Exact(26)
While resistance to PZA in MDR-TB is associated with poor treatment outcome, bacillary susceptibility to PZA along with the use of fluoroquinolone (FQ) and second-line injectable drugs (SLIDs) may predict improved treatment success in MDR-TB.
Furthermore, the synergistic activity of PZA with newly developed agents such as the diarylquinoline bedaquiline suggests that the use of PZA in regimens including novel agents could improve efficacy substantially, if the organism retains susceptibility to PZA.
The real time application of the sensor was explored by successful detection of PZA in pharmaceutical and human blood serum, plasma and urine samples.
Previous studies [42] [44] have shown that mutations in the structural gene or promoter region of pncA, leading to an amino acid substitution, confer resistance to PZA in 72 97% of the cases.
According to this mechanism, the binding of the drug would be mostly ensured by (i) the hydrogen bonding interaction formed between the pyridyl nitrogen atom of PZA and the water molecule HOH220 coordinated to the Fe2+ ion and (ii) the strong interaction of the carbonyl-oxygen atom of PZA in the Ala134-Cys138 oxyanion hole.
panD may encode another target of PZA in addition to RpsA.
Similar(34)
Recently, we identified a new gene, panD encoding aspartate decarboxylase and involved in β-alanine biosynthesis, mutations in which are associated with PZA resistance in M. tuberculosis.
Despite the potential importance of PZA resistance in MDR-TB treatment outcome, standard phenotypic PZA susceptibility testing is seldom performed owing to technical challenges.
Mutations in pncA represent the major mechanism of PZA resistance in M. tuberculosis [3] [8].
Mutations in pncA are the major mechanism of PZA resistance in M. tuberculosis.
To identify new mechanisms of PZA resistance, in this study, we isolated a large number of in vitro generated mutants resistant to PZA and characterized these strains for novel mutations in their genomes by whole genome sequencing.
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