淋球菌氟喹诺酮耐药性的分子机制探讨

The molecular mechanism of fluoroquinolone-resistance in Neisseria gonorrhoeae

目的 : 探讨GyrA、ParC基因变异与淋球菌氟喹诺酮耐药性的相关关系。方法 : 首先对 78株淋球菌临床分离株环丙沙星最低抑菌浓度 (MIC)进行检测和GyrA、ParC基因进行PCR扩增 ,然后分别将 2株敏感菌、2株中介菌和 8株耐药菌的GyrA、ParC基因进行DNA序列测定。结果 : 所有 78株淋球菌均扩增出GyrA、ParC基因 ;2株敏感菌和 1株中介菌的GyrA、ParC基因未发现突变 ,另外 1株中介菌中和 8株耐药菌中GyrA、ParC基因发现有一个或多个位点突变。结论 : GyrA、ParC基因变异可能是导致淋球菌氟喹诺酮耐药的重要分子机制。

Objective: To explore the correlation between GyrA, ParC gene mutation and fluoroquinolone-resistence in Neisseria gonorrhoeae. Methods: Firstly the MIC of ciprofloxacin was determined and GyrA, ParC genes were amplified by PCR of 78 clinical isolates of N. gonorrhoese, then the fragments of GyrA and ParC genes from 2 sensitive strains, 2 intermediate strains and 8 resistant strains were directly sequenced. Results: Of all 78 strains, the GyrA and ParC genes were amplified. There was no mutation in GyrA or ParC gene of 2 sensitive strains and 1 intermediate strain; one or multi-dot mutation of GyrA or ParC gene was found in another intermediate strain and all 8 resistant strains. Conclusion: GyrA, ParC gene mutation may be the important molecular mechanism resulting in resistance to fluoroquinolone in Neisseria gonorrhoeae.