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A correction has been published: N Engl J Med 2006;354(20):2200.

Original Article
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Volume 353:2442-2449 December 8, 2005 Number 23
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A Predominantly Clonal Multi-Institutional Outbreak of Clostridium difficile–Associated Diarrhea with High Morbidity and Mortality
Vivian G. Loo, M.D., Louise Poirier, M.D., Mark A. Miller, M.D., Matthew Oughton, M.D., Michael D. Libman, M.D., Sophie Michaud, M.D., M.P.H., Anne-Marie Bourgault, M.D., Tuyen Nguyen, M.D., Charles Frenette, M.D., Mirabelle Kelly, M.D., Anne Vibien, M.D., Paul Brassard, M.D., Susan Fenn, M.L.T., Ken Dewar, Ph.D., Thomas J. Hudson, M.D., Ruth Horn, M.D., Pierre René, M.D., Yury Monczak, Ph.D., and André Dascal, M.D.

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ABSTRACT

Background In March 2003, several hospitals in Quebec, Canada, noted a marked increase in the incidence of Clostridium difficile–associated diarrhea.

Methods In 2004 we conducted a prospective study at 12 Quebec hospitals to determine the incidence of nosocomial C. difficile–associated diarrhea and its complications and a case–control study to identify risk factors for the disease. Isolates of C. difficile were typed by pulsed-field gel electrophoresis and analyzed for binary toxin genes and partial deletions in the toxin A and B repressor gene tcdC. Antimicrobial susceptibility was evaluated in a subgroup of isolates.

Results A total of 1703 patients with 1719 episodes of nosocomial C. difficile–associated diarrhea were identified. The incidence was 22.5 per 1000 admissions. The 30-day attributable mortality rate was 6.9 percent. Case patients were more likely than matched controls to have received fluoroquinolones (odds ratio, 3.9; 95 percent confidence interval, 2.3 to 6.6) or cephalosporins (odds ratio, 3.8; 95 percent confidence interval, 2.2 to 6.6). A predominant strain, resistant to fluoroquinolones, was found in 129 of 157 isolates (82.2 percent), and the binary toxin genes and partial deletions in the tcdC gene were present in 132 isolates (84.1 percent).

Conclusions A strain of C. difficile that was resistant to fluoroquinolones and had binary toxin and a partial deletion of the tcdC gene was responsible for this outbreak of C. difficile–associated diarrhea. Exposure to fluoroquinolones or cephalosporins was a risk factor.


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From McGill University Health Center (V.G.L., M.D.L., P.B., S.F., K.D., T.J.H., R.H., P.R.); McGill University (V.G.L., M.A.M., M.O., M.D.L., P.B., K.D., T.J.H., R.H., P.R., Y.M., A.D.); Hôpital Maisonneuve-Rosemont (L.P.); Université de Montréal (L.P., A.-M.B.); Sir Mortimer B. Davis–Jewish General Hospital (M.A.M., Y.M., A.D.); St. Mary's Hospital (M.D.L.); Centre Hospitalier Universitaire de Montréal Hôpital St. Luc (A.-M.B.); Hôpital Jean Talon (M.K.); McGill University and Genome Québec Innovation Center (K.D., T.J.H.) — all in Montreal; Cité de la Santé de Laval, Laval, Que., Canada (T.N.); Centre Hospitalier Universitaire de Sherbrooke (S.M.) and Université de Sherbrooke (S.M., C.F.) — both in Sherbrooke, Que., Canada; Hôpital Charles LeMoyne, Longueuil, Que., Canada (C.F.); and Réseau Santé Richelieu-Yamaska, St. Hyacinthe, Que., Canada (A.V.).

Address reprint requests to Dr. Loo at the Department of Microbiology, McGill University Health Center, 1650 Cedar Ave., Rm. D16.168, Montreal, QC H3G 1A4, Canada, or at vivian.loo{at}muhc.mcgill.ca.

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Related Letters:

Epidemic Clostridium difficile
Musher D. M., Logan N., Mehendiratta V., Polk R. E., Oinonen M., Pakyz A., Wilcox M. H., Freeman J., Iwata K., Doi A., Furuya N., McDonald L. C., Gerding D. N., Loo V. G., Libman M. D., Dascal A.
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N Engl J Med 2006; 354:1199-1203, Mar 16, 2006. Correspondence

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