肺炎支原体对大环内酯类抗生素耐药机制的研究进展  

Progress on resistance mechanisms of Mycoplasma pneumoniae to macrolide antibiotics

作　　者：潘明安[1] 张天托[1] 

机构地区：[1]中山大学附属第三医院呼吸内科,广州510630

出　　处：《国际呼吸杂志》2008年第4期214-218,共5页International Journal of Respiration

摘　　要：肺炎支原体（MP）是社区获得性呼吸道感染的常见病原体之一，其对影响细菌蛋白质合成的抗生素如大环内酯类敏感。然而近年来MP的耐药现象逐渐增多，国内外都已经分离出对大环内酯类的耐药菌株。目前体内外的研究表明核糖体上23S rRNA的基因突变和核糖体蛋白的氨基酸改变是MP对大环内酯类抗生素耐药的主要机制。由于新型大环内酯类抗生素的广泛应用，在药物选择压力下以及检测技术的不断进步，新型耐药机制不断涌现，有待进一步深入研究。Mycoplasma pneumoniae（MP） is one of the common pathogens responsible for respiratory tract infections acquired in the community. It is susceptible to macrolide antibiotics which influence the synthesis of protein. However, resistance related to MP is increasing in recent years and macrolide resistance strains have been isolated home and abroad. The research in vivo and vitro shows that the main mechanisms of MP to macrolide antibiotics resistance are genetic mutation in 23S rRNA and the amino acids alteration of ribosome protein. Followed by the wide use of new macrolide antibiotics which lead to the pressure of drug selection and progress of the detection, new types of resistance mechanisms will come up for further research.

关 键 词：肺炎支原体 大环内酯类抗生素 耐药机制 

分 类 号：R725.6[医药卫生—儿科]