This document summarizes several important veterinary diseases. It provides details on the etiology, clinical signs, pathogenesis, lesions, and samples needed for diagnosis for diseases such as foot and mouth disease, rinderpest, malignant catarrhal fever, infectious bovine rhinotracheitis, bovine viral diarrhea, blue tongue, and peste des petits ruminants among others. Information on the causative agents, susceptible hosts, transmission routes, and characteristic gross and microscopic lesions is highlighted.

1. Veterinary Pathology
Dr.A.Arulmozhi, Ph.D., Diplomate ICVP.,
Associate Professor
Department of Veterinary Pathology
Veterinary College and Research Institute
Salem – 636 112.

2. Foot and mouth disease (FMD) Syn: Apthous fever
• The FMDV – Aphthovirus in the family of Picorna viridae. It is a non-enveloped, single stranded RNA
(ss RNA)
• There are seven immunologically distinct serotypes – O, A, C, SAT 1, SAT 2, SAT 3 and ASIA 1.
• Serotypes- O, A, C & Asia 1 are prevalent in India. In cattle, “O” is predominant type and then Asia 1.
• Cattle are usually the most important maintenance hosts for FMDV
Sources of virus: All secretions and excretions -including expired air, saliva, milk, urine, faeces and semen.
Large quantities in vesicle fluid and peak transmission usually occurs when vesicle rupture
Routes of spread:
• Inhalation of aerosolized virus, Ingestion, through skin abrasions or mucous membrane
Pathogenesis:
Tongue -------- multiplication in stratum spinosum causing cytolysis ------- viraemia -----hoof
In calves - There is heavy mortality in young calf due to cardiac damage with absence of appreciable
vesicular lesions.
Heart musculature shows striped appearance – “Tiger heart / Tigroid heart” (necrotising myocarditis /
myocardial necrosis/ fatty infiltration/ thrush breast heart).
Symptoms: vesicles (blisters) on: the feet, in and around the mouth, and on the mammary gland.
Excessive salivation (due to difficulty in swallowing because of painful lesions in the mouth), Abortion
Panters – Thyroid endocrine dysfunction – thermo regulation activity hampered by long grown hair
Pig: Most severe lesions on the feet. Mouth lesions are usually small and less apparent than in cattle, and
drooling is rare
Sheep and goat: Mild in sheep and goats.

3. Foot and mouth disease (FMD)
• Lesions are limited to the epithelium – Hydropic degeneration/balloon
degeneration” middle of the stratum spinosum of the epithelium (intra cellular
edema) and inter cellular edema
• Liquifactive necrosis with leukocytes produce “vesicles”. Small vesicles
(aphthae) coalesce and form large vesicles - “Bullae”
• Loss of epithelium is most common on the dorsal surface of the anterior two-
thirds of the bovine tongue
• Loss of epithelium → red surface → oozing of blood → “anorexia“
• Vesicles = virus + epithelium + leukocytes + RBCs + bacteria (later)
• Foot-and-mouth disease virus does not produce any observable viral inclusions
Samples collection:
• The preferred sample is: epithelium from unruptured or freshly ruptured
vesicles or vesicular fluid.
• If vesicles are not available, blood (serum) and esophageal-pharyngeal fluid

