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Chandra, S., & Laughlin, D. C. (1975). Virus-like particles in cystic mammary adenoma of a snow leopard. Cancer Res, 35(11 Pt 1), 3069–3074.
Abstract: Virus-like particles were observed in the giant cells of a mammary adenoma of a snow leopard kept in captivity. Particles that measured 115 to 125 nm in diameter budded from the lamella of endoplasmic reticulum and were studded on their inner surfaces with dense granules (approximately 12 nm) that gave them their unique ultrastructural morphology. Such particles were not observed extracellularly. Type B or type C particles were not seen in the tumor tissue.
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Gosselin, S. J., Loudy, D. L., Tarr, M. J., Balistreri, W. F., Setchell, K. D., Johnston, J. O., et al. (1988). Veno-occlusive disease of the liver in captive cheetah. Vet Pathol, 25(1), 48–57.
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.
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Munson, L., & Worley, M. B. (1991). Veno-occlusive disease in snow leopards (Panthera uncia) from zoological parks. Vet Pathol, 28(1), 37–45.
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.
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Pollock, R. V., & Carmichael, L. E. (1983). Use of modified live feline panleukopenia virus vaccine to immunize dogs against canine parvovirus. Am J Vet Res, 44(2), 169–175.
Abstract: Modified live feline panleukopenia virus (FPLV) vaccine protected dogs against canine parvovirus (CPV) infection. However, unlike the long- lived (greater than or equal to 20-month) immunity engendered by CPV infection, the response of dogs to living FPLV was variable. Doses of FPLV (snow leopard strain) in excess of 10(5.7) TCID50 were necessary for uniform immunization; smaller inocula resulted in decreased success rates. The duration of immunity, as measured by the persistence of hemagglutination-inhibiting antibody, was related to the magnitude of the initial response to vaccination; dogs with vigorous initial responses resisted oronasal CPV challenge exposure 6 months after vaccination, and hemagglutination-inhibiting antibodies persisted in such dogs for greater than 1 year. Limited replication of FPLV in dogs was demonstrated, but unlike CPV, the feline virus did not spread to contact dogs or cats. Adverse reactions were not associated with living FPLV vaccination, and FPLV did not interfere with simultaneous response to attenuated canine distemper virus.
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Schmidt, R. E., Eisenbrandt, D. L., & Hubbard, G. B. (1984). Tyzzer's disease in snow leopards. J Comp Pathol, 94(1), 165–167.
Abstract: Tyzzer's disease was diagnosed histologically in 2 litters of newborn snow leopard kittens. The gross and histological lesions were similar to those reported in domestic cats and other animals. No signs of illness was noted in either of the snow leopard dams.
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Isenbugel, E., & Weilemann P. (1988). Treatment of Bladder Diverticulum and Ascites in a Female Snow Leopard. In H.Freeman (Ed.), (pp. 171–172). India: International Snow Leopard Trust and Wildlife Institute of India.
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Maity, B., Chakraborty, G., & Pradhan, K. K. (1994). Toxocariasis in snow leopard (Panthera unica). Indian Veterinary Journal, 71(5), 499–501.
Abstract: Spontaneous occurrence of toxocariasis (Toxocaracati) in captive snow leopards with symptoms of diarrhoea, general malaise, letherapy, dehydration, partial or complete anorexia, vomiting with or without expulsion of the ascarid is reported. Response to anthelmintic drug pyrantal pamoate along with antibacterial drug sulphadimethyl pyrimidine and supportive therapy is recorded.
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Paul, H. A., Bargar, W. L., & Leininger, R. (1985). Total hip replacement in a snow leopard. J Am Vet Med Assoc, 187(11), 1262–1263.
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White, S. D., Stannard, A. A., Ihrke, P. J., & Rosser, E. J. (1981). Therapy of demodicosis in snow leopard challenged. J Am Vet Med Assoc, 178(9), 877–878.
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Hast, M. H. (1989). The Larynx of Roaring and Non-Roaring Cats. The Journal of Anatomy, Summer.
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