Journal Article

Antimicrobial-Associated Risk Factors for <i>Clostridium difficile</i> Infection

Robert C. Owens, Curtis J. Donskey, Robert P. Gaynes, Vivian G. Loo and Carlene A. Muto

in Clinical Infectious Diseases

Published on behalf of Infectious Diseases Society of America

Volume 46, issue Supplement_1, pages S19-S31
Published in print January 2008 | ISSN: 1058-4838
Published online January 2008 | e-ISSN: 1537-6591 | DOI: http://dx.doi.org/10.1086/521859
Antimicrobial-Associated Risk Factors for Clostridium difficile Infection

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Antimicrobial therapy plays a central role in the pathogenesis of Clostridium difficile infection (CDI), presumably through disruption of indigenous intestinal microflora, thereby allowing C. difficile to grow and produce toxin. Investigations involving animal models and studies performed in vitro suggest that inhibitory activity against C. difficile and differences in the propensity to stimulate toxin production may also influence the likelihood that particular drugs may cause CDI. Although nearly all antimicrobial classes have been associated with CDI, clindamycin, third-generation cephalosporins, and penicillins have traditionally been considered to harbor the greatest risk. Recent studies have also implicated fluoroquinolones as high-risk agents, a finding that is most likely to be related in part to increasing fluoroquinolone resistance among epidemic strains (i.e., restriction-endonuclease analysis group BI/North American PFGE type 1 strains) and some nonepidemic strains of C. difficile. Restrictions in the use of clindamycin and third-generation cephalosporins have been associated with reductions in CDI. Because use of any antimicrobial has the potential to induce the onset of CDI and disease caused by other health care–associated pathogens, antimicrobial stewardship programs that promote judicious use of antimicrobials are encouraged in concert with environmental and infection control–related efforts.

Journal Article.  8285 words.  Illustrated.

Subjects: Infectious Diseases ; Immunology ; Public Health and Epidemiology ; Microbiology

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