Mechanisms of resistance to antifungal agents: Yeasts and filamentous fungi
Mechanisms of resistance to antifungal agents: Yeasts and filamentous fungi
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DOI：
10.1016/s1130-1406(08)70027-5
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发表时间：
2008-06-01
影响因子：
1.9
通讯作者：
Espinel-Ingroff, Ana
中科院分区：
文献类型：
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作者：
Espinel-Ingroff, Ana
抗真菌治疗失败可能是由于体外耐药性（内在的或治疗过程中产生的）或临床耐药性；后者与宿主、抗真菌剂或感染分离株相关的许多因素有关。最近，出现了敏感 MIC 断点（2 mu g/ml）。在其中一些病例中，临床失败与下述基因突变有关。当通过 CLSI 标准化方法测试分离株时，唑和氟胞嘧啶断点以及棘白菌素敏感断点非常有用；断点也可通过 EUCAST 方法获得。最近，体外耐药 MIC 断点已被指定用于丝状病毒 真菌（霉菌）与五种抗真菌药物，但这些类别并非基于体外与体内治疗反应的相关性。然而，伊曲康唑（杨森）、两性霉素 B（百时美施贵宝）和伏立康唑（辉瑞）治疗曲霉菌病的临床失败与 MIC > 2 μg/ml 相关。本文对报告的阻力进行了回顾 自2005年以来抗真菌药物的分子机制；还列出了以前的相关评论。
Failure to respond to antifungal therapy could be due to in vitro resistance (intrinsic or developed during therapy) or clinical resistance; the latter is associated with numerous factors related to the host, the antifungal agent, or the infecting isolate. Recently, a susceptible MIC breakpoint ( 2 mu g/ml. In some of these cases, clinical failure was associated with the genetic mutations described below. Azole and flucytosine breakpoints, and the echinocandin susceptible breakpoint, are useful when isolates are tested by CLSI standardized methods; breakpoints are also available by the EUCAST method. More recently, in vitro resistant MIC breakpoints have been assigned for filamentous fungi (moulds) vs. five antifungal agents, but these categories are not based on correlations of in vitro with in vivo response to therapy. However, itraconazole (Janssen), amphotericin B (Bristol-Myers) and voriconazole (Pfizer) clinical failures in aspergillosis have been correlated with MICs > 2 mu g/ml. This article provides a review of reported resistance molecular mechanisms to antifungal agents since 2005; previous related reviews are also listed.