Australian Group on Antimicrobial Resistance Australian Enterococcal Sepsis Outcome Programme annual report, 2014.

IF 1.6 Q4 INFECTIOUS DISEASES Communicable Diseases Intelligence Pub Date : 2016-06-30
Geoffrey W Coombs, Denise A Daley, Yung Thin Lee, Stanley Pang, Julie C Pearson, J Owen Robinson, Paul Dr Johnson, Despina Kotsanas, Jan M Bell, John D Turnidge
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Abstract

From 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.

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2014年澳大利亚肠球菌败血症结果规划年度报告。
2014年1月1日至12月31日,澳大利亚27家机构参加了澳大利亚肠球菌败血症结局项目(AESOP)。AESOP 2014的目的是确定澳大利亚耐药肠球菌菌血症分离株的比例,并表征粪肠球菌分离株的分子流行病学特征。在所调查的952例独特的菌血症发作中,94.4%由粪肠杆菌(54.9%)或粪肠杆菌(39.9%)引起。0.6%的粪肠杆菌和89.4%的粪肠杆菌对氨苄西林耐药。粪肠杆菌和粪肠杆菌万古霉素不敏感检出率分别为0.2%和46.1%。51.1%的粪肠杆菌携带vanA或vanB基因。在vanA/B阳性的粪肠杆菌分离株中,81.5%携带vanB基因,18.5%携带vanA基因。澳大利亚对万古霉素耐药的粪肠杆菌菌血症分离株的百分比明显高于大多数欧洲国家。粪肠杆菌共有113个脉冲场凝胶电泳脉冲型,其中68.9%的分离株可分为14个主要脉冲型,且分离株数≥5株。多位点序列分型将14个主要脉冲型归为克隆聚类17,这是一个主要的医院适应型多克隆屎肠杆菌聚类。4种优势序列类型(ST203、ST796、ST555和ST17)的地理分布各不相同,在澳大利亚大部分地区仅发现ST203。总体而言,属于四种优势STs的74.7%分离株含有vanA或vanB基因。总之,2014年AESOP显示澳大利亚肠球菌菌血症通常由多克隆耐氨苄西林高水平庆大霉素耐药vanA或vanB E. faecium引起,治疗选择有限。
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Communicable Diseases Intelligence
Communicable Diseases Intelligence INFECTIOUS DISEASES-
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