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In the Clinic |

Clostridium difficile Infection

Margaret Trexler Hessen, MD
Ann Intern Med. 2010;153(7):ITC4-1. doi:10.7326/0003-4819-153-7-201010050-01004
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Antibiotic-associated diarrhea was described in the 1950s. By 1978, Clostridium difficile had been established as the most common cause of infection, accounting for 15% to 25% of cases (1). The reported incidence and severity as measured by total mortality and colectomy rates rose steadily from 1993 to 2003 (2). A national survey in 2008 of 648 U.S. hospitals reported an overall C. difficile prevalence of 13.1 per 1000 inpatients (3). In the past decade, a strain with increased virulence has been described in relation to outbreaks in Canada, the United States, and Europe. This strain, designated NAP1/BI/027, produces a binary toxin not previously associated with C. difficile and produces substantially (15- to 20-fold) more toxin A and B than other strains. This strain is associated with more severe disease and mortality rates of 7% or more. It also seems to be more readily transmissible, and has been associated with community-acquired disease in persons with no established risk factors, including peripartum women and children. It is very resistant to fluoroquinolones, and emergence is believed to have been fostered by extensive use of these drugs in health care settings and in the community (4–6). This emergence of a hypervirulent form of C. difficile should prompt increased caution in prescribing fluoroquinolones in addition to those agents previously identified as frequent triggers of C. difficile diarrhea.

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Figure.

Treatment strategies for Clostridium difficile diarrhea. GI = gastrointestinal; ID = infectious disease; IV = intravenous; PO = oral; QID = four times daily; TID = three times daily.

*Leukocyte count ≥ 15 × 109 cells/L or creatinine level ≥ 1.5 times baseline.

†Associated with significant ileus, toxic megacolon, hypertension, or shock.

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