4. Rinderpest (Syn: Cattle plague)
• Rinderpest virus is a member- Morbillivirus;Paramyxoviridae family, RNA virus. RP virus is a very fragile
• Antigenically closely related to the viruses of Measles (in humans) Canine distemper, Peste-des-petits-ruminants
(PPR) (in sheep & Goats) & Equine morbillivirus
Spread:
• Close contact between infected and non-infected. Virus is excreted through urine, faeces, nasal discharge, and
sweat.
Transmission: ingestion of contaminated feed, or inhalation of aerosol (infected droplets)
Pathogenesis:
• “Great affinity of virus for lymphoid tissue (Marked leukopaenia) and alimentary mucosa (Focal necrotic
stomatitis and enteritis) ”
• Immunosuppression (due to lymphocytolysis) aggravates these infections, Death is usually due to severe
dehydration
• Immunity is associated with first IgM, and later IgG and IgA (HI).
Lesion:
Large intestine: large intestine – is more affected . Streaks of congestion along the folds of mucosa produce a
characteristic “Zebra-striped” (Zebra markings), or “barred” appearance in rectum. No vesicle formation
Peyer’s patches: Haemorrhages → Sloughening →“Ulcers” in the intestinal wall (deep craters)
Histopathology lesion:
• Eosinophilic both intracytoplasmic inclusion and intranuclear inclusions bodies in mucosal epithelium & giant
cells. multinucleated giant cells in St. spinosum
Samples collection:
• Live animals (preferably before the onset of diarrhoea) , Blood sample, Swabs of lachrymal fluid, Necrotic tissue
of oral cavity, Aspirations of superficial lymph nodes
• Dead animals: Spleen, lymph node, tonsil

5. Malignant catarrhal fever (MCF)
Synonym: Bovine malignant catarrh (BMC);Malignant head catarrh; Snotsiekte
Etiology: Gamma-herpes virus – Double stranded DNA virus
Characterised by catarrhal and mucopurulent inflammation of the eyes and nostrils, erosions of nasal
mucosa, rapid emaciation, enlargement of lymph nodes, corneal opacity and nervous symptoms
• In Africa: Wildebeest ,gnu serves as the source of infection for cattle. Hence, (Wildebeest-
associated virus). Alcelaphine herpesvirus 1 (AlHV-1),
• In USA: Sheep act as the source of this infectious agent. Hnce, (sheep-associated virus) – Ovine
Herpes Virus 2(OHV-2)
• The disease is always fatal, MCF affected ruminants are dead end hosts
Transmission:
Transmitted mainly by close contact with wildebeest calves or sheep or in aerosols during close contact
Clinical signs: Bilateral corneal opacity, Erosions at the tips of oral papillae,muzzle and nares
Nervous signs – hyperaesthesia, incoordination, disorientation, tremors, nystagmus or head pressing
Histopathoology: Arteries and arterioles in almost all organs are affected, and often there is medial
necrosis and endothelial swelling; Marked perivascular and intramural infiltration of mononuclear
cells, chiefly lymphocytes.
Sample collection
• For PCR: Anticoagulated blood, kidney, lymph nodes, intestinal wall and brain
• Sick animals: 10 – 20 ml of blood.

6. Infectious Bovine Rhinotracheitis (IBRT)
Synonym: infectious pustular vulvovaginitis, coital exanthema, vesicular venereal disease, vesicular vaginitis, coital
vesicular vaginitis or coital vesicular exanthema & Red nose
Etiology: Bovine herpesvirus type 1 – Double stranded DNA virus
Characterised by : upper respiratory disease, conjunctivitis, encephalitis, mastitis, infectious pustular vulvovaginitis
and balanoposthitis, abortion, and systemic infection in calves.
Source: nasal exudate and coughed-up droplets, genital secretions, semen and foetal fluids
Route of infection: Aerosol (droplet) infection-respiratory disease; Venereal transmission is genital diseases. The IBR
virus may survive for up to 1 year in frozen semen.
Bovine Viral Diarrhoea / Mucosal Disease
Synonym: BVD, MD and Hynea disease
Etiology: Pestivirus, single stranded RNA, Antigenically related with Border disease of sheep; hog cholera -pig
Two pathotypes: (Based on tissue culture)
1. Cytopathogenic BVDV (cp BVDV) – Virus diarrhoea – transient acute infection, highly contagious between 6 months
and 2 years of age
2. Non cytopathogenic BVDV (non-cp BVDV)- Mucosal disease – occurs in utero with non-cp BVDV persistent infection
to which they are immnunotolerant.
Clinical signs: Severe leukopenia, Abortions, stillbirths, mummified fetuses, Severe metritis
In foetus: Congenital cerebellar hvpoplasia, cataract, retinal atrophy, microphthalmia and optic neuritis
Acute : The principal gross lesions are seen in the gastrointestinal tract.
In chronic condition: skeletal disorder of cattle, termed “hyena disease” - premature growth plate (physis) closure

