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dc.contributor.authorMarbach, Hen_US
dc.contributor.authorVizcay-Barrena, Gen_US
dc.contributor.authorMemarzadeh, Ken_US
dc.contributor.authorOtter, JAen_US
dc.contributor.authorPathak, Sen_US
dc.contributor.authorAllaker, RPen_US
dc.contributor.authorHarvey, RDen_US
dc.contributor.authorEdgeworth, JDen_US
dc.date.accessioned2018-11-12T14:42:36Z
dc.date.available2018-10-20en_US
dc.date.issued2019-02en_US
dc.date.submitted2018-11-09T10:26:13.183Z
dc.identifier.urihttp://qmro.qmul.ac.uk/xmlui/handle/123456789/49983
dc.description.abstractOBJECTIVES: Information on genetic determinants of chlorhexidine tolerance (qacA carriage and MIC) in vitro is available, although evidence of the clinical impact and mechanisms remain poorly understood. We investigated why, following chlorhexidine intervention, prevalent epidemic MRSA ST22 and ST36 clones declined at an ICU, whilst an ST239-TW clone did not. The chlorhexidine tolerant ST239-TW phenotypes were assessed for their protein binding, cell adhesion and intracellular uptake potential. METHODS: Six ST22, ST36 and ST239-TW bloodstream infection isolates with comparable chlorhexidine MICs were selected from a 2-year outbreak in an ICU at Guy's and St. Thomas' Hospital. Isolates were tested for fibrinogen and fibronectin binding, and adhesion/internalization into human keratinocytes with and without biocide. RESULTS: Binding to fibrinogen and fibronectin, adhesion and intracellular uptake within keratinocytes (P < 0.001) and intracellular survival in keratinocytes under chlorhexidine pressure (ST22 3.18%, ST36 4.57% vs ST239-TW 12.79%; P < 0.0001) was consistently higher for ST239-TW. CONCLUSIONS: We present evidence that MRSA clones with similarly low in vitro tolerance to chlorhexidine exhibit different in vivo susceptibilities. The phenomenon of S. aureus adhesion and intracellular uptake into keratinocytes could therefore be regarded as an additional mechanism of chlorhexidine tolerance, enabling MRSA to evade infection control measures.en_US
dc.description.sponsorshipThis work was supported by a Health Schools PhD Studentship at King's College London, UK, awarded to RD Harvey, JD Edgeworth and H Marbach. Jonathan D. Edgeworth received funding from the National Institute for Health Research (NIHR), Guy's and St Thomas’ NHS Foundation Trust and Kings College London, Biomedical Research Centre and the Programme of Infection and Immunity (grant no. RJ112/N027).en_US
dc.format.extent119 - 126en_US
dc.languageengen_US
dc.language.isoenen_US
dc.relation.ispartofJ Infecten_US
dc.rights© 2018. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectAdhesionen_US
dc.subjectBiocide evasionen_US
dc.subjectChlorhexidine toleranceen_US
dc.subjectDecolonizationen_US
dc.subjectIntracellular uptakeen_US
dc.subjectST239-TWen_US
dc.titleTolerance of MRSA ST239-TW to chlorhexidine-based decolonization: Evidence for keratinocyte invasion as a mechanism of biocide evasion.en_US
dc.typeArticle
dc.rights.holder© 2018 The British Infection Association. Published by Elsevier Ltd. All rights reserved.
dc.identifier.doi10.1016/j.jinf.2018.10.007en_US
pubs.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/30367885en_US
pubs.issue2en_US
pubs.notesNot knownen_US
pubs.publication-statusPublisheden_US
pubs.volume78en_US
dcterms.dateAccepted2018-10-20en_US


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