Pulmonary medicine · 2026
Rapid Detection of Resistance Mutations in Multidrug-Resistant Tuberculosis With GenoType MTBDRsl Assay.
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Gaikwad Shaina, Tiwari Antisha, Singh Jitendra, Khurana Alkesh Kumar, Khadanga Sagar, Purwar Shashank, Biswas Debasis, Maurya Anand Kumar
Аннотация
BACKGROUND: Multidrug-resistant tuberculosis (MDR-TB) is becoming a major threat to the global control of tuberculosis (TB). The situation worsens when fluoroquinolone (FQ) and second-line injectable (SLID) resistant strains are involved. This study assesses the utility of MTBDRsl V2.0 line probe assay (LPA) in identifying resistance patterns to FQ and SLID in MDR-TB isolates.
METHODS: A total of 74 MDR-TB isolates were tested for genetic mutations that confer resistance to FQs and against SLIDs by applying the GenoType MTBDRsl V2.0 LPA. This assay targets resistance-associated mutations in the gyrA and gyrB genes for FQ resistance, and in the rrs and eis genes for resistance to aminoglycosides and capreomycin.
RESULTS: Of the 74 isolates examined, 14 (18.9%) had FQ resistance. Most of these isolates had mutations in the gyrA gene, most commonly at codon A90V (6.7%), followed by D94G (5.4%), and various D94 variations. No mutations were found in the rrs, gyrB, or eis genes, and no resistance to SLIDs was found. With no discernible contribution from rrs, gyrB, or eis genes, our results emphasize gyrA mutations, particularly A90V and D94G, as important molecular markers of FQ resistance.
CONCLUSION: The MTBDRsl V2.0 assay demonstrated operational utility for rapid detection of resistance-associated mutations related to FQs and SLID drugs in MDR-TB isolates. Its rapid turnaround time expanded mutation coverage, and applicability in routine diagnostic settings make it a useful tool for molecular resistance profiling in high TB-burden settings.
METHODS: A total of 74 MDR-TB isolates were tested for genetic mutations that confer resistance to FQs and against SLIDs by applying the GenoType MTBDRsl V2.0 LPA. This assay targets resistance-associated mutations in the gyrA and gyrB genes for FQ resistance, and in the rrs and eis genes for resistance to aminoglycosides and capreomycin.
RESULTS: Of the 74 isolates examined, 14 (18.9%) had FQ resistance. Most of these isolates had mutations in the gyrA gene, most commonly at codon A90V (6.7%), followed by D94G (5.4%), and various D94 variations. No mutations were found in the rrs, gyrB, or eis genes, and no resistance to SLIDs was found. With no discernible contribution from rrs, gyrB, or eis genes, our results emphasize gyrA mutations, particularly A90V and D94G, as important molecular markers of FQ resistance.
CONCLUSION: The MTBDRsl V2.0 assay demonstrated operational utility for rapid detection of resistance-associated mutations related to FQs and SLID drugs in MDR-TB isolates. Its rapid turnaround time expanded mutation coverage, and applicability in routine diagnostic settings make it a useful tool for molecular resistance profiling in high TB-burden settings.