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Journal of Clinical Microbiology, January 2005, p. 229-234, Vol. 43, No. 1
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.1.229-234.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Comparison of Helicobacter spp. in Cheetahs (Acinonyx jubatus) with and without Gastritis

K. A. Terio,1* L. Munson,1 L. Marker,2 B. M. Aldridge,1 and J. V. Solnick3

Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine,1 Departments of Internal Medicine and Medical Microbiology and Immunology, Center for Comparative Medicine, School of Medicine, University of California, Davis, California,3 Cheetah Conservation Fund, Otjiwarongo, Namibia2

Received 26 May 2004/ Returned for modification 6 July 2004/ Accepted 8 September 2004

Chronic gastritis causes significant morbidity and mortality in captive cheetahs but is rare in wild cheetahs despite colonization by abundant spiral bacteria. This research aimed to identify the Helicobacter species that were associated with gastritis in captive cheetahs but are apparently commensal in wild cheetahs. Helicobacter species were characterized by PCR amplification and sequencing of the 16S rRNA, urease, and cagA genes and by transmission electron microscopy of frozen or formalin-fixed paraffin-embedded gastric samples from 33 cheetahs infected with Helicobacter organisms (10 wild without gastritis and 23 captive with gastritis). Samples were screened for mixed infections by denaturant gel gradient electrophoresis of the 16S rRNA gene and by transmission electron microscopy. There was no association between Helicobacter infection and the presence or severity of gastritis. Eight cheetahs had 16S rRNA sequences that were most similar (98 to 99%) to H. pylori. Twenty-five cheetahs had sequences that were most similar (97 to 99%) to "H. heilmannii" or H. felis. No cheetahs had mixed infections. The ultrastructural morphology of all bacteria was most consistent with "H. heilmannii," even when 16S rRNA sequences were H. pylori-like. The urease gene from H. pylori-like bacteria could not be amplified with primers for either "H. heilmannii" or H. pylori urease, suggesting that this bacteria is neither H. pylori nor "H. heilmannii." The cagA gene was not identified in any case. These findings question a direct role for Helicobacter infection in the pathogenesis of gastritis and support the premise that host factors account for the differences in disease between captive and wild cheetah populations.


* Corresponding author. Present address: Zoological Pathology Program, University of Illinois, LUMC Bldg. 101, Rm. 0745, 2160 S. First St., Maywood, IL 60153. Phone: (708) 216-1185. Fax: (708) 216-5934. E-mail: kterio{at}lumc.edu.


Journal of Clinical Microbiology, January 2005, p. 229-234, Vol. 43, No. 1
0095-1137/05/$08.00+0     doi:10.1128/JCM.43.1.229-234.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.




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