The following are the supplementary

The following are the supplementary data related to this article.
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Author contributions
Acknowledgements This work was supported by the Defense Advanced Research Projects Agency (DARPA) grant N66001-11-1-4180 and the Wyss Institute for Biologically Inspired Engineering at Harvard University. We thank A. Dinis for microbiology assistance; P. Snell, M. Rhodas, B. Dusel for protein production assistance; and B. Boettner for editorial comments for the manuscript. Statistical assistance was provided by R. Betensky, conducted with support from Harvard Catalyst/The Harvard Clinical and Translational Science Center (National Center for Research Resources, National Center for Advancing Translational Sciences, National Institutes of Health Award UL1 TR001102) and Harvard University.
Introduction The genus Mycobacterium is separated into the pathogenic GSK-J1 sodium salt Mycobacterium tuberculosis complex, Mycobacterium leprae, and Mycobacterium ulcerans, and various nontuberculous mycobacteria (NTM) (Manual of Clinical Microbiology, 2015). Mycobacterium tuberculosis (MTB) is the causative agent of tuberculosis. Global priorities for tuberculosis (TB) care and control are to improve case-detection and to enhance rapid diagnosis of tuberculosis disease (WHO, 2014). Directly observed standardized short-course chemotherapy (DOTS) is an effective treatment for drug-susceptible tuberculosis disease, with cure rates >95.0% (Hopewell et al., 2006). However, the current situation is characterized by increasing numbers of drug-resistant tuberculosis disease. The treatment of multidrug-resistant (MDR) or extensively drug-resistant (XDR) TB requires the use of second-line drugs, which are less effective, more expensive, and more toxic than first-line drugs (WHO, 2014; Hopewell et al., 2006). NTM are ubiquitously present in the environment. Their pathogenic potential is variable and infections predominantly occur in patients with underlying disorders or immunocompromising conditions, although individuals without predisposing risk factors can also be affected (Griffith et al., 2007; Aksamit et al., 2014). Diseases caused by NTM include lung disease (e.g. Mycobacterium abscessus, Mycobacterium kansasii), cutaneous ulcers (e.g. Mycobacterium marinum, M. ulcerans), disseminated infections (e.g. Mycobacterium genavense), lymphadenitis (e.g. Mycobacterium avium), and joint infections (e.g. Mycobacterium haemophilum) (Tortoli, 2009; Tortoli, 2014). The variety of diseases caused by NTM, the association of NTM infections with underlying disorders such as bronchiectasis and severe immunosuppressive conditions, and the difficulty to distinguish NTM pulmonary infections from MTB pulmonary infections on the basis of clinical symptoms and imaging alone, all of these underline the need for detection and proper identification of NTM in addition to that of MTB in clinical specimens (Griffith et al., 2007). Laboratory diagnosis of mycobacterial infections is done in designated and specialized laboratories not the least due to the need for biosafety conditions, and the same isolation procedures and cultural techniques are used for recovery of M. tuberculosis and all of the NTM pathogens. Traditionally, detection of mycobacteria and drug susceptibility testing (DST) is based on culture, which is a time consuming, complicated, resource costly and lengthy process. Recovery of mycobacteria by culture and identification takes about 2–4weeks, followed by an additional 1–2weeks for drug susceptibility testing (Manual of Clinical Microbiology, 2015). PCR-based diagnostic procedures for direct detection of MTB in clinical specimens have been introduced >20years ago (Boddinghaus et al., 1990; Thierry et al., 1990). A number of genetic assays for detection of MTB DNA in clinical specimens are commercially available, e.g. AMTD Amplified Mycobacterium Tuberculosis Direct Test (Gen-Probe Inc., San Diego, USA), COBAS™ TaqMan™ MTB test (Roche, Basel, Switzerland), BD ProbeTec ET system (Becton Dickinson, Baltimore, USA), Abbott LCx M. tuberculosis assay (Abbott Laboratories, Chicago, USA), and Fluorotype MTB (Hain Lifescience GmbH, Nehren, Germany), as are numerous studies comparing molecular and culture-based methods for detection of MTB (Reischl et al., 1998; Goessens et al., 2005; Kim et al., 2011; Tortoli et al., 2012; Bloemberg et al., 2013; Hofmann-Thiel and Hoffmann, 2014). In contrast to MTB, molecular genetic assays for detection of NTM are only infrequently implemented in routine diagnostics, although various in-house assays have been described (Kirschner et al., 1996; Del Portillo et al., 1996; Stauffer et al., 1998; Shrestha et al., 2003; Peter-Getzlaff et al., 2010).