目的　研究伤寒杆菌DNA旋转酶A亚单位基因 (gyrA)变异与其耐喹诺酮类的关系。方法　应用聚合酶链反应 (PCR)检测、限制性片段长度多态性 (RFLP)、单链构象多态性分析 (SSCP)及序列测定 ,对伤寒杆菌S2 75 (临床分离敏感菌株 )及其自发耐药突变株RG1,DNAgyrA喹诺酮类耐药决定区进行了研究。结果　伤寒杆菌S2 75 gyrA第 12 8～ 42 6位碱基与大肠杆菌KL 16高度同源 ,仅 7.49%有差异 ,且大部分为静变异 ,最终仅使DNA旋转酶A亚单位产生Thr 45→His、Arg 49→Leu及Val 5 6→Gly ,均位于喹诺酮耐药决定区 (第 6 7～ 10 6位氨基酸 )外。RG1仅有第 2 47位碱基T→G变异 ,相应Ser 83→Ala ,使萘啶酸、氧氟沙星及环丙沙星对伤寒杆菌的MIC由 2、0 .0 6、<0 .0 3mg/L上升为 5 12、2、1mg/L。Ala替换与文献报道沙门杆菌该位以苯丙氨酸、酪氨酸替换为主不同。PCR RFLP及SSCP分析结果与上述情况类似。结论　gryA第 83位变异为其耐药主要原因 Objective To study the relationship between DNA gyrase A subunit gene (gyrA) mutation and fluoroquinolones resistance in Salmonella typhi. Methods Polymerase chain reaction (PCR), restriction fragment length polymorphism (RFLP), single strand conformation polymorphism (SSCP) and sequencing were used to detect the susceptibility of Salmonella typhi S2 75 Resistance mutant RG1, DNAgyrA quinolone resistance-determining regions were studied. Results The results showed that the 12th to the 42th bases of Salmonella typhi of S2 75 gyrA were highly homologous to KL 16 of Escherichia coli with a difference of only 7.49%, and most of them were static variations. Eventually, DNA gyrase A subunit only produced Thr 45 → His, Arg 49 → Leu and Val 5 6 → Gly all located outside the quinolone resistance-determining region (amino acids 67 to 106). RG1 has only the base T → G mutation at position 2 47, and the corresponding Ser 83 → Ala, so that the nalidixic acid, ofloxacin and ciprofloxacin against the typhoid bacillus MIC from 2,0. 0 3mg / L increased to 5 12,2,1 mg / L. Ala replacement and reported in the literature Salmonella this position to phenylalanine, tyrosine replacement mainly different. PCR RFLP and SSCP analysis results similar to the above. Conclusion The 83rd mutation of gryA is the main reason of its resistance