An assessment of nucleic acid amplification testing for active mycobacterial infection

Drug-resistant mycobacterial infections

MDR-TB² and extensively drug-resistant TB³ are serious global public health problems (Abubakar et al. 2013). In Australia MDR-TB occurs in 2–3% of cases and extensively drug-resistant TB is uncommon (Lumb et al. 2013). Treatment of drug-resistant TB is difficult to manage, requires a long duration, requires the use of drugs that are less potent and more toxic, and may result in poor health outcomes.

Resistance to anti-TB drugs is the result of spontaneous mutations in the genome of MTB and is caused by inappropriate monotherapy and intermittent treatment with anti-TB drugs (Abubakar et al. 2013; Lemos & Matos 2013). Resistance occurs at rates that are predictable for each drug, varying from 1 in every 10^2–4 bacilli for pyrazinamide to 1 in every 10^7–8 bacilli for rifampicin (Lemos & Matos 2013).

Combination treatments can successfully prevent the emergence of resistance during the treatment of TB. Any MTB that becomes resistant to one drug can be killed by the other drug and vice versa (Lemos & Matos 2013; Mitchison 2012).