Resistance acquiring Mycobacterium tuberculosis in human body during drug therapy: resistance mechanism and future anticipations

Abstract

Acquiring of the resistance to the variant line of the drugs used in drug therapy for M. tuberculosis is becoming a crucial problem for the entire globe. Mutation in cord factor led to the bacterium resistant against antibiotics therapy. These changes drive the chromosomal mutations resultant, the drugs which are sensitive against the M. tuberculosis becomes the resistant via overexpression or modification of the drug target. Essential for viability and virulence, enzyme involved in the biosynthesis of mycolic acid represents novel target for drug development. This is particularly relevant to the impact on global health given the rise of MDR and XDR strains of M. tuberculosis. According to the intrinsic drug resistance mechanism the unusual composition and structure of the bacterial cell envelop and the low numbers of the porins assign notably to the envelope’s low compound permeability. For better diffusion of antibiotics across the cell envelope there are require a high membrane fluidity. Though, the lipid-rich nature builds the cell wall exceedingly hydrophobic and prevents the permeation of hydrophilic compounds. Acquired resistance accomplish when a bacterium has the ability to resist the activity of an antimicrobial agent to which it was previously susceptible. The acquisition of the acquired resistance follows up the case of successful gene mutations. Although M. tuberculosis has low genetic diversity as compare to the other pathogens but the genetic diversity of the M. tuberculosis can influence multiple aspects in therapy of drug resistance tuberculosis. From mono drug resistant to MDR and XDR, is threatening to make TB once again an untreatable disease if new therapeutic option does not soon become available.