D104-01 When Vaping Meets Vulnerability: Necrotizing Pneumonia and E-cigarette or Vaping-Associated Lung Injury (EVALI) in a Patient With Selective IgA Deficiency

Abstract Introduction Selective IgA deficiency (sIgAD) is the most common primary immunodeficiency frequently associated with recurrent respiratory infections due to impaired mucosal immunity. E-cigarette or vaping-associated lung injury (EVALI) is an emerging cause of acute lung injury characterized by lipid-mediated alveolar inflammation and diffuse lung injury. We describe the synergistic effects of vaping-related injury and underlying immunodeficiency as contributors to severe pulmonary infection. Description A 24-year-old man with childhood asthma and recurrent pneumonias presented with pleuritic chest pain, productive cough, and fever following a recent transition from cigarette smoking to heavy vaping (approximately 3,000 puffs per week). On presentation, he was febrile, tachypneic, and hypoxemic, requiring supplemental oxygen. Chest CT revealed left lower-lobe necrotizing consolidation with a loculated pleural effusion. Serum immunoglobulin testing demonstrated selective IgA deficiency. Empiric intravenous piperacillin-tazobactam and vancomycin were initiated. Interventional radiology placed a pleural drain, and pleural fluid analysis was consistent with empyema (glucose 20 mg/dL, LDH 3,000 U/L). Initial cultures were negative. Despite antibiotics and intrapleural fibrinolytic therapy (tPA and dornase alfa), his respiratory failure progressed, necessitating endotracheal intubation. On hospital day 11, he underwent video-assisted thoracoscopic surgery (VATS) with decortication. During single-lung ventilation, he developed refractory hypoxemia and was placed on veno-venous extracorporeal membrane oxygenation (VV-ECMO). Next-generation sequencing (MicroGenDx) of pleural fluid identified Paenibacillus lautus, Fusobacterium necrophorum, Streptococcus intermedius, Parvimonas micra, and Fusobacterium periodonticum, consistent with a polymicrobial anaerobic infection, possibly secondary to aspiration. Bronchoalveolar lavage cytology demonstrated numerous lipid-laden macrophages, consistent with EVALI. Following surgical source control, he completed a two-week course of targeted antibiotics (amoxicillin-clavulanate and doxycycline). His course was complicated by deep venous thromboses in the right femoral and left brachial veins, managed with anticoagulation. He was successfully weaned from ECMO on day 16, extubated the following day, and discharged home on day 19 with full clinical and radiographic recovery. Discussion This case highlights the potential synergistic impact of selective IgA deficiency and vaping in the development of severe necrotizing pneumonia and empyema. Impaired mucosal immunity may amplify the inflammatory and infectious consequences of vaping-related lung injury, predisposing to infection and respiratory failure. Early recognition of refractory infection, prompt surgical source control, and multidisciplinary management—including ECMO—were critical to our patient’s survival. Clinicians should consider immunodeficiency and vaping exposure in young adults with fulminant pneumonia, and public health efforts must continue to emphasize the pulmonary risks of vaping, particularly among vulnerable populations. This abstract is funded by: None