Staphylococcus aureus response and adaptation to vancomycin.

Advances in microbial physiology Pub Date : 2024-01-01 Epub Date: 2024-06-01 DOI:10.1016/bs.ampbs.2024.04.006
Anaëlle Fait, Stephanie Fulaz Silva, Jack Åke Harry Abrahamsson, Hanne Ingmer
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Abstract

Antibiotic resistance is an increasing challenge for the human pathogen Staphylococcus aureus. Methicillin-resistant S. aureus (MRSA) clones have spread globally, and a growing number display decreased susceptibility to vancomycin, the favoured antibiotic for treatment of MRSA infections. These vancomycin-intermediate S. aureus (VISA) or heterogeneous vancomycin-intermediate S. aureus (hVISA) strains arise from accumulation of a variety of point mutations, leading to cell wall thickening and reduced vancomycin binding to the cell wall building block, Lipid II, at the septum. They display only minor changes in vancomycin susceptibility, with varying tolerance between cells in a population, and therefore, they can be difficult to detect. In this review, we summarize current knowledge of VISA and hVISA. We discuss the role of genetic strain background or epistasis for VISA development and the possibility of strains being 'transient' VISA with gene expression changes mediated by, for example, VraTSR, GraXSR, or WalRK signal transduction systems, leading to temporary vancomycin tolerance. Additionally, we address collateral susceptibility to other antibiotics than vancomycin. Specifically, we estimate how mutations in rpoB, encoding the β-subunit of the RNA polymerase, affect overall protein structure and compare changes with rifampicin resistance. Ultimately, such in-depth analysis of VISA and hVISA strains in terms of genetic and transcriptional changes, as well as changes in protein structures, may pave the way for improved detection and guide antibiotic therapy by revealing strains at risk of VISA development. Such tools will be valuable for keeping vancomycin an asset also in the future.

金黄色葡萄球菌对万古霉素的反应和适应。
抗生素耐药性是人类病原体金黄色葡萄球菌面临的一个日益严峻的挑战。耐甲氧西林金黄色葡萄球菌(MRSA)克隆已在全球蔓延,越来越多的克隆对治疗 MRSA 感染的首选抗生素万古霉素的敏感性降低。这些万古霉素中间型金黄色葡萄球菌(VISA)或异型万古霉素中间型金黄色葡萄球菌(hVISA)菌株是由多种点突变积累而成,导致细胞壁增厚,万古霉素与细胞壁构筑物脂质 II 的结合力降低。它们对万古霉素的敏感性仅有微小变化,群体中不同细胞对万古霉素的耐受性各不相同,因此很难被检测到。在本综述中,我们总结了目前有关 VISA 和 hVISA 的知识。我们讨论了遗传菌株背景或外显子对 VISA 发展的作用,以及菌株可能是 "瞬时 "VISA,由 VraTSR、GraXSR 或 WalRK 信号转导系统等介导的基因表达变化导致暂时的万古霉素耐受性。此外,我们还研究了对万古霉素以外的其他抗生素的附带敏感性。具体来说,我们估算了编码 RNA 聚合酶 β 亚基的 rpoB 基因突变对整个蛋白质结构的影响,并比较了这些变化与利福平耐药性之间的关系。最终,从基因和转录变化以及蛋白质结构变化的角度对 VISA 和 hVISA 菌株进行这种深入分析,可以揭示有可能发展成 VISA 的菌株,从而为改进检测和指导抗生素治疗铺平道路。未来,这些工具对于保持万古霉素的价值也将是非常宝贵的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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