The periacinar hepatic parenchyma is more susceptible to necrosis than is the portal triad region for an unknown reason. Corneal edema and interstitial nephritis may also occur in infected dogs. Necrosis, centrilobular, diffuse, with eosinophilic and basophilic magenta intranuclear inclusions, Chow Chow, canine, etiology consistent with adenovirus. Canine adenovirus-1, the etiology of canine infectious hepatitis, causes severe disease in dogs and other canids, although fatal infection seldom occurs among dogs older than two years of age. Occasionally, the tonsillitis is severe and causes prominent pharyngeal and laryngeal edema.
Viremia is associated with leukopenia.
Hepatic necrosis begins about seven days after infection. Peracute disease with sudden death may be seen. CAV-1 persists in the kidney and is shed into the urine for up to 9 months. The pathologic features of edema, hemorrhage, and hepatic necrosis are primarily due to the cellular tropism of CAV-1 for endothelium, mesothelium, Kupffer cells, and hepatocytes. Large, solid, deeply acidophilic or basophilic intranuclear inclusion bodies are present in hepatocytes, endothelial cells, and in other cell types such as glomerular endothelial cells, alveolar endothelial and epithelial cells, and collecting tubule epithelium.