Aliment Pharmacol Ther 2011; 34: 1269–1281

Summary
Background  The use of proton pump inhibitors (PPIs) is increasing worldwide. Suppression of gastric acid alters the susceptibility to enteric bacterial pathogens.

Aim  This systematic review was undertaken to examine the relationship between PPI use and susceptibility to enteric infections by a specific pathogen based on published literature and to discuss the potential mechanisms of PPI enhanced pathogenesis of enteric infections.

Methods  PubMed, OVID Medline Databases were searched. Search terms included proton pump inhibitors and mechanisms of, actions of, gastric acid, enteric infections, diarrhoea, Clostridium difficile, Salmonella, Shigella and Campylobacter.

Results  The use of PPIs increases gastric pH, encourages growth of the gut microflora, increases bacterial translocation and alters various immunomodulatory and anti-inflammatory effects. Enteric pathogens show variable gastric acid pH susceptibility and acid tolerance levels. By multiple mechanisms, PPIs appear to increase susceptibility to the following bacterial enteropathogens: Salmonella, Campylobacter jejuni, invasive strains of Escherichia coli, vegetative cells of Clostridium difficile, Vibrio cholerae and Listeria. We describe the available evidence for enhanced susceptibility to enteric infection caused by Salmonella, Campylobacter and C. difficile by PPI use, with adjusted relative risk ranges of 4.2–8.3 (two studies); 3.5–11.7 (four studies); and 1.2–5.0 (17 of 27 studies) for the three respective organisms.

Conclusions  Severe hypochlorhydria generated by PPI use leads to bacterial colonisation and increased susceptibility to enteric bacterial infection. The clinical implication of chronic PPI use among hospitalized patients placed on antibiotics and travellers departing for areas with high incidence of diarrhoea should be considered by their physicians.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2036.2011.04874.x

Systematic review: the use of proton pump inhibitors and increased susceptibility to enteric infection.

The protective efficacy of oral B subunit killed whole-cell (BS-WC) and killed whole-cell (WC) cholera vaccines was assessed in 63 498 Bangladeshi children aged 2-15 years and women aged over 15 years. Each received three doses of BS-WC, WC, or placebo in a randomised, double-blinded fashion. Surveillance for cases seeking medical care up to six months after the third dose revealed 26 cases of confirmed cholera in the placebo group, 4 cases in the BS-WC group (protective efficacy 85%; p less than 0.0001), and 11 cases in the WC group (protective efficacy 58%; p less than 0.01). For each vaccine protective efficacy was consistent in different age-groups (2-10 years versus greater than 10 years) and for different severities of cholera.

Field trial of oral cholera vaccines in Bangladesh

Cholera is a substantial health burden on the developing world and is endemic in Africa, Asia, South America, and Central America. The exact scale of the problem is uncertain because of limitations in existing surveillance systems, differences in reporting procedures, and failure to report cholera to WHO; official figures are likely to greatly underestimate the true prevalence of the disease. We have identified, through extensive literature searches, additional outbreaks of cholera to those reported to WHO, many of which originated from the Indian subcontinent and southeast Asia. Such underestimation of cholera can have important implications for decisions on provision of health interventions for indigenous populations, and on risk assessments for travellers. Furthermore, until recently, it has not been possible to implement public-health interventions in low-income countries to eliminate disease, and the prevention of cholera in travellers has been limited to restrictive guidelines. However, a vaccine against cholera is now available that has proven efficacy and tolerability in mass vaccination campaigns in low-income countries, and among travellers.

https://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(07)70138-X.pdf

The true burden and risk of cholera: implications for prevention and control

Epidemiology of cholera

To cause the diarrheal disease cholera, Vibrio cholerae must effectively colonize the small intestine. In order to do so, the bacterium needs to successfully travel through the stomach and withstand the presence of agents such as bile and antimicrobial peptides in the intestinal lumen and mucus. The bacterial cells penetrate the viscous mucus layer covering the epithelium and attach and proliferate on its surface. In this review, we discuss recent developments and known aspects of the early stages of V. cholerae intestinal colonization and highlight areas that remain to be fully understood. We propose mechanisms and postulate a model that covers some of the steps that are required in order for the bacterium to efficiently colonize the human host. A deeper understanding of the colonization dynamics of V. cholerae and other intestinal pathogens will provide us with a variety of novel targets and strategies to avoid the diseases caused by these organisms.

/pdf/intestinal-colonization-dynamics-of-vibrio-cholerae-4lxe4kolco.pdf

Intestinal Colonization Dynamics of Vibrio cholerae

Low gastric acid as a rise factor for cholera transmission: Application of a new non-invasive gastric acid field test

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Low gastric acid as a rise factor for cholera transmission: Application of a new non-invasive gastric acid field test