7. Blue Tongue
Synonym: Catarrhal fever of sheep & Sore muzzle
Etiology: Orbivirus, double stranded RNA virus; Endotheliotropic virus (Gross and microscopic lesion)
Transmission: Arthropod borne – Biting insect - Culicoides
Characterised by: Catarrhal stomatitis, rhinitis, enteritis and lameness, but adults seem to be affected
more than lambs
Pathogenesis:
Lesions originate from replication of the virus in endothelial cells
↓
Edema, hyperaemia, haemorrhage and infarction
Lesions:
- The striking lesion is edema and cyanosis of the tongue (bluish).
- Flushing of coronet
- Petechiae haemorrhage at the base of the pulmonary artery
In pregnant animals (in utero infection):
• Foetus abnormality : Cerebral abnormalities, hydrocephalus, Porencephaly (cavities in brain),
Retinal dysplasia due to retinal necrosis

8. Peste des Petits Ruminants (PPR)
Synonyms: Pseudo rinderpest, Goat Plague, erosive stomatitis
Etiology: PPR virus is a member of the genus Morbillivirus in the family Paramyxoviridae; PPRV is closely
related to rinderpest virus; Antibodies to PPRV and rinderpest are cross-protective and vaccination for
rinderpest can mask the presence of PPR.
Transmission:
Close contact, Inhalation, through the conjunctiva and oral mucosa. PPRV is shed in nasal and ocular
secretions, saliva, urine and faeces. It probably occurs in milk.
Clinical signs: Serous nasal and ocular discharges ; Matting is common around the eyes, ; profuse diarrhoea
and Necrotic and ulcerative lesion in mouth, nasal cavity, vulva and vagina, In the late stages of the
disease, small nodules resembling contagious ecthyma or sheep/goat pox can appear in the skin around
the muzzle.
Gross lesions:
GI tract: inflammatory and necrotic lesions in the oral cavity – lips, gums, abomasum, duodenum and the
terminal ileum
Respiratory lesions - bronchopneumonia. (Pneumonic lesions are prominent than GI form- Differ from RP)
The lymph nodes- of respiratory and gastrointestinal tracts, congested, enlarged and edematous.
Histopathology lesions:
- Syncytial cells (multinucleated giant cells) in early stage of the disease.(in stratified Squamous epithelium of
the Upper respiratory tract
- Intracytopalsmic inclusions in intestinal epithelium; Intranuclear inclusions in respiratory epithelium
Samples to be collected:
1. Swabs of conjunctival, nasal, buccal and rectal discharges Whole blood collected on heparin
2. Lymph nodes, especially mesenteric and bronchial nodes, Spleen, Large intestine and lungs Transport
under refrigeration
Pasteurellosis can also be a secondary complication of PPR.

9. Equine Infectious Anemia
Synonym: Swamp Fever, Mountain Fever, Slow Fever, Equine Malarial Fever, Coggins
Disease
Etiology: Equine infectious anemia virus (EIAV): lentivirus family Retroviridae – RNA virus
Transmission: Vector borne – Biting insects - Tabanus, stomoxys and mosquitoes
Pathogenesis: In horses, this virus persists in blood leukocytes for life, and also occurs in
plasma
Clinical signs: Based on clinical signs: Acute, subacute and chronic; Acute phase is
characterised by normocytic and normochromic anaemia
- Anaemia due to hameolysis, erythrophagocytosis, decreased production of
erythrocytes, thrombocytopaenia and elevation of serum immunoglobulin level.
- Coombs’ test results are positive (Antiglobulin test; Immune mediate haemolytic
anaemia)
Diagnosis:
- Coombs’ test results are positive (Antiglobulin test; Immune mediate haemolytic anaemia-
to detect antibody and complement
Coggins’ test (agar immunodiffusion) is a sensitive diagnostic test for equine infectious
anemia developed by Dr. Leroy Coggins.

