Helicobacter pylori infection is typically acquired in early childhood, and a predominantly intrafamilial transmission has been postulated. To what extent family members share the same strains is poorly documented. Our aim was to explore patterns of shared strains within families by using molecular typing. Family members of H. pylori-infected 10-to 12-year-old index children identified in a school survey were invited to undergo gastroscopy. Bacterial isolates were typed with random amplified polymorphic DNA and PCRrestriction fragment length polymorphism of the genes ureA-B, glmM, or flaA. The presence or absence of the cag pathogenicity island, a bacterial virulence factor, was determined by PCR. GelCompar II software, supplemented with visual inspection, was used in the cluster analysis. In 39 families, 104 individuals contributed 208 bacterial isolates from the antrum and corpus. A large proportion, 29 of 36 (81%) of the offspring in a sibship, harbored the same strain as at least one sibling. Mother-offspring strain concordance was detected in 10 of 18 (56%) of the families. Of 17 investigated father-offspring relations in eight families, none were strain concordant. Spouses were infected with the same strains in 5 of 23 (22%) of the couples. Different strains in the antrum and corpus were found in 8 of 104 (8%) of the subjects. Our family-based fingerprinting study demonstrates a high proportion of shared strains among siblings. Transmission between spouses seems to be appreciable. The data support mother-child and sib-sib transmission as the primary transmission pathways of H. pylori.Helicobacter pylori colonizes half of the world's population, and the infection is associated with chronic gastritis, peptic ulcer, gastric cancer, and gastric lymphoma. In-depth knowledge of the transmission patterns may constitute important information for future intervention strategies.In the absence of consistent and verified environmental reservoirs, a predominantly person-to-person transmission has been postulated. H. pylori infection is associated with poor living conditions, and possible transmission routes are fecaloral, oral-oral, or gastro-oral, but firm evidence is lacking (36). The infection clusters in families and is usually acquired in early childhood. A child's risk of being infected is largely determined by the presence or absence of infected family members. Having an infected mother has been suggested to be a more prominent risk factor than having an infected father (30,35). Indications of sib-sib transmission have been reported (14). Transmission between spouses occurs but its significance is unclear (5, 9, 19).Molecular typing of pathogens can corroborate and further characterize the transmission pathways suggested by epidemiologic data based on infection status. Shared strains among individuals indicate person-to-person transmission or acquisition from a common source. Unrelated individuals harbor distinct H. pylori isolates (1), while clonal lineages can be discerned within families (2,7,11,16,20,22,24,2...

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This study aimed to disentangle the independent contributions of Helicobacter pylori infections in mothers, fathers and siblings to the risk for the infection in the 11-13 years age group. Index children from a cross-sectional Stockholm school survey and their family members completed questionnaires and contributed blood samples. H. pylori serostatus was determined with an enzyme-linked immunosorbent assay and immunoblot. Fifty-four seropositive and 108 seronegative index children were included and 480 out of 548 family members contributed blood. In multivariate logistic regression modelling, having an infected mother (OR 11.6, 95% CI 2.0-67.9) or at least one infected sibling (OR 8.1, 95% CI 1.8-37.3) were risk factors for index child infection, whilst the influence of infected fathers was non-significant. Birth in high-prevalence countries was an independent risk factor (OR 10.4, 95% CI 3.4-31.3). H. pylori infections in mothers and siblings and birth in high-prevalence countries stand out as strong markers of infection risk amongst children in Sweden.

A cohort of Swedish children was monitored from 6 months to 11 years of age. Immunoglobulin G (IgG) and IgA antibodies to Helicobacter pylori were measured in 1,857 serum samples, drawn at the ages of 6, 8, 10, 18 months and 2, 4, and 11 years. Of the 294 children, 40 (13.6%) were found to have been infected at some time. However, at 11 years of age, only 6 of 201 (3%) children were seropositive. The highest seroprevalence of positive results, 10%, was found at 2 years of age, and the highest incidence of 13.3% could be calculated for the period between 18 months and 2 years of age. There were no confirmed additional cases for children between 4 and 11 years of age. Infection with H. pylori thus occurs at an early age in a developed country (as well as in developing countries), and spontaneous clearance seems to be common.