What question did this study set out to answer?

To identify mutations in the ethA, inhA, and katG genes and correlate them with phenotypic resistance levels to ethionamide and isoniazid in clinical Mycobacterium tuberculosis isolates.

November 24, 2003Antimicrobial Agents and ChemotherapyOpen Access

ethA , inhA , and katG Loci of Ethionamide-Resistant Clinical Mycobacterium tuberculosis Isolates

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Authors

GMGlenn P. MorlockCenters for Disease Control and Prevention BMBeverly MetchockCenters for Disease Control and Prevention DSDavid SikesCenters for Disease Control and Prevention

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Implication

Genomic analysis uncovers distinct ethA and inhA structural mutations conferring high-level ethionamide resistance in Mycobacterium tuberculosis isolates, highlighting diverse resistance pathways.

Key Points

To identify mutations in the ethA, inhA, and katG genes and correlate them with phenotypic resistance levels to ethionamide and isoniazid in clinical Mycobacterium tuberculosis isolates.
Sequenced the complete ethA structural gene, two regions of inhA, and all or part of katG in 41 ethionamide-resistant M. tuberculosis isolates.
Measured minimum inhibitory concentrations (MICs) for ethionamide (ETH) and isoniazid (INH) to link specific genetic variations to resistance phenotypes.
Fifteen isolates harbored unique, previously unreported mutations distributed across the ethA gene, all displaying ETH MICs ≥50 µg/ml.
Structural inhA missense mutations occurred in 8 isolates (7 with ETH MICs ≥100 µg/ml and INH MICs ≥8 µg/ml), while an inhA promoter mutation was detected in 14 isolates.
Mutations in katG occurred in 15 isolates (14 with INH MICs ≥32 µg/ml) without association to ETH resistance, whereas ethA or inhA structural mutations accounted for ~76% of isolates with ETH MICs ≥50 µg/ml.

Cite This Study

Morlock et al. (2003) studied this question.

synapsesocial.com/papers/6a8c120ac716e89f35df0ebb https://doi.org/10.1128/aac.47.12.3799-3805.2003

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Implication

Genomic analysis uncovers distinct ethA and inhA structural mutations conferring high-level ethionamide resistance in Mycobacterium tuberculosis isolates, highlighting diverse resistance pathways.

ethA , inhA , and katG Loci of Ethionamide-Resistant Clinical Mycobacterium tuberculosis Isolates

Discussion

Member takes

Implication

Key Points

Cite This Study

ethA , inhA , and katG Loci of Ethionamide-Resistant Clinical Mycobacterium tuberculosis Isolates

Discussion

Member takes

Implication

Key Points

Cite This Study

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