Annals of Tropical Medicine and Public Health
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Year : 2016  |  Volume : 9  |  Issue : 5  |  Page : 307-311

Frequency of mutations associated with isoniazid-resistant in clinical Mycobacterium tuberculosis strains by low-cost and density (LCD) DNA microarrays

1 Student Research Committee, Kermanshah University of Medical Sciences, Kermanshah, Iran
2 Department of Microbiology, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
3 Department of Microbiology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran

Correspondence Address:
Parviz Mohajeri
Department of Microbiology, Faculty of Medicine, Kermanshah University of Medical Sciences, Shirudi Shahid Boulevard, Daneshgah Street, Kermanshah
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1755-6783.190166

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Background: Isoniazid (INH) is one of the main line drugs used in the treatment of tuberculosis (TB) and the development of resistance against this compound can result in serious problems in the treatment procedures. Resistance to INH is associated with a variety of mutations. Objectives: The aim of the present study is to determine the frequency of major drug resistance mutations across katG and inhA loci of multidrug-resistant (MDR)-MTB isolates using a molecular test. Materials and Methods: 125 Mycobacterium Tuberculosis (MTB) clinical isolates were studied. The Centers for Disease Control and Prevention (CDC) standard conventional proportional method was implied to test drug susceptibility. DNA extraction, katG and InhA amplification, and microarray were performed. Results: From 125 MTB clinical isolates, 34 strains were INH-resistant and 91 strains were INH-sensitive. Of 34 INH-resistant strains, the mutation was identified in 32% KatG 315 (Ser→Thr), in 14% KatG315 (Ser→ Asn), in 52% InhA 15 (C→T), and in 2.9% InhA 17 (G→T). Conclusions: Rapid diagnosis of MDR-TB is essential for the prompt initiation of effective second-line therapy to improve the treatment outcome and limit transmission of this obstinate disease. A range of molecular methods that aid in rapid detection of mutations implicated in MDR-TB have been developed. The sensitivity of the methods is dependent, in principle, on the repertoire of mutations being detected, which is typically limited to mutations in the genes katG and the promoter region of inhA.

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