Whole-genome sequencing revealed independent emergence of vancomycin-resistant Enterococcus faecium causing sequential outbreaks over 3 years in a tertiary care hospital

• Published in: European journal of clinical microbiology & infectious diseases 2019-06, Vol.38 (6), p.1163-1170
• Main Authors: Abdelbary, Mohamed H. H., Senn, Laurence, Greub, Gilbert, Chaillou, Gregory, Moulin, Estelle, Blanc, Dominique S.
• Format: Article
• Language: English
• Subjects: Antibiotic resistance; Antibiotics; Biomedical and Life Sciences; Biomedicine; Cloning; Cross Infection - epidemiology; Cross Infection - microbiology; Disease Outbreaks; Emergence; Enterococcus faecium; Enterococcus faecium - classification; Enterococcus faecium - genetics; Enterococcus faecium - isolation & purification; Epidemiology; Gene sequencing; Genome, Bacterial - genetics; Genomes; Genotype; Genotypes; Gram-Positive Bacterial Infections - epidemiology; Gram-Positive Bacterial Infections - microbiology; Humans; Internal Medicine; Medical Microbiology; Molecular Epidemiology; Nosocomial infection; Original Article; Outbreaks; Phylogeny; Polymorphism, Single Nucleotide; Recombination; Recombination, Genetic; Single-nucleotide polymorphism; Switzerland - epidemiology; Tertiary Care Centers; VanB gene; Vancomycin; Vancomycin Resistance - genetics; Vancomycin-Resistant Enterococci - classification; Vancomycin-Resistant Enterococci - genetics; Vancomycin-Resistant Enterococci - isolation & purification; Whole Genome Sequencing
• ISSN: 0934-9723; 1435-4373
• DOI: 10.1007/s10096-019-03524-z

Vancomycin-resistant Enterococcus faecium (VREfm) emerged as an important cause of nosocomial infections worldwide. Previous studies based on molecular typing revealed that VREfm outbreaks are mainly associated with a particular genetic lineage, namely clonal complex 17 (CC17), which harbours either vanA or vanB gene cluster. The University Hospital of Lausanne faced several VREfm episodes of transmissions between 2014 and 2017. In this study, we used whole-genome sequencing (WGS) to investigate the relatedness of 183 VREfm isolates collected from 156 patients. Sequence types (ST) 17, ST80 and ST117 were the most predominant clones. Based on epidemiological data, 10 outbreaks were identified, which were caused by at least 13 distinct genotypes. The majority of isolates involved in outbreaks (91%) differed by only 0 to 3 SNPs. Four outbreaks involved more than one genotype and half of the cases considered as sporadic were possibly linked to an outbreak. By sequencing all isolates, we were able to better understand our local epidemiology of VREfm. The polyclonal structure observed between the different outbreaks strains, the high level of recombination detected in isolates, the time elapsed between admission and the first VREfm detection and the negative screening at admission support the hypothesis of the emergence of new VREfm clones within the hospitalised population.