Relationship between oral and gastric yeasts and their role in colonization of H. pylori in stomach was studied.

Four groups of 221, 7, 44 and 10 patients were used for isolation of H. pylori and oral and gastric yeasts. In group one, gastric biopsies were used for isolation of H. pylori and yeast, urease activity and staining with Gram’s, hematoxylin & eosin (H&E) and immunohistochemistry (IHC) methods. Gram-stained gastric biopsies were examined with light microscope to observe H. pylori, yeast and released extracellular vesicles (EVs). In other 3 groups, DNAs extracted from H. pylori and yeasts were used for amplification of H. pylori-specific genes; 16S rRNA, VacA (s1/s2), vacA (m1/m2), cagA and jhp947.Wet mounts of yeasts in group 2 were examined for observing intracellular bacteria and released EVs.

Among 221 patients, 65 (29.3%) had oral yeasts (69.23% C. albicans and 30.76% Candida spp.) followed by H. pylori (35, 15.8%) and gastric yeasts (31, 14%) (67.75% C. albicans and 32.25% Candida spp.) (p value > 0.05). Compared with gastric yeast, culture of oral yeast showed a significant correlation with positive results of H. pylori detected by IHC (10.3%), Gram stain (9%), RUT (6.3%), H&E (4.9%) and culture (4%) (p value < 0.05). Detection of H. pylori genes in yeast isolates from other 3 groups showed that oral and gastric yeasts carried similar H. pylori genes, thus could have a common source. Detection of H. pylori genes in different species of Candida showed that harboring H. pylori is not species- or site- specific. Microscopic examination of Gram-stained gastric biopsies and wet mount preparations of yeasts showed release of EVs that could carry H. pylori.

Oral yeast protects its intracellular H. pylori and releases it inside EVs to safely reach gastric mucosa. These results may clarify the environmental reservoir of H. pylori and explain bacterial reinfection after successful eradication.