viral disease of dogs morbilivirus of paramyxoviridae

1. CANINE DISTEMPER
ABHIJITH SP
CVAS POOKODE

2. INTRODUCTION
 Contagious and acute febrile viral disease of
dogs.
 Characterized by biphasic fever, severe immune
suppression, catarrh of mucous membranes of
respiratory, GI, urogenital tracts, skin lesions and
nervous symptoms.
 Synonyms – Carre’s disease, Hard pad disease,
old dog encephalitis.
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3. AETIOLOGY
 Agent—Paramyxoviridae—Morbilivirus—CDV
 SS RNA virus.
 The virus is pantropic virus.
 Pantropic with peculiar affinity for lymphoid tissues,
epithelial tissue (respiratory, gastrointestinal and
urogenital tracts, skin) and nervous tissue.
 Antigenically related to PPR virus of goats, RP virus
of cattle and measles virus of humans.
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4. Susceptible Hosts
 Primarily affects dogs.
 Small pups with less developed immune system more
susceptible than adult dogs with fully developed immune
system.
 Pups are mostly affected.
 Also affects wild animals like lion tiger leopard.
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5. Incubation Period
• The incubation period is 3–7 days: usually 5 days.
• Pups with weak immune system will have lesser
incubation period.
• Duration of disease depends on intensity of
infection, health status and secondary infection.
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6. TRANSMISSION
 All secretions and excretions contain viruses.
 Usual route of infection is aerosol infection-Inhalation of
infected droplets.
 Respiratory signs and lesions are constant, Lung is central to
pathogenesis of CD.
 Lung lesions varies in severity.
 Infection can also occur through ingestion.
 Chance of Bordetella infection as secondary bacterial infection
is high.
 Salmonella infection can also occur.
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7. PATHOGENESIS
 Virus gain access into body through ingestion or
inhalation.
 Following entry virus is taken up by macrophages of
tonsils and bronchial lymph nodes.
 Lymphatic & hematogenous spread occurs to other
lymphoid organs.
 Stage of viremia (presence of virus in blood) 4-5DPI.So
first fever appears.
 Spread beyond lymphoid tissues depends on the immune
status of host.
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8. PATHOGENESIS
• In immunocompromised animals, virus spreads to
the epithelia of respiratory, GI, urogenital tracts and
ultimately reaches skin, brain and optic nerves.
• Viral replication in the target tissues bring about the
characteristic pathological changes.
• Second Fever appears due to localization of virus in
different tissues and also maybe due to secondary
bacterial infection. 12dpi.
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9. CLINICAL SIGNS
 Characterized by two phases esp. in young pups
Visceral Phase
Encephalitic Phase
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10. CLINICAL SIGNS
 Visceral phase – Diphasic/ Biphasic fever-fever for 3/4 days, drops &
remain normal till 11th or 12th day- again rises due to secondary bacterial
infection.
 Conjunctivitis, nasal and ocular discharges initially catarrhal, later
become purulent due to secondary bacterial infection, signs of
pneumonia.
 Diarrhea with blood streaks.
 Vesicles/pustules esp. on the skin of ventral abdomen.
 Marked lymphopenia.
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11. CLINICAL SIGNS
 Encephalitic phase.
 Nervous signs- chewing movements & excess
salivation, epileptic seizures and temporal
twitches – Chorea.
 Blindness, paralysis.
 Nasodigital hyperkeratosis (Hard pad disease)
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12. Hard pad Abdominal pustules
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13. Macroscopic Lesions
• Respiratory tract
Catarrhal exudate which turns purulent in the nasal
and pharyngeal mucosa
Bronchi show serous/ purulent exudate
Broncho interstitial pneumonia – Suppurative
(secondary bacterial infection)
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14. Macroscopic Lesions
• GI tract
Catarrhal to necrotizing gastroenteritis
Swollen mesenteric lymph nodes
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15. Gross lesions
 Other lesions.
Thymic atrophy, Hydropericardium, Nutmeg
appearance of liver, catarrhal conjunctivitis,
corneal ulceration, pan ophthalmitis, meningeal
congestion and edema.
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16. Microscopic lesions
• Respiratory tract – catarrhal rhino tracheitis, bronchitis with ,
bronchiolitis with small purulent plugs- bronchiolitis capillaris.
• Proliferation of type II pneumonocytes and formation of
multinucleated syncytial cells with intracytoplasmic inclusion
bodies and less often intranuclear inclusions.
• In some areas, collection of cells resembling epithelioid cells,
some of which may fuse giving the appearance of giant cell
pneumonia.
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17. Microscopic lesions
• Gastro intestinal tract
Catarrhal to necrotizing inflammation
Formation of intracytoplasmic and intranuclear inclusions in the
epithelia of GI tract
• Urinary tract
Desquamation of epithelium in renal pelvis, Intracytoplasmic &
Intranuclear and inclusions in the epithelia of renal pelvis,
collecting tubules and transitional epithelium of urinary bladder
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18. Microscopic lesions
• Skin- Dermatitis confined to deeper epidermis
(Malpighian layer). Formation of Intracytoplasmic and
intranuclear inclusions. Extensive proliferation of keratin
layer leads to hard pad condition.
Lymphoid tissues – T cell & B cell necrosis of spleen, lymph
nodes. Atrophy of thymus ( Lymphopenia).
• Retina- Congestion, edema, neuritis of optic nerve,
demyelination, gliosis and formation of inclusion bodies.
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19. Microscopic lesions
• Nervous system- Extensive demyelination, vacuolation of white
matter. Myelinated tracts of cerebellum and white columns of
spinal cord are most affected.
• Non suppurative viral encephalitis and perivascular lymphocytic
cuffing.
• Neuronal degeneration, pyknosis, chromatolysis, necrosis
followed by neuronophagia, satellitosis, appearance of Gitter
cells and gemistocytes.
• Intracytoplasmic & intranuclear inclusions mainly in the
astrocytes (targeted cells), ependymal cells and a few neurons.
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20. A. Bronchiole occluded by inflammatory cells,
exudate and cell debris. B. Multiple eosinophilic
intracytoplasmic viral inclusions (arrows) in
bronchiolar epithelium.
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21. (A ) Acute lesions - vacuolization of the white matter due to myelin sheath edema
( B , C ) Progressive myelin loss (pallor and lack of eosinophilia) is present in
subacute lesions.
( D ) Chronic lesions invariably display more than three layers of perivascular
inflammatory cells, accompanying ongoing demyelination and axonal loss.
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22. OLD DOG ENCEPHALITIS
• In mature adult dogs that have survived the acute
infection.
• Persistence of a defective form of virus in the nervous
system.
• Severe lymphocytic encephalitis, perivascular cuffing,
neuronal degeneration affecting gray matter of cerebrum
and brain stem.
• Demyelination is less.
• Only intranuclear inclusions.
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23. DIAGNOSIS
• Finding of Gitter Cells and Gemistocytes
• Clinical signs and post-mortem lesions.
• Demonstration of inclusion bodies.
• Immunological staining.
• Virus isolation and identification.
• CDV antigen – green fluorescence
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