In the last few years, there has been considerable progress in our understanding of the mechanisms of action and resistance to antituberculosis agents. To date, there is information about 11 genes involved in resistance to all major antituberculous drugs in Mycobacterium tuberculosis. Mutations in katG, inhA and ahpC genes are found in up to 90% of isoniazid-resistant strains. Rifampin resistance is associated (>96%) with rpoB mutations, pyrazinamide resistance with pncA mutations (72% to 97%), ethambutol resistance with mutations in embB (47% to 65%), streptomycin resistance with rrs or rpsL mutations (70%), and fluoroquinolone resistance with gyrA substitutions (75% to 94%). Additional genes and mechanisms may play a role, particularly in association with lower levels of resistance. Based on this growing set of information, genotypic analysis of resistance is becoming a real possibility, and novel tests are being developed. Issues such as effectiveness, cost-efficiency, and the appropriate setting for the implementation of these techniques are not yet established.
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The author(s) declare there are no affiliations with or involvement in any organisation or entity with any financial interest in the subject matter or materials discussed in this manuscript.
