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

Subjects: Medicine, Pharmacy >> Preclinical Medicine submitted time 2018-06-14 Cooperative journals: 《协和医学杂志》

刘亚丽 张文娟 王洁 叶莎 4 赵颖 王贺 窦红涛 郭莉娜 王瑶 孙宏莉 刘文静 张小江 谢秀丽 原英 杨启文 徐英春

Abstract： 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.

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