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对腹泻患者的大便培养分离出的非伤寒沙门菌对耐喹诺酮类药物产生耐药性的作用机制进行了综述。非伤寒沙门菌耐喹诺酮类药物的主要作用机制:①细菌细胞中的靶位基因—Ⅱ型拓扑异构酶即DNA促旋酶(GyrA和GyrB)和拓扑异构酶Ⅳ(ParC和ParE)的突变,导致其构型发生改变和功能丧失而使细胞的DNA降解及菌体死亡;②非靶位基因突变导致细菌细胞膜通透性的改变和膜上主动外排泵的激活,使细菌细胞内药物蓄积浓度低于有效浓度导致耐药。
The mechanism of antimicrobial resistance of non-typhoid Salmonella isolated from stool culture of diarrhea patients was reviewed. The main mechanism of action of quinolones resistant to Salmonella typhi is as follows: (1) The targets of bacterial DNA-Ⅱ topoisomerases DNA gyrase (GyrA and GyrB) and topoisomerase IV (ParC and ParE) Mutation, resulting in its configuration change and loss of function and cell DNA degradation and cell death; ② non-target gene mutations lead to changes in bacterial cell membrane permeability and active membrane efflux pump activation, the bacterial intracellular Drug accumulation below the effective concentration results in drug resistance.