Mechanism and management of antibiotic drug resistance tuberculosis

Abstract

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-positive persons is more difficult and may be confused with other pulmonary or systemic infections. Management of patients with mono- or poly-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.