TY - JOUR
T1 - The global dissemination of hospital clones of Enterococcus faecium
AU - van Hal, Sebastiaan J.
AU - Willems, Rob J.L.
AU - Gouliouris, Theodore
AU - Ballard, Susan A.
AU - Coque, Teresa M.
AU - Hammerum, Anette M.
AU - Hegstad, Kristin
AU - Westh, Hendrik T.
AU - Howden, Benjamin P.
AU - Malhotra-Kumar, Surbhi
AU - Werner, Guido
AU - Yanagihara, Katsunori
AU - Earl, Ashlee M.
AU - Raven, Katherine E.
AU - Corander, Jukka
AU - Bowden, Rory
AU - Pinholt, Mette
AU - Loens, Katherine
AU - Xavier, Basil B.
AU - Matheeussen, Veerle
AU - Goossens, Herman
AU - Enterococcal Group
N1 - Funding Information:
Enterococcal Group Collaborators Mette Pinholt 22Katherine Loens23Basil B. Xavier24Veerle Matheeussen23Herman Goossens23,24,22Department of Clinical Microbiology, Hvidovre University Hospital, Hvidovre, Denmark23National Reference Centre for Enterococci, University Hospital Antwerp, Edegem, Belgium24Laboratory of Medical Microbiology, Vaccine & Infectious Disease Institute, Universiteit?Antwerpen, Wilrijk, Belgium [email protected] [email protected]; [email protected]; [email protected]; [email protected] We wish to acknowledge those responsible for all aspects of isolate curation, data collection, typing and sequencing at the different locations. Dr. A. P. Tedim from Spain, Dr. P. Worning from Denmark, Dr. J. K. Bender from Germany and Dr. A. Beukers from Australia.
Funding Information:
No specific funding was obtained for this study. Individual authors have received funding as outlined below. R.J.L.W. was supported by the Joint Programming Initiative in Antimicrobial Resistance (JPIAMR Third call, STARCS, JPIAMR2016-AC16/00039). TMC was supported by the European Commission (JPIAMR - STARCS project); InGEMICS-C (S2017/BMD-3691), funded by Comunidad de Madrid (Spain); CIBERESP (CIBER in Epidemiology and Public Health; CB06/02/0053), and grants AC16/00039 and PI18/01942, integrated in the Spanish 2013–2016 and 2017–2020 R+D+I State Plans and co-funded by Instituto de Salud Carlos III and the European Regional Development Fund (ERDF, “A way to achieve Europe”). SMK acknowledges funding as part of the Methusalem-Excellence consortium VAX–IDEA, and JPIAMR-STARCS (JPIAMR2016-AC16/00039). AE was supported in part by federal funding from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, Department of Health and Human Services, under Contract No. HHSN272200900018C and Grant No. U19AI110818 to the Broad Institute. JC was supported by the ERC grant no. 742158. RB benefited from Victorian State Government Operational Infrastructure Support and Australian Government NHMRC IRIISS to the Walter and Eliza Hall Institute of Medical Research and core funding to the Wellcome Centre for Human Genetics provided by the Wellcome Trust (award 203141/Z/16/Z).
Publisher Copyright:
© 2021, The Author(s).
PY - 2021
Y1 - 2021
N2 - Background: The hospital-adapted A1 group of Enterococcus faecium remains an organism of significant concern in the context of drug-resistant hospital-associated infections. How this pathogen evolves and disseminates remains poorly understood. Methods: A large, globally representative collection of short-read genomic data from the hospital-associated A1 group of Enterococcus faecium was assembled (n = 973). We analysed, using a novel analysis approach, global diversity in terms of both the dynamics of the accessory genome and homologous recombination among conserved genes. Results: Two main modes of genomic evolution continue to shape E. faecium: the acquisition and loss of genes, including antimicrobial resistance genes, through mobile genetic elements including plasmids, and homologous recombination of the core genome. These events lead to new clones emerging at the local level, followed by the erosion of signals of clonality through recombination, and in some identifiable cases producing new clonal clusters. These patterns lead to new, emerging lineages which are able to spread globally over relatively short timeframes. Conclusions: The ability of A1 E. faecium to continually present new combinations of genes for potential selection suggests that controlling this pathogen will remain challenging but establishing a framework for understanding genomic evolution is likely to aid in tracking the threats posed by newly emerging lineages.
AB - Background: The hospital-adapted A1 group of Enterococcus faecium remains an organism of significant concern in the context of drug-resistant hospital-associated infections. How this pathogen evolves and disseminates remains poorly understood. Methods: A large, globally representative collection of short-read genomic data from the hospital-associated A1 group of Enterococcus faecium was assembled (n = 973). We analysed, using a novel analysis approach, global diversity in terms of both the dynamics of the accessory genome and homologous recombination among conserved genes. Results: Two main modes of genomic evolution continue to shape E. faecium: the acquisition and loss of genes, including antimicrobial resistance genes, through mobile genetic elements including plasmids, and homologous recombination of the core genome. These events lead to new clones emerging at the local level, followed by the erosion of signals of clonality through recombination, and in some identifiable cases producing new clonal clusters. These patterns lead to new, emerging lineages which are able to spread globally over relatively short timeframes. Conclusions: The ability of A1 E. faecium to continually present new combinations of genes for potential selection suggests that controlling this pathogen will remain challenging but establishing a framework for understanding genomic evolution is likely to aid in tracking the threats posed by newly emerging lineages.
U2 - 10.1186/s13073-021-00868-0
DO - 10.1186/s13073-021-00868-0
M3 - Journal article
C2 - 33785076
AN - SCOPUS:85103683904
VL - 13
JO - Genome Medicine
JF - Genome Medicine
SN - 1756-994X
IS - 1
M1 - 52
ER -