“…Increased VRE prevalence is partly associated with spread of single, distinct epidemic clones or types (Klare et al, 2005;Top et al, 2007;Bonora et al, 2007;Werner et al, 2007c;Valdezate et al, 2009;Zhu et al, 2010;Johnson et al, 2010;Hsieh et al, 2010). In contrast, VRE outbreaks in single centres tend to be polyclonal suggesting a diverse population of hospital-acquired E. faecium strains and a highly mobile resistance determinant capable of spreading widely among suitable recipient strains (Yoo et al, 2006;Deplano et al, 2007;Kawalec et al, 2007;Borgmann et al, 2007;Werner et al, 2007c;Hsieh et al, 2009). Many facets of VRE and vancomycin resistance epidemiology are currently not fully understood and the question why vancomycin resistance is still mainly limited to E. faecium remains mainly unanswered (Garcia-Migura et al, 2007;Garcia-Migura et al, 2008;Werner et al, 2010b).…”