Abstract / Summary
Abstract Background Pulmonary non-tuberculous mycobacterial disease (NTM-LD) is increasingly recognised as an important cause of chronic pulmonary infection worldwide. However, in tuberculosis (TB)-endemic settings, NTM-LD remains underdiagnosed because clinical algorithms and laboratory services are primarily designed to detect Mycobacterium tuberculosis. Consequently, patients are frequently misdiagnosed, receive repeated empirical anti-tuberculosis treatment, and experience delays in appropriate management. Case presentation We report a 17-year longitudinal case of an immunocompetent Nigerian man whose chronic respiratory illness ultimately proved to be pulmonary NTM disease. The patient had previously completed treatment for pulmonary tuberculosis in 2004 and presented to the University of Port Harcourt Teaching Hospital in 2009 with chronic productive cough, low-grade fever, weight loss, drenching night sweats, and exertional dyspnoea. Chest radiography demonstrated extensive unilateral fibrocavitary lung disease, while three sputum specimens were negative for acid-fast bacilli (AFB). Based on his clinical history and prevailing national tuberculosis treatment guidelines, he was empirically treated for relapsed pulmonary tuberculosis with a Category II anti-tuberculosis regimen. Despite modest clinical improvement, persistent symptoms and progressive radiographic destruction of the left lung prompted further evaluation. Repeat sputum microscopy detected AFB in one of two specimens, raising suspicion of drug-resistant tuberculosis. Mycobacterial culture performed at the Nigerian Institute of Medical Research yielded a non-tuberculous mycobacterium. Subsequent molecular testing confirmed that the isolate was not a member of the Mycobacterium tuberculosis complex; however, species identification and drug susceptibility testing were unavailable due to diagnostic limitations. Given the extensive cavitary lung disease, chronic pulmonary aspergillosis was also considered, and empirical itraconazole therapy was initiated while further investigations were pursued. The patient subsequently received rifampicin- and clarithromycin-based therapy with gradual clinical improvement. However, irreversible structural lung damage resulted in destroyed left lung syndrome and chronic bronchiectasis requiring long-term respiratory follow-up. Conclusions This case highlights the substantial diagnostic and therapeutic challenges of pulmonary NTM disease in resource-limited, TB-endemic settings. It demonstrates the limitations of relying on AFB microscopy and empirical TB treatment, the importance of recognizing discordant microbiological findings, and the consequences of limited access to mycobacterial species identification and drug susceptibility testing. Strengthening laboratory capacity, integrating NTM into national TB diagnostic algorithms, and improving clinician awareness are essential for facilitating timely diagnosis and appropriate management.