Evolutionary dynamics of Enterococcus faecium reveals complex genomic relationships between isolates with independent emergence of vancomycin resistance
, a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which currently is considered first-line therapy. Here, we assess the evolution and resistance acquisition dynamics of in a clinical context using a series of 132 blood...
Saved in:
Published in | Microbial genomics Vol. 2; no. 1 |
---|---|
Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Microbiology Society
19.01.2016
|
Subjects | |
Online Access | Get full text |
Cover
Loading…
Abstract | , a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which currently is considered first-line therapy. Here, we assess the evolution and resistance acquisition dynamics of
in a clinical context using a series of 132 bloodstream infection isolates from a single hospital. All isolates, of which 49 (37 %) were vancomycin-resistant, underwent whole-genome sequencing.
was found to be subject to high rates of recombination with little evidence of sequence importation from outside the local
population. Apart from disrupting phylogenetic reconstruction, recombination was frequent enough to invalidate MLST typing in the identification of clonal expansion and transmission events, suggesting that, where available, whole-genome sequencing should be used in tracing the epidemiology of
nosocomial infections and establishing routes of transmission. Several forms of the Tn
-like element-
gene cluster, which was exclusively responsible for vancomycin resistance, appeared and spread within the hospital during the study period. Several transposon gains and losses and instances of
evolution were inferred and, although usually chromosomal, the resistance element was also observed on a plasmid background. There was qualitative evidence for clonal expansions of both vancomycin-resistant and vancomycin-susceptible
with evidence of hospital-specific subclonal expansion. Our data are consistent with continuing evolution of this established hospital pathogen and confirm hospital vancomycin-susceptible and vancomycin-resistant
patient transmission events, underlining the need for careful consideration before modifying current
infection control strategies. |
---|---|
AbstractList | Enterococcus faecium
, a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which currently is considered first-line therapy. Here, we assess the evolution and resistance acquisition dynamics of
E. faecium
in a clinical context using a series of 132 bloodstream infection isolates from a single hospital. All isolates, of which 49 (37 %) were vancomycin-resistant, underwent whole-genome sequencing.
E. faecium
was found to be subject to high rates of recombination with little evidence of sequence importation from outside the local
E. faecium
population. Apart from disrupting phylogenetic reconstruction, recombination was frequent enough to invalidate MLST typing in the identification of clonal expansion and transmission events, suggesting that, where available, whole-genome sequencing should be used in tracing the epidemiology of
E. faecium
nosocomial infections and establishing routes of transmission. Several forms of the Tn
1549
-like element–
vanB
gene cluster, which was exclusively responsible for vancomycin resistance, appeared and spread within the hospital during the study period. Several transposon gains and losses and instances of
in situ
evolution were inferred and, although usually chromosomal, the resistance element was also observed on a plasmid background. There was qualitative evidence for clonal expansions of both vancomycin-resistant and vancomycin-susceptible
E. faecium
