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目的 探讨人型支原体 (Mh)对喹诺酮类药物的耐药机理 ,指导合理使用抗生素。方法以含氧氟沙星、左旋氧氟沙星、盐酸环丙沙星的培养基培养标准敏感株及临床敏感株Mh12代后 ,将其gyrA基因、parE基因扩增 ,分析其核苷酸序列。结果 3种药物诱导株均产生耐药及交叉耐药性 ,氧氟沙星、左旋氧氟沙星诱导Mh发生 70位G→A的突变 ,导致 42 6位的天冬氨酸转变为天冬酰胺 ;盐酸环丙沙星诱导Mh发生 113位C→T的突变 ,导致 83位的丝氨酸转变为亮氨酸。结论 Mh长期接触低浓度喹诺酮类药物会产生耐药性 ,gyrA、parE基因中的点突变可能是耐药机制的一部分。
Objective To investigate the mechanism of drug resistance of quinolone (Mh) to quinolones and to guide the rational use of antibiotics. Methods The standard sensitive strain and the sensitive clinical strain Mh12 were cultured in the medium containing ofloxacin, levofloxacin and ciprofloxacin. The gyrA gene and parE gene were amplified and the nucleotide sequence was analyzed . Results All three kinds of drug-induced strains were resistant and cross-resistant. Ofloxacin and levofloxacin induced a G → A mutation at position 70 of Mh, resulting in the transformation of aspartate at position 42 6 to asparagus Amide; ciprofloxacin hydrochloride induced Mh mutation 113 C → T, resulting in 83 serine into leucine. Conclusion Mh exposure to low concentrations of quinolones can cause drug resistance. The point mutations in gyrA and parE genes may be part of the drug resistance mechanism.