Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/16199
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dc.contributor.authorCoombs, Geoffrey W-
dc.contributor.authorDaley, Denise A-
dc.contributor.authorThin Lee, Yung-
dc.contributor.authorPang, Stanley-
dc.contributor.authorPearson, Julie C-
dc.contributor.authorRobinson, J Owen-
dc.contributor.authorJohnson, Paul D R-
dc.contributor.authorKotsanas, Despina-
dc.contributor.authorBell, Jan M-
dc.contributor.authorTurnidge, John D-
dc.date2016-06-
dc.date.accessioned2016-09-06T06:06:43Z-
dc.date.available2016-09-06T06:06:43Z-
dc.date.issued2016-06-
dc.identifier.citationCommunicable Diseases Intelligence 2016; 40 (2): E236-243en_US
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/16199-
dc.description.abstractFrom 1 January to 31 December 2014, 27 institutions around Australia participated in the Australian Enterococcal Sepsis Outcome Programme (AESOP). The aim of AESOP 2014 was to determine the proportion of enterococcal bacteraemia isolates in Australia that were antimicrobial resistant, and to characterise the molecular epidemiology of the Enterococcus faecium isolates. Of the 952 unique episodes of bacteraemia investigated, 94.4% were caused by either E. faecalis (54.9%) or E. faecium (39.9%). Ampicillin resistance was detected in 0.6% of E. faecalis and in 89.4% of E. faecium. Vancomycin non-susceptibility was reported in 0.2% and 46.1% of E. faecalis and E. faecium respectively. Overall 51.1% of E. faecium harboured vanA or vanB genes. For the vanA/B positive E. faecium isolates, 81.5% harboured vanB genes and 18.5% vanA genes. The percentage of E. faecium bacteraemia isolates resistant to vancomycin in Australia is significantly higher than that seen in most European countries. E. faecium consisted of 113 pulsed-field gel electrophoresis pulsotypes of which 68.9% of isolates were classified into 14 major pulsotypes containing 5 or more isolates. Multilocus sequence typing grouped the 14 major pulsotypes into clonal cluster 17, a major hospital-adapted polyclonal E. faecium cluster. The geographical distribution of the 4 predominant sequence types (ST203, ST796, ST555 and ST17) varied with only ST203 identified across most regions of Australia. Overall 74.7% of isolates belonging to the four predominant STs harboured vanA or vanB genes. In conclusion, the AESOP 2014 has shown enterococcal bacteraemias in Australia are frequently caused by polyclonal ampicillin-resistant high-level gentamicin resistant vanA or vanB E. faecium, which have limited treatment options.en_US
dc.subjectDrug Resistance, Microbialen_US
dc.subjectEnterococcus faeciumen_US
dc.subjectVancomycin-Resistant Enterococcien_US
dc.titleAustralian Group on Antimicrobial Resistance Australian Enterococcal Sepsis Outcome Programme annual report, 2014en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleCommunicable Diseases Intelligenceen_US
dc.identifier.affiliationAustin Health, Heidelberg, Victoria, Australiaen_US
dc.identifier.affiliationAustralian Collaborating Centre for Enterococcus and Staphylococcus Species (ACCESS) Typing and Research, School of Veterinary and Life Sciences, Murdoch University, Murdoch, Western Australia, Australiaen_US
dc.identifier.affiliationDepartment of Microbiology and Infectious Diseases, PathWest Laboratory Medicine-WA, Fiona Stanley Hospital, Murdoch, Western Australia, Australiaen_US
dc.identifier.affiliationAustralian Group on Antimicrobial Resistance, Fiona Stanley Hospital, Murdoch, Western Australia, Australiaen_US
dc.identifier.affiliationMicrobiologyen_US
dc.identifier.affiliationInfectious Diseases, Monash Health, Monash Medical Centre, Clayton, Victoria, Australiaen_US
dc.identifier.affiliationSA Pathology, Department of Microbiology and Infectious Diseases, Women's and Children's Hospital, North Adelaide, South Australia, Australiaen_US
dc.identifier.affiliational Sciences, UniverDepartments of Pathology, Paediatrics and Molecular and Biomedicsity of Adelaide, Adelaide, South Australia, Australiaen_US
dc.identifier.affiliationInfectious Diseasesen_US
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/27522135en_US
dc.contributor.corpauthorAustralian Group on Antimicrobial Resistance-
dc.type.contentTexten_US
dc.type.austinJournal Articleen_US
local.name.researcherJohnson, Paul D R
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextWith Fulltext-
item.grantfulltextopen-
item.openairetypeJournal Article-
crisitem.author.deptInfectious Diseases-
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