10. African Horse Sickness
• African horse sickness is a highly fatal, infectious disease of horses, mules, and donkeys, caused
by an orbivirus.
Etiology: - orbivirus belonging to the family Reoviridae - double-stranded RNA
Susceptible host: Horses  Mules  Donkeys
Transmission: Vector borne – Biting insects (midges) of Culicoides namely Culicoides imicola, C.
bolitinos; C. variipennis
Clinically, the disease may occur in one of the four forms :
1) Acute pulmonary form – DUNKOP – most common type ; The most characteristic features are the
Severe dyspnoea caused by pulmonary edema, often with frothy exudates in the nostrils.
2) Sub acute cardiac form- DIKKOP - characterized by edema of the head, neck, lips, eyelids, cheek,
and tongue; edematous bulging of the supra orbital fossa
3) Mild form- known as horse sickness fever
4) Mixed form.
Gross lesions: The most prominent changes are seen in the respiratory system, hydrothorax, frothy
fluid from nostrils and hydropericardium
Equine Encephalomyelitis
Etiology: - Arbo virus (Arthopod borne) belonging to the family Reoviridae - double-stranded RNA
Three strains: Western” strain , “Eastern” strain and “Venezuelan” strain.
Transmission: Vector – Mosquitoes (Culex, Aedes); Wild birds – Resorvoir
Pathogenesis: Affect central nervous system and neurological disorder. It has zoonotic potential

11. Pseudorabies
Synonym: “infectious bulbar paralysis”, “Aujeszky’s disease”, “mad itch”
Etiology: herpesvirus suis – ds DNA virus
Host: Natural infection occurs in cattle, sheep, pigs, dogs, cats, and rats, but it is of greatest
importance in cattle, in which the disease is almost always fatal. Pigs (Natural host) and
rats (reservoir hosts) for herpesvirus suis
Route of infection: Abraded skin; Zoonotic Significance
Transmission: Direct contact ; Pigs serve as the source of infection for cattle and sheep; Pig
is a lifetime carrier
Pantropism - mainly in the respiratory tract and other organs like skin and brain
(olfactory, glosso- pharyngeal, or trigeminal nerves).
Signs: Pig – only nervous signs (non-purulent encephalitis); Pruritis is not common
Cattle – violent itching, bulbar involvement (i.e., of medulla oblongata), hence the
name “bulbar paralysis
Histopathology : Pig – Brain – Intranuclear inclusions; Cattle – skin- Intranuclear inclusions
Rabies Pseudorabies
Long incubation period, virus seen in saliva Short incubation period, virus not seen in
saliva
No itching present Itching present
Paralysis of larynx often Paralysis of larynx not often

12. Classical Swine fever
Synonym: Hog Cholera, Swine Plague
Etiology: Pestivirus of the family Flaviviridae, single stranded RNA and is closely related to the viruses
of bovine viral diarrhoea and Border disease.
Source of infection: Blood, secretions and excretions
Route of infection: ingestion (most common), conjunctiva or mucous membranes, skin abrasions,
genital transmission, artificial insemination, percutaneous blood transfer
Pathogenesis: vascular endothelial damage (Endotheliotropic) --- congestion, haemorrhage and
infarction); Thrombosis of small and medium-sized arteries is another feature
Gross lesions: Button ulcer in intestine, Petechiae in kidneys (Turkey egg), infarction in spleen and
haemorrhagic lymph nodes are due to vascular endothelial damage caused by the virus.
Congenital form :
• Central dysmyelinogenesis, cerebellar hypoplasia, microencephaly, Pulmonary hypoplasia,
hydrops and other malformations
Microscopic lesion: The most constant change is swelling and proliferation of endothelial cells. The
capillary wall may become completely hyalinized, resulting in partial or complete occlusion
Diagnosis:
• Live animals: whole blood from multiple febrile cases; Refrigerate and ship to laboratory as quickly
as possible in EDTA or Heparin (live cases)
• Tissues from recently dead animals- Tonsil, Lymph nodes (pharyngeal, mesenteric), spleen,
kidney and distal ileum

