, dehydration, unthriftness and vomiting.
Necropsy findings
• Most outstanding findings are hemorrhagic enteritis with congestion and thickening of mucosa of
the caecum, colon , rectum and ileum.
• In severe cases ulceration and sloughing of the mucosa can occur.
Diagnosis
a) Calves- dysentery, mild systemic involvement and dehydration, Detection of a large number of
oocysts in the faeces
b) In sheep- clinical signs of diarrhoea and dysentery, large number of oocysts in faeces and the
intestinal lesions at necropsy. Lambs which may have been in contact with coccidian and are
immune, other causes of diarrhoea may be considered; E. coli, Salmonellosis, Clostridium
perfrigens type C and helminthosis should be considered.
c) In pigs- outbreak of diarrhoea at 5-8 days of age and responding poorly to treatment Coccidiosis
should be considered.
Control
a) Prevention of excessive faecal contamination of the environment e.g. avoid overcrowding, feed
and water troughs should be high enough to prevent faecal contamination, avoid wet conditions
which favour sporulation and survival of oocysts.
b) Lambing and calving ground should be well drained and kept as dry as possible.
c) These coccidiostat are : sulphonamides, monensin, lasalocid, decoquinate, Toltrazuril and
Amprolium.
BOVINE PETECHIAL FEVER
Synonyms: Ondiri disease, Transmissible petechial fever, Hemorrhagic diathesis, Bushbuck disease
Definition- Acute or Subacute disease of cattle characterized by high fever followed by appearance of
hemorrhages on visible mucous membranes and occasionally followed by bloody diarrhea
Aetiology and distribution

• Ehrlichia ondiri
• The disease is found in the Kenyan highlands (1500-3000m) and in Tanzania-Bushbuck disease.
• It occurs where cattle graze inside or near indigenous forests and scrublands.
• Occurs in cattle that break out from fenced pastures and graze the adjacent forest or bush land
at end of the dry season

Hosts and transmission

• Naturally only affects cattle

• Natural vectors not yet identified but ticks are suspected.

• Indigenous cattle appear to develop resistance

• Reservoirs - bushbuck, dik dik

Clinical signs

• High fever 40.5-41.5°C

• Partial anorexia

• Drop in milk yield up to 1 month

• Profuse lacrimation

• Grunting and glinding of teeth.

• Petechial hemorrhages on visible mucous membranes 24 after temperature rise up to 10d.

• Some animals show spontaneous nasal bleeding (epitaxis)

• Some have slight diarrhea (with melena)

• Coughing,

• Edema in eyes

• Harsh respirations

• Edema of conjunctiva may be marked

• “Poached egg” in 10% of the cases, when there is bleeding in anterior chambers of eye and
eversion of eyelids appearance

• Frank dysentery

• Elevated pulse and respiratory rate

P.M. findings

➢ There is marked endothelial damage – most outstanding sign

 ➢ Sub-mucosal and sub serosal hemorrhage

➢ Edema of brisket, lungs and intramuscular fascia

➢ Heart, endo and epicardial heomorrhages.

➢ Petechial and ecchymotic hemorrhages in mucosa of urinary bladder and gall bladder

Differential diagnosis

• Trypanosomoses

• Bracken fern poisoning

• Senecio poisoning

Diagnosis

a) Epidemiology
b) Clinical signs
c) Clinical pathology.
d) Post mortem
e) Demonstration of organism in granulocytes and monocytes during the peak of infection but
cannot be cultured
Control
a) Keep animals away from wild ruminants.
b) Clear bushes in ranching areas
Heartwater (Cowdriosis)

Definition-is an infectious, noncontagious, tickborne rickettsial disease of ruminants and wildlife

Etiology: Ehrlichia ruminantium (formerly Cowdria ruminantium), is an obligate intracellular rickettsial

agent

Transmission: E ruminantium is transmitted by Amblyomma ticks

Clinical Findings:

• The incubation period in sheep and goats varies, ranging between 14 and 17 days.
• Three different clinical forms of heartwater disease: Peracute, acute, and subacute
• Per acute occurs in naive exotic breeds of ruminants in a heartwater-endemic area
• sudden death with no premonitory signs or fever and convulsions. Occasionally severe diarrhea
may be seen
• Acute is the most common
• Pyrexia of sudden onset, followed by anorexia, depression, and respiratory distress, with
resultant rapid breathing and cyanosis
 • Clinical signs may develop in a few days and include chewing movements, twitching of the
eyelids, protrusion of the tongue, behavior changes, circling and high-stepping gait, wide-based
stance, and muscle fasciculations.
• Hyperesthesia, nystagmus, frothing at the mouth, recumbency, seizures, and coma can occur in
terminal stages of the disease. Death usually occurs within 1 week of onset of clinical signs.
• Subacute form (heartwater fever) is seen in some indigenous breeds of sheep with high natural
resistance to the disease
• This form is characterized by a transient fever.

Diagnosis

a) Identification of the tick vector

b) microscopic demonstration of E. ruminantium in histologic sections of brain cortex stained with
Giemsa stain

Prevention
Tick control in pastures is the mainstay of cowdriosis prevention.
TRICHOMONIASIS

Definition: is a venereal disease of cattle characterized primarily by early fetal death and infertility,
resulting in extended calving intervals

Etiology: The causative protozoan, Tritrichomonas foetus,

Transmission: T foetus is found in the genital tracts of cattle. When cows are bred naturally by an
infected bull, 30%–90% become infected

Clinical Findings:

• infertility caused by embryonic death, this results in repeat breeding

• Fetal death and abortions can also occur but are not as common as losses earlier in gestation

Diagnosis

• History and clinical signs

• Confirmation depends on isolation of T foetus, which may be difficult to differentiate from
other trichomonads resident in the digestive tract

Control

• Control consists of eliminating the infection from the bull battery by culling all bulls and
replacing them with virgin bulls or by testing and culling positive bulls.

GASTROINTESTINAL PARASITES OF RUMINANTS

The common stomach worms of cattle are Haemonchus placei (barber’s pole worm, large stomach
worm, wire worm), Ostertagia ostertagi (medium or brown stomach worm), and Trichostrongylus axei
(small stomach worm,

Clinical Findings:
 • Young animals are more often affected, but adults not previously exposed to infection
frequently show signs and succumb
• Ostertagia and Trichostrongylus infections are characterized by profuse, watery diarrhea that
usually is persistent
• In haemonchosis and Mecistocirrus infection, there may be little or no diarrhea but possibly
intermittent periods of constipation. Anemia of variable degree is a characteristic sign of both
these infections.

Lesions:
• Worms can readily be seen and identified in the abomasum, and small petechiae may be
visible where the worms have been feeding

• The most characteristic lesions of Ostertagia infection are small, umbilicated nodules 1–2 mm
in diameter

• These may be discrete, but in heavy infections they tend to coalesce and give rise to a
“cobblestone” or “morocco leather” appearance
• impaired weight gain.

Diagnosis

• Infection usually can be confirmed by demonstrating nematode eggs or tapeworm segments

on fecal examination

General Control Measures

• Control” generally implies the suppression of parasite burdens in the host below that level at
which economic losses occur.
• The goals of control are as follows: 1) prevent heavy exposure in susceptible hosts (recovery
from heavy infection is always slow), 2) reduce overall levels of pasture contamination, 3)
minimize the effects of parasite burdens, and 4) encourage the development of immunity in
the animals (less important in fattening animals than in those to be kept for breeding
purposes).
• The strategic use of anthelmintics is designed to reduce the buildup of worm burdens and, as
a result, pasture contamination.

FLUKE INFECTIONS IN RUMINANTS

• Fasciola hepatica, the most important trematode of domestic ruminants, is the most common
cause of liver fluke disease in temperate areas of the world.
• Fasciola gigantica is economically important in Africa and Asia

Fasciola gigantica in Ruminants

• Fasciola gigantica is similar in shape to Fasciola hepatica but is longer (75 mm), with less
clearly defined shoulders, and is 12 mm wide. It is found in warmer climates (Asia, Africa) in
cattle and buffalo
 • it is responsible for chronic fasciolosis, and in sheep, in which the disease is frequently acute
and fatal

Clinical Findings:

• Acute disease occurs 2–6 wk after the ingestion of large numbers of metacercariae (usually
>2,000) over a short period. In sheep, acute fasciolosis occurs seasonally and is manifest by a
distended, painful abdomen; anemia; and sudden death occurring 2–6 wk after infection.
• In subacute disease, large numbers (500–1,500) of metacercariae are ingested over longer
periods of time; survival is longer (7–10 wk), even in cases with significant hepatic damage,
but deaths occur due to hemorrhage and anemia.
• Chronic fasciolosis occurs as a result of ingesting moderate numbers (200–500) of
metacercariae over longer periods of time; signs include anemia, unthriftiness, submandibular
edema, and reduced milk production,
• heavily infected cattle may show no clinical signs although their immunity to other pathogens
(eg, Salmonella spp) may be reduced

Diagnosis:

• Demonstration of golden-brown eggs in feaces

• Diagnosis can be aided by an ELISA (commercially available in Europe) that enables detection
~2–3 wk after infection

Control

• Reduction of the intermediate host snail population, and prevention of livestock access to
snail-infested pasture
• Although molluscicides can be used to reduce lymnaeid snail populations, those that are
available all have disadvantages that restrict their use.
• Copper sulfate, if applied before the snail population multiplies each year, is effective but
toxic to sheep, which must be kept off treated pasture for 6 wk after application.
• Other such chemicals are generally too expensive and have ecologically undesirable effects.
• Prevention of livestock access to snail-infested pasture is frequently impractical because of
the size of the areas involved and the consequent expense of erecting adequate fencing.

PORCINE CYSTICERCOSIS

Definition: Porcine Cysticercosis is a zoonotic infestation with the larval form of tapeworm in pigs

Etiology: Porcine Cysticercosis is caused by Taenia solium. Taenia spp. are long, segmented, parasitic
tapeworms (family Taeniidae, subclass Cestoda). These parasites have an indirect life cycle, cycling
between a definitive and an intermediate host. Humans are the definitive hosts for Taenia solium.

Distribution

Cysticercosis is most common in Latin America, Southeast Asia and Africa. It is particularly prevalent in
rural areas where domestic pigs are allowed to roam freely.
Epidemiology

The definitive hosts (humans) for Taenia solium are infected when they ingest tissues from the
intermediate host (pig) that contain larvae (cysticerci). Intermediate hosts become infected when they
ingest eggs that were shed in the faeces of the definitive host.

Clinical signs

T. solium cysticerci are found mainly in the skeletal or heart muscles, liver, and brain. The symptoms of
cysticercosis are caused mainly by inflammation associated with degenerating larvae and by the
mechanical effects of the parasites.

Control

Increasing awareness about the risk factors and measures to address public hygiene, especially through
making the use of adequate latrines is essential to combat this parasitic disease.

Also, antiparasitic medications are available and a vaccine against Taenia solium is being developed.

ECHINOCOCCOSIS OR HYDATIDOSIS

Definition:Echinococcosis, or Hydatid disease, is an infection caused by tapeworms of the genus

Echinococcus, a tiny tapeworm just a few millimetres long. Echinococcosis is a zoonosis, a disease of
animals that affects humans

Etiology: Echinococcus granulosus. Like all tapeworms the life cycle involves two animals. A carnivore is
the definitive host – where the adult worms live in the intestines – and almost any mammal, including
humans, can be the intermediate host - where the worms form cysts in various organs

How is the disease transmitted and spread?

