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dc.contributor.authorChua, K.
dc.contributor.authorMonk, I.
dc.contributor.authorLin, Y.
dc.contributor.authorSeemann, T.
dc.contributor.authorTuck, K.
dc.contributor.authorPorter, J.
dc.contributor.authorStepnell, J.
dc.contributor.authorCoombs, Geoffrey
dc.contributor.authorDavies, J.
dc.contributor.authorStinear, T.
dc.contributor.authorHowden, B.
dc.date.accessioned2017-01-30T13:40:22Z
dc.date.available2017-01-30T13:40:22Z
dc.date.created2015-10-29T04:10:00Z
dc.date.issued2014
dc.date.submitted2015-10-29
dc.identifier.citationChua, K. and Monk, I. and Lin, Y. and Seemann, T. and Tuck, K. and Porter, J. and Stepnell, J. et al. 2014. Hyperexpression of a-hemolysin explains enhanced virulence of sequence type 93 community-associated methicillin-resistant Staphylococcus aureus. BMC microbiology. 14 (31): pp. 1-13.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/33941
dc.identifier.doi10.1186/1471-2180-14-31
dc.description.abstract

The community-associated methicillin-resistant S. aureus (CA-MRSA) ST93 clone is becoming dominant in Australia and is clinically highly virulent. In addition, sepsis and skin infection models demonstrate that ST93 CA-MRSA is the most virulent global clone of S. aureus tested to date. While the determinants of virulence have been studied in other clones of CA-MRSA, the basis for hypervirulence in ST93 CA-MRSA has not been defined. Here, using a geographically and temporally dispersed collection of ST93 isolates we demonstrate that the ST93 population hyperexpresses key CA-MRSA exotoxins, in particular a-hemolysin, in comparison to other global clones. Gene deletion and complementation studies, and virulence comparisons in a murine skin infection model, showed unequivocally that increased expression of a-hemolysin is the key staphylococcal virulence determinant for this clone. Genome sequencing and comparative genomics of strains with divergent exotoxin profiles demonstrated that, like other S. aureus clones, the quorum sensing agr system is the master regulator of toxin expression and virulence in ST93 CA-MRSA. However, we also identified a previously uncharacterized AraC/XylS family regulator (AryK) that potentiates toxin expression and virulence in S. aureus. These data demonstrate that hyperexpression of a-hemolysin mediates enhanced virulence in ST93 CA-MRSA, and additional control of exotoxin production, in particular a-hemolysin, mediated by regulatory systems other than agr have the potential to fine-tune virulence in CA-MRSA.

dc.titleHyperexpression of a-hemolysin explains enhanced virulence of sequence type 93 community-associated methicillin-resistant Staphylococcus aureus.
dc.typeJournal Article
dcterms.dateSubmitted2015-10-29
dcterms.source.volume14
dcterms.source.titleBMC microbiology
curtin.digitool.pid233328
curtin.note

This open access article is distributed under the Creative Commons license http://creativecommons.org/licenses/by/2.0/

curtin.pubStatusPublished
curtin.refereedTRUE
curtin.departmentSchool of Biomedical Sciences
curtin.identifier.scriptidPUB-VC-ORD-SA-23059
curtin.identifier.elementsidELEMENTS-84803
curtin.accessStatusOpen access


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