Editorial Commentary:Decreased Effectiveness of Metronidazole for the Treatment ofClostridium difficileInfection?

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Abstract
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 infection in patients, and the use of this agent may be an important factor contributing to the persistence and spread of this strain [7].

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