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首页> 美国卫生研究院文献>Clinical Microbiology Reviews >Reduced Vancomycin Susceptibility in Staphylococcus aureus Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms Laboratory Detection and Clinical Implications
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Reduced Vancomycin Susceptibility in Staphylococcus aureus Including Vancomycin-Intermediate and Heterogeneous Vancomycin-Intermediate Strains: Resistance Mechanisms Laboratory Detection and Clinical Implications

机译：降低了金黄色葡萄球菌中万古霉素的敏感性包括中度万古霉素和间质性万古霉素中间菌株：耐药机制实验室检测和临床意义

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Summary: The emergence of vancomycin-intermediate Staphylococcus aureus (VISA) and heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA) over the past decade has provided a challenge to diagnostic microbiologists to detect these strains, clinicians treating patients with infections due to these strains, and researchers attempting to understand the resistance mechanisms. Recent data show that these strains have been detected globally and in many cases are associated with glycopeptide treatment failure; however, more rigorous clinical studies are required to clearly define the contribution of hVISA to glycopeptide treatment outcomes. It is now becoming clear that sequential point mutations in key global regulatory genes contribute to the hVISA and VISA phenotypes, which are associated predominately with cell wall thickening and restricted vancomycin access to its site of activity in the division septum; however, the phenotypic features of these strains can vary because the mutations leading to resistance can vary. Interestingly, changes in the staphylococcal surface and expression of agr are likely to impact host-pathogen interactions in hVISA and VISA infections. Given the subtleties of vancomycin susceptibility testing against S. aureus, it is imperative that diagnostic laboratories use well-standardized methods and have a framework for detecting reduced vancomycin susceptibility in S. aureus.
机译：简介：在过去的十年中，出现了万古霉素中间型金黄色葡萄球菌（VISA）和异种万古霉素中间型金黄色葡萄球菌（hVISA），这给诊断微生物学家发现这些菌株，治疗由这些菌株引起的感染的患者提供了挑战。研究人员试图了解耐药机制。最新数据显示，这些菌株已在全球范围内检测到，并且在许多情况下与糖肽治疗失败有关。然而，需要更严格的临床研究来明确定义hVISA对糖肽治疗结果的贡献。现在已经清楚的是，关键的全球调节基因中的顺序点突变会导致hVISA和VISA表型，这主要与细胞壁增厚和限制万古霉素进入其在分隔隔膜中的活性位点有关。但是，这些菌株的表型特征可能会发生变化，因为导致抗药性的突变可能会发生变化。有趣的是，葡萄球菌表面和agr表达的变化可能会影响hVISA和VISA感染中宿主与病原体的相互作用。鉴于万古霉素对金黄色葡萄球菌敏感性测试的微妙之处，诊断实验室必须使用标准化的方法，并具有检测金黄色葡萄球菌对万古霉素敏感性降低的框架。

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