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A spiral- or helix-shaped bacterium that colonizes the stomachs of cats has been isolated in pure culture for the first time. The organism is tightly coiled with tufts of 10 to 17 polar flagella positioned slightly off center at the end of the cell. The body of the cell is entwined with unique periplasmic fibrils that usually occur in pairs, although groupings of one and three fibrils were also seen. The organism is strongly urease, catalase, and oxidase positive and is likely to belong to an as yet unclassified group of bacteria that are specifically adapted to the ecological niche provided by gastrointestinal mucus. Isolation of this organism will allow study of the factors influencing colonization of gastric mucosae, information relevant to the association of another mucus colonizer, Campylobacter pylori, with the human stomach. Recent reports of the isolation of other bacteria with the characteristic periplasmic surface structures suggests that the group may be more widespread than was hitherto thought. Bacteria with the morphology of the organisms seen in the cat stomach have been seen in gastric biopsies from humans. The organism whose isolation is reported here has been used in previous serological studies to support the hypothesis that spiral bacteria from animals can colonize the human stomach.

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Background and aims-Helicobacter pylori is a major cause of peptic ulcers and gastric cancer. Vaccine development is progressing but there is concern that immunisation may exacerbate Helicobacter induced gastritis: prophylactic immunisation followed by challenge with H felis or H pylori can induce a more severe gastritis in mice than seen with infection alone. The aim of this study was to investigate the relationship between immunity to Helicobacter infection and postimmunisation gastritis. Methods-(1) C57BL/6 mice were prophylactically immunised before challenge with either H felis or H pylori. Histopathology and colonisation were assessed one month post-challenge. (2) C57BL/6 mice were prophylactically immunised against H felis infection and gastritis assessed up to 18 months post-challenge. Results-Prophylactic immunisation induced a reduction in bacterial colonisation following H felis challenge which was associated with increased severity of active gastritis with neutrophil infiltration and atrophy. However, immunised mice challenged with H pylori SS1 had little evidence of pathology. Long term follow up showed that post-immunisation gastritis was evident at three months. However, from six months onwards, although immunised/challenged mice still developed gastritis, there was no significant diVerence between inflammation in these mice and infected controls. Postimmunisation gastritis was not associated with the serum antibody response. Immunisation prevented the formation of secondary lymphoid aggregates in the gastric tissue. Conclusion-The H felis mouse model of post-immunisation gastritis is the most extreme example of this type of pathology. We have shown in this model that postimmunisation gastritis is a transient event which does not produce long term exacerbation of pathology. (Gut 2001;49:467-473)

SUMMARYFaecal oral spread is claimed by many to be the mode of transmission of the gastric pathogenHelicobacter pylori. This idea is based not on experimental data but because the epidemiology ofH. pyloriinfection resembles that of other pathogens known to be spread by the faecal-oral route. This is in spite of the observation that no-one has been successful in culturingH. pylorifrom human stool. In this study, a series of transmission experiments are reported on animals infected with the gastric spirilla,Helicobacter felisand ‘Gastrospirillum hominis’. Germfree mice and rats infected withH. felisdid not transmit their infection to uninoculated mice despite prolonged contact in the same cage nor could the bacterium be isolated from their intestinal contents. This was confirmed in specific pathogen free mice where infected dams did not pass the helicobacter to their progeny. Similarly, mice infected with a human isolate of ‘Gastrospirillum hominis’ did not transmit the infection while in close contact with uninoculated mice. In contrast, in a limited series of experiments, bothH. pyloriandH. feliswere transmitted from infected gnotobiotic Beagle puppies to uninfected animals in the same enclosure. In addition, the gastric mucus from a cat with indigenous ‘Gastrospirillum’-like organisms was infectious for mice, whereas faecal content from the same animal was not. It is suggested that the difference between the murine and canine experiments is that the dogs are more likely to have oral-oral contact than rodents. Unlike dogs, mice and rats do not vomit and are coprophagous. It is concluded that the case for faecal-oral spread ofHelicobacterspecies is ‘not proven’ and that the inter-oral route is more likely.