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dc.contributor.authorOteo-Iglesias, Jesus 
dc.contributor.authorGonzález-López, Juan José
dc.contributor.authorOrtega, Adriana 
dc.contributor.authorQuintero-Zárate, J Natalia
dc.contributor.authorBou, Germán
dc.contributor.authorCercenado, Emilia
dc.contributor.authorConejo, María Carmen
dc.contributor.authorMartínez-Martínez, Luis
dc.contributor.authorNavarro, Ferran
dc.contributor.authorOliver, Antonio
dc.contributor.authorBartolomé, Rosa M
dc.contributor.authorCampos, Jose 
dc.date.accessioned2019-11-14T10:47:51Z
dc.date.available2019-11-14T10:47:51Z
dc.date.issued2014-07
dc.identifier.citationAntimicrob Agents Chemother. 2014 Jul;58(7):3874-81. doi: 10.1128/AAC.02738-13. Epub 2014 Apr 28.es_ES
dc.identifier.issn0066-4804es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8589
dc.description.abstractIn a previous prospective multicenter study in Spain, we found that OXA-1 and inhibitor-resistant TEM (IRT) β-lactamases constitute the most common plasmid-borne mechanisms of genuine amoxicillin-clavulanate (AMC) resistance in Escherichia coli. In the present study, we investigated the population structure and virulence traits of clinical AMC-resistant E. coli strains expressing OXA-1 or IRT and compared these traits to those in a control group of clinical AMC-susceptible E. coli isolates. All OXA-1-producing (n = 67) and IRT-producing (n = 45) isolates were matched by geographical and temporal origin to the AMC-susceptible control set (n = 56). We performed multilocus sequence typing and phylogenetic group characterization for each isolate and then studied the isolates for the presence of 49 virulence factors (VFs) by PCR and sequencing. The most prevalent clone detected was distinct for each group: group C isolates of sequence type (ST) 88 (C/ST88) were the most common in OXA-1 producers, B2/ST131 isolates were the most common in IRT producers, and B2/ST73 isolates were the most common in AMC-susceptible isolates. The median numbers of isolates per ST were 3.72 in OXA-1 producers, 2.04 in IRT producers, and 1.69 in AMC-susceptible isolates; the proportions of STs represented by one unique isolate in each group were 19.4%, 31.1%, and 48.2%, respectively. The sum of all VFs detected, calculated as a virulence score, was significantly higher in AMC-susceptible isolates than OXA-1 and IRT producers (means, 12.5 versus 8.3 and 8.2, respectively). Our findings suggest that IRT- and OXA-1-producing E. coli isolates resistant to AMC have a different and less diverse population structure than AMC-susceptible clinical E. coli isolates. The AMC-susceptible population also contains more VFs than AMC-resistant isolates.es_ES
dc.description.sponsorshipThis study was supported by the Plan Nacional de I+D+i 2008-2011 and the Instituto de Salud Carlos III, Subdirección General de Redes y Centros de Investigación Cooperativa, Ministerio de Economía y Competitividad, Spanish Network for Research in Infectious Diseases (REIPI RD12/0015). The study was cofinanced by the European Development Regional Fund (ERDF; A way to achieve Europe) and the Fondo de Investigación Sanitaria (grant PI09/0917).es_ES
dc.language.isoenges_ES
dc.publisherAmerican Society for Microbiology (ASM) es_ES
dc.type.hasVersionAMes_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAmoxicillin-Potassium Clavulanate Combination es_ES
dc.subject.meshAnti-Bacterial Agents es_ES
dc.subject.meshDrug Resistance, Bacterial es_ES
dc.subject.meshEscherichia coli es_ES
dc.subject.meshEscherichia coli Infections es_ES
dc.subject.meshHumans es_ES
dc.subject.meshMolecular Epidemiology es_ES
dc.subject.meshMultilocus Sequence Typing es_ES
dc.subject.meshPhylogeny es_ES
dc.subject.meshVirulence es_ES
dc.subject.meshVirulence Factors es_ES
dc.subject.meshbeta-Lactamase Inhibitors es_ES
dc.subject.meshbeta-Lactamases es_ES
dc.titleInhibitor-resistant TEM- and OXA-1-producing Escherichia coli isolates resistant to amoxicillin-clavulanate are more clonal and possess lower virulence gene content than susceptible clinical isolateses_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución-NoComercial-CompartirIgual 4.0 Internacional*
dc.identifier.pubmedID24777096es_ES
dc.format.volume58es_ES
dc.format.number7es_ES
dc.format.page3874-81es_ES
dc.identifier.doi10.1128/AAC.02738-13es_ES
dc.contributor.funderInstituto de Salud Carlos III 
dc.contributor.funderRETICS-Investigación en Patología Infecciosa (REIPI-ISCIII) (España) 
dc.contributor.funderUnión Europea. Fondo Europeo de Desarrollo Regional (FEDER/ERDF) 
dc.description.peerreviewedes_ES
dc.identifier.e-issn1098-6596es_ES
dc.relation.publisherversionhttps://doi.org/10.1128/AAC.02738-13es_ES
dc.identifier.journalAntimicrobial agents and chemotherapyes_ES
dc.repisalud.centroISCIII::Centro Nacional de Microbiologíaes_ES
dc.repisalud.institucionISCIIIes_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/REIPI RD12/0015es_ES
dc.relation.projectIDinfo:eu-repo/grantAgreement/PI09/0917es_ES
dc.rights.accessRightsopen accesses_ES


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