ANIP 3724

ANIMAL HEALTH

Leon Kruger
082 663 2664
[email protected]
 SECTION A
PRINCIPLES OF DISEASE DEVELOPMENT,
PREVENTION AND TREATMENT

Chapter 1: Livestock disease

pathogenesis and aetiology
 Why do animals get sick?
• Due to infections from pathogens ?
• Due to compromised immunity ?
• Due to poisonous plants ?
• Due to… Due to… Due to…
 Introduction
• Despite the immunisation (vaccination) of animals for diseases
for which there are efficient vaccines available some still get
sick and even die.
• Why? One reason may be because the animal does not have
adequate or specific immunity against the specific infectious
agent.
• There are many reasons why vaccination failed that will be
discussed later on in the course material.
 Introduction…
• There are diseases for which immunisation is not an option in
preventing the disease for example internal parasite infestation
and metabolic diseases.

• Despite our best efforts to prevent animal diseases, there will

always be individual animals or even flocks and herds (epidemic)
of animals that get sick.

• One has to understand the aetiology and pathogenesis of

infectious agents in order to understand animal diseases, whether
it has viral, bacterial, protozoal, parasitical or metabolic origin.
 Definitions
Pathogen: a bacterium, virus, or other microorganism that can
cause disease.
Disease: Any state of ill health where one or more parts of the
body do not function optimally and normally.
Epidemic: A widespread occurrence of an infectious disease in a
community at a particular time i.e. recent anthrax in Lesotho
Aetiology: The cause, set of causes, or manner of causation of a
disease or condition.
Pathogenesis: The pathogenesis of a disease is the biological
mechanism (or mechanisms) that lead to the diseased state.
 Viral disease pathogenesis
• Viruses are very small micro-organisms, only visible with an
electron microscope.
• Outside of an infected cell, viruses exist in the form of
independent particles.

Capripoxvirus Orbivirus Phlebovirus Aphtovirus

Lumpy skin disease Bluetongue Rift valley fever Foot and mouth disease
 Viral disease pathogenesis
Viruses consist of two or three
parts:
• The genetic material made from
either DNA or RNA, long
molecules that carry genetic
information;
• A protein coat, called the capsid,
which surrounds and protects the
genetic material
• In some cases an envelope of
lipids that surrounds the protein
coat.
 Successful viral infection of a host cell
depends on three requirements
(i) There must be sufficient viruses available to initiate the infection.
(ii) Host cells at the site of infection must be available and
susceptible.
(iii) The host’s anti-viral defence systems must be
compromised(stress), ineffective or absent (not vaccinated).

Lumpy skin disease Rift valley fever Bluetongue

 Mechanisms involved with viral disease
development
Implantation at Portal of Entry:
• The virus must implant at the entry portal into the body.
• Implantation is the earliest stage of pathogenesis.
• Implantation frequency is at its greatest where viruses have direct
contact to living cells.
• Virus implantation occurs frequently on cells of respiratory
(bluetongue, IBR), gastrointestinal (Rota,Corona,BVD), skin(lumpy
skin) and genital tissues (orf)

Foot and mouth disease

Mechanisms involved with viral disease
development
Local Replication and Local Spread
• Local replication and spread of the virus follows implantation.
• Replicated viruses from the initially infected cell has the capability to
disperse to neighbouring extracellular fluids or cells and in the
process can destroy, damage, or change the cells.
• Spread occurs by neighbouring cells being infected or the virus being
released into extracellular fluid.

Contagious ecthyma, (orf, scabby mouth, vuilbek)

Mechanisms involved with viral disease
development
Dispersal
• The replicated viruses must spread to target organs (disease
sites) throughout the body.
• The most common route of spread from the portal of entry is
the circulatory system, which the virus reaches via the
lymphatic system.
• Viruses can access target organs from the blood capillaries by
multiplying inside endothelial cells, moving through gaps, or
by being carried inside the organ on leukocytes.
• Some viruses, such as herpes, rabies and polio viruses, can
also disseminate via nerves.
Virus replication
 Mechanisms involved with viral disease
development
Shedding
• The viruses must spread to sites where shedding into the
environment can occur.
• The respiratory (coughing), alimentary (diarrhoea) and
urogenital (semen and vaginal fluids) tracts and blood are the
most common sites of virus shedding and distribution.

