Authors : Chirag J Gohil, Ketan C. Parmar, Priyanka R. Patel, Jignakumari J. Gohil
DOI : 10.18231/j.ijpca.2022.020
Volume : 9
Issue : 3
Year : 2022
Page No : 114-118
Drug resistance in tuberculosis has been shown to result from spontaneous mutation in several chromosomal genes of M.Tuberculosis. Mutation may reduce the medications' capacity to bind to the target genes. In many patients polydrug resistance, multidrug resistance, rifampicin resistance (RR) and extensive drug resistance (XDR) were seen. The diagnosis of drug-resistant TB in HIV-ith mono- or positive persons is more difficult and may be confused with other pulmonary or systemic infections. Management of patients wpoly-resistant TB will be done with standard first line chemotherapy. Treatment of latent infection for people suffering from multidrug resistant bacilli is problematic because the only cure by isoniazid and rifampicin. In the recent cases of severe hepatotoxicity associated with preventive treatment comprising either pyrazinamide and rifampicin or pyrazinamide and fluoroquinolone. The use of dilatory fluoroquinolones, such as moxifloxacin, remarkable improved treatment outcomes of XDR-TB.
Keywords: Tuberculosis, Drugresistance TB, Mechanism of drug resistance