Increasing rates of vancomycin resistance among Enterococcus faecium isolated from German hospitals between 2004 and 2006 are due to wide clonal dissemination of vancomycin-resistant enterococci and horizontal spread of vanA clusters

Diversity of Tn 1546 and Its Role in the Dissemination of Vancomycin-Resistant Enterococci in Portugal

“…Difficulties also arise from the different methods used for this purpose, which complicates comparison among studies (14,44,45). Tn1546 may be located in conjugative plasmids (14,20,25,43,47) or in larger composite transposons, as documented for isolates with chromosomally located vanA (15). Horizontal transfer of conjugative plasmids containing Tn1546 seems to have played a relevant role in the recent increase of VRE in Portugal, as vanA was plasmid located in most VRE isolates studied and specific plasmids containing the most prevalent Tn1546 variants were identified in representative distinct clones collected from different cities and years (13).…”

Dispersion of Multidrug-Resistant Enterococcus faecium Isolates Belonging to Major Clonal Complexes in Different Portuguese Settings

“…CC17 is the only recognized E. faecium HiRCC, nowadays globally disseminated, which has been sporadically isolated from nonhospitalized humans (3,(8)(9)(10). Different studies have analyzed the population structure of local enterococci, but they are focused mainly on clinical strains with a specific phenotype, such as vancomycin resistance, generally isolated in a short temporal frame (2,7,16,18,27,29,36).…”

Current Trends of Emergence and Spread of Vancomycin-Resistant Enterococci

“…Retrospective epidemiological analyses in hospitals experiencing larger VRE outbreaks revealed that changes in specific procedures such as antibiotic policy, staffing, infection prevention and control regimes were, in some instances, significantly associated with increasing VRE rates, whereas in other settings this could not be shown. 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).…”

“…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).…”