Mobile genetic elements and their contribution to the emergence of antimicrobial resistant Enterococcus faecalis and Enterococcus faecium

Abstract

Mobile genetic elements (MGEs) including plasmids and transposons are pivotal in the dissemination and persistence of antimicrobial resistance in Enterococcus faecalis and Enterococcus faecium. Enterococcal MGEs have also been shown to be able to transfer resistance determinants to more pathogenic bacteria such as Staphylococcus aureus. Despite their importance, we have a limited knowledge about the prevalence, distribution and genetic content of specific MGEs in enterococcal populations. Molecular epidemiological studies of enterococcal MGEs have been hampered by the lack of standardized molecular typing methods and relevant genome information. This review focuses on recent developments in the detection of MGEs and their contribution to the spread of antimicrobial resistance in clinically relevant enterococci.

Role of House Flies in the Ecology of Enterococcus faecalis from Wastewater Treatment Facilities

“…Enterococci are well recognized as AR gene reservoirs and readily transfer genes both intraand inter-specifically [31,38,73]. A number of mobile genetic elements (MGE) such as plasmids and transposons are present in enterococci which facilitate AR gene transfer [31,73].…”

Peripheral modifications of [Ψ[CH 2 NH]Tpg 4 ]vancomycin with added synergistic mechanisms of action provide durable and potent antibiotics

“…Cell wall penetration or import is not needed, and this feature allows vancomycin to avoid the common resistance mechanisms mediated by expression levels of proteins involved in transport, efflux, and metabolic deactivation by cytosolic enzymes (35). Finally, it has been suggested that there are genetic features that presently make the glycopeptide antibiotics less susceptible to vertical vs. horizontal gene transfer of resistance (36). Regardless of the origins, it is most revealing that the primary mechanism of clinical resistance to vancomycin (VanA and VanB phenotypes) was transferred to pathogenic bacteria from nonpathogenic organisms that produce vancomycin and use this inducible resistance mechanism to protect themselves during vancomycin production (37).…”

Current Trends of Emergence and Spread of Vancomycin-Resistant Enterococci

“…Results of a recent study about horizontal transferability of vanA plasmids among enterococci, other lactic acid bacteria and bifidobacteria revealed a preferred transfer into and a possible host restriction within the species E. faecium (Werner et al, 2010b). In contrast, vanB-type elements preferably integrate into the chromosome, but are mobile as part of integrative and conjugative elements ICE (Paulsen et al, 2003;Hegstad et al, 2010). Occasionally vanB resides on (transferable) plasmids Zheng et al, 2009); as noticed recently associated with larger VanB-type VRE outbreaks (Sivertsen et al, 2011;Bjorkeng et al, 2011).…”

“…vanB could be subdivided into three different allele types (vanB1-3) with vanB-2 the most prevalent type worldwide. The vanB alleles are part of Tn1547 or the conjugative transposon Tn1549/5382 which are mainly chromosomally located and less frequently, on plasmids (Werner et al, 2006;Zheng et al, 2009;Hegstad et al, 2010;Bjorkeng et al, 2011). The main clinical relevant reservoir of vanA and vanB elements is in E. faecium, at least in Europe, Northern and Latin America and Southeast Asia, although they have also been observed occasionally in other enterococcal species (see Table 1 and below) (Zirakzadeh and Patel 2005;Werner et al, 2008a;Werner 2011).…”