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Veterinary Pathology, Vol 34, Issue 6 549-556, Copyright © 1997 by American College of Veterinary Pathologists
ARTICLES |
R. E. Papendick, L. Munson, T. D. O'Brien and K. H. Johnson
Department of Pathology, College of Veterinary Medicine, University of Tennessee, Knoxville, USA.
Ongoing disease surveillance of necropsied captive cheetahs (Acinonyx jubatus) (n = 141) revealed a high prevalence of renal amyloidosis (n = 54 [38%]; age 1 to 16 years). The prevalence increased from 20% in pre- 1990 necropsies to 70% of cheetahs necropsied in 1995. In 74% of the cheetahs with amyloidosis, renal failure was determined to be the sole or partial cause of death. Papillary necrosis was seen only in affected cheetahs and involved 25% of these animals. Amyloid was present predominantly in the medullary interstitium, with minimal glomerular involvement. The amyloid deposits were immunohistochemically identified as AA type using antisera to both human and canine protein AA. A high percentage (52%) of animals with renal amyloid also had subsinusoidal hepatic AA amyloid deposits. Inflammatory diseases were identified in 100% of affected cheetahs. The most common inflammatory disease was chronic lymphoplasmacytic gastritis. The prevalence and severity of gastritis was higher in cheetahs with amyloidosis, and the prevalence of severe gastritis increased from 16% to 43%, coinciding with the increase in prevalence of amyloidosis. These findings suggest that cheetahs have a high prevalence of systemic amyloidosis in response to inflammation and that renal amyloidosis is an increasingly significant cause of morbidity and mortality in captive cheetah populations. Factors of potential importance in the apparent high prevalence of AA amyloidosis in cheetahs are currently being investigated in our laboratories.
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