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15 January 2007

Volume 44, Number 2
Clinical Infectious Diseases 2007;44:238–244
© 2006 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2007/4402-0013$15.00
DOI: 10.1086/510391
MAJOR ARTICLE

A Portrait of the Geographic Disseminationof the Clostridium difficile North American Pulsed‐Field Type 1 Strain and the Epidemiology of C. difficile–Associated Disease in Québec

Bruno Hubert,1,a

Vivian G. Loo,2

Anne‐Marie Bourgault,3

Louise Poirier,4

André Dascal,5

Élise Fortin,1

Marc Dionne,1 and

Manon Lorange6

1Institut National de Santé Publique du Québec, Québec, and 2McGill University Health Centre, 3Centre Hospitalier de l’Université de Montréal Hôpital St. Luc, 4Hôpital Maisonneuve‐Rosemont, 5Sir Mortimer B. Davis–Jewish General Hospital, and 6Laboratoire de Santé Publique du Québec, Institut National de Santé Publique du Québec, Montréal, Canada

Background.An increase in the incidence and severity of Clostridium difficile–associated disease in Québec and the United States has been associated with a hypervirulent strain referred to as North American pulsed‐field type 1 (NAP1)/027.

Methods.In 2005, a prospective study was conducted in 88 Québec hospitals, and 478 consecutive nosocomial isolates of C. difficile were obtained. The isolates were subjected to pulsed‐field gel electrophoresis (PFGE) typing, antimicrobial susceptibility testing, and detection of binary toxin genes and tcdC gene deletion. Data on patient age and occurrence of complications were collected.

Results.PFGE typing of 478 isolates of C. difficile yielded 61 PFGE profiles. Pulsovars A (57%), B (10%), and B1 (8%) were predominant. The PFGE profile of pulsovar A was identical to that of strain NAP1. It showed 67% relatedness with 15 other PFGE patterns, among which 11 had both binary toxin genes and a partial tcdC deletion but different antibiotic susceptibility profiles. Pulsovars B and B1 were identical to strain NAP2/ribotype 001. In hospitals showing a predominant clonal A or B‐B1 PFGE pattern, incidence of C. difficile–associated disease was 2 and 1.3 times higher, respectively, than in hospitals without any predominant clonal PFGE pattern. Severe disease was twice as frequent among patients with strains possessing binary toxin genes and tcdC deletion than among patients with strains lacking these virulence factors.

Conclusions.This study helped to quantify the impact of strain NAP1 on the incidence and severity of C. difficile–associated disease in Québec in 2005. The identification of the geographic dissemination of this predominant strain may help to focus regional infection‐control efforts.

Received 9 August 2006; accepted 28 September 2006; electronically published 6 December 2006.

Reprints or correspondence: Dr. Bruno Hubert, CCECQA‐Hôpital Xavier Arnozan CHU de Bordeaux, 33604 Pessac Cedex, France ().

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  • Present affiliation: CCECQA‐Hôpital Xavier Arnozan CHU de Bordeaux, Pessac, France.

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