The population structure of vancomycin-resistant and -susceptible in a low-prevalence antimicrobial resistance setting is highly influenced by circulating global hospital-associated clones.

Between 2010 and 2015 the incidence of vancomycin-resistant (VRE) in Norway increased dramatically. Hence, we selected (1) a random subset of vancomycin-resistant enterococci (VRE) from the Norwegian Surveillance System for Communicable Diseases (2010-15; =239) and (2) Norwegian vancomycin-susceptible (VSE) bacteraemia isolates from the national surveillance system for antimicrobial resistance in microbes (2008 and 2014; =261) for further analysis. Whole-genome sequences were collected for population structure, gene cluster, mobile genetic element and virulome analysis, as well as antimicrobial susceptibility testing. Comparative genomic and phylogeographical analyses were performed with complete genomes of global strains from the National Center for Biotechnology Information (NCBI) (1946-2022; =272). All Norwegian VRE and most of the VSE clustered with global hospital-associated sequence types (STs) in the phylogenetic subclade A1. The subtype carried by chromosomal Tn integrative conjugative elements was the dominant type. The major Norwegian VRE cluster types (CTs) were in accordance with concurrent European CTs. The dominant -type VRE CTs, ST192-CT3/26 and ST117-CT24, were mostly linked to a single hospital in Norway where the clones spread after independent chromosomal acquisition of Tn. The less prevalent VRE were associated with more diverse CTs and carrying Inc18 or RepA_N plasmids with toxin-antitoxin systems. Only 5 % of the Norwegian VRE were all of which contained . The Norwegian VRE and VSE isolates harboured CT-specific virulence factor (VF) profiles supporting biofilm formation and colonization. The dominant VRE CTs in general hosted more virulence determinants than VSE. The phylogenetic clade B VSE isolates (=21) recently classified as , harboured fewer VFs than in general, and particularly subclade A1 isolates. In conclusion, the population structure of Norwegian isolates mirrors the globally prevalent clones and particularly concurrent European VRE/VSE CTs. Novel chromosomal acquisition of on Tn from the gut microbiota, however, formed a single major hospital VRE outbreak. Dominant VRE CTs contained more VFs than VSE.