Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis and classified as pulmonary and extrapulmonary based on their site of infection. Antituberculosis drugs developed since the 1940s and as their discovery resistance also developed against them. World health organization recognized tuberculosis as emergency public health in 1993.
Acquired and primary drug resistances are the common pathways for the development of anti-tuberculosis drug resistance. Acquired drug resistance is the result of inappropriate treatment, poor quality of the drugs and inadequate drug intake and primary drug resistance is due to exposure to the drug-resistant anti-tuberculosis. Types of anti-tuberculosis drug-resistant are multidrug-resistant tuberculosis is the result of resistance to isoniazid and rifampicin, extensively drug-resistant tuberculosis a consequence of resistance to isoniazid, rifampicin, fluoroquinolones and one of the second-line injectable drugs and totally drug-resistant tuberculosis is a resistance to all first and second-line anti-tuberculosis drugs.
Anti-tuberculosis drugs primarily actions are on protein synthesis, mycolic acid synthesis, DNA synthesis, folic acid synthesis, and ATP synthase. These drugs could produce bacteriostatic or bactericidal effects on the mycobacteria. The main resistance mechanism to the anti-tuberculosis drug is the mutation of the target gene accountable for the action of anti-tuberculosis drugs. This resistance to the antituberculosis drug produces a devastating effect on public health. Therefore, further study should be conducted in the areas of finding a new target for the development of new anti-tuberculosis drugs.