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Clinical and Molecular Epidemiology of an Emerging Panton-Valentine Leukocidin-Positive ST5 Methicillin-Resistant Staphylococcus aureus Clone in Northern Australia
mSphere ( IF 3.7 ) Pub Date : 2021-02-10 , DOI: 10.1128/msphere.00651-20
Sarah L McGuinness 1, 2, 3 , Deborah C Holt 4, 5 , Tegan M Harris 4 , Connor Wright 6 , Rob Baird 7 , Phillip M Giffard 4, 5 , Asha C Bowen 4, 8, 9, 10 , Steven Y C Tong 11, 12, 13
Affiliation  

Recently, we identified a Staphylococcus aureus sequence type 5 (ST5) clone in northern Australia with discrepant trimethoprim-sulfamethoxazole (SXT) susceptibility results. We aimed to identify isolates of this clone using Vitek 2 SXT resistance as a proxy and to compare its epidemiology with those of other circulating S. aureus strains. We collated Vitek 2 susceptibility data for S. aureus isolates collected through our laboratory and conducted a prospective, case-control study comparing clinical, microbiological, epidemiological, and genomic data for subsets of isolates reported as SXT resistant (cases) and SXT susceptible (controls) by Vitek 2. While overall SXT resistance rates remained relatively stable from 2011 to 2018 among 27,721 S. aureus isolates, non-multidrug-resistant methicillin-resistant S. aureus (MRSA) strains almost completely replaced multidrug-resistant MRSA strains as the predominant SXT-resistant MRSA phenotype. Demographic and clinical features of 51 case-control pairs were similar, but genotyping revealed stark differences: clonal complex 5 (CC5) MRSA predominated among SXT-resistant cases (34/51 [67%]), while CC93 MRSA predominated among susceptible controls (26/51 [51%]). All CC5 isolates were an ST5 clonal lineage that possessed the trimethoprim resistance gene dfrG within SCCmec IVo; all were SXT susceptible by Etest. The replacement of Vitek 2 reported SXT-resistant multidrug-resistant MRSA by non-multidrug-resistant MRSA appears related to the emergence of an ST5-MRSA-SCCmec IVo clone that is SXT susceptible by Etest and causes clinical disease similar to that caused by ST93-MRSA-SCCmec IVa. Reliance on Vitek 2 SXT reporting may lead to unnecessary restriction of effective oral treatment options for S. aureus infections. Whether the presence of dfrG within SCCmec IVo provides a selective advantage at the population level is currently unclear.

中文翻译:

澳大利亚北部新兴 Panton-Valentine 杀白细胞素阳性 ST5 耐甲氧西林金黄色葡萄球菌克隆的临床和分子流行病学

最近,我们在澳大利亚北部鉴定了一个金黄色葡萄球菌序列 5 (ST5) 克隆,其对甲氧苄啶-磺胺甲恶唑 (SXT) 的敏感性结果不一致。我们旨在使用 Vitek 2 SXT 抗性作为代理来鉴定该克隆的分离株,并将其流行病学与其他循环金黄色葡萄球菌菌株的流行病学进行比较。我们整理了通过我们实验室收集的金黄色葡萄球菌分离株的Vitek 2 敏感性数据,并进行了一项前瞻性病例对照研究,比较了报告为 SXT 耐药(病例)和 SXT 敏感(对照)的分离株亚群的临床、微生物学、流行病学和基因组数据) 由 Vitek 2. 虽然整体 SXT 阻力率从 2011 年到 2018 年保持相对稳定,其中 27,721金黄色葡萄球菌分离株,非耐多药耐甲氧西林金黄色葡萄球菌(MRSA) 菌株几乎完全取代耐多药 MRSA 菌株,成为主要的 SXT 耐药 MRSA 表型。51 个病例对照对的人口统计学和临床​​特征相似,但基因分型显示出明显的差异:克隆复合体 5 (CC5) MRSA 在 SXT 耐药病例中占主导地位 (34/51 [67%]),而 CC93 MRSA 在易感对照中占主导地位。 26/51 [51%])。所有 CC5 分离株都是 ST5 克隆谱系,在 SCC mec中具有甲氧苄啶抗性基因dfrG静脉;Etest 都对 SXT 敏感。Vitek 2 报道的 SXT 耐药多重耐药 MRSA 被非多重耐药 MRSA 取代似乎与 ST5-MRSA-SCC mec IVo 克隆的出现有关,该克隆对 SXT 易感 Etest 并导致类似于由ST93-MRSA-SCC mec IVa。依赖 Vitek 2 SXT 报告可能会导致对金黄色葡萄球菌感染的有效口服治疗方案的不必要限制。SCC mec IVo中dfrG的存在是否在群体水平上提供了选择性优势目前尚不清楚。
更新日期:2021-02-11
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