Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/12473
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dc.contributor.authorCoombs, Geoffrey W-
dc.contributor.authorPearson, Julie C-
dc.contributor.authorLe, Tam-
dc.contributor.authorDaly, Denise A-
dc.contributor.authorRobinson, James O-
dc.contributor.authorGottlieb, Thomas-
dc.contributor.authorHowden, Benjamin P-
dc.contributor.authorJohnson, Paul D R-
dc.contributor.authorBennett, Catherine M-
dc.contributor.authorStinear, Timothy P-
dc.contributor.authorTurnidge, John D-
dc.date.accessioned2015-05-16T02:10:34Z
dc.date.available2015-05-16T02:10:34Z
dc.date.issued2014-09-30-
dc.identifier.citationCommunicable Diseases Intelligence Quarterly Report 2014; 38(3): E247-52en_US
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/12473en
dc.description.abstractFrom 1 January to 31 December 2011, 29 institutions around Australia participated in the Australian Enterococcal Sepsis Outcome Programme (AESOP). The aim of AESOP 2011 was to determine the proportion of enterococcal bacteraemia isolates in Australia that are antimicrobial resistant, with particular emphasis on susceptibility to ampicillin and the glycopeptides, and to characterise the molecular epidemiology of the Enterococcus faecalis and E. faecium isolates. Of the 1,079 unique episodes of bacteraemia investigated, 95.8% were caused by either E. faecalis (61.0%) or E. faecium (34.8%). Ampicillin resistance was detected in 90.4% of E. faecium but not detected in E. faecalis. Using Clinical and Laboratory Standards Institute breakpoints (CLSI), vancomycin non-susceptibility was reported in 0.6% and 31.4% of E. faecalis and E. faecium respectively and was predominately due to the acquisition of the vanB operon. Approximately 1 in 6 vanB E. faecium isolates however, had an minimum inhibitory concentration at or below the CLSI vancomycin susceptible breakpoint of ≤ 4 mg/L. Overall, 37% of E. faecium harboured vanA or vanB genes. Although molecular typing identified 126 E. faecalis pulsed-field gel electrophoresis (PFGE) pulsotypes, more than 50% belonged to 2 pulsotypes that were isolated across Australia. E. faecium consisted of 73 PFGE pulsotypes from which 43 multilocus sequence types were identified. Almost 90% of the E. faecium were identified as clonal complex 17 clones, of which approximately half were characterised as sequence type 203, which was isolated Australia-wide. In conclusion, the AESOP 2011 has shown that although polyclonal, enterococcal bacteraemias in Australia are frequently caused by ampicillin-resistant vanB E. faecium.en_US
dc.language.isoenen
dc.titleAustralian Enterococcal Sepsis Outcome Progamme, 2011.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleCommunicable Diseases Intelligence Quarterly Reporten_US
dc.identifier.affiliationAustralian Collaborating Centre for Enterococcus and Staphylococcus Species (ACCESS) Typing and Research, School of Biomedical Sciences, Curtin University, Perth, Western Australiaen_US
dc.identifier.affiliationSA Pathology, Department of Microbiology and Infectious Diseases, Women's and Children's Hospital, North Adelaide, South Australia and Departments of Pathology, Paediatrics and Molecular and Biomedical Sciences, University of Adelaide, Adelaide, South Australiaen_US
dc.identifier.affiliationAustralian Collaborating Centre for Enterococcus and Staphylococcus Species (ACCESS) Typing and Research, School of Biomedical Sciences, Curtin University, Perth, Western Australia and Department of Microbiology and Infectious Diseases, PathWest Laboratory Medicine, WA, Royal Perth Hospital, Perth, Western Australiaen_US
dc.identifier.affiliationAustralian Group on Antimicrobial Resistance, Royal Perth Hospital, Perth, Western Australiaen_US
dc.identifier.affiliationDepartment of Microbiology and Infectious Diseases, PathWest Laboratory Medicine, WA, Royal Perth Hospital, Perth, Western Australiaen_US
dc.identifier.affiliationDepartment of Microbiology and Infectious Diseases, Concord Hospital, Concord, New South Wales.en_US
dc.identifier.affiliationDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria.en_US
dc.identifier.affiliationMicrobiologyen_US
dc.identifier.affiliationPopulation Health, Deakin University, Melbourne.en_US
dc.identifier.affiliationDepartment of Microbiology and Immunology, University of Melbourne, Melbourne, Victoria.en_US
dc.description.pagesE247-52en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/25391408en
dc.contributor.corpauthorAustralian Group on Antimicrobial Resistanceen
dc.type.contentTexten_US
dc.type.austinJournal Articleen
local.name.researcherHowden, Benjamin P
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptInfectious Diseases-
crisitem.author.deptMicrobiology-
crisitem.author.deptInfectious Diseases-
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