<abstract xmlns="http://www.w3.org/1999/xhtml">

<p>The emergence of M. tuberculosis strains resistant to Isoniazid (INH) and Rifampicin (RIF), the two most potent drugs of first-line anti-TB treatment is termed multidrug drug-resistant TB (MDR-TB). Multidrug-resistant tuberculosis has been a severe medical and epidemic problem worldwide.</p>
<p>We present a series of clinical cases consisting of two patients diagnosed with isoniazid-resistant tuberculosis. Histopathological examination supports the diagnosis of tuberculous granulomas. The pathology molecular examination revealed the presence of Isoniazid-resistant Mycobacterium tuberculosis 1, 2 via the following mutation c.947G>A; p. Gly316Asp. Isoniazid-resistance is associated with mutations in the furA-katG and fabG1-inhA operons and in the ahpC gene. 64% of the isoniazid-resistance phenotypes were associated with the kat G 315 mutation worldwide. The second most common mutation is inhA-15, reported in 19% of the Isoniazid-resistant isolates. The significant association between the two mutations, inhA c-15 and kat G 315 respectively, and the high-level resistance is of interest in the interpretation of current and future molecular diagnostic testing, as an early prediction of the level of Isoniazid-resistance is essential to decide the benefit of high-dose Isoniazid use.</p>
</abstract>

The emergence of M. tuberculosis strains resistant to Isoniazid (INH) and Rifampicin (RIF), the two most potent drugs of first-line anti-TB treatment is termed multidrug drug-resistant TB (MDR-TB). Multidrug-resistant tuberculosis has been a severe medical and epidemic problem worldwide.
We present a series of clinical cases consisting of two patients diagnosed with isoniazid-resistant tuberculosis. Histopathological examination supports the diagnosis of tuberculous granulomas. The pathology molecular examination revealed the presence of Isoniazid-resistant Mycobacterium tuberculosis 1, 2 via the following mutation c.947G>A; p. Gly316Asp. Isoniazid-resistance is associated with mutations in the furA-katG and fabG1-inhA operons and in the ahpC gene. 64% of the isoniazid-resistance phenotypes were associated with the kat G 315 mutation worldwide. The second most common mutation is inhA-15, reported in 19% of the Isoniazid-resistant isolates. The significant association between the two mutations, inhA c-15 and kat G 315 respectively, and the high-level resistance is of interest in the interpretation of current and future molecular diagnostic testing, as an early prediction of the level of Isoniazid-resistance is essential to decide the benefit of high-dose Isoniazid use.

Isoniazid-Resistant Tuberculosis - A Series of Clinical Cases

University of Medicine and Pharmacy “Carol Davila”

Department of Pneumology II, Division of Cardiothoracic Pathology IV

University of Medicine and Pharmacy “Dunărea de Jos”

Internal Medicine

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

{"article-title":"Isoniazid-Resistant Tuberculosis - A Series of Clinical Cases"}

The emergence of M. tuberculosis strains resistant to Isoniazid (INH) and Rifampicin (RIF), the two most potent drugs of first-line anti-TB treatment is termed...

Isoniazid-Resistant Tuberculosis - A Series of Clinical Cases

Data publikacji: 06 sty 2024

Zakres stron: 85 - 96

DOI: https://doi.org/10.2478/inmed-2023-0271

Słowa kluczowe
multidrug-resistant tuberculosis, genetic mutations, clinical cases

© 2023 Teodora Butnaru et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Isoniazid-Resistant Tuberculosis - A Series of Clinical Cases

Data publikacji: 06 sty 2024

Zakres stron: 85 - 96

DOI: https://doi.org/10.2478/inmed-2023-0271

Słowa kluczowemultidrug-resistant tuberculosis, genetic mutations, clinical cases

© 2023 Teodora Butnaru et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Słowa kluczowe
multidrug-resistant tuberculosis, genetic mutations, clinical cases