The characterization and pathological significance of gastric campylobacter-like organisms in the ferret: a model for chronic gastritis?

Abstract

SUMMARYGastric campylobacter-like organisms (CLO) were isolated from gastric tissues removed at sacrifice from 17 mature ferrets; all animals were colonized, but no macroscopic mucosal lesions or histological features of chronic gastritis were seen. The isolates resembled Campylobacter pylori in many cultural and biochemical characteristics, and produced substantial urease activity, but there were sufficient differences from C. pylori to suggest that ferret gastric CLO represents a separate species. Comparison of human C. pylori and ferret gastric CLO may help to elucidate the pathogenicity of the former in patients with gastritis, and the ferret may serve as a useful animal model for the study of C. pylori infection.

Transfer of Campylobacter pylori and Campylobacter mustelae to Helicobacter gen. nov. as Helicobacter pylori comb. nov. and Helicobacter mustelae comb. nov., Respectively

“…Susceptible to nalidixic acid (30 pg) but resistant to cephalothin (30 pg). Does not exhibit leucine arylamidase activity (45). Isolated from the gastric mucosa of ferrets.…”

Pathogenesis ofHelicobacter pyloriInfection

“…The ferret pathogen H. mustelae was isolated shortly after H. pylori and was originally classified as Campylobacter pylori subsp. mustelae (197,202,630). It was subsequently shown to have characteristics different from H. pylori (198) and was later classified as H. mustelae (234).…”

Isolation ofHelicobacter mustelaeit from ferrets in New Zealand

“…When barrier-raised ferrets are infected with the organism by oral challenge, the gastric mucosa is colonised and an immune response and chronic gastritis result Fox et al, 1991b). However, colonisation by H. mustelae is not invariably linked to gastritis (Tompkins et al, 1988). A minority of studies have reported only moderate, or lack of, inflammation in infected ferrets, perhaps due to uncharacterised host factors affecting inflammatory response (Jeffries et al, 1987;Tompkins, 1989).…”

“…It is now accepted that H. mustelae colonises the gastrointestinal tract in almost 100% of ferrets in North America (Fox et al, 1991a;Fox and Lee, 1997). Helicobacter mustelae has also been isolated from ferrets in England, Canada and Australia (Fox and Lee, 1997;Tompkins et al, 1988). The failure of one study in New Zealand (Morris et al, 1988) to isolate H. mustelae from ferrets has been subsequently cited by others as indicating that this bacterium is not present in this country (Fox and Lee, 1997).…”