澳大利亚抗微生物药物耐药性小组(琼脂)澳大利亚金黄色葡萄球菌监测结果计划(ASSOP)血流感染年度报告2022。

Geoffrey W Coombs, Denise A Daley, Princy Shoby, Shakeel Mowlaboccus
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引用次数: 0

摘要

从2022年1月1日到12月31日,澳大利亚55个机构参加了澳大利亚金黄色葡萄球菌监测结果计划(ASSOP)。ASSOP 2022的目的是确定澳大利亚耐药金黄色葡萄球菌菌血症(SAB)分离株的比例,特别强调对甲氧西林的敏感性和耐甲氧西林分离株的分子流行病学特征。报告了3214例SAB发作,其中77.5%为社区发病。总体而言,15.0%的金黄色葡萄球菌对甲氧西林耐药。耐甲氧西林SAB的30天全因死亡率为21.4%,与甲氧西林敏感SAB的16.8%有显著差异(p = 0.02)。除β-内酰胺类和红霉素外,甲氧西林敏感金黄色葡萄球菌的耐药性罕见。然而,除了β-内酰胺外,大约31%的耐甲氧西林金黄色葡萄球菌(MRSA)对环丙沙星耐药;红霉素占30%;13%为四环素;庆大霉素占11%;2%是复方新诺明。一株达托霉素MIC为1.5 mg/L的MRSA分离物携带A302V mprF和A23V cls2突变。当应用欧洲抗菌素敏感性试验委员会(EUCAST)的断点时,在一株MRSA分离物中检测到对替柯planin的耐药性。未检出对万古霉素或利奈唑胺耐药。对非β-内酰胺类抗菌素的耐药主要归因于医疗相关MRSA (HA-MRSA)克隆ST22-IV [2B] (EMRSA-15),以及社区相关MRSA (CA-MRSA)克隆ST45-V [5C2&5],后者已对环丙沙星、克林霉素、红霉素、庆大霉素和四环素等多种抗菌素产生耐药。ST22-IV [2B] (EMRSA-15)克隆是澳大利亚主要的HA-MRSA克隆。尽管如此,86%的耐甲氧西林SAB发作是由CA-MRSA克隆引起的。虽然是多克隆的,但大约72%的CA-MRSA克隆被鉴定为ST93-IV [2B](昆士兰克隆);ST5-IV (2 b);ST45-V c2&5 [5];ST1-IV (2 b);ST30-IV (2 b);ST97-IV (2 b);ST953-IV (2 b);ST8-IV [2B]。由于CA-MRSA在澳大利亚社区已经建立,因此监测社区和医疗保健相关SAB的抗菌素耐药性模式非常重要,因为这些信息将指导治疗金黄色葡萄球菌菌血症的治疗实践。
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Australian Group on Antimicrobial Resistance (AGAR) Australian Staphylococcus aureus Surveillance Outcome Program (ASSOP) Bloodstream Infection Annual Report 2022.

From 1 January to 31 December 2022, fifty-five institutions across Australia participated in the Australian Staphylococcus aureus Surveillance Outcome Program (ASSOP). The aim of ASSOP 2022 was to determine the proportion of Staphylococcus aureus bacteraemia (SAB) isolates in Australia that were antimicrobial resistant, with particular emphasis on susceptibility to methicillin and on characterisation of the molecular epidemiology of the methicillin-resistant isolates. A total of 3,214 SAB episodes were reported, of which 77.5% were community-onset. Overall, 15.0% of S. aureus were methicillin resistant. The 30-day all-cause mortality associated with methicillin-resistant SAB was 21.4%, which was significantly different to the 16.8% all-cause mortality associated with methicillin-susceptible SAB (p = 0.02). With the exception of the β-lactams and erythromycin, antimicrobial resistance in methicillin-susceptible S. aureus was rare. However, in addition to the β-lactams, approximately 31% of methicillin-resistant S. aureus (MRSA) were resistant to ciprofloxacin; 30% to erythromycin; 13% to tetracycline; 11% to gentamicin; and 2% to co-trimoxazole. One MRSA isolate, with a daptomycin MIC of 1.5 mg/L, harboured the A302V mprF and A23V cls2 mutations. When applying the European Committee on Antimicrobial Susceptibility Testing (EUCAST) breakpoints, teicoplanin resistance was detected in one MRSA isolate. Resistance to vancomycin or linezolid was not detected. Resistance to non-β-lactam antimicrobials was largely attributable to the healthcare-associated MRSA (HA-MRSA) clone ST22-IV [2B] (EMRSA-15), and to the community-associated MRSA (CA-MRSA) clone ST45-V [5C2&5] which has acquired resistance to multiple antimicrobials including ciprofloxacin, clindamycin, erythromycin, gentamicin, and tetracycline. The ST22-IV [2B] (EMRSA-15) clone is the predominant HA-MRSA clone in Australia. Nonetheless, 86% of methicillin-resistant SAB episodes were due to CA-MRSA clones. Although polyclonal, approximately 72% of CA-MRSA clones were characterised as ST93-IV [2B] (Queensland clone); ST5-IV [2B]; ST45-V [5C2&5]; ST1-IV [2B]; ST30-IV [2B]; ST97-IV [2B]; ST953-IV [2B]; and ST8-IV [2B]. As CA-MRSA is well established in the Australian community, it is important to monitor antimicrobial resistance patterns in community- and healthcare-associated SAB as this information will guide therapeutic practices in treating S. aureus bacteraemia.

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