Clostridium difficile infection in hospitals: risk factors and responses

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Abstract
The intuitively obvious explanation for the increased risk of acquiring this common nosocomial pathogen is that the reduction of gastric acidity abrogates a major host defence barrier against intestinal pathogens. As such, a larger proportion of organisms in the vegetative state and acid-resistant spores ever present in the hospital environment could access the lower gastrointesinal tract. Pathogenesis might not be simply a numbers game, however, and other explanations should be sought. Could PPIs have an independent effect within the colon? Whereas most clinicians regard the effect of PPIs as being localized to the gastric mucosa, studies have confirmed that H+,K+-ATPases, the target of PPIs, are present in the colonic mucosa.2 The function of these pumps and their interaction with the PPI class of compounds remains unclear. In several studies, these membrane proteins appear functionally and biochemically distinct from the gastric proton pump,3,4 suggesting that the PPI class of drug may not affect their function. However, there are also data that one PPI (lansoprazole) may bind to the colonic mucosa.5Whether PPIs affect the function of the colonic protein and subsequently alter the intra-colonic biology of C. difficile infection and the production of C. difficile cytotoxins A and B in animals or in man is completely unknown. Although PPIs appear to increase the likelihood of CDAD, it would be premature to link severity of infection to the use of PPIs. Infection with particular strains of C. difficile capable of expressing more toxin(s), or other undefined virulence characteristics should be considered.