Helicobacter pylori is a major human pathogen and a type I carcinogen, the transmission dynamics of which remain incompletely understood. From a One Health perspective, the interaction between environmental reservoirs, human hosts, and antimicrobial resistance represents a major concern. The Bogotá River basin, impacted by pollution and used extensively by communities, constitutes an ecological interface for pathogen circulation and genetic exchange.
Objective: The aim of this study was to characterize the environmental and clinical molecular profiles of H. pylori in the Bogotá River basin, focusing on virulence genotypes and clarithromycin resistance, and to assess the potential role of contaminated water in shaping bacterial diversity and antimicrobial susceptibility.
Methods: Fifty-one water samples from different sections of the Bogotá River and 24 gastric biopsies from exposed residents were analyzed. Detection of H. pylori was performed by PCR, targeting the vacA gene. Virulence genotyping included vacA alleles (s, m, i), cagA, and glmM. Clarithromycin resistance was evaluated by sequencing the 23S rRNA gene to identify resistance-associated mutations.
Results: H. pylori DNA was detected in 41.2% of river water samples and 50% of gastric biopsies, demonstrating dissemination. River samples displayed highly heterogeneous virulence genotypes, dominated by glmM(+) cagA(–) vacA s1m1 (28.6%) and s1m1i1 (19%). No water sample harbored the cagA gene, and viable bacteria could not be cultured, suggesting persistence primarily in non-culturable but potentially infectious states. Critically, all environmental samples exhibited wild-type 23S rRNA sequences, indicating absence of clarithromycin resistance. In contrast, 25% of clinical isolates carried the A2143G mutation, which is a key determinant of clarithromycin resistance.
Conclusions: These findings support a One Health model in which the aquatic environment acts as a reservoir of H. pylori genetic material that may contribute to bacterial evolution and antimicrobial resistance in human hosts through natural transformation. The clear divergence in clarithromycin susceptibility between environmental and clinical samples underscores the role of human-associated selective pressures.