Contagious ecthyma (orf) Bovine: rabies Bovine viral diarrhoea

 Viruses are species specific with regard to disease
development.

Rabies virus

All mammals susceptible

 Viruses are species specific with regard to disease
development.
All cloven hoof
Foot and mouth animals susceptible
disease virus
 Viruses are species specific with regard to disease
development.

No clinical disease
development
Bluetongue virus

clinical disease
development
 Viruses are species specific with regard to disease
development.
Lumpy skin Bovine ephemeral
disease virus disease virus

Bovine viral diarrhoea virus

Viruses are species specific with regard to disease
development.

Orf virus

Zoonosis
Accidental
host
 Treatment and control
• No cure. Why not?
• Treatment only symptomatic i.e. pain, inflammation and fever
• Control only through vaccination in cases where vaccines exist
• Hygiene, stock control, quarantine and regular examination of
herd, stress free handling and husbandry will aid the
prevention or outbreak of viral disease.

• Proverbs 27:23
 Bacterial Disease Pathogenesis
Bacteria are very small organisms visible through a microscope
Bacillus anthracis Mannheimia haemolytica

Anthrax/ miltsiekte
Pasteurellosis/ bontlong
Clostridium perfringens Mycobacterium bovis

Bacterial culture on agar

plate

Enterotoxaemia/ bloednier Tuberculosis

Bacterial Disease Pathogenesis
• They are prokaryotic microorganisms with membranes (cell
wall) around them.
• They do not have a nucleus and most have no organelles.
• They do have DNA and function as independent organisms.
 Bacterial Disease Pathogenesis
• Bacterial infection results from a disturbance in the balance
between bacterial virulence and host resistance.
• Normal inhabitants become virulent due to favourable conditions i.e.
Lactobacillus plantarum in cases of acidosis
• Opportunistic inhabitants get opportunity due to immune suppression,
i.e. Mannheimia haemolytica causing lung infection
• Infection with no immunity, i.e. Clostridium botulinum causing botulism
• Multiplication is the main “objective” of bacteria, and in the case of
pathogenic bacteria it may cause diseases in the process.
 Bacterial Disease Pathogenesis
The virulence of bacteria relies
on certain factors:
(i) invasion of the host,
(ii) multiplication, and
(iii) evasion of host defences
 Virulence factors of bacteria
• Adherence Factors: Many pathogenic bacteria
colonize mucosal sites by using pili (fimbriae) to
adhere to cells.

• Invasion Factors: Surface components that allow

the bacterium to invade host cells can be encoded
on plasmids, but more often are on the
chromosome.

• Capsules: Many bacteria are surrounded by

capsules that protect them from opsonisation and
phagocytosis.
 Virulence factors of bacteria
• Endotoxins: The lipopolysaccharide endotoxins on Gram-negative
bacteria cause fever, changes in blood pressure, inflammation,
lethal shock, and many other toxic events.
 Virulence factors of bacteria
Exotoxins: Exotoxins include several types of protein toxins and
enzymes produced and/or secreted from pathogenic bacteria.
Major categories include cytotoxins, neurotoxins, and enterotoxins.
 Virulence factors of bacteria
Host Susceptibility
• After bacterial infection the host’s resistance rely on
phagocytic cells (white blood cells) and the immune system
to combat the infection.

• Initial resistance is due to nonspecific mechanisms.

