C68-35 Not So (Acid)-Fast: Unmasking a Pleural Mycobacterium Avium Complex Infection

Abstract Mycobacterium avium complex (MAC) is the most common cause of nontuberculous mycobacterial (NTM) pulmonary disease, typically affecting individuals with chronic lung disease or impaired immunity. Pleural involvement is uncommon but, among NTMs, most often attributed to MAC. NTM pleural infection is considerably less frequent than tuberculous pleuritis; in endemic regions, tuberculosis (TB) remains a leading cause of pleural effusion. Because pleural MAC can exhibit overlapping clinical, radiographic, and immunologic features with Mycobacterium tuberculosis (MTB), it may be misdiagnosed as pleural TB, leading to delayed recognition and inappropriate therapy. A 90-year-old man with chronic obstructive pulmonary disease and a remote smoking history presented with one year of progressive exertional dyspnea and a 40-pound unintentional weight loss. Two months earlier, a QuantiFERON-TB test had been positive. Computed tomography revealed a large, loculated left pleural effusion containing proteinaceous and hemorrhagic material, bilateral pleural calcifications, right lower lobe consolidation, and no mediastinal or hilar lymphadenopathy. Positron emission tomography-computed tomography (PET-CT) demonstrated mild fluorodeoxyglucose uptake along the pleural rind and within the consolidation. The patient underwent left-sided robot- and video-assisted thoracoscopic surgery with evacuation of a hemothorax, total pulmonary decortication, and pleural biopsy. Despite negative results for acid-fast bacillus (AFB) smear, culture, and MTB polymerase chain reaction (PCR) from bronchoalveolar lavage of the left lower lobe and two induced sputum samples, pleural tissue AFB smear revealed rare bacilli with necrotizing granulomas on histopathology. MTB PCR from both pleural tissue and fluid remained negative. At this point, empiric rifampin, isoniazid, pyrazinamide, ethambutol, and pyridoxine were initiated for presumed pleural TB. Two weeks later, MAC grew from pleural tissue, pleural fluid, and both sputum cultures, prompting transition to rifampin, ethambutol, and azithromycin. Despite appropriate therapy, the patient’s condition deteriorated, and he ultimately expired. This case highlights the diagnostic challenge of distinguishing pleural MAC from MTB infection. Both can present with chronic respiratory symptoms, weight loss, exudative effusions, and parenchymal opacities. A positive interferon-gamma release assay reflects immune sensitization to MTB but does not differentiate latent from active infection or exclude NTM disease. Pleural MAC, though rare, should remain in the differential for chronic exudative effusions when TB studies are inconclusive. Early microbiologic confirmation is critical to guide therapy, minimize toxicity, and avoid unnecessary isolation and public health interventions. This abstract is funded by: None