Pechère J C
Department of Microbiology and Genetics, University Medical Centre, 1 Rue Michel Servet, CH-1211, Geneva, Switzerland.
Int J Antimicrob Agents. 2001;18 Suppl 1:S25-8. doi: 10.1016/s0924-8579(01)00407-1.
Two principal mechanisms of resistance to macrolides have been identified in Gram-positive bacteria. Erythromycin-resistant methylase is encoded by erm genes. Resultant structural changes to rRNA prevent macrolide binding and allow synthesis of bacterial proteins to continue. Presence of the erm gene results in high-level resistance. Modification of the mechanism whereby antibiotics are eliminated from the bacteria also brings about resistance. Bacteria carrying the gene encoding macrolide efflux (i.e. the mefE gene) display relatively low-level resistance. Azithromycin, because of its ability to achieve concentrations at sites of infections, is capable of eradicating mefE-carrying strains. Other resistance mechanisms, involving stimulation of enzymatic degradation, appear not to be clinically significant.
革兰氏阳性菌中已确定两种主要的大环内酯类耐药机制。红霉素耐药甲基化酶由erm基因编码。rRNA由此产生的结构变化可阻止大环内酯类药物结合，并使细菌蛋白质合成得以继续。erm基因的存在导致高水平耐药。改变抗生素从细菌中清除的机制也会产生耐药性。携带大环内酯类药物外排编码基因（即mefE基因）的细菌表现出相对低水平的耐药性。阿奇霉素因其能够在感染部位达到一定浓度，所以能够根除携带mefE基因的菌株。其他涉及酶促降解刺激的耐药机制似乎在临床上并不重要。
