Physicians are more and more often challenged by difficult-to-treat cases of TB. They include patients infected by strains of Mycobacterium tuberculosis that are resistant to at least isoniazid and rifampicin (multidrug-resistant TB) or to at least one fluoroquinolone (FQ) and one injectable, second-line anti-TB drug in addition to isoniazid and rifampicin (extensively drugresistant TB). The drug treatment of these cases is very long, toxic, andexpensive, and, unfortunately, the proportion of unsatisfactory outcomes is still considerably high. Although FQs and pyrazinamide (PZA) are backbone drugs in the available anti-TB regimens, several uncertainties remain about their mechanisms of action andeven more remain about the mechanisms leading to drug resistance. From a clinical point of view, a better understanding of the genetic basis of drug resistance will aid (1) clinicians to provide quality clinical management to both drug-susceptible and drug-resistant TB cases (while preventingemergence of further resistance), and (2) developers of new molecular-based diagnostic assays to better direct their researcheff orts toward a new generation of sensitive, specific, cheap, andeasy-to-use pointof-care diagnostics. In this review we provide an update on the molecular mechanisms leading to FQ-and PZA-resistance in M tuberculosis.
|Number of pages||9|
|Publication status||Published - Apr 1 2015|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine
- Cardiology and Cardiovascular Medicine