The most widespread cycle exists for E. granulosus between dogs and sheep. When dogs are fed fresh
offal or scavenge infected sheep carcasses containing cysts, they become infected, contaminate the
pasture with their faeces, and sheep are re-infected as they graze

What are the clinical signs of the disease?

Tapeworms in the small intestine of the defi nitive host cause few ill effects. In the intermediate host,
the cysts gradually displace or induce fi brosis in normal tissue, and result in disease manifestation. The
symptoms in humans depend on where in the body the cyst develops, and the size and numbers of cysts
or metacestode mass.

In infected livestock with E. granulosus there can be reduced growth, decreased production of milk,
meat and wool, reduced birth rate and losses due to condemnation of organs at post mortem
examination. However, the cysts grow slowly so that many infected animals are slaughtered before the
cysts ever cause disease problems.

How is the disease diagnosed?

in defi nitive hosts is the demonstration of the adult worm in the intestine at post mortem or in the
mucus after a diagnostic test (arecoline purgation), or fi nding the proglottids (tapeworm segments) in
faeces.

What is being done to prevent or control the disease?

The best control measure is to interrupt the life cycle of the parasyte. For E. granulosus this can be done
by: - preventing access of dogs to livestock carcasses or slaughter wastes from farms, households,
abattoirs or butchers, - treating dogs with an anthelmintic (praziquantel) to kill the adult tapeworm, -
detecting cysts at meat inspection, thus targeting infected farms or communities, - vaccinating sheep
(or other livestock) to protect against the development of the larval stage of E. granulosus.

ANTHRAX

Definition: Anthrax is a zoonotic disease caused by the sporeforming bacterium Bacillus anthracis.
Anthrax is most common in wild and domestic herbivores (eg, cattle, sheep, goats, camels, antelopes)
but can also be seen in people exposed to tissue from infected animals, to contaminated animal
products, or directly to B anthracis spores under certain conditions.

Transmission

Human cases may follow contact with contaminated carcasses or animal products

Clinical Findings:

• the incubation period is 3–7 days (range 1−14 days)

• The clinical course ranges from peracute to chronic
• the peracute form (common in cattle and sheep) is characterized by sudden onset and a
rapidly fatal course. Staggering, dyspnea, trembling, collapse, a few convulsive movements,
and death may occur in cattle, sheep, or goats with only a brief evidence of illness.
• In acute anthrax of cattle and sheep, there is an abrupt fever and a period of excitement
followed by depression, stupor, respiratory or cardiac distress, staggering, convulsions, and
death

Diagnosis:

A diagnosis based on clinical signs alone is difficult. Confirmatory laboratory examination should be
attempted if anthrax is suspected

Control

Anthrax is controlled through vaccination programs, rapid detection and reporting, quarantine,
treatment of asymptomatic animals (postexposure prophylaxis), and burning or burial of suspect and
confirmed cases.

Clostridial Diseases

• Clostridial diseases can be divided into two categories:

o 1) those in which the organisms actively invade or when locally dormant spores are
activated and reproduce in the tissues of the host, with the production of toxins that
 enhance the spread of infection (the gas-gangrene group, the clostridial cellulitides
group); and
o 2) those characterized by toxemia resulting from the absorption of toxins produced by
organisms within the digestive system (the enterotoxemias), in devitalized tissue
(tetanus), or in food or carrion outside the body (botulism).

• Clostridial diseases are not spread from animal to animal.

INFECTIOUS NECROTIC HEPATITIS (BLACK DISEASE)

❑ Acute toxaemia of sheep, cattle, pigs and horses.

Etiology

❑ Toxin of Cl. novyi type B.

❑ Cl. novyi is a resident in soil and may be present in the liver of normal animals.

❑ Necrosis of the liver causes anaerobic condition which causes the organism to proliferate and
produce toxins.

Animal risk factors

❑ Occur in well nourished adult sheep 2-4 years of age.

❑ Lambs and yearlings are rarely affected.

Environmental Risk Factors

❑ Presence of liver flukes

❑ Outbreaks common in warm months

❑ Marshy areas favor occurrence of the disease.

❑ Heavy irrigation is associated with the occurrence of the disease.

Source of infection

❑ Faecal contamination

❑ Cadavers

❑ Flooding

CLINICAL FINDINGS

Sheep

❑ Sudden death

❑ Segregate from the rest of the flock.

❑ Lag behind.
 ❑ Fever 40-420c

❑ Subnormal temperature before death

❑ Hyperesthesia, respiration is rapid but shallow, the course of illness is few hours

CATTLE

❑ Clinical signs same as in sheep but the clinical course is much longer.

❑ Prominent signs include

✓ Sudden severe depression

✓ Reluctance to move

✓ Coldness of the skin

✓ Absence of rumen sounds

✓ Low or normal temperature

✓ Abdominal pain, Periorbital oedema.

CONTROL

❑ Vaccination with an alum-precipitated toxoid.

❑ On an affected farm the initial vaccination if followed by a second vaccination 4-6 weeks later
and subsequently by annual vaccination.

❑ Control the liver flukes through use of molluscicide, flukicides.

❑ Avoid pasture contamination from cadavers by burning the carcasses.

BOTULISM

❑ Fatal intoxication of cattle, sheep, goats, horses, mules, donkeys and very rearly pigs,

❑ Caused by ingestion of the toxin of Clostridium botulinum

❑ There is partial or complete flaccid paralysis of the muscles of locomotion, mastication and
deglutition.

❑ The organism proliferates in decomposing animal tissue and plant material

❑ Cl. Botulinum present in tissues produces toxins which are absorbed and produces the typical
disease-Toxicoinfectious botulism

❑ NB. botulus is the latin word for sausage.

ETIOLOGY

Neurotoxin that is produced by Cl. Botulinum during vegetative growth.

EPIDEMIOLOGY
 ❑ Ingestion of preformed toxin.

❑ Feed may be contaminated with a carrion containing toxin.

❑ Consumption of carrion on pasture by phosphorus-deficient animals.

❑ Rare cases occur from toxin production from organisms in the intestines or wounds.

❑ Occasional outbreaks may occur due to drinking of water.

❑ Botulism is most common in birds.

❑ Cattle, sheep and horses are susceptible,

❑ But pigs, dogs and cats appear to be resistant

CATTLE AND HORSES

Peracute

❑ Signs appear after 3-17 days.

❑ Peracute death in some.

❑ Muscle tremors and fasculations occur.

❑ Progressive symmetrical muscular paralysis.

❑ The muscular weakness and paralysis commences in the hindquarters and progresses to the
forequarters, the head (muscles of the jaw, tongue) and the neck.

SUBACUTE

❑ Restlessness, in-coordination, stumbling, knuckling, and ataxia are followed by inability to rise
or to lift the head.

❑ Skin sensation is retained

❑ Affected animals lie in sternal recumbency with the head on ground or turned into flank.

❑ The tongue becomes paralysed and hangs from mouth and animal is unable to chew and drools
saliva

❑ Defaecation and urination are not affected although there may be constipation

❑ Paralysis of chest muscles results in a terminal abdominal type respiration

❑ course of the disease is 1-4 days.

Chronic form

❑ Animal may recover after an illness of 3-weeks.

❑ Chronic cases show restlessness and respiratory distress followed by knuckling, stumbling and
disinclination to rise.
SHEEP

❑ Sheep do not show the typical flaccid paralysis of the other species until the final stages of the
disease.

❑ Stiffness while walking.

❑ In-coordination.

❑ Salivation.

❑ Serous nasal discharge.

❑ Terminal stages- there is abdominal respiration, limb paralysis and death

PIGS

❑ Staggering

❑ Recumbency.

❑ Vomiting

❑ Pupillary dilatation.

❑ Flaccid muscular paralysis

❑ Pigs do not eat or drink.

GOATS

❑ Protruding tongue is a characteristic sign

Postmortem findings

❑ No specific changes are seen although the presence of suspicious, foreign material in the fore-
stomachs or stomach may be suggestive.

DIAGNOSIS

❑ Clinical signs.

❑ History of pica.

Control

❑ Supplement with phosphorus or protein-rangelands.

❑ Hygienic disposal of carcasses.

❑ In enzootic areas, vaccination with type specific or combined bivalent precipitated toxoid.

❑ Immunity is set in 2 weeks and is solid for 24 months.

TETANUS (lockjaw)

Definition: A highly fatal infectious disease characterized by an acute onset of hypertonia, painful
muscular contractions (usually of jaws and neck) and generalized muscle spasm and convulsions

Aetiology: Potent neurotoxin of Cl. tetani. Organisms form spore which persist in soil for years. Resistant
to many disinfection procedures

Horse most susceptible and cattle least

Cl. Tetani organisms in horse faeces

Portal of entry- deep puncture wounds

Organisms dormant in tissues until conditions are favourable for proliferation

Puncture wounds of hooves in horses, parturition in cattle, castration in pigs, vaccination in sheep

CLINICAL SIGNS:

Incubation period upto several months after introduction of bacilli

Muscle stiffness, Trismus, prolapse of 3rd eyelid, retraction of eyelids, dilation of nostrils, alert
appearance with erect ears, constipation and urine rention, spine curved and tail deviated to one side,
inability to walk, opisthotonus is marked, profuse sweating and spontaneous convulsions

DIAGNOSIS: Clinical signs and history of recent injury

CLOSTRIDIAL ENTEROTOXAEMIAS

CLOSTRIDIUM PERFRINGENS TYPE A

• Type A strains of C. perfringens are found as part of the normal intestinal microflora of animals.
• They lack some of the powerful toxins produced by strains of other types.
• They produce the lethal and necrotizing α toxin and are incriminated in necrotic enteritis in poultry
and dogs, in colitis in horses, and in diarrhea in pigs.
Pathology

• The disease is characterized by necrotic enteritis with massive destruction of the villi and coagulation
necrosis of the small intestine.
• Large numbers of large, gram-positive rods are visible in fecal smears, and large numbers of C.
perfringens type A are recovered on anaerobic culture of feces while other known enteric pathogens
are usually absent.
• Production of enterotoxin by C. perfringens type A can also induce diarrhea in humans.
• Enterotoxin has also been demonstrated in the feces of pigs with diarrhea but not in feces of healthy
pigs. Experimental disease has been produced in pigs challenged orally with C. perfringens type A.

CLOSTRIDIUM PERFRINGENS TYPES B AND C

1. These strains cause severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves,
pigs, and foals.
2. Types B and C produce the highly necrotizing and lethal β toxin that is responsible for severe
intestinal damage.
3. Βeta toxin is sensitive to proteolytic enzymes and disease is associated with inhibited proteolysis in
the intestine (Sow colostrum, which contains a trypsin inhibitor and has been suggested as a factor in
the susceptibility of young piglets).
4. C. perfringens Type C also causes enterotoxemia in adult cattle, sheep, and goats.
5. C. perfringens also has been associated with hemorrhagic enteritis in dogs.

Diseases

• Lamb dysentery: type B in lambs up to 3 wk of age.

• Calf enterotoxemia: types B and C in well-fed calves up to 1 mo.
• Pig enterotoxemia : type C in piglets during the first few days of life.
• Foal enterotoxemia: type B in foals in the first week of life.
• Struck: type C in adult sheep.
• Goat enterotoxemia : type C in adult goats.

