ArticleAntimicrobial agents and chemotherapy2015
Genotypic Analysis of Genes Associated with Independent Resistance and Cross-Resistance to Isoniazid and Ethionamide in Mycobacterium tuberculosis Clinical Isolates.
Article in Antimicrobial agents and chemotherapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Systematic Review of Mutations Associated with Isoniazid Resistance Points to Continuing Evolution and Subsequent Evasion of Molecular Detection, and Potential for Emergence of Multidrug Resistance in Clinical Strains of Mycobacterium tuberculosis.Antimicrobial agents and chemotherapy · 2021Pooled it
- Host oxidative stress primes mycobacteria for rapid antibiotic resistance evolution.Nature communications · 2026Article
- A Comprehensive Review of Genetic Mechanisms ofInfection and drug resistance · 2026Review
- Current drug susceptibility testing in the Löwenstein-Jensen medium leads to underestimating of prothionamide resistance in multi-drug resistant Mycobacterium tuberculosis.BMC microbiology · 2025Article
- Host oxidative stress primes mycobacteria for rapid antibiotic resistance evolution.Research square · 2025Article
- Genome-wide identification of AAAP gene family and expression analysis under abiotic stresses in Avena sativa.BMC genomics · 2025Article
- Effects of mutations in multiple Ethionamide-resistance-associated genes amongFrontiers in cellular and infection microbiology · 2025Article
- Perchlozone Resistance in Clinical Isolates ofAntibiotics (Basel, Switzerland) · 2023Article
- Genetic Characterization Conferred Co-Resistance to Isoniazid and Ethionamide inInfection and drug resistance · 2023Article
- Molecular analysis of thePeerJ · 2023Article
- How a PCR Sequencing Strategy Can Bring New Data to Improve the Diagnosis of Ethionamide Resistance.Microorganisms · 2022Article
- Detection and characterization of mutations in genes related to isoniazid resistance in Mycobacterium tuberculosis clinical isolates from Iran.Molecular biology reports · 2022Article
- Pre-Clinical Tools for Predicting Drug Efficacy in Treatment of Tuberculosis.Microorganisms · 2022Review
- Molecular Determinants of Ethionamide Resistance in Clinical Isolates ofAntibiotics (Basel, Switzerland) · 2022Article
- Article
- The Value of theInfection and drug resistance · 2021Article
- Adverse treatment outcomes in multidrug resistant tuberculosis go beyond the microbe-drug interaction: Results of a multiple correspondence analysis.Biomedica : revista del Instituto Nacional de Salud · 2020Article
- Genetic Variation Putatively Associated withAntibiotics (Basel, Switzerland) · 2020Article
- Genome-wide analysis of the TCP transcription factor genes in five legume genomes and their response to salt and drought stresses.Functional & integrative genomics · 2020Article
- Correlation between GenoType MTBDRTuberculosis and respiratory diseases · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ethionamide (ETH) is an antibiotic used for the treatment of multidrug-resistant (MDR) tuberculosis (TB) (MDR-TB), and its use may be limited with the emergence of resistance in the Mycobacterium tuberculosis population. ETH resistance in M. tuberculosis is phenomenon independent or cross related when accompanied with isoniazid (INH) resistance. In most cases, resistance to INH and ETH is explained by mutations in the inhA promoter and in the following genes: katG, ethA, ethR, mshA, ndh, and inhA. We sequenced the above genes in 64 M. tuberculosis isolates (n = 57 ETH-resistant MDR-TB isolates; n = 3 ETH-susceptible MDR-TB isolates; and n = 4 fully susceptible isolates). Each isolate was tested for susceptibility to first- and second-line drugs using the agar proportion method. Mutations were observed in ETH-resistant MDR-TB isolates at the following rates: 100% in katG, 72% in ethA, 45.6% in mshA, 8.7% in ndh, and 33.3% in inhA or its promoter. Of the three ETH-susceptible MDR-TB isolates, all showed mutations in katG; one had a mutation in ethA, and another, in mshA and inhA. Finally, of the four fully susceptible isolates, two showed no detectable mutation in the studied genes, and two had mutations in mshA gene unrelated to the resistance. Mutations not previously reported were found in the ethA, mshA, katG, and ndh genes. The concordance between the phenotypic susceptibility testing to INH and ETH and the sequencing was 1 and 0.45, respectively. Among isolates exhibiting INH resistance, the high frequency of independent resistance and cross-resistance with ETH in the M. tuberculosis isolates suggests the need to confirm the susceptibility to ETH before considering it in the treatment of patients with MDR-TB.
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