BACKGROUND: Frequent occurrence of Helicobacter pylori in the human gastrointestinal tract and its persistence due to unsuccessful antimicrobial therapy might be related to a stage in the life cycle of H. pylori in which the bacterium establishes itself as an intracellular symbiont in yeast. In this study, occurrence of non-culturable H. pylori in the oral yeast was assessed by targeting vacuolating cytotoxin A (vacA s1s2) and ureAB genes in the total DNAs of yeasts. METHODS: DNAs were extracted from 13 oral yeasts in which bacterium-like bodies, suspected to be H. pylori, were observed microscopically. Primers were recruited to amplify vacA s1s2 and ureAB genes. DNAs from H. pylori and E. coli were used as controls. The amplicons from one yeast and H. pylori were sequenced. Yeasts were identified as Candida albicans. RESULTS: Fragments of vacA s1s2 and ureAB genes were amplified from 13 yeasts. The size of PCR products was 286 bp for vacA s1s2 gene and 406 bp for ureAB gene. Similar bands were obtained from the control H. pylori, and the results for E. coli were negative. The data from sequencing of PCR products showed about 98% homology between the genes amplified from yeast and those from H. pylori. CONCLUSIONS: The results of this study showed the intracellular occurrence of H. pylori in yeast. This endosymbiotic relationship might explain the persistence of H. pylori in the oral cavity, the consequence of which could be reinoculation of the stomach by the bacterium and spread of infection among human populations.
BACKGROUND: Frequent occurrence of Helicobacter pylori in the humangastrointestinal tract and its persistence due to unsuccessful antimicrobial therapy might be related to a stage in the life cycle of H. pylori in which the bacterium establishes itself as an intracellular symbiont in yeast. In this study, occurrence of non-culturable H. pylori in the oral yeast was assessed by targeting vacuolating cytotoxin A (vacA s1s2) and ureAB genes in the total DNAs of yeasts. METHODS: DNAs were extracted from 13 oral yeasts in which bacterium-like bodies, suspected to be H. pylori, were observed microscopically. Primers were recruited to amplify vacA s1s2 and ureAB genes. DNAs from H. pylori and E. coli were used as controls. The amplicons from one yeast and H. pylori were sequenced. Yeasts were identified as Candida albicans. RESULTS: Fragments of vacA s1s2 and ureAB genes were amplified from 13 yeasts. The size of PCR products was 286 bp for vacA s1s2 gene and 406 bp for ureAB gene. Similar bands were obtained from the control H. pylori, and the results for E. coli were negative. The data from sequencing of PCR products showed about 98% homology between the genes amplified from yeast and those from H. pylori. CONCLUSIONS: The results of this study showed the intracellular occurrence of H. pylori in yeast. This endosymbiotic relationship might explain the persistence of H. pylori in the oral cavity, the consequence of which could be reinoculation of the stomach by the bacterium and spread of infection among human populations.