with evidence of hospital-specific subclonal expansion. Our data are consistent with continuing evolution of this established hospital pathogen and confirm hospital vancomycin-susceptible and vancomycin-resistant
E. faecium
patient transmission events, underlining the need for careful consideration before modifying current
E. faecium
infection control strategies. Enterococcus faecium, a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which currently is considered first-line therapy. Here, we assess the evolution and resistance acquisition dynamics of E. faecium in a clinical context using a series of 132 bloodstream infection isolates from a single hospital. All isolates, of which 49 (37 %) were vancomycin-resistant, underwent whole-genome sequencing. E. faecium was found to be subject to high rates of recombination with little evidence of sequence importation from outside the local E. faecium population. Apart from disrupting phylogenetic reconstruction, recombination was frequent enough to invalidate MLST typing in the identification of clonal expansion and transmission events, suggesting that, where available, whole-genome sequencing should be used in tracing the epidemiology of E. faecium nosocomial infections and establishing routes of transmission. Several forms of the Tn1549-like element-vanB gene cluster, which was exclusively responsible for vancomycin resistance, appeared and spread within the hospital during the study period. Several transposon gains and losses and instances of in situ evolution were inferred and, although usually chromosomal, the resistance element was also observed on a plasmid background. There was qualitative evidence for clonal expansions of both vancomycin-resistant and vancomycin-susceptible E. faecium with evidence of hospital-specific subclonal expansion. Our data are consistent with continuing evolution of this established hospital pathogen and confirm hospital vancomycin-susceptible and vancomycin-resistant E. faecium patient transmission events, underlining the need for careful consideration before modifying current E. faecium infection control strategies.Enterococcus faecium, a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which currently is considered first-line therapy. Here, we assess the evolution and resistance acquisition dynamics of E. faecium in a clinical context using a series of 132 bloodstream infection isolates from a single hospital. All isolates, of which 49 (37 %) were vancomycin-resistant, underwent whole-genome sequencing. E. faecium was found to be subject to high rates of recombination with little evidence of sequence importation from outside the local E. faecium population. Apart from disrupting phylogenetic reconstruction, recombination was frequent enough to invalidate MLST typing in the identification of clonal expansion and transmission events, suggesting that, where available, whole-genome sequencing should be used in tracing the epidemiology of E. faecium nosocomial infections and establishing routes of transmission. Several forms of the Tn1549-like element-vanB gene cluster, which was exclusively responsible for vancomycin resistance, appeared and spread within the hospital during the study period. Several transposon gains and losses and instances of in situ evolution were inferred and, although usually chromosomal, the resistance element was also observed on a plasmid background. There was qualitative evidence for clonal expansions of both vancomycin-resistant and vancomycin-susceptible E. faecium with evidence of hospital-specific subclonal expansion. Our data are consistent with continuing evolution of this established hospital pathogen and confirm hospital vancomycin-susceptible and vancomycin-resistant E. faecium patient transmission events, underlining the need for careful consideration before modifying current E. faecium infection control