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Decreased effectiveness of metronidazole for the treatment of Clostridium difficile infection?

Since the emergence of a new virulent strain of Clostridium difficile characterized as toxinotype III, North American PFGE type 1 (NAP1), restriction endonuclease analysis group type BI, and PCR ribotype 027 (type 027) multiple outbreaks have been reported in North America and Europe [1, 2]. The first reports were from Canada, where the province of Quebec was the earliest and most severely affected [3]. In the United States, at least 38 states have been affected by the new emerging strain [4]. Outbreaks in the United Kingdom and The Netherlands have been followed by a rapid spread of the strain throughout Europe, now including 18 countries [5]. A worrisome new development is outbreaks in Europe attributable to clindamycin-resistant NAP1/027 strains (MIC, >256 mg/L) that harbor the ermB gene [6]. Clindamycin has been considered to be a "protective" antibiotic for the development of C. difficile-associated disease (CDAD) attributable to NAP1/027, but resistance to this agent increases the risk of C. difficile in-