Canine distemper is a contagious viral disease of dogs caused by the canine distemper virus. It is characterized by two phases - a visceral phase with fever, nasal and ocular discharge, diarrhea, and skin lesions. This is followed by an encephalitic phase with neurological signs like seizures and paralysis. Pups are more susceptible than adults. Microscopic lesions include inflammation of respiratory, gastrointestinal, and nervous tissues along with intracytoplasmic and intranuclear viral inclusions. There is currently no treatment for canine distemper, making prevention through vaccination very important.

1. CANINE DISTEMPER
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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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