Clinical Findings

1. Lamb dysentery-An acute disease of lambs <3 wk old. Many may die before signs are seen. Some
newborn lambs stop nursing, become listless, and remain recumbent. Fetid, blood-tinged
diarrhea is common, and death usually occurs within a few days.
2. Calves-Acute diarrhea, dysentery, abdominal pain, convulsions, and opisthotonos. Death occurs
in a few hours-less severe cases survive for a few days, and recovery over a period of several days
is possible.
3. Pigs-acutely illness within a few days of birth. Diarrhea, dysentery, reddening of the anus, and a
high fatality rate; most piglets die within 12 hr.
4. In foals, there is acute dysentery, toxemia, and rapid death.
5. Struck in adult sheep is characterized by death without premonitory signs.

Lesions

• Hemorrhagic enteritis with mucosal ulceration is the major lesion in all species.
• The affected portion of the intestine is deep blue-purple and at first glance appears to be an
infarction associated with mesenteric torsion.
• Smears of intestinal contents have large numbers of gram-positive, rod-shaped bacteria; filtrates
are collected for detection of toxin and subsequent identification by neutralization with specific
antiserum.

Control

• Treatment is ineffective because of the severity of the disease,.

• Specific hyperimmune serum is indicated together with oral administration of antibiotics may be
helpful.
 • Controlled by vaccination of the pregnant dam during the last trimester of pregnancy: initially, 2
vaccinations 1 mo apart, and annually thereafter.
• When outbreaks occur in newborn animals from unvaccinated dams, antiserum should be
administered immediately after birth.

TYPE D ENTEROTOXEMIA(PULPY KIDNEY DISEASE, OVEREATING DISEASE)

Introduction

• This is the classic enterotoxemia of sheep. It is seen less frequently in goats and rarely in cattle.
• Distribution is worldwide and may occur in animals of any age.
• It is most common in lambs that are either <2 wk old, weaned in feedlots and on a high-
carbohydrate diet or on lush green pastures.
• The disease has been suspected in well-nourished beef calves nursing high-producing cows,
grazing lush pasture and in sudden death syndrome in feedlot cattle.

Aetiology

• C. perfringens type D.
• The predisposing factors also are the ingestion of excessive amounts of feed or milk in the very
young and grain in feedlot lambs.
• The disease usually occurs in single lambs, because ewes with twins seldom give enough milk per
lamb to allow enterotoxemia to develop.
• In feedlots, the disease usually is seen in lambs switched rapidly to high-grain diets. Increase in
starch intake it provides a suitable medium for growth of the causative bacteria, which produce
toxin.
• The toxin causes vascular damage especially of brain capillaries.
• Many sheep are carriers of C. perfringens type D as part of the normal intestinal microflora of the
intestine and serve are the source of infection to the newborn.

Clinical Findings

• Sudden deaths in the best-conditioned lambs are the first indication of enterotoxemia.
• Some cases, nervous signs of excitement, incoordination, and convulsions occur before death.
Opisthotonus, circling, and pushing the head against fixed objects are common.
• Hyperglycemia or glycosuria may occur.
• Diarrhea may or may not develop.
• Adult sheep-When affected, they present with weakness, incoordination, and convulsions and die
within 24 hr.
• Goats- Course of disease ranges from peracute to chronic. Signs vary from sudden death to watery
diarrhea with or without blood. Nervous signs are seen and death in several weeks
• Calves not found dead show mania, convulsions, blindness, and death in a few hours. Subacutely-
calves are stuporous for a few days and may recover.
• Type D enterotoxemia can occur in young horses that have overeaten.
Lesions

• Only a few hyperemic areas on the intestine and a fluid-filled pericardial sac on necropsy of young
lambs.
• Older animals, hemorrhagic areas on the myocardium may be found as well as petechiae and
ecchymoses of the abdominal muscles and serosa of the intestine. Bilateral pulmonary edema
and congestion frequently occur in adults.
• The rumen and abomasum contain increased feed and undigested feed is found in the ileum.
• Edema and malacia can be detected microscopically in the basal ganglia and cerebellum of lambs.
• Rapid postmortem autolysis of the kidneys has led to the popular name, pulpy kidney disease in
lambs but this isn’t found in all cases.
• Goats or cattle rarely present with pulpy kidneys and hemorrhagic or necrotic enterocolitis may
be seen in goats.

Diagnosis

• A tentative diagnosis of type D enterotoxemia is based on sudden, convulsive deaths in lambs on

carbohydrate-rich feed or lush pasture.
• Smears of intestinal contents reveal many short, thick gram-positive rods. Confirmation requires
demonstration of toxin in the small-intestinal fluid. Fluid is collected in a sterile vial within a few
hours after death and sent under refrigeration to a laboratory for toxin identification. Chloroform,
added at 1 drop for each 10 mL of intestinal fluid, will stabilize any toxin present.
• P.C.R. is also used to differentiate the serotypes.

Control

• The method used depends on the age of the lambs, the frequency with which the disease appears
on a farm and the method of husbandry.
• Ewe immunization is the most satisfactory method of control. Breeding ewes should be given 2
injections of type D toxoid their first year, and 1 injection 4-6 wk before lambing and each year
thereafter.
• Enterotoxemia in feedlot lambs can be controlled by reducing the amount of concentrate in the
diet. This may not be economical thus immunization of all lambs with toxoid when they enter
feedlot will reduce losses to an acceptable level. Two injections, 2 wk apart, will protect lambs
through the feeding period.

SALMONELLOSIS IN DOMESTIC ANIMALS

INTRODUCTION

• Salmonellosis is caused by many species of salmonellae.

• It is characterized clinically by one or more of 3 major syndromes
1.septicemia
 2. acute enteritis,

3.and chronic enteritis.

• The disease occurs worldwide and in all animals and the incidence has increased with the
intensification of livestock production.
• Young calves, piglets, lambs, and foals usually develop the septicemic form.
• Adult cattle, sheep, and horses commonly develop acute enteritis, and chronic enteritis may develop
in growing pigs and occasionally in cattle and pregnant animals may abort.
• The clinically normal carrier animals pose a serious problem in all host species.
• In dogs and cats, salmonellosis is seen infrequently and is characterized by acute diarrhea with or
without septicemia.
• Incidence of human salmonellosis has increased in recent years; animals have been incriminated as
the principal reservoir. Transmission to humans occurs via contaminated drinking water, milk, meat,
and foods such as cake mixes that use contaminated ingredients; poultry and eggs are particularly
important sources of infection.

Etiology and Epidemiology

• Many Salmonella spp may cause disease but the more common ones in each species are
1. Cattle— Salmonella typhimurium , Salmonella dublin , and Salmonella newport
2. Sheep and goats— Salmonella typhimurium , Salmonella dublin , Salmonella anatum and Salmonella
montevideo
3. Pigs— S. typhimurium and S. choleraesuis
4. Horses— S. typhimurium , S anatum , S newport , S. enteritidis , and Salmonella serovar IIIa 18:z4z23.
• The resulting clinical patterns of these pathogens are not distinct however different species of
salmonellae tend to differ in their epidemiology.
• Plasmid profile and drug-resistance patterns are sometimes useful markers for epidemiologic studies.
• Feces of infected animals contaminate feed and water sources, milk, fresh and processed meats from
abattoirs, plant and animal products used as fertilizers or feedstuffs, pasture and rangeland, and many
inert materials.
• The organisms may survive for months in wet, warm areas such as feeder pig barns or in water
dugouts but survive <1 wk in composted cattle manure.
• Rodents and wild birds also are sources of infection.
• Pelleting of feed reduces the level of contamination by salmonellae.
• Prevalence of infection varies among species and countries and is much higher than the incidence of
clinical disease, which is commonly precipitated by stressful situations such as sudden deprivation of
feed, transportation, drought, crowding, parturition, and the administration of some drugs.
• Animals subjected to prolonged surgical procedures are at an increased risk as is the use of oral
antimicrobial agents.
• Route of infection-Oral and, after infection, the organism multiplies in the intestine and causes
enteritis.
• High gastric pH, absence of stable intestinal flora and limited immunity may predispose younger
animals to the disease.

Cattle and Sheep

• In calves and lambs, disease is usually endemic on a farm, with sporadic explosive outbreaks.
• Subclinical infection with occasional herd outbreaks may be seen in adult cattle.
• Stressors that precipitate clinical disease
1. deprivation of feed and water
2. minimal levels of nutrition
3. long transport times,
4. calving
5. mixing and crowding in feedlots.

Pigs

• Outbreaks of septicemic salmonellosis are rare and usually can be traced to a purchased, infected pig.
• Purchase of feeder pigs from salmonellae-free herds and use of “all-in/all-out” policy in finishing units
minimize exposure.

Horses

• Many horses may be carriers.

• Adults-cases develop after the stress of surgery or transport, especially when horses are moved
through sales yards, deprived of feed and water and then overfed at their destination.
• Mares may be inapparent shedders and despite several negative cultures before foaling, may shed
the bacteria at parturition and infect the newborn foal.
• Salmonellosis in horses hospitalized for other causes is a major problem for equine clinics and stud
farms since
1. carriers are constantly reintroduced
2. the environment is persistently contaminated and
3. a large population of vulnerable horses is at risk.
• Septicemic salmonellosis is also common in foals; it may be endemic on a given premises or there may
be outbreaks.

Dogs and Cats

• Many dogs and cats are asymptomatic carriers.

• Clinical disease is uncommon. When it occurs, it is associated with
-hospitalization

-concurrent infections

-debilitating condition in adults

-exposure to large numbers of the bacteria in puppies and kittens.

Pathogenesis

• Bacteria penetrate into the lamina propria, produce a cyto and enterotoxin which causes gut damage
to and diarrhea.
• The inflammatory response is marked, and salmonellae are engulfed by phagocytic cells; but, the
bacteria survive and multiply in them.
• Septicemia may follow with subsequent localization in brain and meninges(meningoencephalitis),
pregnant uterus (abortion), distal aspects of the limbs (osteitis) and tips of the ears and tails(dry
gangrene)
• The organism frequently localizes in the gallbladder and mesenteric lymph nodes, and
survivors/carriers intermittently shed the organism in the feces.
• Infected adults become carriers and shed the organism for variable periods
—up to 10 wk in sheep and cattle and

-up to 14 mo in horses.

• Adult cattle infected with S. dublin excrete the organism for years.
• Infection may persist in lymph nodes or tonsils, with no salmonellae in the feces.
• Latent carriers begin shedding the organism or develop clinical disease under stress.
• Passive carriers acquire infection from the environment but is not invaded, if removed from the
environment, it ceases to be a carrier.

Clinical Findings

Septicemia

• In newborn calves, lambs, foals, and piglets; outbreaks may occur in pigs up to 6 mo old.
• Illness is acute, marked depression, fever [40.5-41.5°C] and death occurs in 24-48 hr.
• In pigs, a dark red to purple discoloration of the skin is common, especially of the ears and ventral
abdomen (differential for swine erysipelas, African and classical swine fever and pasteurellosis).
• Nervous signs and pneumonia may be seen in calves and pigs; Mortality may reach 100%.

Acute enteritis

• Common form in adults as well as calves that are ≥1 wk old.