13. Swine influenza (“Swine flu”)
• Swine influenza is a specific, highly contagious disease of pigs characterized clinically by
fever and signs of respiratory involvement. mostly in young pigs of 2 -4 months.
Etiology: Swine influenza is caused by influenza A viruses in the family Orthomyxo viridae.
Influenza A - is an RNA virus that causes influenza in birds and swine (pigs)
The virus uses two cell surface proteins to mediate entry and exit from host cells
• The protein haemagglutinin allows the virus to bind to the cell that is being infected:
there are 16 different haemagglutinin subtypes (H1 — H16).
• The protein neuraminidase, an enzyme that cleaves sialic acid from host and viral
proteins, facilitates viral exit from the host cell: there are 9 neuraminidase subtypes
(N1 — N9).
Swine influenza subtypes: H1N1, H1N2, H2N3, H3N1 and H3N2
• Route: Pig to pig contact(Nose to nose contact)
• Intermediate host and reservoir host: Swine lungworms – Metastrongylus apri
• Infection is provoked by the presence of H. influenzae suis (Bacteria).

14. Vesicular Exanthema of Swine
Characteristic feature: Fever, Vesicle formation
Etiology: Calcivirus
VE: Spread: Feeding uncooked garbage to pigs
• Sea lion virus  Calcivirus.
• Sea lion carcasses -----Pigs -----Scraps -----wide outbreak
VE: Sources:
• Infected live pigs ( direct contact); Infected pork
Gross lesions:
• Vesicles are full of clear fluid;Affected feet are very sensitive and there is severe
lameness.
• No systemic involvement; Never fatal
Vesicular stomatitis
• Infectious disease is characterised by vesicles on mouth and feet.
• Etiology: Vesiculo virus; Rhabdo virus
• Horses are more susceptible than cattle and pigs.
• Transmission by arthropods – eg: Mosquitoes, Sand flies
• Two serotypes: New jersey, Indiana

15. Rabies
Synonym: Hydrophobia, Lyssa, Mad dog disease
Etiology: Rhabdo viridae, Lyssa virus, neurotropic, relatively fragile, susceptible to
most disinfectants, dies in dried saliva in a few hours and propagated in tissue
culture and chick embryos
Characterised by : acute, viral encephalomyelitis (inflammation of both brain and
spinal cord), which affects all warm-blooded animals, including humans. It is
highly fatal disease, mortality rate being close to 100%.
Strains of rabies virus:
• Street virus: Isolated from naturally occurring cases.
• Fixed virus: Attenuated laboratory strains .
Spread: By the bite of a rabid animal.
Sources: Dog, minor extent the cat, foxes, wolves, skunks, blood-sucking vampire bats
The virus may appear in the milk of affected animals
Pathogenesis: It depends on 1) virulence of the strain 2) distance between the bite site
and the CNS 3) the severity of the bite 4) amount of infectious virus in the saliva
Bites to the head are much more likely to lead to rabies, than those of the extremities

16. Rabies
• Bite Replication in myocytes Entering into nervous system at motor end plates entry
into peripheral & cranial nerves viral spread to spinal cord Dissemination thro’ CNS(Brain
stem, cerebral cortex, and hippocampus) Centrifugal spread(away from the centre. i.e. from
centre to the periphery) Salivary gland, cornea & tonsil
The clinical symptoms usually appear in one of two forms:
1) dumb or paralytic form 2) furious form
Dumb or paralytic form : stupor (unconsciousness), and has a peculiar staring expression.
paralysis of the throat and muscles of mastication, usually with profuse salivation and inability
to swallow, dropping of the lower jaw, rarely attempt to bite, paralysis progresses rapidly to all
parts of the body, coma and death follow in a few hours.
Furious form” : (“mad-dog syndrome”)
Aggressive, rages (violent anger), biting and slashing at a fly moving object or even
inanimate objects, such as sticks and trees. Champing of the jaws (i.e., chewing noisely)
Cattle - characteristic bellowing ; Horses - rolling as with colic.
Gross lesion: There are no gross lesions; only microscopic lesions , limited to the CNS
Histopathology: Lesions in the gasserian ganglia are specific; proliferating glial cells are known as
“Babes’ nodules”. Negri body – Intracytoplasmic eosinophilic inclusion bodies;
Negri bodies seen : Dog - neurons of hippocampus; Purkinje cells of the cerebellum. In
Impression smears: Hippocampus – Dog; Cattle : Purkinje cells – Cerebellum
Cytology smear: Seller’s stain is effective.

