Clostridium

in the clinic

Clostridium difficile Infection
Prevention Diagnosis Treatment Practice Improvement CME Questions
Section Editors Barbara J. Turner MD, MSED Sankey Williams, MD Section Editors Darren Taichman, MD, PhD Physician Writer Margaret Trexler Hessen, MD

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The content of In the Clinic is drawn from the clinicalinformation and education resources of the American College of Physicians (ACP), including PIER (Physicians’ Information and Education Resource) and MKSAP (Medical Knowledge and Self-Assessment Program). Annals of Internal Medicine editors develop In the Clinic from these primary sources in collaboration with the ACP’s Medical Education and Publishing Division and with the assistance of science writers andphysician writers. Editorial consultants from PIER and MKSAP provide expert review of the content. Readers who are interested in these primary resources for more detail can consult http://pier .acponline.org, http://www.acponline.org/products_services/ mksap/15/?pr31, and other resources referenced in each issue of In the Clinic. CME Objective: To review current evidence for the prevention,diagnosis, and treatment of Clostridium difficile infection The information contained herein should never be used as a substitute for clinical judgment. © 2010 American College of Physicians

in the clinic

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ntibiotic-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. Thisstrain, 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 establishedrisk 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 asfrequent triggers of C. difficile diarrhea.

Prevention
How does a patient acquire C. difficile infection? Colonization with C. difficile occurs through the fecal–oral route, usually by person-to-person transmission. Contaminated fomites and the hands of health care workers are another source of transmission (7).
A prospective 11-month study of C. difficile transmission in hospitalizedpatients showed that 21% of patients who initially had negative test results acquired the organism during admission; C.  difficile was cultured from environmental surfaces in 49% of hospital rooms of symptomatic patients and from the hands of 59% of the health care workers caring for these patients (8).

1. Bartlett JG, Gerding DN. Clinical recognition and diagnosis of Clostridium difficile infection.Clin Infect Dis. 2008;46 Suppl 1:S12-8. [PMID: 18177217] 2. Ricciardi R, Rothenberger DA, Madoff RD, et al. Increasing prevalence and severity of Clostridium difficile colitis in hospitalized patients in the United States. Arch Surg. 2007;142:624-31; discussion 631. [PMID: 17638799] 3. Jarvis WR, Schlosser J, Jarvis AA, et al. National point prevalence of Clostridium difficile in US health care...