• Specific immunity develops over time.
• The immune system will be discussed in more detail later on
the course.
 Virulence factors of bacteria
Host Resistance:
• The host possess physical and chemical attributes to protect it
against bacterial infection.
• This includes antibacterial factors in secretions covering
mucosal surfaces and rapid rate of replacement of skin and
mucosal epithelial cells.
SO PLEASE STOP THE UNCONTROLLED USE OF ANTIBIOTICS
Host-mediated Pathogenesis
• In some bacterial infections such as tuberculosis, tissue
damage develops from the toxic mediators released by
lymphoid cells rather than from bacterial toxins.
 Virulence factors of bacteria
Intracellular Growth
• Some bacteria such as Salmonella species invade cells but do
not require them for growth.
• Most pathogenic bacteria multiply in tissue fluids and not in
host cells.
 Conclusion
• Disease causing bacteria are referred to as pathogenic
bacteria.
• Many bacteria species are beneficial and necessary for
digesting food (gut flora or rumen flora in case of ruminants)
• Some are necessary for production of livestock fodder such
as silage.
• Most bacterial diseases can be treated with antibiotics, BUT
a diagnosis is required before it is used.
• Vaccination is the best method of controlling and prevention
of bacterial diseases.
 Definitions
Prokaryotes: The simplest living things such as bacteria. They
generally do not have a cell nucleus, nuclear membrane or cell
organelles.
Plasmid: A small, circular, double-stranded DNA molecule that is
distinct from a cell's chromosomal DNA. Plasmids naturally exist in
bacterial cells, and they also occur in some eukaryotes. Often, the
genes carried in plasmids provide bacteria with genetic
advantages, such as antibiotic resistance.
Virulence: The severity or harmfulness of a disease causing
organism.
Opsonisation: The process by which the pathogen is marked for
ingestion and eliminated by the phagocytes
 Definitions
Phagocytosis: The process by which certain living cells called
phagocytes ingests or engulfs other cells or particles.
Cytotoxin: a toxin or antibody having a specific toxic action upon
cells of special organs
Neurotoxins: Toxins that are poisonous or destructive to nerve
tissue.
Enterotoxin: A toxin produced in or affecting the intestines
Phagocytic cells: Any of various organisms or specialized cells that
engulf and ingest other cells or particles. In vertebrate animals,
phagocytes are white blood cells that break down bacteria and
other microorganisms, foreign particles, and cellular debris. These
include monocytes, macrophages, and granulocytes.
 Protozoal disease pathogenesis
• Protozoa are an extremely diverse group of microscopic
unicellular eukaryotic organisms.
• Most animals harbour one or more species of protozoa.
• Pathogenic protozoa has the potential to cause a wide
array of clinical diseases ranging from sub-clinical to life
threatening, depending on the species and strain of the
parasite and the resistance of the host.

Trichomonas spp. Eimeria spp. Babesia spp. Anaplasma spp. Ehrlichia spp. Theileria spp.
 Protozoal disease pathogenesis
They are generally divided into:

• Intestinal protozoa e.g. Eimeria crandallis

• Urogenital protozoa e.g. Trichomonas foetus

• Blood and tissue protozoa e.g. Babesia bigemina

 Protozoal disease pathogenesis
Virulence of pathogenic protozoa rely on:
(i) invasion of the host
Haematophagous vectors – ticks, stable flies

(ii) T

per os coitus
 Protozoal disease pathogenesis
Virulence of pathogenic Schizogeny
protozoa rely on:
(ii) Multiplication

Binary fission
 Protozoal disease pathogenesis
Virulence of pathogenic protozoa rely on:
(iii) evasion of the host defences
 Protozoal disease pathogenesis
The infection routes of parasitic protozoa vary between
the various protozoa species.
• Intestinal protozoa infection occurs via the oral route
for example Cryptosporidium parvum taken in with
contaminated water.

• Urogenital tract infection and transmission occur

during coitus for example Trichomonas foetus.

• Blood and tissue infection and transmission occurs via

blood inoculants, mostly by means of vectors
(haematophagous flies and ticks) feeding on the
mammal host, i.e. Babesia spp. Anaplasma spp.
 Protozoal disease pathogenesis
• The infection usually causes tissue damage to the mucosa (intestinal
and urogenital tract) and destruction of erythrocytes (blood).

