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dc.contributor.authorHtun, Htet Lin
dc.contributor.authorHon, Pei Yun
dc.contributor.authorHolden, Matthew T. G.
dc.contributor.authorAng, Brenda
dc.contributor.authorChow, Angela
dc.identifier.citationHtun , H L , Hon , P Y , Holden , M T G , Ang , B & Chow , A 2019 , ' Chlorhexidine and octenidine use, qac genes carriage, and reduced antiseptic susceptibility in methicillin-resistant Staphylococcus aureus isolates from a healthcare network ' , Clinical Microbiology and Infection , vol. 25 , no. 9 , pp. 1154.e1-1154.e7 .
dc.identifier.otherPURE: 257339549
dc.identifier.otherPURE UUID: 814f96d2-01e2-4147-a8db-839d0319dec0
dc.identifier.otherRIS: urn:7C9E4BE876F015A04E83D574761C1721
dc.identifier.otherScopus: 85060348768
dc.identifier.otherORCID: /0000-0002-4958-2166/work/60196420
dc.identifier.otherWOS: 000481643000015
dc.descriptionFunding: This research was supported by the Small Innovative Grant (SIG/15033) and Communicable Diseases – Public Health Research Grant (CDPHRG/0008/2014) awarded by the National Healthcare Group and Ministry of Health Singapore respectively.en
dc.description.abstractObjectives With the widespread use of antiseptics in healthcare facilities for the prevention of methicillin-resistant Staphylococcus aureus (MRSA) transmission, there are concerns for antiseptic tolerance and resistance. We sought to understand the use of chlorhexidine and octenidine, qac genes carriage and reduced antiseptic susceptibilities. Methods A serial cross-sectional study was conducted in an acute care hospital and three extended-care facilities of a healthcare network in June-July, 2014-2016. Two of the extended-care facilities were exposed to intranasal octenidine and universal daily chlorhexidine/octenidine bathing. The minimum inhibitory concentration (MIC) levels and qac genes were determined by broth microdilution tests and whole genome sequencing respectively. Multivariable logistic regression was used to assess for the independent associations between antiseptic exposures, qac genes and reduced antiseptic susceptibilities. Results A total of 878 MRSA isolates were obtained. There were associations between qacA/B carriage and chlorhexidine (adjusted odds ratio [aOR]: 7.80; 95% confidence interval [CI]: 3.25-18.71) and octenidine (aOR: 11.79; 95%CI: 5.14-27.04) exposures. Chlorhexidine exposure was associated with reduced chlorhexidine susceptibility (MIC≥4mg/L) (aOR: 3.15; 95%CI: 1.14-8.74). Carriage of qacA/B (aOR: 10.65: 95%CI: 4.14-27.40) or qacC (aOR: 2.55; 95%CI: 1.22-5.32) had an association with reduced chlorhexidine susceptibility; while MRSA sequence type modified the association. However, we found no direct association between (i) antiseptics use and qacC carriage, (ii) octenidine exposure and reduced susceptibility and (iii) reduced octenidine susceptibility and qacA/B or qacC carriage. Conclusions Antiseptic exposures were associated with qac genes carriage. Chlorhexidine exposure was associated with reduced chlorhexidine susceptibility, requiring continued surveillance for the emergence of resistance.
dc.relation.ispartofClinical Microbiology and Infectionen
dc.rights© 2019, European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. This work has been made available online in accordance with the publisher's policies. This is the author created accepted version manuscript following peer review and as such may differ slightly from the final published version. The final published version of this work is available at
dc.subjectAntiseptic resistanceen
dc.subjectBiocide tolerance and resistanceen
dc.subjectMethicillin-resistant S. aureas (MRSA)en
dc.subjectAntiseptic resistance genesen
dc.subjectqac genesen
dc.subjectQH426 Geneticsen
dc.subjectQR Microbiologyen
dc.titleChlorhexidine and octenidine use, qac genes carriage, and reduced antiseptic susceptibility in methicillin-resistant Staphylococcus aureus isolates from a healthcare networken
dc.typeJournal articleen
dc.contributor.institutionUniversity of St Andrews.Infection and Global Health Divisionen
dc.contributor.institutionUniversity of St Andrews.Biomedical Sciences Research Complexen
dc.contributor.institutionUniversity of St Andrews.Infection Groupen
dc.contributor.institutionUniversity of St Andrews.School of Medicineen
dc.description.statusPeer revieweden

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