An HIV-exposed uninfected 20-month-old boy presented to Chris Hani Baragwanath Academic Hospital in Johannesburg, South Africa, with a 2-day history of shortness of breath, cough and noisy breathing. He had also experienced night sweats, fever and vomiting for a week. Two weeks prior to this presentation, he had been diagnosed with bacteriologically unconfirmed PTB at a primary healthcare clinic and was empirically started on a four-drug antituberculosis treatment regimen (rifampicin, isoniazid, pyrazinamide and ethambutol). The diagnosis was based on a chest X-ray (Fig. 1A) and a positive Mantoux test. His father (a household contact) had been diagnosed with PTB, and had been on first-line antituberculosis treatment for 4 months.  The boy had had normal growth and development up to 1 year of age, but had subsequently lost weight, and fallen from a weight-for-height z-score +2 to the median over the preceding 8 months. 
 On admission, he was apyrexial, tachycardic and in moderate respiratory distress, with oxygen saturations of 97% in room air. He had marked chest wall indrawing and bilateral posterior cervical and axillary lymph nodes (<0.5 cm in diameter). He was clinically hyperinflated, with bilateral wheezing. The rest of his clinical examination was normal. 
 He was diagnosed with viral bronchiolitis, and therefore a chest X-ray was not performed. He was started on oxygen and hypertonic saline nebulisation. He responded poorly to this initial treatment and was therefore started on oral corticosteroids and amoxicillin on day 2 of hospitalisation, and his first-line antituberculosis treatment was continued. Gastric aspirate samples for microscopy for acid-fast bacilli, Xpert MTB/RIF (Cepheid, USA) and culture for mycobacteria were negative. 
 During his hospital admission period his wheezing persisted, and he remained in moderate respiratory distress. On the fifth day of admission, he developed percussion dullness and absent breath sounds over the right hemithorax. 
 A chest X-ray at this point revealed a large right-sided pleural effusion (Fig. 1B). A computed tomography scan of the chest revealed hilar lymphadenopathy and a large right-sided pleural effusion. The thoracic duct could not be visualised. Diagnostic pleurocentesis confirmed a chylothorax. It was suspected that tuberculous lymph nodes had eroded the thoracic duct causing the chylothorax, and therefore a bronchoscopy was performed, which revealed caseating lymph nodes in the right main bronchus suggestive of TB, and 90% obstruction of the left main bronchus. The Xpert MTB/RIF (Cephaid, USA) test on a bronchoalveolar lavage specimen identified rifampicinresistant Mycobacterium tuberculosis. Gastric aspirates, pleural fluid and bronchoalveolar lavage samples were all smear-negative for acidfast bacilli and mycobacterial culture-negative. 
 The chylothorax was managed with a low-fat diet (with additional medium-chain triglycerides), therapeutic taps for worsening respiratory distress and an octreotide infusion. The boy was commenced on multidrug-resistant TB (MDR-TB) treatment (amikacin, levofloxicin, ethionamide, terizidone, pyrazinamide, ethambutol and high-dose isoniazid) and oral steroids. 
 For further management, he was transferred to a hospital dedicated to the care of MDR-TB patients. One month later, he showed marked clinical improvement, with almost complete radiological resolution of the chylothorax, and reduced hilar lymphadenopathy (Fig. 1C). The full case overview is shown in Fig. 2.