Bingen Edouard, Leclercq Roland, Fitoussi Frédéric, Brahimi Naïma, Malbruny Brigitte, Deforche Dominique, Cohen Robert
Service de Microbiologie, Hôpital Robert Debré, Paris, France.
Antimicrob Agents Chemother. 2002 May;46(5):1199-203. doi: 10.1128/AAC.46.5.1199-1203.2002.
The mechanisms of resistance to macrolides in seven group A streptococcal (Streptococcus pyogenes) isolates that were the cause of pharyngitis in children who were unsuccessfully treated with azithromycin (10 mg/kg of body weight/day for 3 days) were evaluated. All posttreatment strains were found to be genetically related to the pretreatment isolates by random amplified polymorphism DNA analysis and pulsed-field gel electrophoresis. Two isolates had acquired either a mef(A) or an erm(B) gene, responsible for macrolide efflux and ribosomal modification, respectively. Three isolates displayed mutations in the gene encoding the L4 ribosomal protein that is part of the exit tunnel within the 50S subunit of the bacterial ribosome. In the two remaining posttreatment strains, the mechanisms of macrolide resistance could not be elucidated.
对七株A组链球菌(化脓性链球菌)分离株的大环内酯类耐药机制进行了评估,这些分离株是阿奇霉素治疗失败(10mg/kg体重/天,共3天)的儿童咽炎的病因。通过随机扩增多态性DNA分析和脉冲场凝胶电泳发现,所有治疗后的菌株与治疗前的分离株存在遗传相关性。两株分离株分别获得了mef(A)或erm(B)基因,分别负责大环内酯类外排和核糖体修饰。三株分离株在编码L4核糖体蛋白的基因中出现突变,该蛋白是细菌核糖体50S亚基出口通道的一部分。在其余两株治疗后的菌株中,大环内酯类耐药机制尚不清楚。