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Chromosomally and Extrachromosomally Mediated High-Level Gentamicin Resistance in Streptococcus agalactiae

2016-01-04Journal article Open access
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dc.contributor.authorSendi, Parham
dc.contributor.authorFuritsch, Martina
dc.contributor.authorMauerer, Stefanie
dc.contributor.authorFlorindo, Carlos
dc.contributor.authorKahl, Barbara C.
dc.contributor.authorShabayek, Sarah
dc.contributor.authorBerner, Reinhard
dc.contributor.authorSpellerberg, Barbara
dc.date.accessioned2017-03-07T15:20:42Z
dc.date.available2017-03-07T15:20:42Z
dc.date.issued2016-01-04
dc.descriptionFree PMC Articlept_PT
dc.description.abstractStreptococcus agalactiae (group B Streptococcus [GBS]) is a leading cause of sepsis in neonates. The rate of invasive GBS disease in nonpregnant adults also continues to climb. Aminoglycosides alone have little or no effect on GBS, but synergistic killing with penicillin has been shown in vitro. High-level gentamicin resistance (HLGR) in GBS isolates, however, leads to the loss of a synergistic effect. We therefore performed a multicenter study to determine the frequency of HLGR GBS isolates and to elucidate the molecular mechanisms leading to gentamicin resistance. From eight centers in four countries, 1,128 invasive and colonizing GBS isolates were pooled and investigated for the presence of HLGR. We identified two strains that displayed HLGR (BSU1203 and BSU452), both of which carried the aacA-aphD gene, typically conferring HLGR. However, only one strain (BSU1203) also carried the previously described chromosomal gentamicin resistance transposon designated Tn3706. For the other strain (BSU452), plasmid purification and subsequent DNA sequencing resulted in the detection of plasmid pIP501 carrying a remnant of a Tn3 family transposon. Its ability to confer HLGR was proven by transfer into an Enterococcus faecalis isolate. Conversely, loss of HLGR was documented after curing both GBS BSU452 and the transformed E. faecalis strain from the plasmid. This is the first report showing plasmid-mediated HLGR in GBS. Thus, in our clinical GBS isolates, HLGR is mediated both chromosomally and extrachromosomally.pt_PT
dc.description.sponsorshipVelux Stiftung provided funding to Parham Sendi under grant number 724pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationAntimicrob Agents Chemother. 2016 Jan 4;60(3):1702-7. doi: 10.1128/AAC.01933-15pt_PT
dc.identifier.doi10.1128/AAC.01933-15pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.18/4545
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherAmerican Society for Microbiologypt_PT
dc.relation.publisherversionhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4775929/pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by-nc/4.0/pt_PT
dc.subjectAnti-Bacterial Agentspt_PT
dc.subjectBacterial Proteinspt_PT
dc.subjectDNA Transposable Elementspt_PT
dc.subjectEnterococcus faecalispt_PT
dc.subjectGentamicinspt_PT
dc.subjectHumanspt_PT
dc.subjectKanamycin Kinasept_PT
dc.subjectMicrobial Sensitivity Testspt_PT
dc.subjectPlasmidspt_PT
dc.subjectStreptococcal Infectionspt_PT
dc.subjectStreptococcus agalactiaept_PT
dc.subjectInfecções Sexualmente Transmissíveispt_PT
dc.titleChromosomally and Extrachromosomally Mediated High-Level Gentamicin Resistance in Streptococcus agalactiaept_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage1707pt_PT
oaire.citation.issue3pt_PT
oaire.citation.startPage1702pt_PT
oaire.citation.titleAntimicrobial Agents and Chemotherapypt_PT
oaire.citation.volume60pt_PT
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT

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