Characterization of Global Patterns and the Genetics of Fusidic Acid Resistance
Characterization of Global Patterns and the Genetics of Fusidic Acid Resistance
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DOI：
10.1093/cid/cir164
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发表时间：
2011-06-01
影响因子：
11.8
通讯作者：
Chopra, Ian
中科院分区：
文献类型：
--
作者：
Farrell, David J.;Castanheira, Mariana;Chopra, Ian
夫西地酸与延伸因子G（EF-G）结合，阻止其从核糖体释放，从而阻止细菌蛋白质合成。在葡萄球菌中，高水平的夫西地酸耐药通常是由编码EF-G、fusA的基因突变引起的，而低水平的耐药通常是由水平转移机制fusB和fusC引起的，它们对EF-G具有假定的保护作用。此外，fusD是造成金黄色葡萄球菌中的内在抗性的原因，并且rplF的L 6部分（fusE）的改变在夫西地酸抗性中起作用。夫西地酸在欧洲和澳大利亚已经使用了几十年。最近，它也被用于其他国家和地区，但不是在美国。全球夫西地酸耐药性发展缓慢，耐药性水平和遗传机制通常反映了自引入以来的时间、治疗适应症、给药途径和处方实践。
Fusidic acid binds to elongation factor G (EF-G), preventing its release from the ribosome, thus stalling bacterial protein synthesis. In staphylococci, high-level fusidic acid resistance is usually caused by mutations in the gene encoding EF-G, fusA, and low-level resistance is generally caused by the horizontally transferable mechanisms fusB and fusC that have a putative protective role on EF-G. In addition, fusD is responsible for intrinsic resistance in Staphylococcus saprophyticus, and alterations in the L6 portion of rplF (fusE) have a role in fusidic acid resistance. Fusidic acid has been used in Europe and Australia for decades. More recently, it has also been used in other countries and regions, but not in the United States. Worldwide fusidic acid resistance has been slow to develop, and the level of resistance and genetic mechanisms responsible generally reflect the time since introduction, indications for treatment, route of administration, and prescribing practices.