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山东大学学报(医学版) ›› 2010, Vol. 48 ›› Issue (3): 39-43.

• 论文 • 上一篇    下一篇

体外诱导肺炎支原体对喹诺酮类药物耐药机制的研究

王鑫1,吴大玮1,公衍文2   

  1. 1. 山东大学齐鲁医院呼吸内科, 济南 250012;
    2. 济南军区总医院实验诊断科, 济南 250031
  • 收稿日期:2009-11-25 出版日期:2010-03-16 发布日期:2010-03-16
  • 通讯作者: 吴大玮(1960- ),男,教授,硕士,主要从事肺部感染和病 原菌耐药机制的研究。
  • 作者简介:王鑫(1976- ),男,主治医师,硕士研究生,主要从事肺部感染和病原菌耐药机制的研究。
  • 基金资助:

    山东省科技攻关计划项目(2006GG2202008);山东省医药卫生科技发展计划项目(2005HW057)。

Induction and mechanisms of resistance to quinolones in Mycoplasma pneumoniae

WANG Xin 1, WU Dawei 1, GONG Yanwen 2   

  1. 1. Department of Respiratory, Qilu Hospital of Shandong University, Jinan 250012, China;
    2. Department of Laboratory Diagnosis, General Hospital of Jinan Military Command, Jinan 250031, China
  • Received:2009-11-25 Online:2010-03-16 Published:2010-03-16

摘要:

目的    探讨在亚抑菌浓度喹诺酮类药物多代培养后,肺炎支原体(MP)标准株FH对喹诺酮类药物敏感性的变化及其机制。方法    将标准株FH在含有亚抑菌浓度环丙沙星、左氧氟沙星和加替沙星的液体培养基中传代培养后,检测其对3种药物的MIC值。提取标准株及诱导耐药株的DNA,PCR扩增喹诺酮耐药决定区的gyrA、gyrB、parC和parE基因。测序分析耐药株的基因突变情况。结果    经亚抑菌浓度喹诺酮类药物多代培养诱导后,FH出现对诱导药物的耐药及交叉耐药。6株药物诱导耐药株,其中在左氧氟沙星诱导的耐药株gyrA基因编码的95位蛋氨酸转变为异亮氨酸,parC基因编码的87位天门冬氨酸转变为酪氨酸。在加替沙星诱导的耐药株中gyrB基因编码的464位精氨酸转变为赖氨酸。parE基因未检出错义突变。结论    亚抑菌浓度喹诺酮类药物可诱导肺炎支原体出现耐药及交叉耐药。其产生可能与喹诺酮耐药决定区的基因突变有关。

关键词: 肺炎,支原体;喹诺酮类;抗药性,微生物;点突变

Abstract:

Objective    To investigate the effect of the subinhibitory concentration of quinolones on resistance to quinolones in Mycoplasma pneumoniae (MP) and its mechanisms. Methods    To induce resistance to quinolones, the reference strain FH was cultured for several passages with three different quinolones at sub-inhibitory concentrations. DNA was extracted from the FH strain and in vitro drug-induced quinolone-resistant strains. The quinolone resistancedetermining regions(QRDR) of gyrA, gyrB, parC and parE in each strain were amplified with the corresponding primers by PCR and then sequenced. Results    The  FH  strain exhibited resistance or crossresistance to the three quinolones after  induction. In 6 drug-induced quinolone-resistant strains,the strains induced by levofloxacin had a substitute of Met95→Ile in the gyrA gene and a substitute of Asp87→Tyr in the parC gene; and the strains induced by Gatifloxacin had a substitute of Arg→Lys in the gyrB gene. No mis-sense mutation was detected in the parC gene. Conclusion    Longterm use of quinolones at sub-inhibitory concentration can contribute to resistance and cross-resistance of MP. The mutation of QRDR is closely associated with  quinolone-resistance.

Key words: Pneumonia, mycoplasma; Quinolones; Drug resistance, microbial; Point mutation

中图分类号: 

  • R375+.2
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