JMI Laboratories, North Liberty, Iowa 52317, USA.
Clin Infect Dis. 2011 Jun;52 Suppl 7:S487-92. doi: 10.1093/cid/cir164.
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.
夫西地酸与延伸因子 G（EF-G）结合，阻止其从核糖体上释放，从而阻断细菌蛋白质合成。在葡萄球菌中，高水平的夫西地酸耐药性通常是由编码 EF-G 的基因 fusA 突变引起的，而低水平的耐药性通常是由 FusB 和 FusC 等水平转移机制引起的，这些机制对 EF-G 具有潜在的保护作用。此外，fusD 负责屎肠球菌的固有耐药性，rplF（fusE）的 L6 部分的改变在夫西地酸耐药性中起作用。几十年来，夫西地酸一直在欧洲和澳大利亚使用。最近，它也在其他国家和地区使用，但不在美国。全球夫西地酸耐药性的发展速度较慢，耐药水平和相关的遗传机制通常反映了引入时间、治疗指征、给药途径和处方实践。
