McDonald et al. [1] collected a total of 187 Clostridium difficile isolates from 8 health care facilities in 6 states (Georgia, Illinois, Maine, New Jersey, Oregon, and Pennsylvania) in which outbreaks of C. difficile-associated disease occurred between 2000 and 2003. The isolates were characterized by restriction-endonuclease analysis (REA), pulsed-field gel electrophoresis (PFGE), and toxinotyping, and the results were compared with those from a database of more than 6000 isolates obtained before 2001. Polymerase chain reaction was used to detect the recently described binary toxin CDT and a deletion in the pathogenicity locus gene, tcdC, which might result in increased production of toxins A and B. Isolates that belonged to 1 REA group (BI) and had the same PFGE type (NAP1) were identified in specimens collected from patients at all 8 facilities and accounted for at least half of the isolates from 5 facilities. REA group BI, which was first identified in 1984, was uncommon among isolates from the historic database (14 cases). Both historic and current (obtained since 2001) BI/NAP1 isolates were of toxinotype III, were positive for the binary toxin CDT, and contained an 18-bp tcdC deletion. Resistance to gatifloxacin and moxifloxacin was more common in current BI/NAP1 isolates than in non-BI/NAP1 isolates (100% versus 42%, P <.001), whereas the rate of resistance to clindamycin was the same in the 2 groups (79%). All of the current but none of the historic BI/NAP1 isolates were resistant to gatifloxacin and moxifloxacin (P <.001). The authors' conclusions were that a previously uncommon strain of C. difficile with variations in toxin genes has become more resistant to fluoro-quinolones and has emerged as a cause of geographically dispersed outbreaks of C. difficile-associated disease. In March 2003, Loo et al. [2] reviewed several hospitals in Quebec, Canada, that noted a marked increase in the incidence of C. difficile-associated diarrhea (CDAD). In 2004, the authors conducted a prospective study at 12 Quebec hospitals to determine the incidence of nosocomial CDAD and its complications and a case-control study to identify risk factors for the disease. Isolates of C. difficile were typed by PFGE 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. The authors identified a total of 1703 patients with 1719 episodes of nosocomial CDAD. The incidence was 22.5 per 1000 admissions. The 30-day attributable mortality rate was 6.9%. Case patients were more likely than matched controls to have received fluoroquinolones (odds ratio [OR], 3.9; 95% confidence interval [CI], 2.3-6.6) or cephalosporins (OR, 3.8; 95% 95% CI, 2.2-6.6). A predominant strain, resistant to fluoroquinolones, was found in 129 of 157 isolates (82.2%), and the binary toxin genes and partial deletions in the tcdC gene were present in 132 isolates (84.1%). The authors' concluded that 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 CDAD and that exposure to fluoroquinolones or cephalosporins was a risk factor.
