A Predominantly Clonal Multi-Institutional Outbreak of Clostridium difficileAssociated 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.
Background In March 2003, several hospitals in Quebec, Canada,noted a marked increase in the incidence of Clostridium difficileassociateddiarrhea.
Methods In 2004 we conducted a prospective study at 12 Quebechospitals to determine the incidence of nosocomial C. difficileassociateddiarrhea and its complications and a casecontrol studyto identify risk factors for the disease. Isolates of C. difficilewere typed by pulsed-field gel electrophoresis and analyzedfor binary toxin genes and partial deletions in the toxin Aand B repressor gene tcdC. Antimicrobial susceptibility wasevaluated in a subgroup of isolates.
Results A total of 1703 patients with 1719 episodes of nosocomialC. difficileassociated diarrhea were identified. Theincidence was 22.5 per 1000 admissions. The 30-day attributablemortality rate was 6.9 percent. Case patients were more likelythan matched controls to have received fluoroquinolones (oddsratio, 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 foundin 129 of 157 isolates (82.2 percent), and the binary toxingenes and partial deletions in the tcdC gene were present in132 isolates (84.1 percent).
Conclusions A strain of C. difficile that was resistant to fluoroquinolonesand had binary toxin and a partial deletion of the tcdC genewas responsible for this outbreak of C. difficileassociateddiarrhea. Exposure to fluoroquinolones or cephalosporins wasa risk factor.
Source Information
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. DavisJewish 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.
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.
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