A 50-year-old male presented with a 2-month history of worsening breathlessness and a chronic productive cough. He also reported general malaise, weight loss, and night sweats, but no haemoptysis or chest pain. The patient was an active smoker (30+ pack years) with long-standing COPD and a history of crack cocaine use and alcohol misuse (although he stopped drinking 15 years ago). The patient was taking methadone 35 ml per day and inhaled steroids plus long-acting bronchodilator and anti-muscarinic agents once daily, and had no known drug allergies. He lived in sheltered accommodation and could only move with a mobility scooter.
On examination he was found to be cachectic and tachypnoeic at rest on air (88% O2 saturation). He had a BMI of 14 kg/m2, a respiratory rate of 20, and a pulse rate of 110 beats per minute. He had widespread respiratory wheeze, and no palpable lymphadenopathy. A chest X-ray showed right mid-zone consolidation with hyper-inflation and emphysema, in keeping with COPD and a history of smoking and drug use (Fig. 3B).
The patient was admitted to hospital with Type 2 respiratory failure (tachypnoeic and oximetry: 85% in room air; arterial blood gas: pH 7.16, pO2 6.9 kPa, pCO2 10 kPa, HCO3 31.6 mmol/L). He responded well to 2 L of oxygen via nasal cannula, nebulisers, steroids, and antibiotics, based on a diagnosis of community-acquired pneumonia. The patient had been symptomatic for the past two months with worsening productive cough. He tested negative for COVID-19 (both from a throat swab and a serology test), was HIV negative, and had no prior history of tuberculosis or contact with tuberculosis-infected individuals. However, sputum samples were sent for acid fast bacilli (AFB) testing; one smear sample was positive for AFB and two samples 9 days apart were culture positive for mycobacteria. A polymerase chain reaction (PCR) test was performed for M. tuberculosis, which was negative, suggesting potential infection with NTM. A sample was therefore sent for analysis by matrix assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry, which can rapidly speciate culture isolates, and this identified M. avium. This was subsequently confirmed by the reference laboratory through whole-genome sequencing and drug susceptibility testing showed no macrolide resistance.
Following the NTM-PD diagnosis, an HRCT scan was performed (Fig. 3B) and showed fibrocavitary disease. Based on this, and the smear-positive sputum sample, an initial 2 weeks of amikacin therapy plus the standard three drug regimen for M. avium infection (azithromycin, ethambutol and rifampicin) was started. Due to challenges with methadone administration, rifampicin was changed to clofazimine. At the time of writing, the patient is undergoing further tests for potential fungal infection ten months into NTM treatment, due to newly increased levels of Aspergillus antibodies, and he is being supported to stop smoking.