An overview of the pattern of first- and second-line anti-tuberculosis drug resistance gene mutations

Shuaibu Abdullahi Hudu *

Department of Medical Microbiology and Parasitology, Faculty of Basic Medical Sciences College of Health Sciences, Usmanu Danfodiyo University, Sokoto, 840232 Sokoto State, Nigeria.
 
Review
International Journal of Frontline Research in Multidisciplinary Studies, 2022, 01(01), 035–042.
Article DOI: 10.56355/ijfrms.2022.1.1.0031
Publication history: 
Received on 10 May 2022; revised on 14 June 2022; accepted on 16 June 2022
 
Abstract: 
Tuberculosis is still the most prevalent infectious cause of mortality, and it has a significant medical, societal, and economic impact MDR-TB is a type of tuberculosis (TB) infection produced by bacteria resistant to at least two of the most important first-line anti-TB treatments, isoniazid, and rifampin. Extensively drug-resistant tuberculosis (XDR-TB) is a type of tuberculosis that is resistant to second-line treatments. MDR-TB is a type of tuberculosis (TB) infection produced by bacteria resistant to at least two of the most important first-line anti-TB treatments, isoniazid, and rifampin. Extensively drug-resistant tuberculosis (XDR-TB) is a type of tuberculosis that is resistant to second-line treatments. Because resistant cases have significant morbidity and mortality, multidrug-resistant tuberculosis poses a significant threat to treatment. The most effective anti-tuberculosis drugs are first-line essential anti-tuberculosis drugs, which must be included in any short-term treatment plan. Rifampicin, ethambutol, Isoniazid, streptomycin, and pyrazinamide are among the medications in this group. Ethionamide, amikacin, capreomycin, and para-aminosalicylic acid are Second-line anti-tuberculosis that are clinically ineffective and cause severe responses far more commonly than first-line drugs. Resistance to first-line drugs was connected to mutations in the pncA, emb­­­­, rpsL, and rrs genes, while rrs, gyrA, eis, tlyA and gryB are associated with second-line drugs.
 
Keywords: 
Mutations; Mechanism; Resistance; Tuberculosis; Drug-resistance
 
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