• This form presents with
- initial fever [40.5-41.5°C],
- followed by severe watery diarrhea, sometimes dysentery and often tenesmus.
- Feces may vary considerably, have a putrid odor and contain mucus, fibrinous casts, shreds
of mucous membrane, and in some cases, large blood clots.
- Rectal examination causes severe discomfort, tenesmus, and dysentery.
- Milk production often declines precipitously in dairy cows.
- Horses-Abdominal pain/colic is common and severe; horses are severely dehydrated and may
die within 24 hr of the onset of diarrhea; mortality may reach 100%.
- Clin. Path.-marked leukopenia and neutropenia are characteristic of the acute Salmonellosis
in horses.
- Dogs and cats-acute diarrhea with septicemia and is seen occasionally in puppies and kittens
or in adults stressed by concurrent disease. Pneumonia may occur. Abortion may occur in
pregnant bitches or queens. Conjunctivitis may occur in affected cats.
Subacute enteritis-may develop in adult horses and sheep on farms where the disease is endemic.
Signs
 1. mild fever [39-40°C]
2. soft feces
3. inappetance
4. dehydration.
5. high incidence of abortion in cows and ewes,
6. some deaths in ewes after abortion
7. high mortality rate due to enteritis in lambs younger than a few weeks of age.
In cattle, the first signs may be fever and abortion, followed several days later by diarrhea.

Chronic enteritis

- Is a common form in pigs and adult cattle.

- Presents with
1. persistent diarrhea
2. severe emaciation
3. intermittent fever
4. poor response to treatment.
5. feces scant and may be normal or contain mucus, casts, or blood.
- In growing pigs, rectal stricture may be a sequela if the terminal part of the rectum is involved. Affected
pigs are anorectic and lose weight; the abdomen becomes grossly distended and the animal has tenesmus.
The stricture is obvious on digital palpation and necropsy.

-Several rodents ( guinea pigs, hamsters, rats, and mice) and rabbits are susceptible and commonly act
as a source of infection on farms where the disease is endemic.

Diagnosis

-Is based on

-the clinical signs presented

-laboratory examination of feces, tissues from affected animals, feed (including all

mineral supplements used), water supplies, and feces from wild rodents and birds

that may inhabit the premises.

-Culture techniques that involve suppression of fecal E coli are usually necessary and several daily fecal
cultures may be necessary to isolate the organism due to intermittent shedding.. Blood cultures in
septicaemic animals may be rewarding but are costly.

-Serologic testing is difficult to interpret.

DDXs
-The clinical syndromes usually are characteristic but must be differentiated from several similar
diseases in each species:

Cattle—diarrhea due to enterotoxigenic Escherichia coli , dysentery due to verotoxigenic E coli ,

coccidiosis, cryptosporidiosis, the alimentary tract form of infectious bovine rhinotracheitis, bovine viral
diarrhea, hemorrhagic enteritis due to Clostridium perfringens types B and C, paratuberculosis among
others.

Sheep—enteric colibacillosis, septicemia due to Haemophilus sp or pasteurellae, and coccidiosis.

Pigs—enteric colibacillosis of newborn pigs and weanlings, swine dysentery, campylobacteriosis and the
septicemias of growing pigs (which include erysipelas, classical swine fever, and pasteurellosis);

Horses—septicemia due to E coli , Actinobacillus equuli , Streptococci and colitis.

Treatment

-Early treatment is essential for septicaemic Salmonellosis.

-Recent research findings have shown that oral antibiotics may alter the intestinal microflora thus
interfering with competitive antagonism and prolong shedding of the organism. Concern has also been
raised that antibiotic-resistant strains of salmonellae selected by oral antibiotics may subsequently infect
humans. Most nosocomial infections often involve highly drug-resistant organisms.

-Broad-spectrum antibiotics are used parenterally to treat the septicemia based on knowledge of the drug
resistance pattern found in the area.

- Trimethoprim-sulfonamide combinations are often effective.

- Ampicillin
- Fluoroquinolones
- Third-generation cephalosporins.
- Treatment should be continued daily for up to 6 days.
- Oral medication are given in drinking water because affected animals are thirsty due to dehydration.
- Fluid therapy to correct acid-base imbalance and dehydration is necessary.
- Antibiotics such as ampicillin or cephalosporins lead to bacterial lysis and release of endotoxins thus
NSAIDs may be used to reduce the effects of endotoxemia.
- Horses with acute intestinal salmonellosis are severely acidotic and hyponatremic and may need to
be treated initially with 5% sodium bicarbonate, IV, at 5-8 L/450 kg body wt. This is followed by
balanced electrolytes containing potassium to correct the hypokalemia that may follow correction of
the acidosis.
- In horses, flunixin meglumine is recommended for its antiendotoxic properties.
N.B.-Corticosteroids are not recommended because of their immunosuppressive effects and their
potential to exacerbate laminitis. Administration of plasma with a high titre of Salmonella
lipopolysaccharide core antibodies may be beneficial in horses. Plasma with serotype-specific antibodies
is even more beneficial.

Septicemic salmonellosis in pigs usually responds favorably if treated early.

N.B. The intestinal form is difficult to treat effectively in all species; clinical cure may be achieved but
bacteriologic cure is difficult, particularly in adult animals because the organisms become established in
the biliary system and are intermittently shed into the intestinal lumen, which causes chronic relapsing
enteritis and contamination of the environment.

Control and Prevention

- Control and prevention of Salmonellosis is complicated by carrier animals and contaminated

feedstuffs.
- Drain swabs or milk filters are often cultured to monitor the salmonellae status of a herd.
- The two methods used in control are prevention of introduction and limitation of spread within a
herd.
1. Prevention of Introduction

Is achieved by preventing the introduction of a carrier animals. Animals should be purchased directly only
from farms known to be free of the disease and should be isolated for ≥1 wk while their health status is
monitored. Feed supplies should be free of salmonellae and procured from reliable sources.

2. Limitation of Spread within a Herd:

In an outbreak, the following procedures should be implemented

a) Carrier animals should be identified and either culled or isolated and treated vigorously. Treated
animals must be rechecked several times before there can be confidence that they are not carriers.

b) The prophylactic use of antibiotics in feed or water supplies may be considered

c) Movement of animals around the farm should be restricted to limit infection to the smallest group.
Random mixing of animals should be avoided.

c) Feed and water supplies must be protected from fecal contamination.

e) Contaminated buildings must be vigorously cleaned and disinfected.

f) Contaminated material must be disposed of carefully.

g) All persons should be aware of the hazards of working with infected animals and the importance of
personal hygiene.

h) Use of a vaccine should be considered, particularly in an outbreak involving pregnant cattle in where a
vaccine has been shown to confer some protection in adults and calves. Commercial killed bacterins or
autogenous bacterins may be used.

i) Stresses should be minimized.

j) Fetal membranes of mares should be placed in a plastic bag until the mare eliminates them, and the
foal should be fed colostrum before contact with the mare.
Vaccines:

Several studies with live attenuated Salmonella vaccines in pigs, cattle, and chickens have shown them to
be effective in stimulating a strong cell-mediated immune response and protecting animals against
disease. The commercial vaccines available for use in cattle are bacterins and appear to induce a modest
level of protection. When given to pregnant cows, they induce antibodies in colostrum, which provide an
important measure of protection to calves, which are most susceptible in the first week of life.

Brucellosis in Cattle

(Contagious abortion, Bang's disease)

The disease in cattle, water buffalo, and bison is caused almost exclusively by Brucella abortus

Natural transmission occurs by ingestion of organisms, which are present in large numbers in aborted
fetuses, fetal membranes, and uterine discharges. Cattle may ingest contaminated feed and water or
may lick contaminated genitals of other animals. Venereal transmission by infected bulls to
susceptible cows appears to be rare. Transmission may occur by artificial insemination when Brucella-
contaminated semen is deposited in the uterus

Clinical Findings:

Abortion is the most obvious manifestation. Infections may also cause stillborn or weak calves,
retained placentas, and reduced milk yield. Usually, general health is not impaired in uncomplicated
abortions.

Diagnosis:

Diagnosis is based on bacteriology or serology. B abortus can be recovered from the placenta but
more conveniently in pure culture from the stomach and lungs of an aborted fetus.

Control:

Efforts are directed at detection and prevention, because no practical treatment is available. Eventual
eradication depends on testing and eliminating reactors. The disease has been eradicated from many
individual herds and areas by this method. Herds must be tested at regular intervals until two or three
successive tests are negative.
LEPTOSPIROSIS

Defination: This is an infectious, zoonotic disease of domestic animals caused by Leptospira serotypes
characterized by changes in milk consistency and colour, abortions, haemoglobinuria, jaundice in most
domestic animals and periodic opthalmia in horses.

Etiology

It is caused by different serotypes belonging to L.interrogans group-pathogenic types and L. biflexa-

saprophytic

Leptospira are spirochaetes found in the soil and their survival is dependant on moist environment and
thrive in neutral to alkaline soils. They are found in moist warm and humid climate where soil is alkaline
and there is abundant surface water. The disease is sporadic and was first reported in Kenya in 1958.
Mortality rate in cattle is low especially in adult but the morbidity rate may be high.

In the Pigs, the morbidity rate is 20% by serology. The disease is rarely reported in shoats except in
Israel. The disease is an occupational hazard because it affects man including, farmers, butchers and
veterinarians.

Transmission

Sources of infection are contaminated feed, pastures and water. These are contaminated through urine,
aborted fetuses and uterine discharges. The routes of infection are via ingestion-the main route and
skin abrasion. The reservoir are rats, wild pigs, wild dogs, jackals and foxes. It has been reported of the
disease transmission through semen infected by the bacteria. There is also transplacental transmission
and transmission to calves through the milk especially in septicaemic stage.

Pathogenesis

There are two phases of the disease- .Leptospiraemia and Leptospiruria

Leptospiraemia- The organism multiplies in the blood stream. After 7 days, the organism can be cultured
from the blood. There is an increase in temperature ( fever). Antibodies start appearing 7 – 14 days after
infection. After 21 days, the organisms start appearing in the urine ( leptospiruria).The organisms
localize in several organs- kidney, liver and may also localize in the CNS or cross placenta leading to
placentitis. Leptospiruria may last upto 3 months. In the pigs may last upto 4-6 months. Localisation in
the kidney results in Interstitial nephritis and in the liver results in liver necrosis. In the nervous tissue
there is meningitis and abortion when in the placenta. Hemolysin factor isolated is the cause of
erythrocyte hemolysis.

Clinical signs

Cattle: The disease may be acute,subacute or chronic. Acute in calves upto 1 month old. There is
septicaemia with temperature of 40.5-41.5., anorexia, depression, petechiation of mucus membrane,
acute hemolytic anaemia with jaundice and hemoglobinuria,dyspnoea, loud heart sounds and
decreased rate.The mortality is high in calves. Abortion occurs in pregnant cows in the last trimester.
There is decreased or cessation of milk production or secretion. Milk is yellowish, reddish in colour,
udder is soft or flaccid and shows no evidence of inflammation on palpation. This is atypical mastitis.
Localisation in the joint is severe. There is also necrotic dermatitis especially in non pigmented animal.
There is a long convalescent period.

Subacute disease in cattle is the same as acute but mild. It is common in adult cattle.

Chronic stage is characterized by abortion storm. Most cows have retained afterbirth. Leptospira
Eliminate sources of infection by draining damp, standing water areas. Proper manure disposal and
hygiene. If water from water holes, it should be fenced off to minimize urine. Proper disposal of aborted
fetuses.

