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目的探讨GyrA基因突变与体外诱导人型支原体(Mh)氟喹诺酮耐药的相关关系。方法将Mh标准株PG21在分别含有4种次抑菌浓度氟喹诺酮类药物的液体培养基中传代培养3代和l2代后,筛选诱导株并分别检测其对4种药物的最低抑菌浓度(MIC)值;对所有诱导株GyrA基因PCR扩增后进行DNA测序分析。结果经体外诱导后,共筛选出8株诱导株。其中4株短期诱导株呈现低度的耐药和交叉耐药,仅SPX诱导株G3发生GyrA基因Ser83→Leu变异,4株长期诱导株呈现高度的耐药和交叉耐药,除CFX诱导株C12外,均发生GyrA基因Ser83→Leu变异。SPX诱导株G12同时还出现GyrA基因Ser84→Trp变异。结论体外长时间、次抑菌浓度的氟喹诺酮类药物刺激将诱导Mh产生耐药和交叉耐药。GyrA基因83位上丝氨酸(Ser)→亮氨酸(Leu)的变异可能是Mh体外获得性氟喹诺酮耐药的重要分子机制。
Objective To investigate the relationship between GyrA gene mutation and fluoroquinolone resistance induced by Mycoplasma hominis (Mh) in vitro. Methods The Mh standard strain PG21 was subcultured for 3 and 12 generations respectively in liquid medium containing four Fubonin concentrations. The induced strains were screened and their minimum inhibitory concentration (MIC) against four drugs MIC) values; GyrA gene of all induced strains after PCR amplification of DNA sequencing analysis. Results After in vitro induction, a total of 8 strains were selected. Four of the short-term induced strains showed low resistance and cross-resistance. Only the SP83-induced GyrA gene Ser83 → Leu was mutated. Four long-term induced strains showed high resistance and cross-resistance. Except CFX-induced C12 In addition, mutation of Ser83 → Leu occurred in GyrA gene. SPX induced strain G12 also appeared GyrA gene Ser84 → Trp variation. Conclusion Long-term and secondary inhibitory concentrations of fluoroquinolones in vitro will induce Mh resistance and cross-resistance. The mutation of serine → leucine at position 83 of GyrA gene may be an important molecular mechanism of acquired fluoroquinolone resistance in vitro.