Changes

====Pathogenesis====

====Pathogenesis====

Canine adenovirus 1 (CAV1) initially infects and replicates in the cells of the oropharynx, before establishing a viraemia. A tropism for endothelial cells exists, leading to attack of the liver sinusoids and the lining of the gall bladder. Kuppfer cells are also affected. This results in hepatitis.

Canine adenovirus 1 (CAV1) initially infects and replicates in the cells of the oropharynx, before establishing a viraemia. A tropism for endothelial cells exists, leading to attack of the liver sinusoids and the lining of the gall bladder. Kuppfer cells are also affected. This results in hepatitis.

In foxes, the virus replicates in the endothelial cells of the brain resulting in neuronal damage, fits, and paralysis.

In foxes, the virus replicates in the endothelial cells of the brain resulting in neuronal damage, fits, and paralysis.

====Gross====

====Gross====

*the virus has a tropism for endothelium and hepatocytes

The liver is enlarged and friable on post-mortem examination. Extensive centrilobular necrosis leads to a pale, mottled appearance, but widespread haemorrhage is also apparent. These haemorrhages are located particularly on the serosal surface. Fibrinous or fibrino-haemorrhagic strands may be seen between the lobes of the liver.

**widespread haemorrhages, especially on serosal surface

 

*distinctly pale mottled appearance

 

**from extensive necrosis, characteristically periacinar (centrilobular) in distribution - the reason for the increased susceptibility of this area is not known

*fibrinous or fibrino-haemorrhagic strands between lobes

*[[Gall Bladder - Anatomy & Physiology|gall bladder]]

*[[Gall Bladder - Anatomy & Physiology|gall bladder]]

**wall usually shows oedema (up to 2cm diameter)

**wall usually shows oedema (up to 2cm diameter)