Johne’s disease (Paratuberculosis)

• This disease occurs in adult dairy cows and beef cattle older than 2-3years of age

Etiology

• The disease is caused by Mycobacterium paratuberculosis

Epidemiology

• Disease is worldwide in distribution

• Affects mainly cattle

• Also occurs in Goats and sheep

Clinical findings

• Early clinical disease presents as intermittent or continous watery or “pea-soup” diarrhoea

associated with stress (e.g., parturition)

• Vital signs are normal, and appetite is good to excellent

• Emaciation becomes progressive

• And milk production decreases

• Terminal signs include profound emaciation, profuse waterly diarrhoea, and dependent edema

Diagnosis

• Clinical signs alone are not reliable for diagnosis

• Laboratory tests confirm the diagnosis

• Postmortem examination of a specifically sacrificed animal is most reliable diagnostic tool.

Laboratory tests

• Fecal culture is the most reliable and frequently used diagnostic test for infection in individual
cattle

• Serological tests offer some value in determining herd status of infection but often must be
carried out as a series of tests.

Prevention

(a) Methods of herd management

 • The disease may be kept in check on a herd basis by test and slaughter method

• Removal of reactor or culture positive animals and their offspring is necessary.

• This need to be combined with improved hygienic practices, which decrease the fecal-oral
spread of the organism

• Calves must be removed from the dam at birth and reared separately

• The herd should be maintained as a closed herd or replacement animals purchased from known
Johne’s-free herds.

(b) Problems with herd management

• The disease may be effectively eliminated from a herd, but the management changes required
are intensive, rigorous, and expensive.

• Because of the inaccuracies in diagnostic tests, there is as yet no test and slaughter program
that effectively eliminates all carriers

• Therefore, the only effective method of elimination is one of repopulation of a new

environment with unexposed or known negative animals.

(C) Vaccination-if the legislation allows- of calves may provide protection against clinical disease and
reduce the rate of spread of infection. A major complication of a vaccination program is that vaccines
are positive to the tuberculin test for bovine tuberculosis

Mastitis

Mastitis, or inflammation of the mammary gland, is predominantly due to the effects of infection by
bacterial pathogens, although mycotic or algal microbes play a role in some cases

Almost any microbe that can opportunistically invade tissue and cause infection can cause mastitis.
However, most infections are caused by various species of streptococci, staphylococci,

Intramammary infections are often described as subclinical or clinical mastitis.

Subclinical mastitis is the presence of an infection without apparent signs of local inflammation or
systemic involvement.

Clinical mastitis is an inflammatory response to infection causing visibly abnormal milk (eg, color,
fibrin clots). As the extent of the inflammation increases, changes in the udder (swelling, heat, pain,
redness) may also be apparent.

Control

• Dry cow therapy

• Hygiene
• Culling animals with chronic cases

ACTINOBACILLOSIS (WOODEN TONGUE)

Etiology
 • Actinobacillus lignieresii,

• Gram-negative rod

• Normal inhabitant of the mouth of ruminants

Epidemiology

• Common only in cattle and sheep

• Can occur in swine and horses, chicken and rarely in man

• World wide in distribution

• Sporadic disease

• Infected discharges are the source of infection and transmission is effected by ingestion of
contaminated pasture or feed

• Injury to the buccal mucosa, especially when animals are fed on dry sharp feeds, permits easy
entry of the infection

Clinical findings

• Onset is acute and characterised by:

✓ Ptyalism

✓ Excessive tongue movement

✓ Inability to eat

✓ In cattle, the tongue is swollen, hard, and painful on manipulation

✓ The tongue may be enlarged, particulary at the base, early in the course of the disease, but
later it becomes shrunken and firm.

✓ Manipulation of the tongue will cause pain and resentment

✓ Nodules and ulcers may be present.

✓ Suppuration occurs and pus is discharged from the affected areas

Sheep

• Tongue not usually affected

• Lesions up to 8 cm in diameter occur on the lower jaw, face and nose or in the skin folds from
the lower jaw to the sternum

• Viscid, yellow-green pus containing granules is discharged through a number of small

openings

Diagnosis
 • Use clinical presentation

• Consider the DDX, rabies, Foreign body, tuberculosis abscesses of the throat

Control

• Quick treatment of affected animals

• Prevention of contamination of pasture and feed troughs by discharging animals

• Isolation or disposal of animals with discharging lesions

ACTINOMYCOSIS (LUMPY JAW

Etiology

• Actinomyces bovis

Epidemiology

• Common in cattle, however occasional cases occur in pigs, horses, dogs and human

• Actinomyces bovis is a common inhabitant of the bovine mouth and infection is thought to
occur through wounds to the bucal mucosa caused by sharp pieces of feed or foreign material

Clinical finding

• Actinomycosis of the jaw commences as a painless, bony swelling which appears on the
mandible and maxilla

• Some lesions enlarge rapidly within a few weeks, others slowly over a period of months

• The swellings are very hard, are immovable and in the later stages, painful to the touch

• They usually break through the skin and discharge through one or more openings

• The discharge of pus is small in amount and consists of sticky, honey-like fluid containing
minute, hard, yellow-white granules

• There is tendency for sinuses to heal and for fresh ones to develop periodically

Diagnosis

• Use clinical signs

• Consider the DDX especially feed jammed between the cheek and teeth

• Consider other causes of indigestion

• To confirm the diagnosis make a smear of the discharging pus and stain with Gram’s stain

• Gram-positive filaments are seen

FOOT ROT IN CATTLE, GOATS

  Footrot is a highly contagious disease affecting the interdigital (between the toes) tissue of
ruminants.

 It is one of the most common causes of lameness in cattle and sheep and can result in serious
economic loss.

Etiology and predisposing factors

 Mechanical injury or softening and thinning of the interdigital (between the toes) skin by
puncture wounds

 continuous exposure to wet conditions are necessary to provide entrance points for infectious
agents.

 Fusobacterium necrophorum is the main causative agent, also including Bacteroides

melaninogenicus, Bacteroides nodosus,Corynebacterium pyogenes and Sphaerophorus
necrophorus

Clinical finding

❖ Lameness is usually the first sign of an infected animal, varying from scarcel noticeable to
severe in one or more feet.

❖ Lameness is typically followed by reddening of the interdigital tissue and swelling of the foot,
causing spreading of the toes. One or more feet may be affected simultaneously.

❖ Spreading of the dewclaws due to swelling is a classic sign of foot rot.

DIAGNOSIS

❖ Examination of the foot, looking at the characteristic signs of sudden onset of lameness
(usually in one limb)

❖ Elevated body temperature

❖ Interdigital swelling

❖ Separation of the interdigital skin

Control

 CONTROL

 Removal of predisposing factors such as nails, broken bottles, stones from the animal’s
environment

 Regular hoof trimming

 Footbath with 5% copper sulphate

 Zinc supplementation in the diet

INFECTIOUS KERATOCONJUCTIVITS IN CATTLE(PINK EYE)

 • Pinkeye disease is a painful debilitating condition that can severely affect animal productivity

 It is caused by a bacteria called Moraxella bovis.

 The bacterium causes inflammation of the eye and in severe cases results in temporary or
permanent blindness.

Predisposing Factors

Host-Lack of eye pigmentation, age

Environmental:

- High solar radiation.

- Dusty conditions.

- Flies.

- Physical irritation by foreign bodies

Clinical findings

 Cornea was cloudy with a bluish-grey discolouration .

 Central Ulceration of cornea.

 Congested and inflamed conjunctiva

Control

 Prompt treatment.

 Fly control (hygiene, tags).

 Isolation (sick, age-groups).

 Pasture management (long grass, dust).

 Eye flaps.

CONTAGIOUS BOVINE PLEUROPNEUMONIA (CBPP)

Definition: Contagious bovine pleuropneumonia (CBPP) is a highly infectious acute, subacute, or

chronic disease, primarily of cattle, affecting the lungs and occasionally the joints, and caused by
Mycoplasma mycoides mycoides.

Transmission

❖ Contagious bovine pleuropneumonia is spread by inhalation of droplets from an infected,

coughing animal.

❖ Consequently, relatively close contact is required for transmission to occur.

❖ Outbreaks usually begin as the result of movement of an infected animal into a naive herd
CLINICAL SIGNS

▪ fever up to 41.5°C

 Anorexia and painful, difficult breathing.

 Head lowered and extended

 Percussion of the chest is painful, respiration is rapid, shallow, and abdominal.

 The disease progresses rapidly, animals lose condition, and breathing becomes very labored,
with a grunt at expiration.

 Animals are inclined to stand with elbows abducted in an attempt to decrease thoracic pain
and increase chest capacity.

 The animal becomes recumbent and dies after 1–3 wk.

PATHOLOGY:

 There is usually extensive and marked inflammation of the lung.

 There is consolidation, or thickening, of individual lobules,

 Thoracic cavity may contain up to 10 L of clear yellow or turbid fluid mixed with fibrin flakes

 In severe cases there can be abundant fluid in the thoracic cavity.

 The organs in the thorax covered by thick deposits of fibrin.

 The disease is largely unilateral, with more than 80%–90% of cases affecting only one lung.

 DIAGNOSIS

 Based on clinical signs and the characteristic gross pathologic lesions of the lungs

CONTROL

 Vaccination, quarantine, blood testing, and slaughter

Contagious caprine pleuropneumonia

• Contagious caprine pleuropneumonia is a highly fatal disease that occurs in goats

AETIOLOGY

 Mycoplasma capricolum capripneumoniae (Mycoplasma biotype F38)

 Transmitted by infective aerosol.

CLINICAL SIGNS

 Weakness

 Anorexia
  Cough

 hyperpnea

 nasal discharge accompanied by fever (104.5°–106°F [40.5°–41.5°C])

 Exercise intolerance progresses to respiratory distress with open-mouth breathing and frothy
salivation.

PATHOLOGY

 Excess of straw-colored pleural exudate and acute fibrinous pneumonia.

 Consolidation is sometimes confined to one lung just like in CBPP

DIAGNOSIS

 Clinical signs, epidemiology, and necropsy findings

 Culture of causative organism

 PCR

 Serologic tests are complement fixation, passive hemagglutination, and ELISA

CONTROL

 Quarantine of affected flocks.

