Disease caused by Adenovirus

• G. adeno = gland
• two genera
• 1. Mast-adenovirus (G. masto = mammal)
• 2. Avi-adenovirus or (L. avi = bird)
• non-enveloped, ds DNA
• Replicated in nucleus, where a characteristic
inclusion body is produced
• highly species specific
 Infectious Canine Hepatitis
• k/a hepatitis contagiosa canis, Rubarth disease,
and canine adenovirus infection
• ICH is a contagious disease of dogs caused by
canine adenovirus-1
• Rubarth in 1947, from Sweden pointed out that
fox encephalitis virus, infective for dogs, was
the same as virus of canine hepatitis
• Spread:
• spread mainly by excretion of virus in the urine
• acquired as a naso-oral infection
• Contamination of urine, faeces, or saliva
• Pathogenesis:
• Initial infection occurs in the tonsillar crypts and
Peyer's patches
• Followed by viraemia and infection of
endothelial cells in many tissues
• This initiates infection of visceral organs
• Liver, kidneys, spleen, and lungs are main
target organs
• Chronic kidney lesions and corneal clouding
("blue eye") result from immune-complex
reactions following recovery from acute disease
• Sign:
• affects mainly young dogs
• illness is manifested for several days before
death, or recovery occurs
• lack of interest, listlessness, anorexia and
intense thirst
• Severe s/c oedema of head, neck, and ventral
aspects of trunk is prominent, but is a rare
• vomiting, diarrhoea with haemorrhage,
abdominal pain expressed by moaning sounds,
and fever at onset, but may fall suddenly to
subnormal levels as death approaches
• Signs in CNS are uncommon, clonic spasms of
extremities & neck, paralysis of hindquarters
and extreme agitation
• mucous membranes appear anaemic, icteric
• Tonsils are reddened and swollen, & tonsillitis
• lachrymation with hyperaemic conjunctiva
• diffuse, opaque cloudiness of cornea (blue eye)
develops 1-3 weeks after initial signs
• Albuminurea, Severe hypoglycemia
Neutropaenia & lymphopaenia during the
course, with Iymphocytosis during recovery
• prolonged bleeding and coagulation times; and
elevation of SGOT and SGPT
• Lesions:
• affinity for parenchymal & Kupffer cells of liver,
and endothelial cells
• Affected cells develop specific basophilic I/N
bodies, and become necrotic
• Gross lesions are dominated by haemorrhage,
mainly of stomach and serosal surfaces,
resulting from endothelial damage and loss of
coagulation factors of hepatic origin
• spleen and LN are oedematous & congested
• liver congested and enlarged
• gallbladder wall oedematous and thickened
• Lesions:
• microscopic lesion is focal hepatic necrosis, in
periportal region
• Recovery is followed by complete regeneration
of the liver
 Haemorrhages in the stomach
and serosal surface of GI tract

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 FOCAL NECROSIS IN LIVER

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Oedema and haemorrhage of the gall bladder
(11infectious canine hepatitis )
 “Blue eye”- A result of
Immunological reaction

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 NORMAL ABNORMAL

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 FOCAL NECROSIS IN LIVER

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 FOCAL NECROSIS IN LIVER

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 INTRA NUCLEAR INCLUSION BODIES

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• Diagnosis:
• Diagnosis in the living animal is difficult
because of the non-specific nature of symptoms
• Microscopic demonstration of I/N inclusion
bodies in surgically removed tonsils, or liver
biopsy specimens
• confirmed by isolation & immunofluorescence
• disease can occur in association with CD, or
leptospirosis, and has to be differentiated