摘要
目的研究Uu临床株对氟喹诺酮类药物的耐药机制.方法从184个临床Uu株中筛选出13株对6种氟喹诺酮类药物呈不同程度耐药的菌株,PCR扩增其gyrA, gyrB, parC 和 parE基因的QRDR区.产物测序后和标准敏感株进行序列比较.结果序列比较结果表明 gyrA QRDR第87位核苷酸C到A的突变导致GyrA第95位天冬氨酸被谷氨酸替代,parC QRDR 的第50位核苷酸C到T的突变导致ParC第80位丝氨酸被亮氨酸所替代.结论这些结果表明gyrA QRDR第87位核苷酸C到A的突变与parC QRDR 的第50位核苷酸C到T的突变和Uu对氟喹诺酮类药物的耐药相关.
OBJECTIVE: To study the resistance mechanism of clinical isolates of Ureaplasma urealyticum resistant to fluoroquinolones. METHODS: Thirteen isolates of Ureaplasma urealyticum resistant to six fluoroquinolones were selected out of 184 clinical isolates and their QRDRs (quinolone resistance-determining region) gyrA, gyrB, parC and parE were amplified by PCR. Sequencing results were compared to those susceptible reference strains and a comparison of deduced amino acid sequences were performed. RESULTS: Sequence comparison revealed a C to A change at 87nt of gyrA QRDR leading to the substitution of Asp95 with glutamic acid and a C to T change at 50nt of parC QRDR leading to the substitution of Ser80 with leucine. CONCLUSION: These results suggest that a C to A change at 87nt of gyrA QRDR and a C to T change at 50nt of parC QRDR are associated with fluoroquinolone resistance of Ureaplasma urealyticum.
关键词
突变位点
解脲脲原体
基因结构
基因突变
耐药性
氟喹诺酮类药物
合理用药
Mutation
Amino Acid Substitution
Anti-Infective Agents
DNA Gyrase
DNA Topoisomerase IV
Drug Resistance, Multiple, Bacterial
Fluoroquinolones
Humans
Polymerase Chain Reaction
Research Support, Non-U.S. Gov't
Ureaplasma urealyticum
