ABSTRACT

One major barrier to efficient treatment and disease control is multi-drug resistance (MDR) in Mycobacterium leprae (ML) and Mycobacterium tuberculosis (MTB). An overview of the MDR mechanisms in these infections and the medications used to combat their resistance is given in this abstract. Mutations in the genes that code for the targets of drugs or the activation enzymes of drugs or metabolism are frequently the cause of MDR in MTB. Important first-line medications like rifampicin and isoniazid target essential cellular functions including RNA transcription and cell wall formation. Resistance mechanisms, such as changes in genes like rpoB and katG, impair the effectiveness of drugs. Gene alterations such as gyrA and rrs impair second-line medications, such as fluoroquinolones and injectable treatments, increasing treatment obstacles and resulting in extensively drug-resistant tuberculosis (XDR- TB). Similar to this, drug target genes, such as folP1 for dapsone and rpoB for rifampicin, as well as efflux pumps and metabolic pathways, are mutated in M. Leprae resistance mechanisms. Many different types of medications with different mechanisms of action are used to fight MDR in MTB and M.Leprae. Novel treatments targeting alternate routes are being developed in addition to traditional antibiotics. To reduce resistance and improve treatment effectiveness, combination medicines that are customized to each patient's unique resistance profile are crucial. Molecular assays and whole-genome sequencing are two examples of diagnostic breakthroughs that enable prompt therapeutic interventions by facilitating the quick identification of drug resistance mutations. Keywords: Multi drug resistance, M.tuberculosis, M.leprae, Mechanism of drug resistance
Publication date: 01/09/2025

https://ijbpas.com/pdf/2025/September/MS_IJBPAS_2025_9377.pdf

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https://doi.org/10.31032/IJBPAS/2025/14.9.9377