• In chronic infections the tissue damage is often due to an immune

response and/or to host antigens as well as to changes in cytokine
profiles.
• Alternatively, it may be due to toxic protozoal products and/or to
mechanical damage.
 Protozoal disease pathogenesis
• Reproduction occurs through binary fission, an asexual way of
reproduction.
• Multiple asexual divisions occur in some forms.
• In protozoa species of the phylum: Apicomplexa, both sexual
(gametogony) and asexual (shizogony)reproduction occurs.
 Protozoal disease pathogenesis
Protozoal parasites possess various escape
mechanisms from the host’s immune system:
Antigenic Masking

• The protozoa parasite has the ability to escape

immune detection by covering itself with host
antigens.
 Protozoal disease pathogenesis
Protozoal parasites possess various escape
mechanisms from the host’s immune system:
Blocking of Serum Factors

• Some protozoa parasites acquire a coating of

antigen-antibody complexes or non-cytotoxic
antibodies that blocks the binding of specific
antibody or lymphocytes to the parasite surface
antigens.
 Protozoal disease pathogenesis
Protozoal parasites possess various escape
mechanisms from the host’s immune system:
Intracellular Location
• The intracellular habitat of some protozoa
parasites protects them from the direct
effects of the host's immune response. By
concealing the parasite antigens, this strategy
also delays detection by the immune system.
 Protozoal disease pathogenesis
Protozoal parasites possess various escape
mechanisms from the host’s immune system:
Antigenic Variation
• Some protozoan parasites change their
surface antigens during the course of an
infection.
• Parasites carrying the new antigens escape
the immune response to the original
antigens.
 Protozoal disease pathogenesis
Protozoal parasites possess various escape
mechanisms from the host’s immune system:
Immunosuppression
• Parasitic protozoan infections generally produce
some degree of host immunosuppression.
• This reduced immune response may delay
detection of antigenic variants.
• It may also reduce the ability of the immune
system to inhibit the growth of and/or to kill the
parasites.
 Protozoal disease pathogenesis
• Resistance of a host to defend it against protozoan
parasites involves three interrelated mechanisms:
• nonspecific factors
• cellular immunity
• humoral immunity

The physiology of immunity will be discussed later in the

course.
 Protozoal disease pathogenesis
Conclusion
• Protozoal infections can be treated with certain
antimicrobial and antiprotozoal drugs with varied
success rates.

• Vaccination as a means of control exists for certain

protozoa species such as Babesia bigemina (red-water
blood vaccine), Anaplasma marginale (Gall-sickness
blood vaccine) and Ehrlichia ruminantium (heart-
water blood vaccine).
 Definitions
Haematophagous: Referring to an organism or animal,
especially an insect or tick feeding on blood.
Infestation: The presence of an unusually large number
of insects or parasites in a place, typically so as to cause
damage or disease.
Erythropoiesis: The process which produces red blood
cells (erythrocytes). It is stimulated by decreased O2 in
circulation, which is detected by the kidneys, which
then secrete the hormone erythropoietin.
 Nematode disease pathogenesis
• Nematodes (Roundworms, Helminths), of animals are a group of
worms of which thousands of species have been described
worldwide.
• Some species such as Haemonchus contortus (wireworm) is
responsible for severe production loss and mortalities in small
stock.
• Haemonchus contortus are visible to the naked eye with the adult
female 18–30 mm long and the adult male 10–20 mm long.
 Nematode disease pathogenesis
• Infestation of parasitic roundworms occurs via the oral route with
some exceptions for example;
• Strongyloides papillosus (white bankrupt worm) that infest the
host either by oral route or penetrate through the skin.
• Gaigeria pachyscelis (hookworm) only infest the host through skin
penetration.

