Biliary cirrhosis caused by Campula spp. in a dolphin and four porpoises.

Biliary cirrhosis produced by Campula spp. is described in 1 striped dolphin Stenella coeruleoalba and 4 harbour porpoises Phocoena phocoena. The hepatic lesions consisted of severe proliferation of fibrous connective tissue with loss of the lobular pattern, nodular regeneration of the hepatic tissue, bile duct hyperplasia and severe inflammatory infiltrate composed of eosinophils, macrophages, lymphocytes and plasma cells. These lesions were associated with severe infestation by Campula spp. Although inflammatory and degenerative hepatic lesions are frequently found in stranded dolphins, biliary cirrhosis has not been previously reported in cetaceans. Massive infestation by these parasites should be included as a cause of hepatic failure resulting in stranding of marine mammals.

Biliary cirrhosis secondary to obstruction of the common bile duct by ectopic pancreas in a cow.

A 10-year-old Japanese Black cow showed icterus with gradual emaciation for a period of 3 months. Ultrasonography demonstrated increased "echogenicity" of the entire liver, with marked dilatation of the gall-bladder. At necropsy, the common bile duct was found to be obstructed by focally thickened fibrous tissue adjacent to a flesh-like mass (9 x 4 x 4 mm) attached to the wall of the duct. The mass consisted of normal pancreatic tissue. The liver showed moderate fibrosis, with nodular regeneration of the hepatic tissue and bile duct hyperplasia. A diagnosis of biliary cirrhosis secondary to ectopic pancreas in the common bile duct was made.

Use of technetium-99m sulfur colloid to evaluate changes in reticuloendothelial function in dogs with experimentally induced chronic biliary cirrhosis and portosystemic shunting.

Technetium-99m sulfur colloid scintigraphy was used to study alterations of reticuloendothelial function in 7 dogs with experimentally induced biliary cirrhosis and portosystemic shunting. Scintigraphic studies were performed before and 6 weeks after common bile duct ligation. Radiocolloid plasma clearance rate was determined by measuring activity in plasma samples and by analyzing the rate of liver uptake on dynamic scintigraphic image sequences. Percentage of uptake in the liver, spleen, and lungs, as well as the ratio of hepatic-to-extrahepatic uptake, was determined from static equilibrium images. Relative to preoperative values, there were significant decreases in plasma clearance rate, percentage of liver uptake, and ratio of hepatic-to-extrahepatic uptake and significant increases in percentage of spleen and lung uptake on postoperative studies. The mechanism of technetium-99m-labeled sulfur colloid extraction by the liver is different from that of other radiocolloids; it does not require active phagocytosis or pinocytosis. Thus, liver uptake of this tracer principally reflects effective liver blood flow. Portosystemic shunting was documented in these dogs at the time of the postoperative radiocolloid scans, and we believed was responsible for the decrease in liver reticuloendothelial activity. Possible mechanisms for the increased splenic and pulmonary reticuloendothelial activities are discussed.

Feline cholangiohepatitis complex.

Feline cholangiohepatitis complex causes a diffuse intrahepatic cholestasis of unknown etiology. Recognized histologic forms include acute suppurative cholangitis/cholangiohepatitis, long-term nonsuppurative cholangitis/cholangiohepatitis, and biliary cirrhosis. Treatment of cholangiohepatitis complex varies based on histologic type. Thus a liver biopsy is necessary for definitive diagnosis and treatment. Because cholangiohepatitis complex causes diffuse hepatic change, percutaneous needle biopsies are often sufficient for obtaining a diagnosis. Antibiotics are used to treat all forms of feline cholangiohepatitis complex, but steroids may be of equal or greater importance for use in the treatment of long-term nonsuppurative cholangiohepatitis. Prognosis is guarded for cats with any form of cholangiohepatitis complex due to the variable response to treatment seen in many cats. Spontaneous remission occasionally occurs.

Chylous ascites in cats: nine cases (1978-1993).

Medical records of 9 cats with chylous ascites that underwent exploratory celiotomy were reviewed. In 7 cats, chylous ascites was associated with intra-abdominal neoplasia: 4 cats had an unresectable tumor (hemangiosarcoma, 3 cats; paraganglioma, 1 cat) within the mesenteric root; 2 had malignant lymphoma of the small intestine and mesenteric lymph nodes; and 1 had lymphangiosarcoma of the abdominal wall. In 2 cats, chylous ascites was associated with nonneoplastic diseases: 1 cat had severe biliary cirrhosis and an extrahepatic portosystemic shunt; the other had steatitis caused by vitamin E deficiency. Three cats were euthanatized or died at the time of surgery, and 5 cats were euthanatized within 3 months of surgery. One cat with malignant lymphoma responded well to chemotherapy and lived for 14 months after surgery.

Feline hepatic disease.

Species differences in anatomy, physiology, and biochemistry lead to many dissimilarities between the canine and feline liver. Major differences exist in the interpretation of liver function tests, the significance of biochemical jaundice, the consequences of anorexia, and the efficiency of hepatic metabolic systems. Biochemical alterations in total bilirubin, ALT, and SAP may indicate the presence of disease in the feline liver. It is, however, impossible to make accurate diagnoses without liver biopsy. A liver biopsy can provide a diagnosis and prognosis and can guide the therapeutic plan. The feline hepatic diseases most frequently seen in our hospital are hepatic lipidosis, cholangiohepatitis complex, toxic hepatopathy, and hepatic neoplasia. Less common diseases of the feline liver include extrahepatic biliary obstruction, portacaval vascular anomalies, hepatic parasites, hepatic cysts, and diaphragmatic hernia. Systemic diseases that can effect the liver of cats are feline infectious peritonitis, multicentric lymphosarcoma, myeloproliferative diseases, hemolytic anemia, infectious panleukopenia, and systemic fungal infections.

Spontaneous "primary biliary cirrhosis" in rabbits.

A syndrome resembling human Primary Biliary Cirrhosis (PBC) and occurring spontaneously in a strain of domesticated rabbits from the Faenza region in Italy, is reported. The syndrome is characterized by histological liver changes consisting of chronic non-suppurative destructive cholangitis and copper accumulation, biochemical and immunological abnormalities mainly represented by an elevation of serum alkaline phosphatase and a positive antimitochondrial antibody test. The abnormalities were not observed in newborn rabbits from the same area nor in control rabbits from the island of Sardinia. A toxic effect related to some environmental factor may be responsible for the disease. Alternatively, a continuous process of partial inbreeding among consanguineous animals may have resulted in a selection of a strain genetically predisposed to the development of PBC. Whatever the etiology, the domesticated Faenza rabbit proves to be an interesting animal model for a chronic nonsuppurative destructive cholangitis, very similar to the human disease known as PBC.