Antimicrobial-Associated Risk Factors for Clostridium difficile Infection

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 s...

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Bibliographic Details
Published in:Clinical infectious diseases 2008-01, Vol.46 (Supplement-1), p.S19-S31
Main Authors: Owens, Robert C., Donskey, Curtis J., Gaynes, Robert P., Loo, Vivian G., Muto, Carlene A.
Format: Article
Language:English
Subjects:
Adult
Anti-Infective Agents - adverse effects
Anti-Infective Agents - therapeutic use
Antimicrobials
Cephalosporins
Clostridium
Clostridium difficile
Clostridium difficile - drug effects
Clostridium difficile - growth & development
Clostridium difficile - pathogenicity
Diarrhea
Disease Management
Drug Resistance, Bacterial
Drug Therapy, Combination
Ecosystem
Enterocolitis, Pseudomembranous - drug therapy
Enterocolitis, Pseudomembranous - epidemiology
Enterocolitis, Pseudomembranous - etiology
Enterocolitis, Pseudomembranous - prevention & control
Epidemiology
Fluoroquinolones
Humans
Infections
Intestines - microbiology
Microorganisms
Predisposing factors
Risk Factors
Time Factors
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Summary: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.
ISSN:1058-4838
1537-6591
DOI:10.1086/521859