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旷凌寒, 母丽媛, 苏敏等. 孕晚期妇女产道定植性B群链球菌的耐药性及耐药机制研究[J]. 四川大学学报(医学版), 2015, 46(5): 692-696.
引用本文: 旷凌寒, 母丽媛, 苏敏等. 孕晚期妇女产道定植性B群链球菌的耐药性及耐药机制研究[J]. 四川大学学报(医学版), 2015, 46(5): 692-696.
KUANG Ling-han, MU Li-yuan, SU Min. et al. Epidemiology and Resistance Mechanisms of Group B Streptococci in Late-pregnant Maternal Birth Canal[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(5): 692-696.
Citation: KUANG Ling-han, MU Li-yuan, SU Min. et al. Epidemiology and Resistance Mechanisms of Group B Streptococci in Late-pregnant Maternal Birth Canal[J]. Journal of Sichuan University (Medical Sciences), 2015, 46(5): 692-696.

孕晚期妇女产道定植性B群链球菌的耐药性及耐药机制研究

Epidemiology and Resistance Mechanisms of Group B Streptococci in Late-pregnant Maternal Birth Canal

  • 摘要: 目的 了解孕晚期妇女产道内B群链球菌(group B Streptococci,GBS)的耐药现状和相关耐药机制,为国内孕妇产道GBS预防治疗及抗生素的合理应用提供理论及数据支持。方法 纳入31例产道有GBS定植的孕晚期妇女,对分离出的GBS菌株进行药物敏感实验,对红霉素和克林霉素耐药的菌株进行耐药表型分析和耐药基因检测。结果 21株(67.7%)对红霉素耐药,12株(38.7%)对克林霉素耐药,其中有12株为固有型耐药表型(cMLS型),9株为主动外排型耐药表型(MS型)。在红霉素耐药菌株中有11株检测到mef(A)基因,12株检测到erm(B)基因,其中有3株同时检测到erm(C)基因。结论 孕晚期妇女产道内分离出的GBS菌株对大环内酯类抗生素耐药率较高,对红霉素耐药的GBS菌株的耐药机制以erm(B)基因介导的核糖体靶位改变和mef(A)基因介导的特异大环内酯类外排机制增强为主。

     

    Abstract: Objective To study the antibiotic-resistant rate of group B Streptococci (GBS) in obstetric canal of late-pregnant women, evaluate the antibiotic-resistant status and finally to support the GBS prevention and curing by proper antibiotics. Methods 31 pregnant women between 35 to 37 gestational weeks were included, for whom the antibiotic sensitivity as well as the drug (erythromycin and clindamycin) resistance genes of GBS in obstetric canal was analyzed. Results 12 (38.7%) strains of GBS were resistant to clindamycin, while 21 (67.7%) to erythromycin, within which 12 strains were intrinsic phenotype ——cMLS type-clindamycin resistance, other 9 were active efflux phenotype ——MS type-clindamycin sensitive and all of which were confirmed by Double disk diffusion method. Eleven strains were mef (A) positive, and 12 strains were erm (B) positive, in which 3 with erm (C). Conclusions In our research the GBS strains show a high erythromycin and clindamycin resistance rate. The resistance of our GBS strains are mainly caused by the ribosomal target changes induced by erm (B) and the increased efflux of clindamycin induced by mef (A).

     

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