| Autor: |
Terio, K. A., Munson, L., Marker, L., Aldridge, B. M., Solnick, J. V. |
| Zdroj: |
Journal of Clinical Microbiology; January 2005, Vol. 43 Issue: 1 p229-234, 6p |
| Abstrakt: |
ABSTRACTChronic 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 Helicobacterspecies that were associated with gastritis in captive cheetahs but are apparently commensal in wild cheetahs. Helicobacterspecies were characterized by PCR amplification and sequencing of the 16S rRNA, urease, and cagAgenes and by transmission electron microscopy of frozen or formalin-fixed paraffin-embedded gastric samples from 33 cheetahs infected with Helicobacterorganisms (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 Helicobacterinfection 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. pyloriurease, suggesting that this bacteria is neither H. pylorinor “H. heilmannii.” The cagAgene was not identified in any case. These findings question a direct role for Helicobacterinfection in the pathogenesis of gastritis and support the premise that host factors account for the differences in disease between captive and wild cheetah populations. |
| Databáze: |
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