ArticleAntimicrobial agents and chemotherapy2011
Molecular investigation of resistance to the antituberculous drug ethionamide in multidrug-resistant clinical isolates of Mycobacterium tuberculosis.
Article in Antimicrobial agents and chemotherapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Xpert MTB/XDR for detection of pulmonary tuberculosis and resistance to isoniazid, fluoroquinolones, ethionamide, and amikacin.The Cochrane database of systematic reviews · 2022Pooled it
- Key Proteins and Enzymatic Mechanisms Underlying Drug Resistance in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 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
- Trends in Antituberculosis Drug Resistance and Associated Factors: A 31-Year Observational Study at a Tertiary Hospital in Barcelona.Antibiotics (Basel, Switzerland) · 2025Article
- Xpert MTB/XDR Assay for Detection of Resistance to Isoniazid, Fluoroquinolone, Aminoglycoside, and Ethionamide Among Patients with Pulmonary Tuberculosis in Bangladesh.Infectious diseases and therapy · 2025Article
- Effects of mutations in multiple Ethionamide-resistance-associated genes amongFrontiers in cellular and infection microbiology · 2025Article
- How do Mutations of Mycobacterium Genes Cause Drug Resistance in Tuberculosis?Current pharmaceutical biotechnology · 2024Review
- Drug-resistant Mycobacterium tuberculosis among Nepalese patients at a tuberculosis referral center.PloS one · 2024Article
- Clustering minimal inhibitory concentration data through Bayesian mixture models: An application to detectStatistical methods in medical research · 2023Article
- A pro-oxidant property of vitamin C to overcome the burden of latentFrontiers in cellular and infection microbiology · 2023Review
- Genetic Characterization Conferred Co-Resistance to Isoniazid and Ethionamide inInfection and drug resistance · 2023Article
- Tools to Alleviate the Drug Resistance inMolecules (Basel, Switzerland) · 2022Review
- How a PCR Sequencing Strategy Can Bring New Data to Improve the Diagnosis of Ethionamide Resistance.Microorganisms · 2022Article
- Significance of the coexistence of non-codon 315 katG, inhA, and oxyR-ahpC intergenic gene mutations among isoniazid-resistant and multidrug-resistant isolates of Mycobacterium tuberculosis: a report of novel mutations.Pathogens and global health · 2022Article
- MDR Tuberculosis Treatment.Medicina (Kaunas, Lithuania) · 2022Review
- Molecular Determinants of Ethionamide Resistance in Clinical Isolates ofAntibiotics (Basel, Switzerland) · 2022Article
- Heterologous Expression ofAntimicrobial agents and chemotherapy · 2021Article
- Genome analyses of 174 strains ofMicrobial genomics · 2021Article
- Structure-based drug design, synthesis and screening of MmaA1 inhibitors as novel anti-TB agents.Molecular diversity · 2021Article
- Application of Computational Methods in Understanding Mutations inFrontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ethionamide (ETH) needs to be activated by the mono-oxygenase EthA, which is regulated by EthR, in order to be active against Mycobacterium tuberculosis. The activated drug targets the enzyme InhA, which is involved in cell wall biosynthesis. Resistance to ETH has been reported to result from various mechanisms, including mutations altering EthA/EthR, InhA and its promoter, the NADH dehydrogenase encoded by ndh, and the MshA enzyme, involved in mycothiol biosynthesis. We searched for such mutations in 87 clinical isolates: 47 ETH-resistant (ETH(r)) isolates, 24 ETH-susceptible (ETH(s)) isolates, and 16 isolates susceptible to ETH but displaying an intermediate proportion of resistant cells (ETH(Sip); defined as ≥1% but <10% resistant cells). In 81% (38/47) of the ETH(r) isolates, we found mutations in ethA, ethR, or inhA or its promoter, which mostly corresponded to new alterations in ethA and ethR. The 9 ETH(r) isolates without a mutation in these three genes (9/47, 19%) had no mutation in ndh, and a single isolate had a mutation in mshA. Of the 16 ETH(Sip) isolates, 7 had a mutation in ethA, 8 had no detectable mutation, and 1 had a mutation in mshA. Finally, of the 24 ETH(s) isolates, 23 had no mutation in the studied genes and 1 displayed a yet unknown mutation in the inhA promoter. Globally, the mechanism of resistance to ETH remained unknown for 19% of the ETH(r) isolates, highlighting the complexity of the mechanisms of ETH resistance in M. tuberculosis.
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