The global burden of active TB occurs on a background of quiescent or latent TB infection (LTBI), affecting one third of the world's population and a higher proportion of the population of TB-endemic areas [3] . Respiratory and constitutional symptoms overlapping with those of pulmonary TB are very common in communities where TB is endemic [4] . In this scenario the challenge is to distinguish symptomatic patients with active TB from those with latent disease but whose presenting symptomatology is attributable to some other infectious or inflammatory process. In terms of rapid diagnosis, sputum microscopy will only identify approximately 50% of patients with active pulmonary TB. Conversely, while the interferon gamma release assays (IGRAs) represent a major advance in the detection of latent TB, they cannot distinguish active TB from symptomatic patients with latent infection in this context [5, 6] . This overlap between LTBI, active TB and non-specific clinical manifestations presents a formidable obstacle to the rapid recognition of active TB and the timely and appropriate targeting of anti-TB chemotherapy or chemoprophylaxis. In practice this difficulty may give rise to 2 types of therapeutic error. In the first instance, erroneous diagnosis of active TB in a symptomatic patient with LTBI may result in inappropriate administration of full course TB treatment. Conversely, offering chemoprophylaxis to a patient with supposed LTBI in whom active TB has not been recognized, will drive emergence of drug resistance.