Molecular techniques in the diagnosis of drug-resistant tuberculosis.
In the last few years, there has been considerable progress in our understanding of the mechanisms of action and resistance to anti-tuberculosis agents. To date, there is information about 11 genes involved in resistance to all major anti-tuberculous 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 appropriate setting for the implementation of these techniques are not yet established.
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Institute of Medical Microbiology, University of Berne, Switzerland.
Telenti
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D000995:Antitubercular Agents / Q000627:therapeutic use; D005838:Genotype; D006801:Humans; D009154:Mutation; D009169:Mycobacterium tuberculosis / Q000187:drug effects* / Q000235:genetics*; D016133:Polymerase Chain Reaction; D018088:Tuberculosis, Multidrug-Resistant / Q000188:drug therapy* / Q000235:genetics
D000995:Antitubercular Agents