17. Canine Distemper
Synonym: Carre’s disease, Hard pad disease
Etiology: Morbilli viruses in the paramyxo viridae family (RNA). Closely related to
measles virus (MV), rinderpest virus (RPV) and peste de petits ruminants virus
(PPRV).
Characterised by: very serious, potentially fatal disease. Bi-phasic fever, Lymphopenia,
Gastrointestinal and/or respiratory signs, Neurologic signs, Hyperkeratosis
(Pantropic)
Spread: Ingestion and inhalation
Sources: All secretions and excretions contains virus
Pathogenesis: Pantropic – It affect all germinal layers
Clinical signs: Twisting of muscle – chorea; Convulsion – Chewing gum fits; Chronic
distemper encephalitis (old dog encephalitis)
Gross lesions: Thymic atrophy , Hyperkeratosis of the nose and footpads
bronchopneumonia, enteritis, and skin pustules
Histopathology: Intracytoplasmic and intranuclear acidophilic inclusion bodies in
respiratory, urinary and GI epithelium.
Brain – Gemistocyte – Intranuclear inclusion in astrocytes

18. Infectious Canine Hepatitis(ICH)
Synonym: Hepatitis contagiosa canis, Rubarth disease (by Rubarth), Blue eye
Etiology: canine adenovirus-1, ds DNA
Spread: Ingestion of contaminated matherial urine, faeces and saliva; transmitted
by parasites such as mosquitoes, ticks and fleas
Sources: excretion of virus in the urine,faeces or saliva from infected animal
• Pathogenesis: Tropism for endothelial cells in many tissue ---- infection of
visceral organs(Liver, kidneys, spleen, and lungs)
• Immune-complex ----Chronic kidney lesions and corneal clouding (“blue eye”)
Clinical signs: affects mainly young dogs; anaemic and icteric
Clinical pathology: Proteinuria, neutropaenia, lymphopaenia during the course,
with lymphocytosis during recovery; prolonged bleeding and coagulation
times; elevation of SGOT and SGPT.
• Gross lesions: an affinity for endothelial cells generally, parenchymal and
Kupffer cells of the liver; and Liver and Gall bladder: congested and enlarged
Histopathology:Basophilic intranuclear inclusion bodies&necrosis of affected cells.

19. Canine Parvovirus Infection
Etiology: Parvo virus, ds DNA, The virus is more than 98% identical in DNA with feline
panleukopaenia virus
Characterised by: two different clinico-pathological forms of the disease.
1) Intestinal form, which is the main form (Adult dog)
2) Cardiac form – Affect young puppies
Spread: Direct dog to dog; contaminated faeces of from the environment
Pathogenesis:
Intestinal Form :Necrotizing enteritis of the small intestine; This form occurs in dogs
of all ages, severe more than 6 weeks.
• It i s characterized by vomiting, diarrhoea, and dehydration. There may be fever
and leukopaenia.
• Intranuclear inclusion bodies - intestinal epithelial cells
Cardiac Form : Affect younger dogs - puppies of 2-8 weeks of age. Death is due to
myocardial necrosis. This form may exist with or without, signs or lesions in the
small intestine
Histopathology: multiple foci of myocardial necrosis; Intranuclear inclusion bodies are
present in muscle fibres

