Molecular basis of clarithromycin-resistance in Mycobacterium avium intracellulare complex
Molecular basis of clarithromycin-resistance in Mycobacterium avium intracellulare complex
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DOI：
10.1054/tuld.1999.0227
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发表时间：
2000-01-01
期刊：
影响因子：
--
通讯作者：
Kashiwabara, Y
中科院分区：
文献类型：
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作者：
Jamal, MA;Maeda, S;Kashiwabara, Y
在体外构建的突变株和具有克拉霉素耐药性的禽分枝杆菌和胞内分枝杆菌临床分离株中，测定了23S rRNA基因V区和II区的核苷酸序列。所有实验室制备的突变株都对克拉霉素表现出高水平的抗药性(>；150mug ml(-1))，并在V区2058位(与大肠杆菌碱基同源)发生突变。在临床分离株中，敏感株在V区无突变，而耐药株在2058或2059处发生突变。6株耐药水平较低的菌株在V区无突变，所有受试菌株均无II区突变。这些结果表明，大多数耐药性来自23S rRNA基因V区的突变，但在分枝杆菌中也存在其他未知的机制。(C)2000 HarCourt出版有限公司。
Nucleotide sequences of domain V and domain II regions of the 23S rRNA gene were determined in both in vitro-made mutants and clinical isolates of Mycobacterium avium and M. intracellulare conferring clarithromycin-resistance. All laboratory-made mutants showed high level resistance to clarithromycin (>150 mug ml(-1)) and mutation at position 2058 (cognate with Escherichia coli base) in domain V region. In the clinical isolates, while the susceptible ones had no mutation in domain V, the resistant strains showed mutation at 2058 or 2059. Six isolates with low level of resistance exhibited no mutation in domain V. AII strains tested had no mutation in domain II region. These results suggested that most of the resistance arose from the mutation in domain V of the 23S rRNA gene, but other unknown mechanisms evidently exist in mycobacteria. (C) 2000 Harcourt Publishers Ltd.