Abstract: Two adult snow leopards (Panthera uncia), male and female, both with vaccinations current, became infected with feline panleukopenia virus (FPV) at the Blank Park Zoo, Des Moines, Iowa, in late 1988. Clinical signs included weakness, hemorrhagic feces, fever, seizures, and nasal discharge. Blood analysis revealed severe lymphopenia and mild anemia. A positive enzyme-linked immunosorbent assay (ELISA) test for FPV on fecal contents from the male leopard confirmed the diagnosis. In spite of intensive therapy, both animals died. Necropsy of the female, which survived for 1 wk after onset of signs, revealed intestinal crypt necrosis, pulmonary consolidation, necrotizing laryngitis, and diffuse lymphoid depletion. The male leopard, which lived 3 wk after onset of illness, had similar enteric and lymphoid lesions. In addition, there was a severe interstitial pneumonia, with syncytial cells containing eosinophilic intracytoplasmic inclusion bodies. Ultrastructural characteristics of these inclusions featured tubular structures consistent with a paramyxovirus. Although repeated virus isolation attempts from the affected lung were negative, polyclonal and monoclonal fluorescent antibody tests were strongly positive for canine distemper virus (CDV). Frozen paired sera from each leopard demonstrated very high acute and convalescing titers to FPV; both animals also seroconverted to CDV, with titers in the male leopard higher than those in the female. Additional tests for toxoplasmosis, feline infectious peritonitis, feline rhinotracheitis, feline calicivirus, feline leukemia, canine parainfluenza, and bovine respiratory syncytial virus were all negative. The neurologic signs present in these leopards remained unexplained, but may have been attributable to CDV infection. A feral cat trapped on zoo property had feces positive for FPV by ELISA. Although the specific contributions of FPV and CDV toward the development of this case are unknown, it is likely that initial FPV-induced immunosuppression allowed the subsequent development of CDV in these snow leopards. The likelihood that initial FPV infection came from feral cats underscores the importance of feral animal control on zoo premises.

Abstract: Liver tissues from 126 captive cheetah were evaluated by light microscopy and histochemistry; eight animals were evaluated by electron microscopy. The main hepatic lesion, a vascular lesion resembling veno- occlusive disease (VOD) of the liver and characterized by subendothelial fibrosis and proliferation of smooth muscle-like cells in the central veins, was seen in 60% of the sexually mature cheetah. Although this hepatic vascular lesion was seen in cheetah as young as 1 year of age, the most severe lesions, usually associated with liver failure, were found in cheetah between the ages of 6 and 11. There was no sex predisposition, and in approximately 40% of the VOD cases, liver disease was not suspected clinically or at necropsy. VOD was found in other felidae, especially in the snow leopard. High levels of vitamin A in livers, as well as in diets of the cheetah, could be a contributing factor in the development of VOD in some groups of cheetah.

Abstract: Livers from 54 snow leopards, 4 days to 23 years old, that had died in 23 US zoos, were evaluated histopathologically to determine if the hepatic fibrosis, which has been noted to be prevalent in this species, was due to chronic active hepatitis from hepadnaviral infection, Ito cell proliferation, or hemosiderosis. Forty-two of 54 snow leopards had subintimal vascular fibrosis with partial or total occlusion of central and sublobular veins (veno-occlusive disease) of unknown origin. All 21 leopards older than 5 years were affected. Four leopards had chronic active hepatitis, and 12 leopards had cholangiohepatitis; but these lesions were not connected anatomically to central and sublobular venous fibrosis. Hepatocellular and Kupffer cell siderosis and Ito cell proliferation were prevalent and often coexisted with perisinusoidal, central, and sublobular venous fibrosis; but fibrosis was present in leopards without siderosis or Ito cell proliferation. The pattern and prevalence of veno-occlusive disease in these leopards was similar to that reported in captive cheetah (Acinonyx jubatus), suggesting that a common extrinsic factor may cause the majority of hepatic disease in these large felid animals in captivity.