Systemic AA Amyloidosis in Captive Cheetahs (Acinonyx jubatus)

R. E. Papendick, L. Munson, T. D. O'Brien, K. H. Johnson

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78 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)549-556
Number of pages8
JournalVeterinary pathology
Issue number6
StatePublished - Nov 1997

Bibliographical note

Funding Information:
We thank the following institutions and their veterinarians for contributing tissues or slides for this study: Audubon Park and Zoological Gardens (Dr. S. Mikota, Dr. R. Aguilar), Binder Park Zoo (Dr. D. Rost), Cheetah Conservation Fund (L. Marker-Kraus), Cincinnati Zoo and Botanical Garden (Dr. M. Campbell, Dr. K. Cameron), Columbus Zoological Gardens (Dr. L. Kramer, Dr. R. Wack), Detroit Zoological Park (Dr. D. Agnew), Dickerson Park Zoo (Dr. D. Hardy), Fort Wayne Children's Zoo (Dr. K. Brown), Fossil Rim Wildlife Center (Dr. E. Blumer), Henson Robinson Zoo (Dr. G. Hurst), Honolulu Zoo (Dr. B. Okimoto), Kansas City Zoological Gardens (Dr. W. K. Suedmeyer), Knoxville Zoological Gardens (Dr. E. Ramsay), Louisville Zoological Gardens (Dr. R. Burns), Metropolitan Toronto Zoo (Dr. K. Mehren), Montgomery Zoo (Dr. B. Fiore), New York Zoological Society (Dr. T. McNamara), Oklahoma City Zoological Park (Dr. M. Barrie), Dr. J. Peddie, Zoological Society of Philadelphia (Dr. G. Pierce), Phoenix Zoo (Dr. K. Orr), Pittsburgh Zoo (Dr. S. Marks), Rio Grande Zoo (Dr. B. Snyder), San Antonio Zoological Gardens and Aquarium (Dr. M. Richardson), Zoological Society of San Diego (Dr. B. Rideout, Dr. I. Stalis), St. Louis Zoological Park (Dr. E. Miller, Dr. R. Junge), Sunset Zoological Park (Dr. J. Carpenter), University of Pretoria (Dr. N. Kriek), White Oak Conservation Center (Dr. S. Citino), Wildlife Safari (Dr. J. Mortenson), and Zoo de Vicennes (Dr. S. Rousselle). We also thank B. Collins and R. Moulton for their histotechnology assistance and P. Snow for photographic expertise. This study was supported in part by funds from the University of Tennessee and the Geraldine R. Dodge Foundation.


  • Acinonyx jubatus
  • Amyloidosis
  • Cheetah
  • Gastritis
  • Immunohistochemistry
  • Kidney
  • Liver


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