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Infectious Canine Hepatitis (ICH) is a highly contagious disease of dogs caused by [[Canine Adenovirus 1]] (CAV-1). This virus is closely related to Canine Adenovirus 2, which causes respiratory disease.

Infectious Canine Hepatitis (ICH) is a highly contagious disease of dogs caused by [[Canine Adenovirus 1]] (CAV-1). This virus is closely related to Canine Adenovirus 2, which causes respiratory disease.

Canine Adenovirus 1 invades via the oronasal route following excretion in the urine and faeces. Urinary excretion can persist for up to nine months after an active infection, and the virus may also be spread by contaminated fomites. Once established, CAV-1 replicates in the cells of the oropharynx before a viraemia causes dissemination to other tissues. A trophism exists for hepatic parenchyma and vascular endothelium: the target organs of CAV-1 are therefore the liver, kidney, vascular endothelium and eye.

Canine Adenovirus 1 invades via the oronasal route following excretion in the urine and faeces and spread via fomites. . Once established, CAV-1 replicates in the cells of the oropharynx before a viraemia causes dissemination to other tissues 4-8 days later. A trophism exists for hepatic parenchyma and vascular endothelium. In the liver, CAV-1 replicates in Kuppfer cells and damages adjacent hepatocytes when released. Other parenchymal organs, namely the kidney, and the eye may also be affected in infectious canine hepaptitis. When an adequate antibody response is mounted, organs may be cleared of virus within 10-14 days, but urinary excretion can persist for up to nine months after an active infection.  

In the liver, the clinical outcome of CAV-1 infection depends on the level of pre-existing immunity. Animals with high antibody titres usually mount an effective neutralising antibody response by day seven post-infection which clears the virus. Outcome is variable when a partial antibody response is mounted four to five days post-infection: both chronic active hepatitis (and ultimately hepatic fibrosis) and latent hepatic infection are possible. Low antibody titres, such as in unvaccinated dogs, fail to prevent infection and pathology and lead to potentially fatal hepatic necrosis. This necrosis is initially widespread and centrilobular, but may progress to become panlobular. In the kidney, virus localisation or deposition of circulating immune complexes causes glomerular damage and thus proteinuria. Immune complexes may also be deposited in the cornea and uveal tract, damaging the eye. In addition to glomerular localisation, CAV-1 persists in the renal tubular epithelium which accounts for the extended period of urinary excretion. Virus replication in the vascular endothelium leads to vasculitis and bleeding diatheses, and direct cytoxic damage to the eye is also possible.

In the liver, the clinical outcome of CAV-1 infection depends on the level of pre-existing immunity. Animals with high antibody titres usually mount an effective neutralising antibody response by day seven post-infection which clears the virus. Outcome is variable when a partial antibody response is mounted four to five days post-infection: both chronic active hepatitis (and ultimately hepatic fibrosis) and latent hepatic infection are possible. Low antibody titres, such as in unvaccinated dogs, fail to prevent infection and pathology and lead to potentially fatal hepatic necrosis. This necrosis is initially widespread and centrilobular, but may progress to become panlobular. In the kidney, virus localisation or deposition of circulating immune complexes causes glomerular damage and thus proteinuria. Immune complexes may also be deposited in the cornea and uveal tract, damaging the eye. In addition to glomerular localisation, CAV-1 persists in the renal tubular epithelium which accounts for the extended period of urinary excretion. Virus replication in the vascular endothelium leads to vasculitis and bleeding diatheses, and direct cytoxic damage to the eye is also possible.