 Vaccination

VIRAL DISEASES OF DOMESTIC ANIMALS

Foot and Mouth Disease

Definition:An extremely contagious acute disease of all cloven footed animals, caused by a virus
and characterized by fever and vesicles in the mouth, feet and teats

Etiology

• Family: Picornaviridae
Genus: aphthovirus
• Virus has 7 serotypes: A, O, C, SAT1, SAT2, SAT3 (South African territories) and ASIA type1
from the far East
Types A,O,C occur in all continents;
SAT1 is found in Africa and Asia
SAT2 and SAT3 occur in Africa.
Asia type 1 Asian continent

Spread from herd to herd

 • Directly by movement of infected animals
• Indirectly by inanimate objects: uncooked and unprocessed meat products and other
animal products
• Flash pasteurization does not inactivate the virus
• Infection also through infected semen during AI

Clinical findings

• Precipitate fall in milk production, high fever (40-41C) accompanied by severe dejection,
anorexia and acute painful stomatitis
• Abundant salivation with saliva hanging in long ropey strings, careful chewing and a
characteristic smacking of the lips
• Vesicles and bullae (1-2mm) appear on buccal mucosa, dental pad and tongue
• Vesicles may also appear on teats Vesicles on teat orifice lead to development of mastitis
• Abortion and this may be followed by infertility
• The animal resumes eating in 2-3 days but convalescence can take up to 6 months

Diagnosis

• any tentative diagnosis reported to director of vet services (DVS) immediately

Epidemiology
Clinical signs especially hypersalivation, vesicles/ulcers in mouth, feet and teats
Laboratory diagnosis
Microplate CFT which gives results in 24hrs
Virus infection associated test (VIAT): detects non- viral antibody in infected and recovered
animals. Important for imported animals
Other serological tests: plaque reduction neutralization test, Radial immunodiffusion, serum
neutralization test (SNT) and ELISA

Control

• Vaccination
• Eradication

Rinderpest

Rinderpest (RP) is a contagious viral disease of cattle, domestic buffalo, and some species of
wildlife. It is characterized by fever, oral erosions, diarrhea, lymphoid necrosis, and high mortality.

Etiology

Rinderpest virus (RPV) is a single-stranded RNA virus in the family Paramyxoviridae, genus
Morbillivirus

Transmission
RP is transmitted by direct and indirect (contaminated ground, waters, equipment, clothing)
contact with infected animals; aerosol transmission is not a significant means of transmission (it
occurs only in a confined area and over a short distance). A major reason RP spreads in Africa is
that the herds are nomadic.

Clinical findings

RP can appear as a peracute, acute, or mild infection

◼ Peracute Form

This form is seen in highly susceptible and young animals. The only signs of illness are a fever of
104-107o F (40-41.7o C), congested mucous membranes, and death within 2 to 3 days after the
onset of fever

Acute or classic form

This form of the disease progresses as follows:

◼ Small amounts of virus may be in nasal and ocular secretions before the onset of fever
◼ Fever of 40-41.1o C
◼ Serous to mucopurulent ocular discharge
◼ Serous to mucopurulent nasal discharge.
◼ Anorexia
◼ Constipation
◼ Oral erosions — Salivation may be abundant and frothy
◼ Diarrhea — May be very watery or hemorrhagic, or both -arched back

Diagnosis

• Clinical signs
• Pm lesions
• Lab diagnosis

Control

Kenya has managed to eradicate the disease through vaccination

RABIES

Introduction

• Rabies comes from Latin word rabidus = mad.

• It is a highly fatal disease of humans and other warm blooded animals.
 • For centuries, the dramatic nature of the clinical signs and symptoms and the invariable fatal
outcome of the infection has been recognized.
• Importance - Rabies is not of major economic importance in farm animals though individual herds
may suffer fatalities. The main importance of rabies is its transmissibility to humans with
invariably fatal consequences if post exposure vaccination is not done. Most human cases result
from contact with/bites from rabid domestic animals and the disease is an occupational hazard
for veterinarians.
• According to a W.H.O. report (1987), Dogs were responsible for 91 % of all human cases, cats-2%,
bats – 2%, other domestic animals 3% and other wild animals < 1%.
Aetiology

• Rabies is caused by a virus in the family Rhabdovirus, Genus Lyssavirus (Lyssa = Greek for rage)
• Other genera in this family are Ephemervirus-Ephemeral fever and Vesiculovirus (Vesicular
stomatitis)
• Members of the genus Lyssavirus are Rabies virus-Lyssavirus genotype I. The rabies related
viruses are
1. Lagos bat virus- Lyssavirus genotype I
Affect bats, shrews and
2. Makola- Lyssavirus genotype II rodents in Africa
3. Duvenhage- Lyssavirus genotype III
4. European bat Lyssavirus 1- Lyssavirus genotype V
5. European bat Lyssavirus 2- Lyssavirus genotype VI
6. Australian bat Lyssavirus
• A Nigerian equine encephalitis virus has recently been identified as rabies virus.
• The genetic relationships between the different species are important because they are reflected
in antigenic relationships e.g. rabies vaccine does protect against Duvenhage, European bat and
Australian bat Lyssaviruses.
• Fixed rabies virus-strains adopted to secondary hosts for experimental purposes. Their biological
behaviour is reproducible and is characteristic of the strain.
• Street rabies virus – stains isolated from naturally infected warm blooded animals.
• Different strains of the virus will produce either the paralytic or the furious form of rabies.
Epidemiology

Occurrence
 • Rabies occurs in most countries except Island nations which are able to exclude it through rigid
quarantine measures or prohibition of entry of dogs.
• The disease has never been reported in Australia or New Zealand. Britain, Hawaii and the
Scandinavian countries are currently free of the disease.
• Several Western European countries are on the verge of eradicating the disease; however; they
all have B.A.L.V. Bats (Vampire, fruit and insectivorous) are normally symptomless carriers of the
virus. The virus can multiply in their fatty tissue without invasion of the nervous system and is the
basis of their “resovoiring” mechanism. The migtratory habits of bats, also helps to introduce the
virus to new areas.
• In the rest of the world, rabies is endemic but there are marked variations in the prevalence and
the host species affected.
NB> The disease is poorly reported and under-monitored in most countries.

• Rabies in most countries has a domestic and a sylvatic cycle. In Kenya and Tanzania, dog rabies is
endemic in both domestic and wild populations. Other important species of affected animals are
cats and the mongoose.
Transmission

• Rabies is ordinarily transmitted by bites from an infected-susceptible host.

• Factors that determine successful transmission are
1. The dose
2. the route of administration
3. the biotype of the virus
4. susceptibility of the recipient
• The occurrence and concentration of the virus in saliva varies with the biotype and the host
species.
1. > 80% salivary gland infection – cattle, kudu and black backed jackal
2. 20-74% in natural and experimental dog cases
3. 70-80% Cats
• The virus is present in saliva from 13 days before onset of clinical signs and may terminate 2 days
before death.
• The susceptibility to the virus varies with the host species
1. Extremely susceptible-Foxes, coyotes and jackals
 2. Highly susceptible-Skunks, raccoons, cats, cattle, mongoose and rodents
3. Moderately susceptible-Dogs, sheep, goats, horses and primates
4. Low susceptibility-Opossums
N.B. This is based on epidemiological data and not laboratory experiments.

• The outcome of potential exposure to infection is also influenced by the severity, location and
multiplicity of the bites inflicted on the victim. Bites on the head and neck are associated with short
incubation periods and the highest mortality rates.
• The other modes of transmission are
1. Oral-Through milk (reported in a lamb and human baby), cannibalism, scavenging and predation
have been reported in the wild.
2. Aerosol transmission-in bat caves or when a susceptible host is in close proximity with a rabid
animal.
3. Transplacental infection.
4. Tissue transplants
5. Skin wound contamination with fresh virus laden saliva.

Pathogenesis

• The sensory nerve endings of the epithelial and subepithelial tissues of the skin and mucus
membranes provide a portal of entry of rabies virus into the nervous system.
• In most species, oral infection is aided by the presence of superficial wounds on the mucus
membranes.
• After deep introduction through a bite, the virus enters the nervous system through the
neuromuscular spindles or motor end plates.
• In the olfactory end organ in the nares, the neuroepithelial cells are in direct contact with the body
surface the cells extend directly to the olfactory bulb in the brain.
• The virus spreads passively to the spinal cord through axons and dendrites then enters the brain. The
immune response during this phase of the disease is minimal hence there is no production of
neutralizing antibody and infiltration by inflammatory cells is absent at the onset of clinical signs.
Antibodies are only detectable in the terminal stages.
• In the spinal cord, there is an ascending wave of neuronal infection and destruction which results in
signs of paresis/paralysis. When the virus reaches the brain, it irritates the higher centers leading to
signs of mania, excitement and convulsions.
• After this, there is centrifugal virus spread to non-neural cells; however, salivary gland infection
coincides with the period of widespread dissemination of the infection to the brain.
• Involvement of the autonomic nervous system and endocrine glands leads to signs of hypersalivation,
indigestion, pica, paralysis of the urinary bladder and anus as well as increased libido (bulls mount
inanimate objects).
• “Virus induced wasting” may explain the cachexia and failure to thrive in infected animals even before
overt clinical signs. It is mainly due to excess cortisol production and impaired growth hormone
production.
• Death will normally result from respiratory failure.

Clinical signs

• Clinical signs of rabies are rarely definitive.

• Rabid animals of all species exhibit typical signs of CNS disturbance, with minor variations among
species.

• The most common findings are

1. acute behavioral changes and
2. unexplained progressive paralysis.
• Behavioral changes include
- sudden anorexia
- signs of apprehension or nervousness
- irritability and
- hyperexcitability (including priapism).
- The animal may seek solitude.
- Ataxia
- altered phonation and excessive bellowing in cattle
 - Changes in temperament such as uncharacteristic aggressiveness may develop or an aggressive
animal becomes docile.
- Rabid wild animals may lose their fear of humans, and species that are normally nocturnal may
be seen wandering about during the daytime.
- The clinical course may be divided into 3 phases
1. prodromal
2. excitative and
3. paralytic/endstage.
- This division is of limited practical value because of the variability of signs and the irregular
lengths of the phases.
- Prodromal phase - which lasts ~1-3 days. Animals show vague CNS signs, which intensify rapidly.
The disease progresses rapidly after the onset of paralysis, and death is virtually certain. Some
animals die rapidly without marked clinical signs.
- Excitative phase - The term “furious rabies” refers to animals in which aggression (the excitative
phase) is pronounced.
- “Dumb or paralytic rabies” refers to animals in which the behavioral changes are minimal, and
the disease is manifest principally by paralysis.
Furious Form

- Is the classic “mad-dog syndrome,” although it may be seen in all species.

- There rarely evidence is of paralysis during this stage.
- The animal becomes irritable and, with the slightest provocation, may viciously and aggressively
use its teeth, claws, horns, or hooves. The posture and expression is one of alertness and anxiety,
with pupils dilated and conjuctiva congested.
- Noise invites attack. Such animals lose caution and fear of other animals.
- Carnivores with this form roam extensively, attack other animals, including people and any
moving object.
- They swallow foreign objects, eg, feces, straw, sticks, and stones. Rabid dogs may chew the wire
and frame of their cages, breaking their teeth, and will follow a hand moved in front of the cage,
attempting to bite.
Cattle
 - Cattle with furious rabies can be dangerous, attacking and pursuing humans and other animals.
Lactation ceases abruptly in dairy cattle. The usual placid expression is replaced by one of
alertness. The eyes and ears follow sounds and movement. A common clinical sign is a
characteristic abnormal bellowing, which may continue intermittently until shortly before death.
- Young pups can seek human companionship and are overly playful, but bite even when petted,
usually becoming vicious in a few hours.
- Rabid skunks may seek out and attack litters of puppies or kittens. Rabid domestic cats and
bobcats can attack suddenly, biting and scratching viciously. As the disease progresses, muscular
incoordination and seizures are common. Death results from progressive paralysis.
Paralytic Form:

- This is first manifest by paralysis of the throat and masseter muscles, often with profuse salivation
and inability to swallow.
- Dropping of the lower jaw is common in dogs. Owners are often tempted to examine the mouth
of dogs and livestock searching for a foreign body or administer medication with their bare hands,
thereby exposing themselves to rabies.
- These animals may not be vicious and rarely attempt to bite. The paralysis progresses rapidly to
all parts of the body, and coma and death follow in a few hours to days.
- They also present with signs of anaesthesia.
Horses and donkeys

- They commonly present with signs of distress and extreme agitation. They may be accompanied
by rolling and confused with colic.
- As in other species, horses may bite or strike viciously and, because of their size and strength,
become unmanageable in a few hours. People have been killed by such animals and these animals
suffer self-inflicted wounds.
- Rabid wild canines often invade homes attacking dogs and people. They may attack porcupines
and finding a canine with porcupine quills can sometimes support a diagnosis of rabies.
Diagnosis

• No ante-mortem laboratory examination tests are of diagnostic value.

