Investigation by long PCR of the genetic elements mediating VaNa glycopeptide resistance in enterococci from uncooked meat in south Manchester.

Abstract

Enterococci resistant to vancomycin and teicoplanin (the VanA phenotype) were first isolated from clinical specimens in 1986 in the UK and France1. Resistance is conferred by the van gene cluster and in the prototypic VanA enterococcus, E. faecium BM4147, this cluster is part of a transposon designated Tn1546 (Figure 1)2. The mobilities of this transposon and the plasmids of which it is often a part have resulted in wide dissemination of this complex resistance mechanism, both in terms of its geographical distribution and the numbers of affected species and strains of enterococci. Although methods such as pulsed-field gel electrophoresis have been used extensively for epidemiological comparisons of VanA enterococci, they do not provide data on the relatedness of the actual elements mediating resistance. Generation of such data has previously required numerous PCR assays and hybridization with multiple probes2–4.