Appelbaum Peter C
Hershey Medical Center, P.O. Box 850, Hershey, PA 17033, USA.
Int J Antimicrob Agents. 2007 Nov;30(5):398-408. doi: 10.1016/j.ijantimicag.2007.07.011. Epub 2007 Sep 20.
Vancomycin and other glycopeptide antibiotics are the current mainstay of therapy for infections caused by methicillin-resistant Staphylococcus aureus (MRSA). However, the high prevalence of MRSA has led to increased use of vancomycin in chronic and seriously ill patients and has resulted in the emergence of MRSA with reduced susceptibility to glycopeptides. Multiple MRSA phenotypes demonstrate reduced susceptibility to glycopeptides. According to the Clinical and Laboratory Standards Institute, vancomycin-intermediate S. aureus (VISA) are now those isolates with minimum inhibitory concentrations (MICs) between 4 microg/mL and 8 microg/mL, whilst heterogeneous VISA (hVISA) strains appear to be susceptible to vancomycin but contain a subpopulation of cells with reduced susceptibility to vancomycin (MICs > or = 4 microg/mL). At this time, MICs for these strains are reported to range between 1 microg/mL and 2 microg/mL. Vancomycin-resistant S. aureus (VRSA) are defined as those having MICs > or = 16 microg/mL. The detection of reduced susceptibility to vancomycin by routine susceptibility testing is unreliable and vancomycin non-susceptibility is most probably being underreported. Reports of reduced clinical efficacy associated with vancomycin MICs between 1 microg/mL and 2 microg/mL have been published. Patients most at risk of infection by hVISA, VISA and VRSA appear to be those with previous exposure to vancomycin. VRSA appears in the elderly and those with chronic leg or decubitus ulcers mainly containing vancomycin-resistant enterococci, which were probably the donor organism of the vanA gene to S. aureus. All MRSA strains recovered from patients whose infections do not respond to vancomycin treatment should be tested accurately for vancomycin susceptibility if these phenotypes are not to be missed. Treatment options for infections due to MRSA with reduced susceptibility to vancomycin are limited. Rapid identification of patients harbouring VRSA, VISA or hVISA as well as prompt isolation and adherence to infection control protocols are paramount in controlling the dissemination of these pathogens.
万古霉素及其他糖肽类抗生素是目前治疗耐甲氧西林金黄色葡萄球菌(MRSA)感染的主要药物。然而,MRSA的高流行率导致万古霉素在慢性和重症患者中的使用增加,并导致对糖肽类药物敏感性降低的MRSA出现。多种MRSA表型显示对糖肽类药物的敏感性降低。根据临床和实验室标准协会的定义,万古霉素中介金黄色葡萄球菌(VISA)是指那些最低抑菌浓度(MIC)在4微克/毫升至8微克/毫升之间的菌株,而异质性VISA(hVISA)菌株似乎对万古霉素敏感,但含有对万古霉素敏感性降低的细胞亚群(MIC≥4微克/毫升)。此时,据报道这些菌株的MIC在1微克/毫升至2微克/毫升之间。耐万古霉素金黄色葡萄球菌(VRSA)被定义为那些MIC≥16微克/毫升的菌株。通过常规药敏试验检测对万古霉素敏感性降低并不可靠,万古霉素不敏感情况很可能被漏报。已发表了关于MIC在1微克/毫升至2微克/毫升之间的万古霉素临床疗效降低的报道。最易感染hVISA、VISA和VRSA的患者似乎是那些先前接触过万古霉素的患者。VRSA多见于老年人以及患有慢性腿部或褥疮溃疡且主要含有耐万古霉素肠球菌的患者,耐万古霉素肠球菌可能是vanA基因转移至金黄色葡萄球菌的供体菌。如果不想漏诊这些表型,那么对于感染后对万古霉素治疗无反应的患者所分离出的所有MRSA菌株,都应准确检测其对万古霉素的敏感性。对于对万古霉素敏感性降低的MRSA感染,治疗选择有限。快速识别携带VRSA、VISA或hVISA的患者,以及及时隔离并遵守感染控制方案,对于控制这些病原体的传播至关重要。
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