Molecular Basis of Rifampin Resistance inStreptococcus pneumoniae
Molecular Basis of Rifampin Resistance inStreptococcus pneumoniae
复制标题
肺炎链球菌利福平耐药的分子基础
DOI：
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发表时间：
1999
影响因子：
4.9
通讯作者：
K. Klugman
中科院分区：
文献类型：
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作者：
Thanugarani Padayachee;K. Klugman
南非肺炎链球菌临床分离株的利福平耐药性是由于rpoB基因的错义突变引起的。对24株利福平耐药菌株的序列分析显示，在群I内存在突变，在一个指定为群III的肺炎球菌区域也存在新的突变。在表征的24个分离株中，仅1个耐药分离株在测序区域中不含任何突变。簇I或簇III突变分别赋予32至128 μg/ml的MIC。临床分离株55（MIC为256 μg/ml）发现含有10个已鉴定突变中的9个，包括簇I和簇III突变。如在大肠杆菌中，可能S. pneumoniae相互作用形成抗生素结合位点的一部分，因此解释了分离株55观察到的非常高的MIC。含有簇I或簇III突变的PCR产物能够转化利福平敏感的S。pneumoniae耐药虽然许多研究的分离株显示相同的序列，脉冲场凝胶电泳分析显示，分离株不是克隆起源。
ABSTRACT Rifampin resistance among South African clinical isolates ofStreptococcus pneumoniae was shown to be due to missense mutations within the rpoB gene. Sequence analysis of 24 rifampin-resistant isolates revealed the presence of mutations within cluster I as well as novel mutations in an area designated pneumococcus cluster III. Of the 24 isolates characterized, only 1 resistant isolate did not contain any mutations in the regions sequenced. Either the cluster I or the cluster III mutations separately conferred MICs of 32 to 128 μg/ml. Clinical isolate 55, for which the MIC was 256 μg/ml, was noted to contain 9 of the 10 mutations identified, which included the cluster I and cluster III mutations. As in Escherichia coli, it is possible that cluster I (amino acids 406 to 434) and cluster III (amino acids 523 to 600) of S. pneumoniaeinteract to form part of the antibiotic binding site, thus accounting for the very high MIC observed for isolate 55. PCR products containing cluster I or cluster III mutations were able to transform rifampin-susceptible S. pneumoniae to resistance. Although many of the isolates studied displayed identical sequences, pulsed-field gel electrophoresis analysis revealed that the isolates were not of clonal origin.