20. Jaagsiekte
Synonym: Ovine pulmonary adenoma, Ovine pulmonary adenomatosis, Pulmonary
carcinoma of sheep; Driving sickness/disease
- Jaagsiekte is a neoplastic disease of older sheep ; hypertrophy and hyperplasia of alveolar
epithelium “jaagsiekte means a “driving sickness/disease” (jaagt = drive; siekte =
sickness).
Etiology: type D oncovirus (a retrovirus) ; RNA virus
Spread and source: Naturally, transmitted by inhalation of infected droplets from respiratory
secretions.
Pathogenesis: Virus --- replication in the type II pneumocytes in the alveolus and Clara cells
in Terminal Bronchioles ---- Transformation of the cells in the terminal bronchioles ---
intra-alveolar and intra-bronchiolar polypoid ingrowths ---- copious production of fluid
The adenomatous ingrowths encroach alveolar space -----Anoxic anoxia
Clinical signs: incubation period in natural cases is 1-3 years; rare in sheep younger than 2
years and is most common at 3-4 years of age; Moist crackles (slowly boiling porridge)
Microscopic lesions: Pronounced thickening of the alveolar walls and partial obliteration of
the alveolar spaces by small adenocarcinomas
Diagnosis: wheelbarrow test where one lifts the hind legs of the animal above the head to
observe lung exudate flow out the nose and mouth.This fluid contains infectious virus.

21. Maedi
Synonym: Progressive interstitial pneumonia; Ovine Progressive Pneumonia,
Marsh’s Progressive Pneumonia, Montana Progressive Pneumonia, Chronic
Progressive Pneumonia
• Visna-means shrinkage or wasting; is a chronic viral encephalomyelitis of sheep
slow, progressive demyelination
• Maedi means dyspnoea; Chronic, slowly progressive interstitial pneumonia
Etiology for Both visna and maedi : Lentivirus, RNA virus; The virus is closely
related to Caprine Arthritis Encephalitis in goats
Maedi Spread: Mainly by the respiratory route; Common victims are adult sheep.
(Goats suffer from CAE).
Maedi Signs: listlessness, emaciation, dyspnoea, coughing, wasting, and the “thin
ewe syndrome”, Induration (hardening) of the mammary glands.
Maedi Gross lesions: Lungs: rubbery consistency of lungs
S.No. Characters Jaaagsiekte Maedi
1. Alveoli show adenamatosis Not seen
2. Inclusions absent Present
3. Lesions Local Diffuse
4. Lymphnodes Not affected Lymphadenitis
5. Course Shorter Longer

22. Prion diseases
• Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family
of rare progressive neurodegenerative disorders that affect both humans and
animals and always fatal
• Features of the disease: long incubation periods, characteristic spongiform
changes with neuronal loss and - a failure to induce inflammatory response.
Etiology: The causative agent of TSEs is believed to be a prion. “Proteinaceous
infective particle” – Proin → Prion
• Prion: is an abnormal, transmissible agent that is able to induce abnormal
folding of normal cellular prion proteins (PrPc) which are found on the surface
of neurons in the brain.
• It has zoonotic potential – in beef eaters- In humans it is called-Creutzfeldt-
Jacob disease (CJD)
Features of Prion: - Lacks nucleic acid (RNA or DNA); Don’t produce inflammatory
or immune reactions in the host
Animal Prion Diseases: Scrapie ; Bovine Spongiform Encephalopathy (BSE); Chronic
Wasting Disease (CWD)

23. Scrapie
Synonym: Ovine Spongiform Encephalopathy
• Scrapie is a fatal, Neuro degenerative disease affecting the central nervous system of
sheep and goats. PrPsc are resistant to the treatments that ordinarily destroy bacteria,
spores, viruses and fungi. sheep - 3-4 years of age group are mainly affected
Pathogenesis: PrP / PrPc(Normal cellular protein) PrPsc /SAF (Scrapie prion/ scrapie-associated
fibril protein –Amyloid) ------- Accumulation in neuron
Clinical signs: Itching and neurological sign
Lesions: No characteristic gross lesions are found in this disease
Microscopic Lesions:
1. Neuronal degeneration - shrinkage of neurons with increased basophilia cytoplasmic vacuolation.
central chromatolysis and Ischaemic cell damage
2. Astrocytosis - hypertrophy and hyperplasia of astrocytes are characteristic
3.Spongiosis:(prominent neuronal and neuropil vacuolation), in grey matter
Bovine Spongiform Encephalopathy (BSE, Mad Cow Disease)
• BSE is a progressive degenerative disease that affects the central nervous system of cattle
• The incubation period is unusually long of about 4-5 years.
• It is because of this peculiar and uncontrollable behaviour of the affected cow that the disease has
been termed ‘mad cow disease”.
• Microcavities, in the neuropil. This spongiosis (i.e., neuropil vacuolation) is a predominant form of
vacuolar change observed, and is a feature of TSEs.

