伊朗伊斯法罕结核分枝杆菌临床分离株中rpsL和rrs基因的遗传模式

B. Salehi, S. Karimi
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引用次数: 1

摘要

耐药结核病被认为是一个普遍存在的主要问题。基于对结核分枝杆菌基因组中某些突变的了解,可以及时检测耐药性。这项研究的目的是确定伊朗伊斯法罕省结核分枝杆菌分离株中可能由链霉素耐药性引起的最常见突变的流行率,以及rpsL和rrs基因的遗传模式。临床标本来自伊斯法罕结核病中心的疑似结核病患者,其中205个分离株通过常规方法被诊断为结核分枝杆菌。用Lowenstein-Jensen培养基,用比例法测定了这些分离株中链霉素的最低抑制浓度。除了随机选择的5个链霉素敏感菌株外,还分析了所有链霉素抗性菌株中rpsL和530环rrs基因的核苷酸序列。6株(6/10,60%)链霉素抗性分离株的rpsL基因和/或rrs530环发生突变。四个(40%)分离株显示rpsL突变(密码子43和88),其中两个(20%)在rrs基因(A514C和C517T)中发生改变。然而,在链霉素易感分离株的两个基因中都没有发现突变。该研究可以成功地强调rpsL和rrs突变作为链霉素耐药性的分子标记在结核分枝杆菌菌株中的积极作用。突变的多样性和存在与否表明,各种菌株可能存在循环,以及其他机制在不同地区对链霉素耐药的作用。
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Genetic Patterns of rpsL and rrs Genes in Clinical Isolates of Mycobacteriumtuberculosis, Isfahanâ Iran
Drug-resistant tuberculosis is considered a major universal problem. Based on knowledge on certain mutations occurring in Mycobacterium tuberculosis genome, drug resistance could be detected timely. The goal of this study was to determine the prevalence of the most common mutations likely to result from resistance to streptomycin in M. tuberculosis isolates, as well as genetic patterns of rpsL and rrs genes, in the province of Isfahan, Iran. Clinical specimens were collected from individuals suspected of tuberculosis who referred to the Tuberculosis Center of Isfahan among whom 205 isolates were diagnosed with M. tuberculosis by conventional methods. The minimum inhibitory concentration of streptomycin in these isolates was determined with proportion method using Lowenstein- Jensen medium from which 10 isolates were recognized with streptomycin-resistant tuberculosis. The nucleotide sequence of rpsL and 530 loop of rrs genes were analyzed in all streptomycin-resistant isolates, in addition to five randomly selected streptomycin-susceptible isolates. Six (6/10, 60%) streptomycin-resistant isolates represented a mutation in either rpsL gene and/or rrs530 loop. Four (40%) isolates showed rpsL mutations (codons 43 and 88), and two (20%) of them alterations in rrs gene (A514C and C517T). However, no mutation was found in streptomycin-susceptible isolates in either of the genes. The study could successfully highlight the positive effects of rpsL and rrs mutations as molecular markers of streptomycin resistance in M. tuberculosis strains. Diversity and presence or absence of mutations suggested possible circulation of a variety of strains and the role of additional mechanisms contributing to strstreptomycin resistance in various regions.
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