1Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA, USA; 2Department of Internal Medicine, Division of Infectious Diseases, School of Medicine, University of California, Davis, CA, USA; 3Cheetah Conservation Fund, Windhoek, Namibia
Abstract
Gastritis continues to be an important disease of captive cheetah populations worldwide. Spiral Helicobacter-like organisms are present in lesions in captive cheetahs but are also seen in wild cheetahs without gastritis. This research aimed to determine if the development of disease in captive cheetahs was associated with specific strains of Helicobacter or the host immune response. To determine the species of Helicobacter in cheetah populations, complete and partial sequences of the 16s rRNA gene and urease genes of Helicobacter spp. present in gastric biopsy and necropsy tissues from 30 cheetahs (8 wild, 22 captive) were compared. No single strain of Helicobacter was associated with gastritis and similar strains were present in cheetahs with and without gastritis. Sequences from captive cheetahs were most homologous with H. pylori or H. heilmannii and only H. pylori-like strains were present in the wild cheetahs. H. acinonychis (previously H. acinonyx), the species of Helicobacter isolated from captive cheetahs at one institution, was not found in this study. The possibility that virulence factors are present in strains within the captive population but absent from strains infecting wild cheetahs is currently being investigated. Alternatively, in captive cheetahs, an aberrant host immune response to normally commensal Helicobacter could account for the development of gastritis. Chronic stress manifested as elevated glucocorticoids is well known to modulate the immune response. Because adrenocortical hyperplasia has been noted in captive but not wild cheetahs, baseline corticoid concentrations were compared between captive (n=20) and wild (n=20) cheetahs. Captive cheetahs were found to have up to four times higher baseline corticoid concentrations than wild cheetahs. The presence of similar organisms in cheetahs with and without disease, and evidence of hypercortisolemia in captive cheetahs suggests that a modulated immune response to Helicobacter, rather than the bacteria alone, may account for the differences in disease prevalence between captive and wild populations.