中华皮肤科杂志 ›› 2007, Vol. 40 ›› Issue (2): 71-73.

• 论著 • 上一篇    下一篇

体外诱导解脲脲原体对喹诺酮类药物交叉耐药的研究

许阳1, 骆丹1, 朱正华1, 孙蔚斌2   

  1. 1. 南京医科大学第一附属医院皮肤科 南京 210029;
    2. 扬中市人民医院皮肤科
  • 收稿日期:2006-02-21 发布日期:2007-02-15
  • 通讯作者: 骆丹,email:dannilu02005@yah00．com．cn E-mail:dannilu02005@yah00．com．cn
  • 基金资助:
    江苏省自然科学基金资助项目(BK2003110)

Induction and mechanisms of cross-resistance to quinolones in Ureaplasma urealyticum

X? Yang1, LUO Dan1, ZHU Zheng-hua1, SUN Wei-bin2   

  1. Department of Dermatology, First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
  • Received:2006-02-21 Published:2007-02-15

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摘要： 目的 探讨经次抑菌浓度喹诺酮类药物多代培养后,解脲脲原体(Uu)敏感株对喹诺酮类药物敏感性的变化及其机制.方法 将3株Uu临床分离株及标准株Uu3在含有次抑菌浓度诺氟沙星、氟罗沙星、环丙沙星或左氧氟沙星的液体培养基中传代培养10-12代后,检测其对4种药物的MIC值.提取标准株及耐药株的DNA,PCR扩增喹诺酮耐药决定区的gyrA和parC基因,测序分析耐药株的基因突变情况.结果 经次抑菌浓度喹诺酮类药物多代培养诱导后,3株临床分离敏感株与Uu3均出现对诱导药物的耐药及交叉耐药,共诱导出16株药物诱导耐药株.在它们及9株临床分离耐药株中,parC基因未检出错义突变,但gyrA基因检出2种错义突变,即:v175A(n=8)和N165D(n=1).结论 次抑菌浓度喹诺酮类药物可诱导解脲脲原体出现交叉耐药,其产生可能与gyrA基因突变有关.

关键词: 解脲支原体, 喹诺酮类, 抗药性, 微生物, 点突变

Abstract: Objective To investigate the effects and mechanisms of the subinhibitory concentration of quinolones on cross-resistance to quinolones in Ureaplasma urealyticum (Uu).Methods To induce resistance to quinolones,three quinolone-sensitive clinical isolates of Uu and the reference strain Uu3 were cultured for 10 to 12 passages with four different quinolones at subinhibitory concentrations (1/2 MIC).DNA was extracted from the strain Uu3,quinolone-resistant clinical isolates,and the in vitro drug-induced quinolone-resistant strains.The quinolone resistance-determining regions (QRDR) of gyrA and parC of each strain were amplified with the corresponding primers by PCR and then sequenced.Results All the quinolone-sensitive clinical isolates and the strain Uu3 exhibited resistance or cross-resistance to the four quinolones after the induction.In 9 quinolone-resistant clinical isolates of Uu and 16 drug-induced quinolone-resistant strains,no missense mutation was detected in the parC gene,whereas 2 missense mutations were detected in the gyrA gene,i.e.V175A (n=8) and N165D (n=1).Conclusion The results suggest that mutations of the gyrA gene may account for the induction of cross-resistance to quinolones in some Uu strains.

Key words: Ureaplasma urealyticum, Quinolones, Drug resistance, microbial, Point mutation