People with TB are said to have drug-resistant disease if their strain of Mycobacterium tuberculosis (M. tuberculosis) is resistant to one or more first-line drugs: isoniazid (INH), rifampin (RMP), pyrazinamide (PZA) and ethambutol (EMB). The impact of drug resistance on the outcome of TB treatment varies according to which drug, or combination of drugs, the isolate is resistant to, and reflects the different, but complementary, role each drug plays in the treatment of TB.1
At the level of the individual patient who begins with TB disease due to drug-susceptible M. tuberculosis organisms, it is commonly believed that drug resistance occurs due to one or more of the following: improper prescription of anti-TB drugs (including drug selection and dosing), their proper prescription but unavailability, the malabsorption of these drugs, treatment interruptions or inadequate treatment supervision. Recent studies suggest that low anti-TB drug concentration exposures, caused by inter-individual pharmacokinetic variability, poor quality drugs, suboptimal drug dosing and/or poor drug penetration into tissues, could be a major cause of acquired drug resistance.2
At the population level, it is likely that the resource-driven use of standardized regimens in the absence of pretreatment drug susceptibility testing (DST) has resulted in a steadily rising global prevalence of drug resistance.3 In a systematic review and meta-analysis of initial drug resistance and TB treatment outcomes, the cumulative incidence of acquired drug resistance with initially pan-sensitive strains was 0.8% (95% CI 0.5 to 1.0%), compared with 6% (CI 4 to 8%) with initially single-drug-resistant strains and 14% (CI 9 to 20%) with initially polydrug-resistant strains.4 In some geographic locations, transmission of organisms that are already drug-resistant in congregate institutions—notably hospitals and prisons—amplifies the problem of drug-resistant TB.
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