临床病原菌磷霉素耐药机制研究进展  

Research progress on the drug resistance mechanism of clinical pathogens to fosfomycin

作　　者：王立新[1] 苏云福 王毅[1] WANG Lixin;SU Yunfu;WANG Yi(Department of Clinical Laboratory,Tianjin Hospital,Tianjin 300211,China;Department of Clinical Laboratory,Hotan District People's Hospital,Hotan 848000,Xinjiang,China)

机构地区：[1]天津医院检验科,天津300211 [2]新疆维吾尔自治区和田地区人民医院检验科,新疆和田848000

出　　处：《检验医学》2022年第10期993-997,共5页Laboratory Medicine

摘　　要：近年来,多重耐药和泛耐药病原菌不断产生,新的抗菌药物研发速度已无法满足临床治疗需求。磷霉素和多黏菌素等抗菌药物被重新用于临床抗感染治疗。磷霉素对革兰阳性菌和革兰阴性菌有独特的作用机制,不易产生交叉耐药,仍有较好的临床应用价值。文章对磷霉素的耐药机制,如murA发生突变引起的磷霉素耐药、膜转运体的结构基因突变、质粒介导的磷霉素修饰酶,以及异质性耐药等耐药机制进行综述。With the spread of multidrug-resistant or extensively drug resistant pathogens and the lack of new antibiotics,many old antibiotics,such as fosfomycin and polymyxin,are reused for anti-infection treatment in clinic.Fosfomycin has a unique mechanism against Gram-positive and Gram-negative bacteria.Cross-resistance is not common.This review mainly focuses on drug resistance mechanism to fosfomycin,such as drug resistance caused by murA mutations,mutations in the chromosomal genes encoding fosfomycin transporters,acquisition of plasmid-encoded genes encoding fosfomycin-modifying enzymes and hetero-resistance to fosfomycin.

关 键 词：磷霉素 耐药机制 murA突变 膜转运体 磷霉素修饰酶 异质性耐药 

分 类 号：R446.5[医药卫生—诊断学]