Vector potential of cockroaches for Helicobacter pylori infection.

OBJECTIVES: The routes of human infection with Helicobacter pylori remain unclear. In the present study, we examined cockroaches as possible vectors for transmission of H. pylori. METHODS: We used a common species of cockroach (Periplaneta fuliginosa). After a 3-day fast, cockroaches were placed on agar plates containing freshly grown H. pylori (Sydney strain) (challenge group) or on sterile agar plates without H. pylori (control group). After 24 h of challenge, cockroaches were moved to disinfected containers, and sterile food and water were provided. The external surfaces (legs and body) and excreta of the cockroaches were sampled for culture, rapid urease test, and polymerase chain reaction (PCR). RESULTS: H. pylori were culturable from the excreta of the challenge group for 24 h postchallenge. Positive rapid urease test results were obtained up to day 3, and PCR analysis was positive for H. pylori DNA up to day 7 from the excreta. In contrast, H. pylori were not culturable from the external surfaces of the cockroaches. The rapid urease test was positive for only 8 h, and PCR analysis was positive for H. pylori DNA for 1 day from the external surface. CONCLUSIONS: Cockroaches usually live in unsanitary environments and may contaminate foods and food containment areas such as pantries. Transmission of H. pylori infection could be achieved via inadvertent ingestion of foods contaminated with cockroach excreta containing viable H. pylori.

Helicobacter pylori infection in mice: Role of outer membrane proteins in colonization and inflammation.

BACKGROUND & AIMS: Mouse models of Helicobacter pylori infection have yielded variable results with respect to colonization and inflammation. We examined whether outer membrane proteins (OMPs) or the cag pathogenicity island (PAI) was responsible for some of this variability. METHODS: C57BL/6 mice received clinical H. pylori isolates with different genotypes for the cag PAI and OMP gene switch status, as well as isogenic gene knockout mutants for cagE, oipA, babA2, hopZ, cagE/oipA, or oipA/hopZ. Bacterial density, histology, and mucosal cytokine/chemokine levels were measured after 4 and 12 weeks. RESULTS: oipA, hopZ, hopO, and hopP switch status influenced both H. pylori density and colonization ability in mice. When 2 or more of the genes were "off," colonization rates were markedly reduced compared with those for strains with all genes "on" (from 58% to 0% after 12 weeks). oipA knockout mutants caused reduced inflammation and decreased mucosal interleukin 6 messenger RNA and KC messenger RNA and protein levels. H. pylori density and colonization ability were reduced if hopO or hopP switch status was changed from "on" to "off." There was a close relationship (r > 0.7) between the H. pylori density of the gastric mucosa of humans and mice when using the same H. pylori strains. CONCLUSIONS: Many of the differences reported with mouse models may reflect subtle unrecognized differences (e.g., switch status of an OMP gene), emphasizing the necessity of characterizing isolates before and after experiments. The mouse model may be suitable for investigating factors related to colonization ability, H. pylori density, and gastric mucosal inflammation.