strategies. , a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which currently is considered first-line therapy. Here, we assess the evolution and resistance acquisition dynamics of in a clinical context using a series of 132 bloodstream infection isolates from a single hospital. All isolates, of which 49 (37 %) were vancomycin-resistant, underwent whole-genome sequencing. was found to be subject to high rates of recombination with little evidence of sequence importation from outside the local population. Apart from disrupting phylogenetic reconstruction, recombination was frequent enough to invalidate MLST typing in the identification of clonal expansion and transmission events, suggesting that, where available, whole-genome sequencing should be used in tracing the epidemiology of nosocomial infections and establishing routes of transmission. Several forms of the Tn -like element- gene cluster, which was exclusively responsible for vancomycin resistance, appeared and spread within the hospital during the study period. Several transposon gains and losses and instances of evolution were inferred and, although usually chromosomal, the resistance element was also observed on a plasmid background. There was qualitative evidence for clonal expansions of both vancomycin-resistant and vancomycin-susceptible with evidence of hospital-specific subclonal expansion. Our data are consistent with continuing evolution of this established hospital pathogen and confirm hospital vancomycin-susceptible and vancomycin-resistant patient transmission events, underlining the need for careful consideration before modifying current infection control strategies. |
Author | van Hal, Sebastiaan J. Ip, Camilla L. C. Espedido, Bjorn A. Bowden, Rory Wilson, Daniel J. Jensen, Slade O. Ansari, M. Azim |
Author_xml | – sequence: 1 givenname: Sebastiaan J. surname: van Hal fullname: van Hal, Sebastiaan J. organization: 2 Antibiotic Resistance & Mobile Elements Group, Ingham Institute for Applied Medical Research, Sydney, NSW, Australia, 1 Department of Microbiology and Infectious Diseases, Royal Prince Alfred Hospital, Sydney, NSW, Australia – sequence: 2 givenname: Camilla L. C. surname: Ip fullname: Ip, Camilla L. C. organization: 3 Oxford Genomics Centre, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK – sequence: 3 givenname: M. Azim surname: Ansari fullname: Ansari, M. Azim organization: 4 Oxford Martin School, University of Oxford, 34 Broad Street, Oxford, UK – sequence: 4 givenname: Daniel J. surname: Wilson fullname: Wilson, Daniel J. organization: 5 Nuffield Department of Medicine, University of Oxford, Oxford, UK – sequence: 5 givenname: Bjorn A. surname: Espedido fullname: Espedido, Bjorn A. organization: 2 Antibiotic Resistance & Mobile Elements Group, Ingham Institute for Applied Medical Research, Sydney, NSW, Australia, 6 Molecular Medicine Research Group, School of Medicine, University of Western Sydney, Sydney, NSW, Australia – sequence: 6 givenname: Slade O. surname: Jensen fullname: Jensen, Slade O. organization: 2 Antibiotic Resistance & Mobile Elements Group, Ingham Institute for Applied Medical Research, Sydney, NSW, Australia, 6 Molecular Medicine Research Group, School of Medicine, University of Western Sydney, Sydney, NSW, Australia – sequence: 7 givenname: Rory surname: Bowden fullname: Bowden, Rory organization: 3 Oxford Genomics Centre, Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27713836$$D View this record in MEDLINE/PubMed |
BookMark | eNp1kU9v1DAQxS1URMu2R67IRy5ZnDixnQsSqhaoVIlL75YzmXSNEjvEyZb9JnxcZtm2aivVB__9zXsjv_fsJMSAjH3IxToXdf15uMWwFmtBozRv2FkhKp1VpjInT_an7CKlX4TklVG1rt6x00LrXBqpztjfzS72y-xjcNOet_vgBg-Jx45vwoxThAiwJN45BL8MfMIduj5xiMPY4x9O_pEK6L53B5G09WPiDc53iIH7FOkaE7_z85b70OKINIWZ44AT1QIenHYukN4efCCd5NNMZzxnbztywov7dcVuvm1uLn9k1z-_X11-vc5AGj1ndVmXBRiotSmE0VI1tTNOY5WbXBaq1KLFEltVd8rkxDRSAXZSia4RACBX7MtRdlyaAVug5ibX23HyA32Ijc7b5y_Bb-1t3NlKlHVFhiv26V5gir8XTLMdfALsexcwLsnmRlZSa2UkoR-fej2aPKRBQHYEYIopTdg9Irmwh8DtIXAr7DFw4uULHvz8Pwdq1fevVP0DIiS1Jw |
