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dc.contributor.authorHarkins, Catriona P.
dc.contributor.authorPettigrew, Kerry A.
dc.contributor.authorOravcová, Katarina
dc.contributor.authorGardner, June
dc.contributor.authorHearn, R. M. Ross
dc.contributor.authorRice, Debbie
dc.contributor.authorMather, Alison E.
dc.contributor.authorParkhill, Julian
dc.contributor.authorBrown, Sara J.
dc.contributor.authorProby, Charlotte M.
dc.contributor.authorHolden, Matthew T. G.
dc.date.accessioned2018-01-19T13:30:06Z
dc.date.available2018-01-19T13:30:06Z
dc.date.issued2018-02
dc.identifier.citationHarkins , C P , Pettigrew , K A , Oravcová , K , Gardner , J , Hearn , R M R , Rice , D , Mather , A E , Parkhill , J , Brown , S J , Proby , C M & Holden , M T G 2018 , ' The microevolution and epidemiology of Staphylococcus aureus colonization during atopic eczema disease flare ' , Journal of Investigative Dermatology , vol. 138 , no. 2 , pp. 336-343 . https://doi.org/10.1016/j.jid.2017.09.023en
dc.identifier.issn0022-202X
dc.identifier.otherPURE: 251160165
dc.identifier.otherPURE UUID: c30a1c5c-3f2c-4386-8583-9e4170f3b9a9
dc.identifier.otherRIS: urn:0CA68F82357F406CC5C910084C8E5EEA
dc.identifier.otherScopus: 85041655628
dc.identifier.otherORCID: /0000-0002-4958-2166/work/60196473
dc.identifier.otherWOS: 000423029700017
dc.identifier.urihttp://hdl.handle.net/10023/12525
dc.descriptionFunding: Wellcome Trust [Grant number 104241/z/14/z] (CPH). Scottish Infection Research Network and Chief Scientist Office through the Scottish Healthcare Associated Infection Prevention Institute consortium funding [CSO Reference: SIRN10] (MTGH, KAP, KO). Bioinformatics and Computational Biology analyses were supported by the University of St Andrews Bioinformatics Unit that is funded by a Wellcome Trust ISSF award [grant 097831/Z/11/Z]. Wellcome Trust grant 098051 (JP, MTGH). Biotechnology and Biological Sciences Research Council grant BB/M014088/1 (AEM). Wellcome Trust Senior Research Fellowship in Clinical Science [106865/Z/15/Z] (SJB).en
dc.description.abstractStaphylococcus aureus is an opportunistic pathogen and variable component of the human microbiota. In atopic eczema (AE) a characteristic of the disease is colonization by S. aureus, with exacerbations associated with an increased bacterial burden of the organism. Despite this, the origins and genetic diversity of S. aureus colonizing individual patients during AE disease flares is poorly understood. To examine the micro-evolution of S. aureus colonization we have deep-sequenced S. aureus populations from nine children with moderate to severe AE, and 18 non-atopic children asymptomatically carrying S. aureus nasally. Colonization by clonal S. aureus populations was observed in both AE cases and controls, with all but one of the individuals containing colonies belonging to a single sequence type. Phylogenetic analysis revealed that disease flares were associated with the clonal expansion of the S. aureus population, occurring over a period of weeks to months. There was a significant difference in the genetic backgrounds of S. aureus colonizing AE patients versus controls (Fisher’s Exact test, p=0.03). Examination of intra-host genetic heterogeneity of the colonizing S. aureus populations identified evidence of within-host selection in the AE patients, with AE variants being potentially selectively advantageous for intracellular persistence and treatment resistance.
dc.language.isoeng
dc.relation.ispartofJournal of Investigative Dermatologyen
dc.rights© 2017 The Authors. Published by Elsevier, Inc. on behalf of the Society for Investigative Dermatology. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).en
dc.subjectRL Dermatologyen
dc.subjectDASen
dc.subject.lccRLen
dc.titleThe microevolution and epidemiology of Staphylococcus aureus colonization during atopic eczema disease flareen
dc.typeJournal articleen
dc.contributor.sponsorThe Wellcome Trusten
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews. School of Medicineen
dc.contributor.institutionUniversity of St Andrews. Infection Groupen
dc.contributor.institutionUniversity of St Andrews. Infection and Global Health Divisionen
dc.contributor.institutionUniversity of St Andrews. Biomedical Sciences Research Complexen
dc.identifier.doihttps://doi.org/10.1016/j.jid.2017.09.023
dc.description.statusPeer revieweden
dc.identifier.grantnumber097831/z/11/zen


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