[1]王强,王跃,刘明方.红霉素体外诱导肺炎链球菌耐药的研究[J].陆军军医大学学报(原第三军医大学学报),2009,31(12):1185-1188.
 WANG Qiang,WANG Yue,LIU Ming-fang.Study on the Streptococcus pneumoniae resistance induced by erythromycin in vitro[J].J Amry Med Univ (J Third Mil Med Univ),2009,31(12):1185-1188.
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红霉素体外诱导肺炎链球菌耐药的研究(/HTML )
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陆军军医大学学报(原第三军医大学学报)[ISSN:1000-5404/CN:51-1095/R]

卷:
31卷
期数:
2009年第12期
页码:
1185-1188
栏目:
论著
出版日期:
2009-06-30

文章信息/Info

Title:
Study on the Streptococcus pneumoniae resistance induced by erythromycin in vitro
作者:
王强王跃刘明方
重庆医科大学:临床检验诊断学教育部重点实验室,基础医学院病原生物学教研室
Author(s):
WANG Qiang WANG Yue LIU Ming-fang
Key Laboratory of Clinical Laboratory Medicine of State Education Commission; Department of Pathogenic Biology, College of Basic Medical Sciences, Chongqing Medical  University, Chongqing 400016, China
关键词:
肺炎链球菌红霉素诱导变异
Keywords:
Streptococcus pneumoniae erythromycin induce mutation
分类号:
R378.12;R965;R978.15
文献标志码:
A
摘要:
目的   通过体外诱导获得肺炎链球菌(Streptococcus pneumoniaeS.pn)耐药菌株,对比分析S.pn诱导耐药前后红霉素结合域的变异。   方法   采用最低抑菌浓度(MIC)递增方法对S.pn标准菌株tigr4、tigr2临床分离敏感株进行红霉素体外诱导耐药,PCR与RT-PCR对诱导前后rplD、rplV基因以及23S rRNA扩增并测序,CPHmodels-2.0蛋白质空间构象预测系统对诱导前后rplD、rplV基因编码的核糖体蛋白L4和L22进行空间构象预测分析。   结果   诱导后tigr4 MIC由0.031 2 mg/L 增加到256 mg/L,而临床分离敏感株MIC均由0.031 2 mg/L 增加到32 mg/L。诱导前后测序结果对比显示标准菌株tigr4核糖体蛋白L4发生V32A变异,L22发生D35G变异,而临床分离敏感株核糖体蛋白L4发生Q67R、K68E变异。空间构象分析L22的D35G及L4的Q67R、K68E变异导致其相应的表面空间构象发生明显改变。   结论   S.pn可通过红霉素体外诱导而导致耐药,其耐药机制与红霉素结合域发生新的变异有关。
Abstract:
Objective   To establish erythromycin resistance models of Streptococcus pneumoniae for analysis of the mutations in the binding domain of erythromycin.     Methods   Streptococcus pneumonia tigr4 and two clinical sensitive isolates were induced with erythromycin by minimum inhibitory concentration (MIC) method for antimicrobial susceptibility, and then the rplD, rplV genes, and 23S rRNA in sensitive and resistant strains were amplified by PCR and RT-PCR for sequencing. CPHmodels-2.0 was used to predict the spatial structures of ribosomal protein L4 and L22 coded by rplD and rplV genes.     Results   MIC of Streptococcus pneumonia tigr4 increased from 0.0312 mg/L to 256mg/L while MICs of the two clinical isolates increased from 0.0312 mg/L to 32 mg/L.  Comparison of the pre- and post-induction results showed V32A mutation in ribosomal protein L4, D35G mutation in ribosomal protein L22, and 67QK68 to 67RE68 mutations in ribosomal protein L4. Changes in spatial structure was found in SiThe ribosomal protein L22 and ribosomal protein L4 due to D35G, Q67R, and K68E mutations respectively.     Conclusion   Streptococcus pneumonia can be induced to resistant to erythromycin in vitro. The mechanisms of resistance may be relate to the new mutations in the binding domain of erythromycin.

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更新日期/Last Update: 2009-05-31