24. Pox virus diseases in Animals
Etiology: The pox viruses are the largest animal viruses

25. Capri-Poxviruses
• Diseases caused by Capri-Poxviruses : Sheep - pox, Goatpox, and Lumpy skin disease.
Sheep-Pox:
• Sheep-pox is highly contagious, and spread by contact with infected animals and
contaminated articles.
• Clinically, the malignant form is more common in lambs. Lesions appear on
unwoolled skin, and on the buccal, respiratory, digestive, and urogenital tract
mucosa. In skin, papules----- nodular----- vesicular----- pustular ----finally scabs.
• In the benign form, common in adults, only skin lesions occur, particularly under
the tail, and there is no systemic reaction
• Localized acanthosis (thickened epidermis) and hyperplasia are followed by
vesiculation (vesicle formation), beginning in the middle layers of epithelium. The
underlying oedematous dermis and subcutis contain many distinctive cells called
“cellules claveleuses” of Borrel, or “sheep-pox cells”.
Goat pox:
• It is usually benign (less severe) compared to sheep-pox.
• The virus is immunologically related to sheep-pox
• Young kids suffer a systemic disease skin, respiratory and alimentary mucosa
• In adults, the disease is mild and lesions are rare
• The skin lesions are smaller in goat pox, and are rarely haemorrhagic

26. Lumpy Skin Disease (LSD)
• Caused by a Capri-poxvirus
• Highly infectious disease of cattle and buffaloes (Neethling virus). Nodules on all parts of
the skin and oral, nasal, genital mucous membranes and enlarged lymphnodes
• Spread by insect vectors, mainly flies.
Lesions:
Acanthosis (thickened epidermis), Parakeratosis (thickened Stratum corneum with pyknotic
nuclei) and hyperkeratosis (thickened s tratum corneum) of the epidermis with necrosis
and vesicle formation.
• Eosinophilic cytoplasmic inclusion bodies in keratinocytes, fibroblasts, and macrophages
Diseases caused by Para-Poxviruses
1) Contagious Pustular Dermatitis: Parapox
Synonyms: “contagious ovine ecthyma”, “infectious labial dermatitis”, scabby mouth’, ‘sore
mouth’ and “orf
Spread: by contact
• There is a severe systemic reaction - alimentary tract -gastroenteritis, and trachea may be
followed by bronchopneumonia
• The epidermis proliferates and becomes several times than normal and deep into the
dermis.
• Although hyperplasia of the epidermis is seen in most poxvirus infections, it is particularly
striking in ecthyma
• Zoonotic: Transmissible to humans. Mild transitory (of short duration) pustular lesions

27. Bovine Papular Stomatitis
Synonym: Infectious ulcerative stomatitis and oesophagitis’.
Characterised by: mild viral disease of young cattle- papules on the muzzle,
nostrils, and in the oral cavity. Lesions also occur in the oesophagus, rumen,
reticulum and omasum.
Etiology: Para-poxvirus. It is closely related to pseudo-cowpox virus.
The affected keratinocytes often contain spherical eosinophilic cytoplasmic
inclusion bodies.
Pseudo-Cowpox
Synonym: Milker’s nodule
Etiology: Para-poxvirus. Pseudo-cowpox is called paravaccinia, but is not related to
vaccinia or cowpox. It is closely related to contagious pustular dermatitis virus
and bovine pustular stomatitis virus
Lesions are limited to the teats and udders of milking cows, and appear as red
papules and vesicles.
Zoonotic Significance: transmissible to humans -“milker’s nodules” on the hand