连续 5 年脲原体属和人型支原体体外药物敏感性回顾性分析及喹诺酮类耐药机制研究
目的 分析北京协和医院连续5年脲原体属和人型支原体培养及体外药物敏感性特点,并分析喹诺酮类耐药的相关机制。方法 该研究针对北京协和医院连续5年通过体外培养方法检测出的脲原体属和人型支原体,结合患者和菌种信息,分析其体外药物敏感性的特 点。同时,针对喹诺酮类药物的耐药特点,检测DNA促旋酶(GyrA/GyrB)和拓扑异构酶Ⅳ (ParC/ParE)序列的突变情况。结果 整体上脲原体属混合人型支原体的敏感性明显低于脲原体属或人型支原体单独的体外敏感性;除大环内酯类外,脲原体属对喹诺酮类、四环素类、交沙霉素、原始霉素、强力霉素的敏感性低于人型支原体。此外,女性患者体内分离的脲原体属对阿奇霉素、红霉素、克拉霉素、氧氟沙星的体外敏感性较男性患者低。微小脲原体对大部分抗菌药物的敏感率高于解脲脲原体的敏感率,尤其是微小脲原体对四环素的敏感率明 显高于解脲脲原体(差值25.8%),且差异有统计学意义(p<0.05)。此外,该研究从GyrA、 GyrB、ParC和ParE的序列中共发现了 21个突变位点。其中,ParC的 S83L突变占96.22%, 为最主要的突变位点;同时,也分别检测到了ParC的A136T和ParE的R448K突变,以及一例 GyrA L176F和ParC S83L的联合突变。此外,该研究还发现了6个新的突变位点(ParC的 L540F、R718W、Q767E、S789N、M828I和I831T)。结论 体外药物敏感性与感染种属、 菌种、患者性别有关。耐药机制的研究结果表明,单独ParC氨基酸序列的改变为该研究的主 要耐药机制,而新发现突变位点,其是否与喹诺酮类耐药相关还需要后续更深入的研究。
Objective To analyze the culture and in vitro antimicrobial susceptibility of Ureaplasma and Mycoplasma hominis in Peking Union Medical College Hospital for 5 consecutive years and mechanisms responsible for fluoroquinolone resistance.Method The study reviewed all of the Ureaplasma and Mycoplasma hominis cases detected by in vitro culture from September 2012 to April 2017 in Peking Union Medical College Hospital, with the information of patients and species, its charactoristics of antimicrobial susceptibility testing were also analyzed. Meanwhile, mutations in DNA gyrase (GyrA/GyrB) and topoisomerase IV (ParC/ParE) which were related to fluoroquinolone resistance were detected in this study.Results The in vitro sensitivity of Ureaplasma mixed with Mycoplasma hominis was significantly lower than that of Ureaplasma or Mycoplasma hominis alone. Except for macrolides, Ureaplasma was less susceptible to quinolones, tetracycline, josamycin, and primycin than that of Mycoplasma hominis. In addition, the susceptibility of Ureaplasma to azithromycin, erythromycin, clarithromycin, ofloxacin in female patients was lower than that in male patients. Ureaplasma parvum were more susceptible than Ureaplasma urealyticum to most antibiotics, especially for tetracycline (25.8% discrepancy), p<0.05. Moreover, twenty-one mutations from sequences of GyrA, GyrB, ParC and ParE were determined. Mutation in ParC, with a S83L substitution being most frequent, 96.22%; A136T substitution in ParC, R448K substitution in ParE, and L176Fof GyrA combined with S83L in ParC was also detected. This study also found Six novel mutations, L540F, R718W, Q767E, S789N, M828I and I831T amino acid substitutions in ParC protein.
王瑶、原英、窦红涛、王洁、王贺、张小江、谢秀丽、赵颖、杨启文、刘亚丽、张文娟、郭莉娜、孙宏莉、刘文静、徐英春、叶莎 4
医学研究方法微生物学药学
脲原体属人型支原体体外药物敏感性耐药机制
王瑶,原英,窦红涛,王洁,王贺,张小江,谢秀丽,赵颖,杨启文,刘亚丽,张文娟,郭莉娜,孙宏莉,刘文静,徐英春,叶莎 4.连续 5 年脲原体属和人型支原体体外药物敏感性回顾性分析及喹诺酮类耐药机制研究[EB/OL].(2018-06-14)[2025-08-18].https://chinaxiv.org/abs/201806.00223.点此复制
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