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The clonal dissemination of VanB-type vancomycin-resistant  Enterococcus faecium  (VREfm) strains in three Swedish hospitals between 2007 and 2011 prompted further analysis to reveal the possible origin and molecular characteristics of the outbreak strain. A representative subset of VREfm isolates (n = 18) and vancomycin-susceptible  E. faecium  (VSEfm, n = 2) reflecting the spread in time and location was approached by an array of methods including: selective whole genome sequencing (WGS; n = 3), multi locus sequence typing (MLST), antimicrobial susceptibility testing, virulence gene profiling, identification of mobile genetic elements conferring glycopeptide resistance and their ability to support glycopeptide resistance transfer. In addition, a single VREfm strain with an unrelated PFGE pattern collected prior to the outbreak was examined by WGS. MLST revealed a predominance of ST192, belonging to a hospital adapted high-risk lineage harbouring several known virulence determinants (n≥10). The VREfm outbreak strain was resistant to ampicillin, gentamicin, ciprofloxacin and vancomycin, and susceptible to teicoplanin. Consistently, a  vanB2 -subtype as part of Tn 1549 /Tn 5382  with a unique genetic signature was identified in the VREfm outbreak strains. Moreover, Southern blot hybridisation analyses of PFGE separated S1 nuclease-restricted total DNAs and filter mating experiments showed that  vanB2- Tn 1549 /Tn 5382  was located in a 70-kb sized  rep   17/pRUM  plasmid readily transferable between  E. faecium . This plasmid contained an  axe-txe  toxin-antitoxin module associated with stable maintenance. The two clonally related VSEfm harboured a 40 kb  rep   17/pRUM  plasmid absent of the 30 kb  vanB2- Tn 1549 /Tn 5382  gene complex. Otherwise, these two isolates were similar to the VREfm outbreak strain in virulence- and resistance profile. In conclusion, our observations support that the origin of the multicentre outbreak was caused by an introduction of  vanB2- Tn 1549 /Tn 5382  into a  rep   17/pRUM  plasmid harboured in a pre-existing high-risk  E. faecium  ST192 clone. The subsequent dissemination of VREfm to other centres was primarily caused by clonal spread rather than plasmid transfer to pre-existing high-risk clones.

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A Multicentre Hospital Outbreak in Sweden Caused by Introduction of a vanB2 Transposon into a Stably Maintained pRUM-Plasmid in an Enterococcus faecium ST192 Clone