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==Description==

==Description==

Infectious Canine Hepatitis (ICH) is a highly contagious disease of dogs caused by [[Canine Adenovirus 1]] (CAV1). 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]] (CAV1). 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, CAV1 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 CAV1 are therefore the liver, vascular endothelium, kidney and eye.

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, CAV1 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 CAV1 are therefore the liver, kidney, vascular endothelium and eye.

 

In the liver, the clinical outcome of CAV1 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. 

 

Damage caused by localisation to the vascular endothelium can lead to vasculitis and bleeding diatheses such as disseminated intravascular coagulation.  

In the kidney, glomerular damage results from localisation of virus or deposition of circulating immune complexes. This can lead to proteinuia. It is also possible for CAV1 to persist in renal tubular epithelium; this is responsible for the extended period of urinary excretion of virus.

In the liver, the clinical outcome of CAV1 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 persists in the renal tubular epithelium, accounting for the extended period of urinary excretion of virus.  The virus may similarly localise to the vascular endothelium, leading to vasculitis and bleeding diatheses.  

Immune complex deposition in the cornea and uveal tract causes damage to the eye. Direct cytotoxic damage to the eye may also occur.

Immune complex deposition in the cornea and uveal tract causes damage to the eye. Direct cytotoxic damage to the eye may also occur.