Gaigeria pachyscelis Strongyloides papillosus

Haemonchus contortus L 3 larvae mouthparts larva migrans
 Nematode disease pathogenesis
• The pathogenesis and effect on the host varies between the
different roundworm species and some of the species of
economic importance is discussed.
• The various roundworm species will be discussed in detail
later on in the course.
 Nematode disease pathogenesis
Haemonchus contortus
• The pathogenesis of haemonchosis is essentially that of
haemorrhagic anaemia due to the blood-sucking habits of the
worms.
• Depending on the number of infective larvae ingested,
haemonchosis can be peracute, acute or chronic.
• Each worm can be responsible for up to 0, 05 ml of blood loss
per day due to ingestion and seepage from the lesion.
• Compensatory erythropoiesis is usually insufficient due to the
iron reserves becoming depleted faster than it is restored.
 Nematode disease pathogenesis
Haemonchus placei
• The pathogenesis of bovine haemonchosis is similar to
Haemonchus contortus in small stock.
• As opposed to H. contortus, H. placei elicits a strong and
lasting immunity.
• The immunity is produced by the 4th and early 5th stages,
while functional antibody is produced by the 5th stage and
adult worms.
• After initial infection, calves develop a marked immunity and
subsequent infestations are retarded in the late 4th stage or
as stunted 5th stage worms.
 Nematode disease pathogenesis
• The treatment and control of roundworm infestations rely
largely on treatment with effective anthelmintics.
• Other control measures are of vital importance and should be
incorporated into the management of roundworms.
• Grazing management especially on planted pastures should
be implemented.
• Faecal egg count (FEC) is an efficient tool to determine
parasite load and effectivity of anthelmintics.
• Yearly faecal egg count reduction tests (FECRT) is necessary to
counteract roundworm resistance to anthelmintics.
• Treatment and control will be discussed in detail later on in
 Metabolic disease pathogenesis
• The most common and significant cause of metabolic diseases
are acquired and not inherited.
• Metabolic diseases are of clinical importance due to an
alteration of the energy production and/or damage to tissues
critical for survival

Pregnancy toxaemia /ketosis

Milk fever / hypocalcaemia Frothy bloat
 Metabolic disease pathogenesis
• The pathogenesis of metabolic diseases is primarily related to
alterations in the animal’s metabolism due to specific production
and management factors.
• The development of the disease is often related to an increased
demand for a specific nutrient that has become deficient.
• Typical metabolic diseases such as hypocalcaemia (milk fever),
hypomagnesaemia (grass tetany), and hypoglycaemia
(pregnancy toxaemia) occur frequently where management
practices strive at improved and increased production.
• It is thus correctly considered production related diseases.
Metabolic disease pathogenesis
• Production-induced metabolic diseases result from a negative
balance of a particular nutrient.
• The production of the animal at its peak is beyond the capacity
of that animal’s metabolic reserves to sustain a particular
nutrient at physiologic concentrations.
• For example, milk fever (hypocalcaemia) in cows occurs when
the mammary secretion of calcium is greater than the cow’s
diet or its skeletal reserves can supply.
• Comparable situations occur with magnesium
(hypomagnesaemia) and glucose (hypoglycaemia) metabolism.
 Metabolic disease pathogenesis
Metabolic diseases must not be confused with nutritional
deficiencies.
• Nutritional deficiencies are long-term, steady-state conditions
that can be corrected through dietary supplementation.
• Metabolic diseases such as milk fever (hypocalcaemia) are usually
acute states that may dramatically respond to the systemic
administration of the deficient nutrient or metabolite.
• This is however not the case for pregnancy toxaemia
(hypoglycaemia) where no treatment is effective to turn the
deficiency around.
 Metabolic disease pathogenesis
• Affected animals may however require subsequent dietary
supplementation to avoid recurrence of the metabolic disease.
• Quick, accurate diagnosis (Dx) and correct treatment (Rx) will
improve the chances of survival of animals with milk fever.
• Control of metabolic diseases relies on sound production and
management practices.
Wrong Rx for milk fever

Correct Rx for milk fever

 Possible test and/or exam questions
• Definitions: i.e. Pathogenesis, pathogen, epidemic, aetiology…
• Describe the mechanisms involved with viral disease
development
• Link the disease with the most probable host
• Describe the virulence factors of bacteria
• Protozoal parasites possess various escape mechanisms from
the host’s immune system. Describe these different
mechanisms