2019Mycobacterial DiseasesOpen access

Detection of Genetic mutations in inhA and katG for Isoniazid and its Association with Rifampicin Resistance in Tuberculosis Confirmed by Line Probe Assay-its Rationality or Isoniazid Prophylaxis Empirical or DST Guided

Prasanta Kumar Das, Somtirtha B Ganguly, Bodhisatya Mandal

Open full text 1 citations

Abstract

Out of 442 cases of rifampicin resistant MTB strains 410 cases showed Isoniazid resistance. Out of which exclusive involvement with inhA was seen in 32 cases. 19 cases showed involvement of both inhA as well as katG resistance 359 cases accounting to 87.5% showed exclusive involvement of katG thereby conferring high degree of resistance. The higher percentage of katG induced Isoniazid resistance among the Rifampicin resistant strains depicts the spread of higher degree of Isoniazid resistance. The question remains how effective would be the Isoniazid prophylaxis in pediatric age group in this scenario. The analysis has shown that only around 14.93% cases reflected exclusive mutations at around 15 and 16 regions of the inhA gene and MUT3 accounted to a percentage of 60.3% among the inhA dependant isoniazid resistance.

About this research paper

What this paper is about

Out of 442 cases of rifampicin resistant MTB strains 410 cases showed Isoniazid resistance. Out of which exclusive involvement with inhA was seen in 32 cases. 19 cases showed involvement of both inhA as well as katG resistance 359 cases accounting to 87.5% showed exclusive involvement of katG thereby conferring high degree of resistance. The higher percentage of katG induced Isoniazid resistance among the Rifampicin resistant strains depicts the spread of higher degree of Isoniazid resistance. The question remains how effective would be the Isoniazid prophylaxis in pediatric age group in this scenario. The analysis has shown that only around 14.93% cases reflected exclusive mutations at around 15 and 16 regions of the inhA gene and MUT3 accounted to a percentage of 60.3% among the inhA dependant isoniazid resistance.

Why it matters

OpenAlex reports 1 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

Out of 442 cases of rifampicin resistant MTB strains 410 cases showed Isoniazid resistance. Out of which exclusive involvement with inhA was seen in 32 cases. 19 cases showed involvement of both inhA as well as katG resistance 359 cases accounting to 87.5% showed exclusive involvement of katG thereby conferring high degree of resistance. The higher percentage of katG induced Isoniazid resistance among the Rifampicin resistant strains depicts the spread of higher degree of Isoniazid resistance. The question remains how effective would be the Isoniazid prophylaxis in pediatric age group in this scenario. The analysis has shown that only around 14.93% cases reflected exclusive mutations at around 15 and 16 regions of the inhA gene and MUT3 accounted to a percentage of 60.3% among the inhA dependant isoniazid resistance.

Key concepts: INHA, Isoniazid, Rifampicin, Mycobacterium tuberculosis, Tuberculosis, Medicine, Genetics, Biology

Related papers

Back to paper searchBrowse research topicsOriginal source
Detection of Genetic mutations in inhA and katG for Isoniazid and its Association with Rifampicin Resistance in Tuberculosis Confirmed by Line Probe Assay-its Rationality or Isoniazid Prophylaxis Empirical or DST Guided — Research Paper | ScholarLens