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以伤寒杆菌临床分离的喹诺酮类敏感株 S2 75与其诱导耐药株 RG1 与 RG2 ,对有关伤寒杆菌耐喹诺酮类机制进行了研究。结果发现与伤寒杆菌 S2 75相比较 ,RG1 与 RG2 对喹诺酮类、四环素、氯霉素敏感性明显降低 ,对头孢唑林 ,亚胺培南敏感性有所增加。喹诺酮类对 DNA旋转酶活性 5 0 %抑制剂量 ,RG1 与RG2 较 S2 75呈 3～ 8倍增加 ,S2 75与 RG1 、RG2 旋转酶亚单位交叉重建及 DNA旋转酶 A亚单位基因 (gyr A)喹诺酮耐药决定区 PCR- RFL P分析表明 A亚单位变异为耐药原因之一。细菌对氧氟沙星聚积测定 ,RG1 与RG2 分别为 S2 75之 1/ 2与 1/ 8,经 CCCP处理后 ,分别上升为 S2 75原水平与 S2 75之 1/ 2水平。外膜蛋白分析示 RG2 5 5 k D蛋白带消失 ,同时伴生化反应改变。表明伤寒杆菌耐喹诺酮类机制存在 DNA旋转酶变异 ,药物主动外运及外膜通透性改变。
Quinolone sensitive isolates S2 75 and RG1 and RG2, which were isolated from Salmonella typhi, were used to study the mechanism of quinolones resistant to Salmonella typhi. The results showed that, compared with Salmonella typhi S2 75, the sensitivity of RG1 and RG2 to quinolones, tetracycline and chloramphenicol was significantly reduced, and their sensitivity to cefazolin and imipenem was increased. Quinolones showed 50% inhibition of DNA gyrase activity, RG1 and RG2 increased by 3 ~ 8 times compared with S2 75, and cross-rebuilding of S275 and RG1 and RG2 gyrase subunits and gyr A gene of DNA gyrase, The quinolone resistance-determining region PCR-RFLP analysis showed that mutation of A subunit was one of the causes of drug resistance. The bacterial accumulation of ofloxacin, RG1 and RG2 were respectively 1/2 and 1/8 of S2 75, respectively. After CCCP treatment, the levels of S2 75 and S2 75 were increased respectively. Outer membrane protein analysis showed RG2 5 5 kD protein band disappeared, accompanied by changes in the response. The results showed that there was DNA gyrase variation in the quinolone resistance mechanism of Salmonella typhi, and the changes of active drug transport and permeability of the outer membrane.