CitedBy_id | crossref_primary_10_1186_s13756_018_0335_z crossref_primary_10_46234_ccdcw2021_277 crossref_primary_10_1099_mgen_0_000855 crossref_primary_10_3389_fmicb_2021_728356 crossref_primary_10_1038_s41598_018_33266_5 crossref_primary_10_1128_spectrum_05107_22 crossref_primary_10_3390_microorganisms9061118 crossref_primary_10_1186_s13073_017_0507_0 crossref_primary_10_1186_s13073_021_00868_0 crossref_primary_10_1099_mgen_0_000283 crossref_primary_10_1186_s12866_024_03243_2 crossref_primary_10_1128_mbio_03771_21 crossref_primary_10_3389_fmicb_2016_00788 crossref_primary_10_1186_s12879_021_06386_z crossref_primary_10_1016_j_drup_2020_100732 crossref_primary_10_1093_jac_dkae023 crossref_primary_10_1101_gr_204024_116 crossref_primary_10_1038_s41598_020_62371_7 crossref_primary_10_1007_s10096_018_3209_7 crossref_primary_10_1099_jmm_0_001731 crossref_primary_10_1186_s13104_019_4136_0 crossref_primary_10_1128_JCM_01520_17 crossref_primary_10_1093_jac_dkw539 crossref_primary_10_1128_spectrum_02131_24 crossref_primary_10_1128_mBio_01780_18 crossref_primary_10_1099_mgen_0_000224 crossref_primary_10_1016_j_nmni_2017_12_001 crossref_primary_10_1016_j_envres_2020_110664 crossref_primary_10_1016_j_diagmicrobio_2016_12_007 crossref_primary_10_1186_s13756_020_00770_1 crossref_primary_10_1007_s10096_019_03524_z crossref_primary_10_1007_s10096_020_03853_4 crossref_primary_10_1186_s13756_019_0604_5 crossref_primary_10_1038_srep43035 |
Cites_doi | 10.1002/0471250953.bi1105s31 10.1101/gr.111120.110 10.2807/ese.13.47.19046-en 10.1093/bioinformatics/btp352 10.1086/593956 10.1093/gbe/evt111 10.1128/mBio.00534-13 10.1086/595011 10.1086/591861 10.5694/mja14.00672 10.1038/nrmicro2761 10.1086/491711 10.1080/00313020600820807 10.1038/ismej.2008.93 10.1086/430909 10.1038/ng.2895 10.1111/j.1574-6976.2011.00284.x 10.1016/j.jinf.2013.12.013 10.1093/jac/dkf229 10.3201/1106.041204 10.1128/JCM.03286-13 10.1371/journal.pone.0011147 10.1038/nrmicro845 10.1128/mBio.00151-12 10.1186/1471-2164-14-595 10.1093/nar/gku1196 10.1089/mdr.1995.1.235 10.1093/bioinformatics/btl446 10.1099/00221287-146-6-1481 10.1371/journal.pcbi.1004041 10.1128/mBio.00412-13 |
ContentType | Journal Article |
Copyright | 2016 The Authors 2016 |
Copyright_xml | – notice: 2016 The Authors 2016 |
DBID | AAYXX CITATION CGR CUY CVF ECM EIF NPM 7X8 5PM |
DOI | 10.1099/mgen.0.000048 |
DatabaseName | CrossRef Medline MEDLINE MEDLINE (Ovid) MEDLINE MEDLINE PubMed MEDLINE - Academic PubMed Central (Full Participant titles) |
DatabaseTitle | CrossRef MEDLINE Medline Complete MEDLINE with Full Text PubMed MEDLINE (Ovid) MEDLINE - Academic |
DatabaseTitleList | MEDLINE - Academic MEDLINE |
Database_xml | – sequence: 1 dbid: NPM name: PubMed url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 2 dbid: EIF name: MEDLINE url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search sourceTypes: Index Database |
DeliveryMethod | fulltext_linktorsrc |
DocumentTitleAlternate | http://mgen.microbiologyresearch.org |
EISSN | 2057-5858 |
ExternalDocumentID | PMC5049587 27713836 10_1099_mgen_0_000048 |
Genre | Research Support, Non-U.S. Gov't Journal Article |
GrantInformation_xml | – fundername: United Kingdom Wellcome Trust – fundername: Wellcome Trust grantid: 101237 – fundername: Wellcome Trust grantid: 090532 |
GroupedDBID | 53G AAVHR AAXYV AAYXX ADBBV ADCDP ALMA_UNASSIGNED_HOLDINGS AOIJS BCNDV CITATION DIK EBS EJD FRP GROUPED_DOAJ H13 HYE M~E OK1 RGM RPM CGR CUY CVF ECM EIF NPM 7X8 5PM |
ID | FETCH-LOGICAL-c387t-94942c8c978208736b9a8a7e5181326470de4ed69f681782b36cef360fb0ccc3 |
