A total of 631 serum samples collected in 1969, 1979, and 1989 from adults and children were screened for Helicobacter pylori by Western blot analysis. Results showed that H. pylori seroprevalence has become less frequent over the 20-year period. By studying seropositivity by year of birth, the magnitude of a cohort effect of H. pylori seropositivity was estimated. The odds of being seropositive decreased by 26% per decade, P = .008 (95% confidence interval, 8%-41%). Estimates of seroprevalence adjusted for both age-specific variation and the cohort effect suggest that most seropositivity in adults occurs by the age of 15 years. The implication of these findings is that H. pylori infection is becoming less frequent and is predominantly acquired in childhood.

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It has been reported that Helicobacter hepaticus infection of mice leads to chronic hepatitis and hepatocarcinoma. Our aim was to monitor a cohort of 80 conventional A/J mice in which half of the mice were infected by H. hepaticus in order to study the evolution of the infection and the pathological changes in comparison to uninfected mice. H. hepaticus was detected by culture only in some colon and cecum specimens after 17 months of age, while PCR detected H. hepaticus in the intestines of all inoculated mice after only 5 months of infection. The percentage of mice in which H. hepaticus was detected in the gallbladder, bile ducts, and liver by PCR, as well as the number of bacteria present in the liver, tended to increase with increasing age and longer infection time. Anti-H. hepaticus immunoglobulin G antibodies were positive by enzyme-linked immunosorbent assay only in inoculated mice. Pathological findings were also more frequent as the mice grew older: fibrosis was present (especially in the peripheral part of the liver), and significant portal inflammation including lymphoid nodules was present in almost all infected animals. Biliary lesions of neutrophilic acute cholangitis or lymphocytic cholangitis were noted. However, lesions were also observed in uninfected animals, although at a significantly lower level, and the only hepatocellular carcinoma occurred in an uninfected mouse. The evolution towards hepatocarcinoma is not always the endpoint and may depend on the bacterial strain and on the environmental conditions.Helicobacter species are responsible for chronic infections. In humans, Helicobacter pylori induces gastritis, which may last for decades and may be a lifelong condition. This infection is the first bacterial infection found to be involved in the development of a carcinogenic process in humans (8).After the occurrence of an unexpected and high level of hepatocellular tumors in mice with chronic active hepatitis, H. hepaticus was cultured from the liver and identified as a new species of Helicobacter that induces carcinoma (5). This bacterium has been the topic of extensive research since then. There have been studies on diagnostic methods (4, 13, 16, 17), pathogenic properties (2, 18), and the process of carcinogenesis (3, 9, 15) but few prospective studies of the natural history of H. hepaticus infection and liver pathology in mice. Therefore, our aim was to study the natural history of this infection for 17 months and to use the LightCycler methodology to quantitate the bacteria present in the liver.Study design. Eighty male A/J mice (3 to 4 weeks old) (not specific pathogen free), obtained from Jackson Laboratory (Bar Harbor, Maine), were maintained in microisolator cages and fed conventional food (Usine d'Alimentation Rabonnelle, Villemoisson-sur-Orge, France). The mice were cared for in accordance with the National Institutes of Health guidelines. Half of the mice were orally inoculated with H. hepaticus (group I), and the other half (group II) were used as controls. H. hepaticus type st...