Understanding the Success of ST203 Vancomycin-resistant <em>Enterococcus Faecium</em> — ASN Events
  1. Schedule
  2. Division 4 – Microbial Genetics, Physiology and Pathogenesis
  3. Symposium 7 - The Evolution of Commensals and Pathogenic Bacteria: Traits Important for Survival
  4. Understanding the Success of ST203 Vancomycin-resistant Enterococcus Faecium

Understanding the Success of ST203 Vancomycin-resistant Enterococcus Faecium (#157)

Margaret Lam 1 , Torsten Seemann 2 , Nicholas Tobias 1 , Susan Ballard 3 , M. Lindsay Grayson 4 5 , Paul D. R. Johnson 1 4 5 , Benjamin Howden 1 3 4 5 6 , Tim Stinear 1 6
  1. University of Melbourne, Parkville, VIC, Australia
  2. Victorian Bioinformatics Consortium, Clayton, Victoria, Australia
  3. Microbiology Department, Austin Hospital, Heidelberg, Victoria, Australia
  4. Infectious Diseases, Austin Centre for Infection Research (ACIR), Heidelberg, Victoria, Australia
  5. Department of Medicine, University of Melbourne, Heidelberg, Victoria, Australia
  6. Department of Microbiology, Monash University, Clayton, Victoria, Australia

Vancomycin-resistant Enterococcus faecium (VRE) is a leading cause of infection in healthcare facilities worldwide. A significant increase in VRE bacteraemia had previously been observed at the Austin Hospital in the years leading up to 2009. MLST analysis revealed replacement of the previously-dominant ST17 E. faecium strains with a recently-emerged ST203 clone. The mechanisms behind the emergence of ST203 VRE and the ensuing apparently clonal outbreak have not been determined. Comparative genomics and phenotypic studies were therefore employed to improve our understanding of the shift in E. faecium genotype and the increase in VRE bacteraemia.

The genome of ST203 strain Aus0085 was completely assembled and annotated. The genome differences between our previously sequenced ST17 strain Aus0004, and Aus0085 were assessed by a suite of bioinformatic tools. Phenotypic differences were assessed by growth curve experiments, biofilm assays and G. mellonella virulence assays. 

Significant differences in genome architecture and 500kb of Aus0085-unique genome content were observed between the two strains. Notably, Aus0085 possesses additional plasmids and genes that encode for resistances against other antimicrobials and other metabolic pathways. The conjugative transposon that carries the vancomycin resistance-conferring genes differs in length and site of insertion between Aus0004 and Aus0085. Phenotypically, the ST203 strains grow significantly faster and outcompete the ST17 strains. 

The differences revealed in this study provide key insights into the emergence of ST203 VRE and suggests the recent success of ST203 E. faecium relates to several genomic differences that promote successful growth and persistence.