Mechanisms and Action of Drug Resistance on Mycobacterium tuberculosis

Tuberculosis (TB) remains the most challenging infection to treat worldwide. The contemporary TB regimens consist of 6–9 months of daily doses of four drugs in the existing regimen that is extremely toxic to patients. The purpose of these longer treatments is to eliminate Mycobacterium tuberculosis, notorious for its ability to resist most antimycobacterial drugs, thereby preventing the formation of drug-resistant clinical strains. On the contrary, prolonged therapies have led to impoverished patient adherence. Furthermore, the severe limitations of drug choices have resulted in the emergence of drug-resistant strains. Unfortunately, the lack of great lethargy toward developing effective antituberculosis regimens with a large-scale prevalence rate is a tremendous challenge to controlling the pandemic. In fact, the current improvement in genomic studies for early diagnosis and understanding of drug resistance mechanisms, and the identification of newer drug targets, is remarkable and promising. Identifying genetic factors, chromosomal mutations, and associated pathways give new hope to current antituberculosis drug discovery. This focused review renders insights into understanding molecular mechanisms underlying the profound drug resistance. This knowledge is essential for developing effective, potent antibiotics against drug-resistant strains and helps shorten the current treatment courses required for drug-susceptible tuberculosis.