Clostridium difficile infection in hospitals: risk factors and responses

• Published in: Canadian Medical Association journal (CMAJ) 2004-07, Vol.171 (1), p.45-46
• Main Authors: Louie, Thomas J, Meddings, Jon
• Format: Article
• Language: English
• Subjects: Anti-Bacterial Agents - adverse effects; Anti-Ulcer Agents - adverse effects; Clostridium difficile; Clostridium Infections - chemically induced; Clostridium Infections - epidemiology; Clostridium Infections - microbiology; Clostridium Infections - prevention & control; Control; Diarrhea; Diarrhea - chemically induced; Diarrhea - epidemiology; Diarrhea - microbiology; Diarrhea - prevention & control; Hospitals; Humans; Infection Control; Infections; Infectious diseases; Proton Pump Inhibitors; Quebec - epidemiology; Risk Factors; Treatment
• ISSN: 0820-3946; 1488-2329
• DOI: 10.1503/cmaj.1040966

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.5 Whether 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. Finally, a word on antibiotics inducing C. difficile diarrhea. With the exception of MRSA, these nosocomial pathogens, along with C. difficile, are microbes that multiply in the intestinal tract under selective antibiotic pressure. Contamination of the hospital environment with a myriad of gut-amplified nosocomial pathogens is an inevitable consequence of the use of antimicrobials. It is to the risk of patients that virtually all antimicrobials used in hospital or in the community can be selectors for this organism, with the exception of the aminoglycosides. Over the last decade we have observed a reduction in the use of aminoglycosides because of their potential for oto- and nephrotoxicity. Clindamycin, cephalosporins as a class (with particular emphasis on second-and third-generation agents) and ampicillin are regarded as the most common inducers.10,11 Q