C69-10 When Hemoptysis Hides a Parasite: Strongyloides Stercoralis Induced Diffuse Alveolar Hemorrhage

Abstract Introduction Evaluation of suspected diffuse alveolar hemorrhage (DAH) requires detailed history, careful examination, and a comprehensive workup to ensure timely diagnosis and treatment. We present a case of DAH secondary to Strongyloides infection—a rare but important consideration in the right clinical context. Case Presentation A 76-year-old Puerto Rican man with recently diagnosed focal segmental glomerulosclerosis (FSGS) on prednisone 50 mg daily and prophylactic apixaban, hypertension, hypothyroidism, type 2 diabetes, nonischemic cardiomyopathy, and prior traumatic brain injury with subarachnoid hemorrhage presented with diarrhea and black, tarry stools.He developed worsening encephalopathy and hypoxemia, leading to postponement of planned endoscopy. Chest X-ray revealed patchy right upper-lobe opacities. Broad-spectrum antibiotics were started, and pulmonary consultation was obtained.On evaluation, he was somnolent, arousable only to stimuli, requiring high-flow nasal cannula (55 L/min, FiO2 85%). Physical exam showed coarse bilateral breath sounds without wheezing and no peripheral edema. CT angiography was performed, and he was transferred to the MICU for intubation and diagnostic bronchoalveolar lavage (BAL).BAL revealed findings consistent with DAH, prompting pulse-dose corticosteroids. Extensive infectious workup, including urine antigens for Legionella and Streptococcus pneumoniae, as well as influenza, COVID-19, and RSV testing, was negative. Laboratory evaluation and BAL analyses demonstrated the key findings described below. Strongyloides larvae were identified on stain, and ivermectin was initiated.Steroids were tapered from methylprednisolone 1 mg/kg/day to his maintenance prednisone dose of 50 mg daily. Although successfully extubated, his mental status remained poor. Serial BALs continued to reveal Strongyloides larvae; albendazole was added to aid eradication and for improved CNS penetration. Despite treatment, his condition deteriorated, and he was transitioned to comfort care. Discussion We presume the patient had asymptomatic Strongyloides infection for years, with reactivation after being started on intravenous methylprednisolone followed by oral prednisone for a recent diagnosis of FSGS. This allowed uncontrolled proliferation of the larvae, leading to Strongyloides hyperinfection syndrome, a condition classically associated with glucocorticoid use. Our patient demonstrated both pulmonary and gastrointestinal involvement, consistent with increased larval migration. In this case, timely recognition of the infectious process, initiation of anti-helminthic therapy and reduction in immunosuppression unfortunately did not prevent death from Strongyloides hyperinfection syndrome. Conclusion Management should be adjusted promptly and guided by clinical suspicion. Strongyloides infection should ideally be screened for prior to initiating immunosuppressive therapy and, if not previously done, must be considered in any patient presenting with diffuse alveolar hemorrhage (DAH) who is immunocompromised and coming from an endemic region. This abstract is funded by: None