The following are our views regarding the "letter to the editor" (Helicobacter is preserved in yeast vacuoles! Does Koch's postulates confirm it?) by Alipour and Gaeini, and the response "letter to the editor" (Candida accommodates non-culturable Helicobacter pylori in its vacuole-Koch's postulates aren't applicable) by Siavoshi and Saniee. Alipour and Gaeini rejected the methods, results, discussion, and conclusions summarized in a review article by Siavoshi and Saniee. The present article reviews and discusses evidence on the evolutionary adaptation of Helicobacter pylori (H. pylori) to thrive in Candida cell vacuoles and concludes that Candida could act as a Trojan horse, transporting potentially infectious H. pylori into the stomach of humans.

Helicobacter pylori infections are generally acquired during childhood and affect half of the global population, but its transmission route remains unclear. It is reported that H. pylori can be internalized into Candida, but more evidence is needed for the internalization of H. pylori in human gastrointestinal Candida and vaginal Candida.

Candida was isolated from vaginal discharge and gastric mucosa biopsies. We PCR-amplified and sequenced H. pylori-specific genes from Candida genomic DNA. Using optical and immunofluorescence microscopy, we identified and observed bacteria-like bodies (BLBs) in Candida isolates and subcultures. Intracellular H. pylori antigen were detected by immunofluorescence using Fluorescein isothiocyanate (FITC)-labeled anti-H. pylori IgG antibodies. Urease activity in H. pylori internalized by Candida was detected by inoculating with urea-based Sabouraud dextrose agar, which changed the agar color from yellow to pink, indicating urease activity.

A total of 59 vaginal Candida and two gastric Candida strains were isolated from vaginal discharge and gastric mucosa. Twenty-three isolates were positive for H. pylori 16S rDNA, 12 were positive for cagA and 21 were positive for ureA. The BLBs could be observed in Candida cells, which were positive for H. pylori 16S rDNA, and were viable determined by the LIVE/DEAD BacLight Bacterial Viability kit. Fluorescein isothiocyanate (FITC)-conjugated antibodies could be reacted specifically with H. pylori antigen inside Candida cells by immunofluorescence. Finally, H. pylori-positive Candida remained positive for H. pylori 16S rDNA even after ten subcultures. Urease activity of H. pylori internalized by Candida was positive.

In the form of BLBs, H. pylori can internalize into gastric Candida and even vaginal Candida, which might have great significance in its transmission and pathogenicity.

Helicobacter pylori (H. pylori), a gram-negative bacterium that colonizes the stomach, can cause chronic gastritis and peptic ulcers, as well as gastric cancer as a Class I carcinogen. However, the modes of H. pylori transmission are not clear. This review aims to clarify the transmission routes and patterns of H. pylori and identify efficacious prevention measures.

Studies of H. pylori transmission were identified using PubMed, the Web of Science, and Cochrane Central; the retrieval deadline was October 2022.

The transmission routes of H. pylori are discussed, focusing on the five primary transmission routes, namely fecal-oral, oral-oral, gastric-oral, anal-oral, and genital-oral. We propose that H. pylori is contracted through multiple transmission routes. Additionally, we summarize the key transmission patterns of H. pylori, including person-to-person and animal-to-human transmission, as well as foodborne and occupational exposure.

Fecal-oral appears to be the most common H. pylori transmission routes. Although the oral-oral pathway is also important, the evidence does not support that this route of transmission is universal. The gastric-oral route occurs primarily in children and patients who are prone to vomiting. Meanwhile, the anal-oral and genital-oral routes remain hypothetical. Person-to-person and foodborne infections represent the predominant transmission patterns of H. pylori, whereas strong environmental and occupational limitations are associated with animal-to-human and occupational exposure.

Polymicrobial biofilms have a significant impact on pathogenesis of infectious microorganisms. Many human diseases are affected by colonization of multi-species communities affecting negatively the treatments and increase the risks for the health. In particular, in the epithelium of the stomach co-existence between C. albicans and H. pylori has been described, which has been associated to a synergistic effect on ulcer pathogenesis.

The objective of this work was to advance in the understanding of surface interaction between H. pylori and C. albicans for the formation of polymicrobial biofilms.

Studies of microbial surfaces both bacterium, yeast and co-cultures of them were carried out by infrared spectroscopy, deconvolution analysis, transmission and scanning electron microscopies, and optic microscopy. Additional methods were used to contrast the results as dynamic light scattering, contact angle, agarose gel electrophoresis and gene amplification.

Several surface interaction mechanisms promote the anchoring of H. pylori on C. albicans, cell co-aggregation, and polymicrobial biofilm formation, main identified interactions were: (i) hydrophobic interactions between non-polar peptide chains and lipid structures, characterized by θ_w among 84.9 ± 1.6 (γ = 22.78 mJ/m² with 95.3 of dispersive contribution) and 76.6 ± 3.8 (γ = 17.34 mJ/m², 40.2 of dispersive contribution) for C. albicans and H. pylori, respectively, (ii) hydrogen bonds between surface components of yeast and bacterium (e.g., -S-H⋅⋅⋅NH₂- or -S-H⋅⋅⋅O[bond, double bond]CO-) and (iii) thiol-mediated surface interactions identified by displacements to lower wavenumbers (Δv = 5 cm^-1). Evidence of internalization and electrostatic interactions were not evidenced. All observations were congruent with the biofilm formation, including the identification of small-size biostructures (i.e., 122-459 nm) associated with extracellular proteins, extracellular DNA, or outer membrane vesicles were observed characteristic of biofilm formation.

It is concluded that biofilm is formed by co-aggregation after anchoring of H. pylori on C. albicans. Several surface interactions were associated with the prevalence of H. pylori, the possibility to find C. albicans in the stomach epithelium infected by H. pylori, but also, strength interactions could be interfering in experimental observations associated with bacterial-DNA detection in culture mixtures.