• Tests can however be done on urine, feaces and blood to rule out lead poisoning.
• Confirmatory diagnosis can be achieved through laboratory examination of fresh brain
Dogs and other animals presenting with signs of rabies are kept in strict isolation for 10 days. Those that
die are submitted for post-mortem examination. The tests carried out include

a) fluorescent antibody test on brain tissue especially the hippocampus, medulla oblongata, cerebellum
or Gasserian nucleus. The test is very accurate. This test can also be used on spinal cord and salivary gland
tissue if brain tissue is not available.

b) Histological examination of brain tissue to screen for Negri bodies in the nucleus of neurons.

c) Intracerebral inoculation of weaned mice with suspect brain tissue. The incubation period is 11-12 days
and death occurs 7-21 days later. The mouse brain is then harvested for the above tests.

Differential diagnosis

There are many diseases in animals that present with signs of abnormal mental state and/or paralysis.
Any such animals should be handled with extreme caution.

Cattle –

1. acute lead poisoning - blindness, convulsions and jaw champing with production of frothy saliva and
twitching of eyelids and ears. There is hyperaethesia.
2. subacute lead poisoning – blindness, stupor, head pressing, teeth grinding and no response to
treatment. There is hyperaesthesia
3. lactation tetany and hypovitaminosis A – get convulsions but no mania.
4. Polioencephalomalacia – blindness, Nystagmus, Opisthotonus and convulsions but hypersalivation,
anaesthesia and tenesmus are not present.
5. listeriosis- has circling and facial nerve paralysis.
6. tetanus- has hyperaesthesia.
7. Nervous form of acetonaemia
8. Other conditions with sialorrhoea
Sheep-

1. Clostridial enterotoxaemia-confined to lambs

2. Tetanus
 3. Pregnancy toxaemia
Pigs-

• Psuedorabies, teschen disease, meningitis (Streptococcus suis type II and Hemophilus spp.),
Glasser’s disease, E. coli septicaemia and Erysipelas.
Horses

• Western equine encephalitis, Eastern equine encephalitis, Venezuelan equine encephalitis and
Japanese encephalitis.
• Herpes virus encephalitis – equine viral rhinopneumonitis
• Hepatic encephalopathy caused by toxic plants such as Senecio ane Clotalaria spp.
• Toxoplasmosis and lead poisoning.
• Cerebellar hypoplasia of Arabian and Swedish Gotland horses.
• Tetanus and botulism.
• Epilepsy.
Dogs-(read)

Treatment

• No treatment should be attempted after clinical signs are evident.

• Immediately after exposure to infection, the wound should be irrigated with copious amounts of
water with soap solution, zepharine or iodine.
• Immediate postexposure vaccination of exposed animals.
• Euthanasia is debatable since one needs the disease to establish and fully develop to enable a
diagnosis.

Control

• Two basic methods are used in farm animals

1. prevention of exposure – This is done by destruction of wild fauna that contain the virus. In the
west, foxes which account for a large proportion of wildlife rabies are annually culled thus the
prevalence of disease is reduced due to lack of a multiplying host. However, this is against most
animal welfare regulations. Restraint and control of the domestic dog population is paramount.
2. Vaccination
 • Mass oral vaccination of terrestrial wild animals offers better hope than culling. The ERA strain
of virus is used since it offers better protection (3 years in cattle and 2 yrs in horses and dogs) than
the H.E.P. Flurry strain.
• In endemic areas, it is recommended that all animals at risk especially dogs and cats are
vaccinated annually. Vaccinated cows pass the antibodies through colostrum and the calves are
1st vaccinated at 6 months, repeated at 10 months then annual boosters.
• Calves from unvaccinated cows are 1st vaccinated at 17 days of age.
• In rabies free countries, dogs are quarantined for 4-6 months and vaccinated

LUMPY SKIN DISEASE

Definition: Lumpy skin disease (LSD) is an acute to chronic viral disease of cattle characterized by
skin nodules that may have inverted conical necrosis (sitfast) with lymphadenitis accompanied by
a persistent fever.

Etiology

The causative agent of LSD is a capripoxvirus.

Host Lumpy skin disease is a disorder of cattle

Transmission

Biting insects play the major role in the transmission of LSDV

Clinical signs

A fever 40-41.5o C can occur and can be transitory or last up to 4 weeks. Generally within 2 days
after the appearance of the fever, swellings or nodules 1 to 5 cm in diameter appear in the skin
and generalization occurs

Depression, anorexia, excessive salivation, oculonasal discharge, agalactia, and emaciation are
presented.

As the disease progresses, the nodules become necrotic, and eventually a deep scab forms; this
lesion is called a sitfast

Secondary bacterial infection can complicate healing and recovery

animals can become lame and reluctant to move

Abortion may occur as the result of prolonged fever.

Diagnosis

A tentative diagnosis of LSD can be made based upon clinical signs. A contagious disease with
generalized skin nodules having a characteristic inverted conical necrosis of skin nodules (sitfast),
persistent fever, emaciation, and low mortality suggests LSD

Control and eradication

▪ The most likely way for LSD to enter a new area is by introduction of infected animals.
Biting insects that have fed on infected cattle may travel and be blown for substantial
distances. It is likely that LSD spread to Israel via contaminated insects blown across the
Sinai Desert (21). The movement of contaminated hides represents another potential
means for this resistant virus to move.
▪ If LSD is confirmed in a new area before extensive spread occurs, the area should be
quarantined, infected and exposed animals slaughtered, and the premises cleaned and
disinfected. Vaccination of susceptible animals within the quarantine should be
considered.
▪ If the disease has spread over a large area, the most effective means of controlling losses
from LSD is vaccination. However, even with vaccination, consideration still should be
given to eliminating infected and exposed herds by slaughter, proper disposal of animals
and contaminated material, and by cleaning and disinfecting contaminated premises,
equipment, and facilities.
▪ In South Africa, the control of insects was not effective in preventing the spread of LSD,
but current insecticides together with repellents aid in the prevention of the spread of
LSD.

RIFT VALLEY FEVER (Epizootic hepatitis

RiftValleyfever (RVF) is a peracute or acute, mosquito-borne, zoonotic disease of domestic and

wild ruminants in Africa usually associated with heavy rainfall and localized flooding

AETIOLOGY: Phlebovirus in the Bunyavirus family

Transmission

Mosquito is the vector

• People are readily infected through blood aerosols from infected animals during
slaughter, or by exposure to infected animal tissues, aborted fetuses, mosquito bites, and
laboratory procedures

CLINICAL SIGNS:

• Listlessness, Anorexia

• Abdominal pain, Rapid Respiration

 • Melena or fetid diarrhoea

• Blood tinged mucopurulent nasal discharge

• Icterus

• Pregnant animals may abort at any stage of pregnancy and the aborted foetuses are
usually autolysed

DIAGNOSIS:

• The occurrence of abortion on a mass scale after heavy rainfall and flooding

• Clinical signs

• Post mortem lesions

• ELISA in virus isolation

CONTROL: Immunization remains the only effective way to protect livestock from RVF

NAIROBI SHEEP DISEASE

Definition: Nairobi sheep disease (NSD) is a noncontagious, tick-borne, viral infection of sheep
and goats characterized by hemorrhagic gastroenteritis and high mortality

Etiology and transmission

Nairobi sheep disease virus (NSDV) is transmitted primarily by the brown tick, Rhipicephalus
appendiculatus. The causative agent is an RNA-containing virus having structural and chemical
characteristics common within the Bunyaviridae viruses . However, it is antigenically independent
of this group but is closely related to the Ganjam virus of goats in India. Ganjam virus is
antigenically related to Dugbe virus isolated from cattle in west Africa. A new genus, Nairovirus,
has been proposed for these three viruses

Distribution

Nairobi sheep disease is usually confined to countries in east Africa, where the principal vector,
R. appendiculatus, is endemic. The disease has been reported most frequently in Kenya in Kikuyu
country between Nairobi and Mount Kenya as well as in Uganda, Tanzania, and Somalia.

Clinical findings

Nairobi sheep disease is characterized by an acute hemorrhagic gastroenteritis (17). Clinical signs
of NSD begin with a temperature rise to 40 to 41° C (104 to 106° F) and, during this stage, a
prominent clinical depression develops followed by a temperature decline and diarrhea. There is
an abundant mucopurulent nasal discharge, and breathing may become rapid and painful
Field Diagnosis

An outbreak of NSD is nearly always associated with movement of susceptible animals into an
endemic area where R. appendiculatus is abundant. When recently introduced small ruminants
become ill with signs of severe enteritis and nasal discharge within an NSD

SHEEP AND GOAT POX

Definition

➢ Sheep and goat pox (SGP) is an acute to chronic disease of sheep and goats characterized
by generalized pox lesions throughout the skin and mucous membranes, a persistent
fever, lymphadenitis, and often a focal viral pneumonia with lesions distributed uniformly
throughout the lungs. Subclinical cases may occur.

Etiology

➢ The virus that causes SGP is a capripoxvirus, one of the largest viruses (170-260 nm by
300-450 nm) . It is closely related to the virus that causes lumpy skin disease; SGP virus
and lumpy skin disease virus cannot be distinguished serologically. There is only one
serotype of SGP virus (SGPV). Various strains of SGPV cause disease only in sheep, others
only in goats, and some in both sheep and goats.
➢ The SGPV is very resistant to physical and chemical agents.

Transmission

Contact is the main means of transmission of SGPV. Inhalation of aerosols from acutely affected
animals, aerosols generated from dust contaminated from pox scabs in barns and night holding
areas, and contact through skin abrasions either by fomites or by direct contact are the natural
means of transmitting SGPV

Clinical findings

The first signs may include fever, depression, conjunctivitis, lacrimation, and rhinitis. Within a few
days of the prodromal signs, pox lesions develop in the skin. These are more easily observed on
the wool-free or hair-free parts of the body such as the perineum, inguinal area, scrotum, udder,
axilla, and muzzle. Lesions do occur in wooled or haired skin. Generally, more severe (extensive)
skin lesions correlate with more severe illness. The skin lesion first appears as an erythematous
area (macula).

➢ Field Diagnosis
➢ A tentative diagnosis of SGP can be made on the basis of clinical signs consisting of skin
lesions, which on, palpation involve the whole thickness of the skin, a persistent fever,
lymphadenitis, and often pneumonia; mortality may approach 50 percent in adults and
95 percent in lambs and kids under 1 month of age.
Control-vaccination

FUNGAL DISEASES OF DOMESTIC ANIMALS

MYCOTIC DERMATITIS

 This is the infection of the epidermis with lesions characterized by exudative dermatitis
with scab formation.
 It is seen in a wide host range, and among domestic animals, cattle, sheep, goats, and
horses are affected most frequently, and pigs, dogs, and cats rarely.
 It is commonly called STREPTOTHRICOSIS in cattle, goats, and horses; in sheep, it is
termed LUMPY WOOL when the wooled areas of the body are affected

AETIOLOGY: The proper name of the disease is DERMATOPHILOSIS and it is caused by a fungus
called Dermatophilus congolensis

CLINICAL SIGNS:

 Pruritus
 Hairs matted together
 Crust or scab formation
 Chronic lumpy wool infections are characterized by pyramid-shaped masses of scab
material bound to wool fibers.

