Results were compared with phenotypic DST data. Nineteen different

mutation types to at least one of the drugs were found; six isolates (6%) were classified as MDR-TB, defined as resistance to at least rifampicin and isoniazid. The rates of concordance of the PCR with the phenotypic susceptibility test were 71.4, 54.5, and 44.4 for isoniazid, rifampicin, and ethambutol, respectively. These results highlight the importance of molecular epidemiology studies of tuberculosis in understudied regions with a tuberculosis burden to uncover the true prevalence of the selleck chemicals llc MDR-TB. The spread of multidrug-resistant tuberculosis (MDR-TB) due to emergence of multidrug-resistant Mycobacterium tuberculosis isolates has increased worldwide and reached epidemic proportions in many countries (Mokrousov et al., 2003). The increasing number of multidrug-resistant isolates over the years has complicated the control of several outbreaks of the disease (WHO, 2000a, b). MDR-TB is defined as resistant to at least rifampicin and isoniazid, which are the backbone of short-course chemotherapy for tuberculosis (Herrera-León et al., 2005). Therefore, immediate identification of these resistant isolates is very important for adjustments in treatment (Herrera-León et al., 2005;

Abe et al., 2008). Rifampicin was introduced in 1972 as an antituberculosis drug and has excellent EPZ-6438 molecular weight sterilizing activity. Rifampicin acts by binding to the β-subunit of RNA polymerase (rpoB) (Ramaswamy & Musser, Bay 11-7085 1998), the enzyme responsible for transcription and expression of mycobacterial genes, resulting in inhibition of the bacterial transcription activity and thereby killing the

organism. Mutations in the 81-bp core region of rpoB were reported to be responsible for resistance in at least 95% of isolates (Sekiguchi et al., 2007). This region is located between codons 507 and 533, with the most common changes in codons Ser531Leu, His526Tyr, and Asp516Val (González et al., 1999). Isoniazid enters the bacterial cell as a prodrug; it is then activated to a toxic substance in the cell by a catalase peroxidase encoded by the katG gene (Wang et al., 1998) and subsequently affects intracellular targets such as mycolic acid biosynthesis, an important component of the cell wall, which eventually results in loss of cellular integrity and the bacterial death. Ethambutol, a first-line-specific antituberculosis drug used in combination with other drugs, inhibits the incorporation of mycolic acids into the mycobacterial cell wall. Genetic and biochemical studies have shown that resistance to ethambutol is mediated by mutations in the embB gene, which encodes arabinosyl transferase, an integral membrane protein that is inhibited by the drug.