Rifampicin
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Pneumonitis: case report A 43-year-old man developed pneumonitis during treatment with rifampicin for tuberculous meningitis. The man presented to the emergency department with headache, shortness of breath, fever and lethargy for 1 week. Two months prior to the presentation, he had been diagnosed with tuberculous meningitis. Sixteen days prior to the admission, his unspecified first-line therapy was switched due to drug-induced hepatitis to the second-line therapy comprising of oral rifampicin 600mg once daily, moxifloxacin, cycloserine, ethionamide and pyridoxine. He was kept on droplet and airborne isolation due to the suspicion of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. He was febrile with bilateral basal crackles in the lungs. His physical examination was unremarkable and his oxygen saturation was 91% at room air. A chest X-ray revealed patchy bilateral consolidation and bilateral pulmonary infiltrates. The sepsis workup was negative for any bacterial growth. PCR tests were negative for respiratory viruses. Nasopharyngeal reverse transcription PCR was negative for SARS-CoV-2. Due to his underlying condition of tuberculosis, drug resistance/reinfection was considered as differential diagnosis. However, PCR and culture from sputum were negative. Due to his negative smoking history, acute eosinophilic pneumonitis was also ruled out. The man started receiving empirical treatment with unspecified antibiotics and was kept on oxygen supplementation through a nasal cannula. He remained afebrile for subsequent days. His CT thorax revealed peri-broncho and perihilar vascular ill-defined opacities with a patchy area of alveolar consolidation. CT thorax also showed small basal pleural thickening, ground-glass opacities at the base of the lungs, and sub-centimetric lymph nodes in the mediastinum. It also revealed air bronchograms and patchy consolidations, consistent with acute respiratory distress syndrome. On day 5 of admission, bronchoscopy was performed. Bronchoalveolar lavage revealed a predominance of lymphocytes with negative results for acid-fast bacilli, viral, fungal and bacterial cultures. Bronchoalveolar lavage analysis ruled out alveolar haemorrhage. Histopathological examination showed chronic inflammatory cells, including histiocytes, rare eosinophils and lymphocytes and widened interstitial septae by loose connective tissue. Additionally, the alveolar sacs and ducts were filled with organising fibrinous material. Type II pneumocyte hyperplasia was evident. Based on the findings, drug-induced pneumonitis secondary to rifampicin was considered. On day 6 of admission, rifampicin was discontinued. He continued receiving other anti-tubercular medications. He was treated with prednisolone. On the second day of prednisolone therapy, he was afebrile with normal oxygen saturation on room air. He was discharged with tapering dose regimen of unspecified steroids. Two weeks after discharge, he was seen in the tuberculosis clinic. He was asymptomatic at the time of discharge. The man
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