ISSN | 2057-5858 |
IngestDate | Thu Aug 21 13:56:03 EDT 2025 Fri Jul 11 00:50:15 EDT 2025 Sat May 31 02:10:11 EDT 2025 Tue Jul 01 02:27:00 EDT 2025 Thu Apr 24 23:05:09 EDT 2025 |
IsDoiOpenAccess | true |
IsOpenAccess | true |
IsPeerReviewed | true |
IsScholarly | true |
Issue | 1 |
Keywords | transposon Enterococcus faecium multi-locus sequence typing infection control recombination vancomycin resistance |
Language | English |
License | This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/). |
LinkModel | OpenURL |
MergedId | FETCHMERGED-LOGICAL-c387t-94942c8c978208736b9a8a7e5181326470de4ed69f681782b36cef360fb0ccc3 |
Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Three supplementary tables and three supplementary figures are available with the online Supplementary Material. We confirm all supporting data, code and protocols have been provided within the article or through supplementary data files. |
OpenAccessLink | http://dx.doi.org/10.1099/mgen.0.000048 |
PMID | 27713836 |
PQID | 1835377683 |
PQPubID | 23479 |
ParticipantIDs | pubmedcentral_primary_oai_pubmedcentral_nih_gov_5049587 proquest_miscellaneous_1835377683 pubmed_primary_27713836 crossref_primary_10_1099_mgen_0_000048 crossref_citationtrail_10_1099_mgen_0_000048 |
ProviderPackageCode | CITATION AAYXX |
PublicationCentury | 2000 |
PublicationDate | 2016-01-19 |
PublicationDateYYYYMMDD | 2016-01-19 |
PublicationDate_xml | – month: 01 year: 2016 text: 2016-01-19 day: 19 |
PublicationDecade | 2010 |
PublicationPlace | England |
PublicationPlace_xml | – name: England |
PublicationTitle | Microbial genomics |
PublicationTitleAlternate | Microb Genom |
PublicationYear | 2016 |
Publisher | Microbiology Society |
Publisher_xml | – name: Microbiology Society |
References | mgen000048-Willems12 mgen000048-Coombs1 mgen000048-McGowan1 mgen000048-Miller1 mgen000048-Willems1 mgen000048-Li1 mgen000048-Willems123 mgen000048-Coque1 mgen000048-Karki1 mgen000048-Howden1 mgen000048-Lunter1 Werner (mgen000048-Werner1) 2008; 13 mgen000048-Didelot1 mgen000048-Lebreton1 mgen000048-Garnier1 (b2) 2015 mgen000048-Hidron1 mgen000048-Chewapreecha1 mgen000048-Darling1 mgen000048-Courvalin1 mgen000048-Vos1 mgen000048-Arias1 mgen000048-Stamatakis1 mgen000048-Lam1 Croucher (mgen000048-Croucher1) 2015; 43 mgen000048-de1 mgen000048-DiazGranados1 mgen000048-Ramsey1 (b1) 2015 mgen000048-Woodford1 mgen000048-Adams mgen000048-Zerbino1 mgen000048-Boucher1 |
References_xml | – ident: mgen000048-Zerbino1 doi: 10.1002/0471250953.bi1105s31 – ident: mgen000048-Lunter1 doi: 10.1101/gr.111120.110 – volume: 13 start-page: 19046 year: 2008 ident: mgen000048-Werner1 article-title: Emergence and spread of vancomycin resistance among enterococci in Europe publication-title: Euro Surveill doi: 10.2807/ese.13.47.19046-en – year: 2015 ident: b1 – ident: mgen000048-Li1 doi: 10.1093/bioinformatics/btp352 – ident: mgen000048-Ramsey1 doi: 10.1086/593956 – ident: mgen000048-de1 doi: 10.1093/gbe/evt111 – ident: mgen000048-Lebreton1 doi: 10.1128/mBio.00534-13 – ident: mgen000048-Boucher1 doi: 10.1086/595011 – ident: mgen000048-Hidron1 doi: 10.1086/591861 – ident: mgen000048-Karki1 doi: 10.5694/mja14.00672 – ident: mgen000048-Arias1 doi: 10.1038/nrmicro2761 – ident: mgen000048-Courvalin1 doi: 10.1086/491711 – year: 2015 ident: b2 – ident: mgen000048-Adams doi: 10.1080/00313020600820807 – ident: mgen000048-Vos1 doi: 10.1038/ismej.2008.93 – ident: mgen000048-DiazGranados1 doi: 10.1086/430909 – ident: mgen000048-Chewapreecha1 doi: 10.1038/ng.2895 – ident: mgen000048-Willems12 doi: 10.1111/j.1574-6976.2011.00284.x – ident: mgen000048-Miller1 doi: 10.1016/j.jinf.2013.12.013 – ident: mgen000048-Coque1 doi: 10.1093/jac/dkf229 – ident: mgen000048-Willems1 doi: 10.3201/1106.041204 – ident: mgen000048-Coombs1 doi: 10.1128/JCM.03286-13 – ident: mgen000048-Darling1 doi: 10.1371/journal.pone.0011147 – ident: mgen000048-McGowan1 doi: 10.1038/nrmicro845 – ident: mgen000048-Willems123 doi: 10.1128/mBio.00151-12 – ident: mgen000048-Lam1 doi: 10.1186/1471-2164-14-595 – volume: 43 start-page: e15 year: 2015 ident: mgen000048-Croucher1 article-title: Rapid phylogenetic analysis of large samples of recombinant bacterial whole genome sequences using Gubbins publication-title: Nucleic Acids Res doi: 10.1093/nar/gku1196 – ident: mgen000048-Woodford1 doi: 10.1089/mdr.1995.1.235 – ident: mgen000048-Stamatakis1 doi: 10.1093/bioinformatics/btl446 – ident: mgen000048-Garnier1 doi: 10.1099/00221287-146-6-1481 – ident: mgen000048-Didelot1 doi: 10.1371/journal.pcbi.1004041 – ident: mgen000048-Howden1 doi: 10.1128/mBio.00412-13 |
SSID | ssj0001586975 |
Score | 2.236125 |
Snippet | , a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which currently is... Enterococcus faecium, a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which... Enterococcus faecium , a major cause of hospital-acquired infections, remains problematic because of its propensity to acquire resistance to vancomycin, which... |
SourceID | pubmedcentral proquest pubmed crossref |
SourceType | Open Access Repository Aggregation Database Index Database Enrichment Source |
SubjectTerms | Bacterial Typing Techniques Enterococcus faecium - genetics Enterococcus faecium - isolation & purification Evolution, Molecular Genome, Bacterial - genetics Multilocus Sequence Typing Phylogeny Species Specificity Vancomycin Resistance - genetics |
Title | Evolutionary dynamics of Enterococcus faecium reveals complex genomic relationships between isolates with independent emergence of vancomycin resistance |
URI | https://www.ncbi.nlm.nih.gov/pubmed/27713836 https://www.proquest.com/docview/1835377683 https://pubmed.ncbi.nlm.nih.gov/PMC5049587 |
Volume | 2 |
hasFullText | 1 |
inHoldings | 1 |
isFullTextHit | |
isPrint | |
link | http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwnV1Nj9MwELXKcuGCFvFVvmQkxKWkNLETO8eqWlQhFnEo0t4ix3FEJJpUtEXL_hL-CP-PGdtJky5IsJeoalwn7byOZ5x5bwh5VZSSyyhkgQ6lCnhesiAtwiIQiWY8nsG9F7ba4mOy_MzfX8QXo9GvXtXSfpdP9dUfeSU3sSq8B3ZFlux_WLabFN6A12BfOIKF4fhPNj777qfH0rfC9Za3pRn2UX8Dvk7vt5NSGV3t18hSMSiWbKvIzSU2T0ZKsqezuLqtbVe4VcGtYxzqdmqrrlvubmI8Y9PuNmAFQbP-oS0tZovBaIuitk1UZaWeAAn-el0Qj8yppe03AB4LVlPwNcilmnZo3biKFNsYafJhOll0p-b1VjmK_Pl0Mr-q1r3tI08hc9z5djq_rxHafY2e9_R354SofAWrW7Osc4wgzgwg1ZF9Tx4dA_ba-gDxMBh1DV94OrPSlU7ms4eVzdqCJRKQvUt2pNJt1_1P54sY8qpYilvkNowbZPKOnC6TVMRe0RUu-XZwQdSf9rMPg6FrGc5xoW4v8lmdkrs-ZaFzh797ZGTq--RnH3u0xR5tStrHHvXYox571GOPeizQAfaoxx5tsUcRe7SHPdphD690wB49YO8BWb07Wy2Wge_yEWgmxS5IecojLXWKyo1SsCRPlVTCxBB7Qm7Bxaww3BRJWiYyhDE5S7QpWTIr85nWmj0kJ3VTm8eESgO-Jsp5KEXJuVCqDKNIG6W0ilQu4jF50_7amfYK-NiI5WvmKjHSDO2UoV4u2mlMXnfDN0765W8DX7amy8A54xM3VZtmv81gvYyZgIyejckjZ8puqhYDYyIGRu4GoPD78ExdfbEC8B5-T278yafkzuEv94yc7L7tzXMIrnf5Cwvl3wLN4GU |
linkProvider | Directory of Open Access Journals |
openUrl | ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Evolutionary+dynamics+of+Enterococcus+faecium+reveals+complex+genomic+relationships+between+isolates+with+independent+emergence+of+vancomycin+resistance&rft.jtitle=Microbial+genomics&rft.au=van+Hal%2C+Sebastiaan+J.&rft.au=Ip%2C+Camilla+L.+C.&rft.au=Ansari%2C+M.+Azim&rft.au=Wilson%2C+Daniel+J.&rft.date=2016-01-19&rft.pub=Microbiology+Society&rft.eissn=2057-5858&rft.volume=2&rft.issue=1&rft_id=info:doi/10.1099%2Fmgen.0.000048&rft_id=info%3Apmid%2F27713836&rft.externalDocID=PMC5049587 |
thumbnail_l | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2057-5858&client=summon |
thumbnail_m | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2057-5858&client=summon |
thumbnail_s | http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2057-5858&client=summon |