It has been wondered how Helicobacter pylori actually spreads from human to human.
Beside the fecal-oral transmission in low hygienic standards, some few people have it in notable amounts even freely in their saliva, from where it can spread by aerosols, kissing or sharing drinks.
Another transmission vector and reservoir, however, appears to be through oral, vaginal, food-borne and environmental spread of H.pylori-infected yeasts, which provide greatly enhanced protection to these bacteria, as shown by these Iranian researchers:
Vacuoles of Candida yeast as a specialized niche for Helicobacter pylori, 2014
[image: 1775649512607-candida-pylori.jpg]
The internalized H.pylori also reproduces inside yeast vacuoles and when the yeast divide, H.pylori is imparted to the daughter generation.
Helicobacter pylori (H. pylori ) have been observed within yeast vacuoles by light and fluorescence microscopy, and their presence has been confirmed by the detection of H. pylori -specific genes and proteins in yeast extracts, such as VacA subunits, UreA, peroxiredoxin and thiol peroxidase.
Moreover, non-culturable H. pylori cells have been found in subsequent generations
of yeasts, indicating the generational transmission of the bacteria is part of the transfer of vacuolar content.
H. pylori are therefore well-equipped to establish in the vacuoles of yeast, which provide them with essential nutrients such as ergosterol for multiplication, as a pre-adaptation for invasion of human cells.
Indeed, H. pylori-specific genes ureAB and babAB were detected in Candida yeasts from Iranian traditional breads (Sangak, Taftoon and Barbary), yogurt, banana skin, grape juice and quince jam, which carried vacuolar fast-moving and non-culturable BLBs (Figure 2)[87].
Thus, foodborne yeasts originating from the environment, which were once considered as harmless microorganisms when ingested through fermented foods such as dairy products[38,89], including kefir and kumis[94,95], could now be pinpointed as a public health problem source. In this regard, occurrence of yeast in food and environment can be considered as an important indicator of contamination with H. pylori and other pathogenic bacteria. Therefore, a key approach for the control of H. pylori infection may be to reduce the yeast content of foods through proper hygienic practice, especially by food handlers and during food processing[87]
Would be interesting to know about the contamination in foods from "Western" sources and if H.pylori also infects saccharomyces boulardii/cerevisiae (baking yeast) and amoeba (water sources). And whether when we go buy goods which have not been baked like beer, (pasteurized) fermented foods or baking yeast (supplements?) they are free from intracellular bacteria?
There's a criticism of the study above which strongly questions the ability of bacteria to enter yeast cells. They do bring up amoeba and water supply, however:
Interestingly, several articles in the literature have shown similarity in prevalence of Acanthamoeba in drinking water sampled from different geographical locations and the prevalence of H. pylori in patients[8-19]. While we cannot observe such overlap between yeast and H. pylori incidences, it is more logical to believe that yeast cannot be a reservoir of H. pylori but that Acanthamoeba can play such a role.
Indeed, in an earlier publication, the same Iranian researchers also showed symbiosis in a co-culture of amoeba and H.pylori.
And they also found H.pylori in saccharomyces cerevisiae (baking + beer yeast) which was meant as a negative control - although in a less virulent, CagA-toxin free variation. Which could be coincidence or not. No testing for VacA-toxin was done in this context.
