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。
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 l0 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. VI75A （ 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.
出处
《中华皮肤科杂志》
CAS
CSCD
北大核心
2007年第2期71-73,共3页
Chinese Journal of Dermatology
基金
江苏省自然科学基金资助项目(BK2003110)
关键词
解脲支原体
喹诺酮类
抗药性
微生物
点突变
Ureaplasma urealyticum
Quinolones
Drug resistance, microbial
Point mutation
