Piatek A S, Telenti A, Murray M R, El-Hajj H, Jacobs W R, Kramer F R, Alland D
Division of Infectious Diseases, Department of Medicine, Montefiore Medical Center, Bronx, New York 10467, USA.
Antimicrob Agents Chemother. 2000 Jan;44(1):103-10. doi: 10.1128/AAC.44.1.103-110.2000.
Past genotypic studies of Mycobacterium tuberculosis may have incorrectly estimated the importance of specific drug resistance mutations due to a number of sampling biases including an overrepresentation of multidrug-resistant (MDR) isolates. An accurate assessment of resistance mutations is crucial for understanding basic resistance mechanisms and designing genotypic drug resistance assays. We developed a rapid closed-tube PCR assay using fluorogenic reporter molecules called molecular beacons to detect reportedly common M. tuberculosis mutations associated with resistance to isoniazid and rifampin. The assay was used in a comparative genotypic investigation of two different study populations to determine whether these known mutations account for most cases of clinical drug resistance. We analyzed samples from a reference laboratory in Madrid, Spain, which receives an overrepresentation of MDR isolates similar to prior studies and from a community medical center in New York where almost all of the resistant isolates and an equal number of susceptible controls were available. The ability of the molecular beacon assay to predict resistance to isoniazid and rifampin was also assessed. The overall sensitivity and specificity of the assay for isoniazid resistance were 85 and 100%, respectively, and those for rifampin resistance were 98 and 100%, respectively. Rifampin resistance mutations were detected equally well in isolates from both study populations; however, isoniazid resistance mutations were detected in 94% of the isolates from Madrid but in only 76% of the isolates from New York (P = 0.02). In New York, isoniazid resistance mutations were significantly more common in the MDR isolates (94%) than in single-drug-resistant isolates (44%; P < 0.001). No association between previously described mutations in the kasA gene and isoniazid resistance was found. The first mutations that cause isoniazid resistance may often occur in sequences that have not been commonly associated with isoniazid resistance, possibly in other as yet uncharacterized genes. The molecular beacon assay was simple, rapid, and highly sensitive for the detection of rifampin-resistant M. tuberculosis isolates and for the detection of isoniazid resistance in MDR isolates.
以往对结核分枝杆菌的基因分型研究可能因多种抽样偏差而错误地估计了特定耐药突变的重要性,这些偏差包括多重耐药(MDR)菌株的过度代表性。准确评估耐药突变对于理解基本耐药机制和设计基因分型耐药检测方法至关重要。我们开发了一种快速闭管PCR检测方法,使用称为分子信标的荧光报告分子来检测据报道与对异烟肼和利福平耐药相关的常见结核分枝杆菌突变。该检测方法用于对两个不同研究人群的比较基因分型调查,以确定这些已知突变是否占临床耐药的大多数病例。我们分析了来自西班牙马德里一家参考实验室的样本,该实验室接收的MDR菌株比例过高,类似于先前的研究,还分析了来自纽约一家社区医疗中心的样本,那里几乎所有耐药菌株和相同数量的敏感对照都可用。还评估了分子信标检测方法预测对异烟肼和利福平耐药的能力。该检测方法对异烟肼耐药的总体敏感性和特异性分别为85%和100%,对利福平耐药的总体敏感性和特异性分别为98%和100%。在两个研究人群的分离株中,利福平耐药突变的检测效果相同;然而,在马德里的分离株中,94%检测到异烟肼耐药突变,而在纽约的分离株中,仅76%检测到异烟肼耐药突变(P = 0.02)。在纽约,异烟肼耐药突变在MDR分离株中(94%)比在单药耐药分离株中(44%)明显更常见(P < 0.001)。未发现kasA基因中先前描述的突变与异烟肼耐药之间存在关联。导致异烟肼耐药的首批突变可能经常发生在与异烟肼耐药通常无关的序列中,可能在其他尚未表征的基因中。分子信标检测方法对于检测耐利福平的结核分枝杆菌分离株以及检测MDR分离株中的异烟肼耐药简单、快速且高度敏感。