The bacterial drug resistance in tuberculosis results from:
Drug resistance: It refers to unresponsiveness of a microorganism to an AMA, and is akin to the phenomenon of tolerance seen in higher organisms. Resistance may be developed by mutation or gene transfer. Mutation: It is a stable and heritable genetic change that occurs spontaneously and randomly among microorganisms. It is not induced by the AMA. Any sensitive population of a microbe contains a few mutant cells which require higher concentration of the AMA for inhibition. These are selectively preserved and get a chance to proliferate when the sensitive cells are eliminated by the AMA. Thus, in time it would appear that a sensitive strain has been replaced by a resistant one, e.g. when a single antitubercular drug is used. Mutation and resistance may be: (i ) Single step.- A single gene mutation may confer high degree of resistance; emerges rapidly, e.g. enterococci to streptomycin, E. coli and Staphylococci to rifampin. (ii ) Multistep.* A number of gene modifications are involved, sensitivity decreases gradually in a stepwise manner. Resistance to erythromycin, tetracyclines and chloramphenicol is developed by many organisms in this manner. Sometimes mutational acquisition of resistance is accompanied by decrease in virulence, e.g. ceain rifampin resistant staphylococci and low grade penicillin-resistant gonococci have decreased virulence
Transduction
Transformation
Plasmid mediated
Mutation
Chemotherapy