Abstract. Ascites and acquired portosystemic shunts were consistent findings in six dogs with a chronic hepatitis of unusual morphology and unknown etiology. The hepatitis was characterized by a mixed inflammatory infiltrate and dissection of the lobular parenchyma by reticulin and fine collagen fibers. While limiting plates were disrupted by this process, portal inflammation was inconstant and seldom marked. Biopsy samples generally had very small, sublobular regenerative nodules, but larger nodules sometimes were present postmortem. Dilated vascular channels, representing sinusoids and portal venous radicles were a prominent feature of most affected livers.The lesions differ from previously documented chronic hepatitis in the dog, and from the chronic hepatitides in man.Portosystemic shunts in the dog may be congenital [8] or acquired. Acquired shunts develop as the result of portal hypertension. They consist of multiple, frequently tortuous, anastomotic vessels which represent the opening up of preexistent portosystemic collaterals [23, 24]. The obstruction to blood flow responsible for the portal hypertension may be extrahepatic or intrahepatic. Acquired shunts resulting from intrahepatic portal hypertension have been described in dogs with chronic hepatitis/ hepatic fibrosis [5,6,10] and overt cirrhosis [5,10,21, 24]. Affected dogs ranged in age from nine months to 15 years.Chronic hepatitis is an etiologically diverse and morphologically variable condition which has been documented extensively in man. By contrast there are few descriptions of chronic hepatitis in the dog, and aggressive forms have been recognized only recently [3,6,13,17]. Portosystemic shunts have not been a common feature of the reports.Over the last five years we have recognized an unusual and histologically distinctive chronic hepatitis in six dogs with acquired portosystemic shunts. Case ReportsAs indicated in table I, three unrelated standard poodles were included. Males and females were represented in equal numbers, although all standard poodles were male. Ages at initial presentation ranged from seven months to five years. The common presenting sign was ascites of three to eight weeks duration. In addition, the dogs were inappetant (refusing, particularly, 179

This paper summarizes the clinical and laboratory data on two adult Bedlington Terriers with liver disease associated with copper toxicosis. The younger dog, at 3 years, had elevated serum levels of alanine aminotransferase and alkaline phosphatase with active parenchymal cell degeneration and hepatitis. The second dog developed chronic hepatic failure at 5 years with advanced cirrhosis. Both dogs had stainable copper granules in the liver and chemical analysis of their livers revealed elevated copper contents (1,027 and 10,728 μg/g dry weight; normal less than 300 μg/g). These are the first published cases of this inherited abnormality of copper metabolism in this breed in this country.

12 marmosets of 3 different species died of hepatitis during a period of 5 months. The lesions closely resembled those of virus hepatitis in man but material from these animals and from in-contact marmosets failed to reveal the presence of hepatitis A. This together with certain aspects of the epidemiology of the disease suggests that the outbreak was not caused by a virus of human origin but possibly by a virus indigenous to the marmoset or tamarin.