A portrait of the geographic dissemination of the Clostridium difficile North American pulsed-field type 1 strain and the epidemiology of C-difficile-associated disease in Quebec

被引:156
作者
Hubert, Bruno
Loo, Vivian G.
Bourgault, Anne-Marie
Poirier, Louise
Dascal, Andre
Fortin, Elise
Dionne, Marc
Lorange, Manon
机构
[1] Inst Natl Sante Publ Quebec, Lab Sante Publ Quebec, Montreal, PQ, Canada
[2] McGill Univ, Ctr Hlth, Hop St Luc, Montreal, PQ, Canada
[3] Hop Maison Neuve Rosemont, Montreal, PQ H1T 2M4, Canada
[4] Sir Mortimer B Davis Jewish Hosp, Montreal, PQ H3T 1E2, Canada
关键词
D O I
10.1086/510391
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background. An increase in the incidence and severity of Clostridium difficile - associated disease in Quebec 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 Quebec 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 Quebec in 2005. The identification of the geographic dissemination of this predominant strain may help to focus regional infection- control efforts.
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页码:238 / 244
页数:7
相关论文
共 30 条
[1]   Prevalence and association of macrolide-lincosamide- streptogramin B (MLSB) resistance with resistance to moxifloxacin in Clostridium difficile [J].
Ackermann, G ;
Degner, A ;
Cohen, SH ;
Silva, J ;
Rodloff, AC .
JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, 2003, 51 (03) :599-603
[2]   Antecedent use of fluoroquinolones is associated with resistance to moxifloxacin in Clostridium difficile [J].
Ackermann, G ;
Tang-Feldman, YJ ;
Schaumann, R ;
Henderson, JP ;
Rodloff, AC ;
Silva, J ;
Cohen, SH .
CLINICAL MICROBIOLOGY AND INFECTION, 2003, 9 (06) :526-530
[3]  
*CLIN LAB STAND I, 2004, METH ANT SUSC TEST A
[4]   Laboratory diagnosis of Clostridium difficile associated diarrhoea:: a plea for culture [J].
Delmée, M ;
Van Broeck, J ;
Simon, A ;
Janssens, M ;
Avesani, V .
JOURNAL OF MEDICAL MICROBIOLOGY, 2005, 54 (02) :187-191
[5]   gyrA and gyrB mutations are implicated in cross-resistance to ciprofloxacin and moxifloxacin in Clostridium difficile [J].
Dridi, L ;
Tankovic, J ;
Burghoffer, B ;
Barbut, F ;
Petit, JC .
ANTIMICROBIAL AGENTS AND CHEMOTHERAPY, 2002, 46 (11) :3418-3421
[6]   Pulsed-field gel electrophoresis can yield DNA fingerprints of degradation-susceptible Clostridium difficile strains [J].
Fawley, WN ;
Wilcox, MH .
JOURNAL OF CLINICAL MICROBIOLOGY, 2002, 40 (09) :3546-3547
[7]   Clindamycin, cephalosporins, fluoroquinolones, and Clostridium difficile-associated diarrhea:: This is an antimicrobial resistance problem [J].
Gerding, DN .
CLINICAL INFECTIOUS DISEASES, 2004, 38 (05) :646-648
[8]   Binary toxin-producing, large clostridial toxin-negative Clostridium difficile strains are enterotoxic but do not cause disease in hamsters [J].
Geric, B ;
Carman, RJ ;
Rupnik, M ;
Genheimer, CW ;
Sambol, SP ;
Lyerly, DM ;
Gerding, DN ;
Johnson, S .
JOURNAL OF INFECTIOUS DISEASES, 2006, 193 (08) :1143-1150
[9]  
GILCA R, 2006, SURVEILLANCE DIARRHE, P1
[10]  
HUBERT B, 2005, SURVEILLANCE DIARRHE, P1