DIAGNOSIS:

 Clinical signs
 Demonstrating the organism in cytologic preparations, isolation via culture, and/or via
skin biopsy
 >ZOONOTIC RISK: Direct contact with an infected animal can lead to infections on the
hands and arms.

PRODUCTION DISEASES

• The term "Production Diseases" referred traditionally to those diseases induced by

management practices, metabolic diseases being typical examples

• Recently, "Production related diseases" have been enhanced to include other traits, such
as infertility, and diseases such as mastitis and lameness (laminitis), retained placenta that
might involve infectious agents but exacerbated by nutritional or managemental factors.

PARTURIENT PARESIS

Other names: milk fever, parturient hypocalcaemia, post-parturient hypocalcaemia

ETIOLOGY
 • Decrease in ionized plasma Ca to below 5mg/dl (normal 9.5mg/dl)
• Due to failure to mobilize enough Ca from bones, loss of Ca in colostrum i.e. increased
demand for Ca

EPIDEMIOLOGY

• Occurs in high yielding cows usually in the 5-10 years age group (peak production,
impaired Ca metabolism –bone resorption, GIT absorption)
• Has sporadic occurrence (incidence in some farms may be 25-30%)
• 70-80% of cases are not complicated
• Complications: aspiration pneumonia, mastitis, limb injuries
• Jersey cows are most susceptible
• Common in certain families of a particular breed
• Occurs in three stages of lactation - prepartum, parturient and postpartum

Risk factors

• Diet high in Ca and low P in the dry period

• Over-steaming with high proteins and carbohydrate diet (obese animals)
• High (negative) cation-anion difference (Na+K)- (Cl- +SO4) i.e. need more anions
• Increasing age of the cow
• Alimentary stasis
• Genetic predisposition (breed)
• Complete stripping 48hrs postpartum
• High poultry manure feeding (>30% dry wt)

Clinical findings

• Has three stages –

1. Excitement
2. Sternal recumbency and
3. Lateral recumbency

Diagnosis

• History
• Clinical signs – recumbency, kinking of the neck, dry muzzle, starring of the eyes, dilated
pupils, hypothermia, cold extremities, reduced intensity of heart sounds
• Response to Ca treatment
• Blood chemistry

CONTROL OF PARTURIENT PARESIS

• Low Ca (20g/day) high P diet pre-partum

• Controlled steaming up (no obesity)
• Feeding feeds mixed with NH4Cl
 • CAD (= cation-anion difference) of about minus 50-100 meq/kg diet
• Injection of Vit. D and Vit. metabolites
• Oral CaCl2 several days before date of calving and 1to 2 days after calving
• Injection of PTH – IM or IV
• Limited milking (in susceptible cows)
• Selecting of animals that are less susceptible to milk fever
• Ca injection at calving followed by high Ca diet

KETOSIS

• Other names; Acetonemia, Post-parturient dyspepsia

• Definition – typical production disease

Etiology

• Increased demand for glucose

• Hypoglycaemia
• Accumulation of keto-acids (acetone, acetoacetic, β-hydroxybutyric acids)

Epidemiology

• Most common 20-30 days after calving in high yielding cows

• Incidence peaks 5th – 6th lactation
• Common in certain individuals (genetic)
• Vague and non-specific clinical signs

Risk factors

• Wet silage with high butyric acid content

• Over-fatness at calving
• Inadequate energy intake in early lactation
• Factors that reduce appetite (e.g. diseases)
• High milk production
• Mineral deficiencies – Co, P
• Dental deformities e.g. due to Fluorosis
• High protein diet (>20% dry matter)
• Interruption of normal routine and access to feed in early lactation

Clinical findings

Two forms:

• Digestive form – loss of appetite, rapid loss of body wt., ↓milk production, firm and dry
faeces, rough hair coat, acetone smell in breath and milk
• Nervous form – sudden onset of nervous signs; circling, head pressing, apparent
blindness, wandering, pica (licking), hypersthesia, bellowing, moderate tremors and
tetany, may be aggressive behaviour
Diagnosis

• Epidemiology – recent calving, high producing cow,

• Clinical signs
• Clinical pathology
• Elimination of similar diseases

Control

• Feeding in the dry period

• Feeding in early lactation
• No interruption to normal routine and access to feed
• Mineral supplementation
• No feeding on wet silage with butyrate content, mouldy or dusty
• Feeding of sodium propionate

LACTATION TETANY

Other Names: Hypomagnesaemic tetany, Grass tetany, Wheat pasture poisoning disease

Definition: highly fatal metabolic disease of ruminants due to low plasma Mg levels
(hypomagnesaemia)

Epidemiology

• Occurs world-wide
• Most common in cattle 4-7 years
• Incidence highest in first 2 months after calving (lactating cows →lactation tetany)
• Incidence high in animals grazing on lush grass pastures (grass tetany)
• Incidence high in animals on cereal crops (wheat pasture poisoning)

Risk factors

• Partial or complete starvation

• Heavy fertilization of pastures with nitrogenous and potassium fertilizers
• Excessive dietary Ca intake
• Feeding of highly proteinous feeds
• Mg chelating agents e.g. ketobutyric acid, citrate

Etiology

• Hypomagnesaemia - low Mg levels in the in plasma and CSF

Clinical signs

There are Four forms

1. Peracute form – No clinical signs are observed, affected animals are found dead where they
collapsed in tetany

2. acute form

Sudden onset of neurological signs

• Affected animal becomes restless and separates from the herd, stops feeding, suddenly
walks or runs for no apparent reason, adopts a posture of unusual alertness
• Twitching of muscles and ears, hyperaesthesia, staggering gait, falling down with tetany
of the limbs, clonic convulsions, opisthotonus, nystagmus, champing of the jaws,
frothing at the mouth, retraction of the eyelids, temp 40-40.5oC, ↑intensity of heart
sounds

3.Subacute form

Gradual onset of clinical signs (3-4 days)

• Slight anorexia, exaggerated limb movement, wild facial expression, spasmodic

urination and frequent urination, mild tetany, muscle tremors of the hind limbs,
unsteady gait, sudden stimulation can lead to violet convulsions, animal may become
recumbent or recover spontaneously,

4 chronic form

There are no obvious clinical signs

• Few animals may show signs of dullness, unthriftness, decreased milk production, mild
signs of tetany and indifferent appetite

Diagnosis

• History
• Clinical signs – nervous signs (incoordination, hypersthesia, tetany)
• Blood chemistry - ↓ Mg and Ca levels

Control

• Oral dosing with Mg to animals at risk

• Dry or cured hay before going to lush pastures
• Incorporation of legume into tetany prone pasture
• Limited application of potash fertilizers to pastures
• Increasing Mg content of pastures (dusting of pastures with finely ground MgO 2)
• Mg alloy bullets to animals that are at risk
VIRAL POULTRY DISEASES

NEWCASTLE DISEASE

 Newcastle disease is an infection of domestic poultry and other bird species with virulent
Newcastledisease virus (NDV).

 It is a worldwide problem that presents primarily as an acute respiratory disease, but

depression, nervous manifestations, or diarrhea may be the common clinical form.

AETIOLOGY: Newcastle disease virus, NDV, synonymous with avian paramyxovirus serotype 1 (PMV-1)

 Virulent NDV strains are endemic in poultry in most of Asia, Africa, and some countries of
North and South America

4 serotypes

 virulent Newcastle Disease

 Mesogenic

 Velogenic neurotropic

 Velogenic viscerotropic

TRANSMISSION:

 Infected birds shed virus in exhaled air, respiratory discharges, and feces.

 Virus may also be present in eggs laid during clinical disease and in all parts of the carcass
during acute NDV infections.

 Chickens are readily infected by aerosols and by ingesting contaminated water or food.

 Movement of infected birds and movement of people and contaminated equipment or litter
are the main methods of virus spread between poultry flocks.

CLINICAL SIGNS:

 Respiratory signs of gasping, coughing, sneezing, and rales predominate.

 Nervous signs of tremors, paralyzed wings and legs, twisted necks, circling, clonic spasms, and
complete paralysis may occur.

 Digestive signs- greenish diarrhoea

DIAGNOSIS:

 Clinical signs, especially respiratory signs and twisting neck

  NDV can be isolated from oropharyngeal or cloacal swabs or tissues from infected birds

PREVENTION: Vaccination via the nares or conjunctival sac.

 Healthy chicks are vaccinated as early as day 1–4 of life.

MAREKS DISEASE

 Marek's disease is one of the most ubiquitous avian infections; it is identified in chicken flocks
worldwide.

 Occasionary it affects quails, gamefowls and turkeys

 >ETIOLOGY: caused by herpes virus .

 Normally infect young birds (12-25weeks)

TRANSMISSION:

The disease is highly contagious, can occur through the air (aerosal route) within poultry house

CLINICAL SIGNS:

 Typically, affected birds show only depression before death,

 lameness

 Transient paralysis syndrome and neurologic signs have been associated with Marek's disease

PATHOLOGY:

Enlarged nerves are one of particularly the vagus, brachial, and sciatic.

Diffuse or nodular lymphoid tumors may be seen in various organs, particularly the liver, spleen,
gonads, heart, lung, kidney, muscle, and proventriculus

DIAGNOSIS:

 It is important to diagnose the tumors and not the infection because Marek's disease is
considered ubiquitous within commercial poultry flocks

 Postmortem - enlarged nerves and lymphoid tumors in various viscera

 Use of PCR to identify the Marek’s virus

PREVENTION: Vaccination at hatching.

AVIAN LEUKOSIS COMPLEX/BIG LIVER/LYMPHOID LEUCOSIS

 Lymphoid leukosis has been the most common form of the leukosis/sarcoma group of
diseases seen in chicken flocks

 Chickens are the natural hosts for all viruses of the leukosis
  >AETIOLOGY: Alpharetrovirus

 Avianleukosis virus is shed by the hen into the albumen or yolk, or both, or can be transmitted
by contaminated faeces and vaccines.

Transmission

 Through vertical transmission

 Horizontal transmission through contact with contaminated environment

CLINICAL SIGNS:

 Palpation often reveals an enlarged bursa and sometimes an enlarged liver

 Affected birds are dull

 Bone maarow tumours make the bird form thickened bowed leggs

 Diffuse or nodular lymphoid tumors are common in the liver, spleen, and bursa and are found
occasionally in the kidneys, gonads, and mesentery

DIAGNOSIS:

 The tumorous involvement of the liver, spleen, or bursa in the absence of peripheral nerve
lesions as is the case with Marek’s disease

 PCR to detect and characterize avianleukosisvirus strains

CONTROL:

 Eradication of avian leukosis virus from primary breeding stocks is the most effective means to
control avianleukosis.

 Eggs from shedder hens are discarded, so that progeny flocks typically have reduced levels of
infection.

 All in and all out production