SESSION TITLE: Diffuse Lung Disease SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 31, 2017 at 01:30 PM - 02:30 PM INTRODUCTION: Acute eosinophilic pneumonia (AEP), first described in 1989, is a rare disorder of accumulated eosinophils within lung interstitium and alveoli. The pathogenesis of this disease is not fully known and continued reporting of clinical cases is beneficial, including AEP in association with the mold, Phoma betae. CASE PRESENTATION: A 20 year old male smoker was admitted for community acquired pneumonia. He reported inhaled marijuana use, acquired from a stranger, the day before admission. Initial chest radiograph showed bilateral consolidations and he was noted to require 2 lpm supplemental oxygen. Broad spectrum antibiotics were initiated. Over the next 24 hours he developed rapidly progressive hypoxic respiratory failure and was transferred to the ICU for high flow oxygen. Physical examination revealed a febrile and tachycardic thin man with bilateral diffuse crackles and expiratory wheezing on lung auscultation. Initial laboratory data showed a leukocytosis with 3% eosinophils. A CT thorax revealed diffuse ground glass and tree-in-bud opacities with bilateral pleural effusions. A thoracentesis revealed a transudative fluid with 30% eosinophils. Serum IgE was 333 and a hypersensitivity pneumonitis panel was positive for Phoma betae. HIV, ANCA, galactomannan and fungitel were negative. Bronchoscopy showed 67% eosinophils with an otherwise negative infectious work up. Antibiotics were discontinued and he received pulse-dose steroids with rapid improvement of his hypoxia and symptoms. He was discharged on an extended prednisone taper over the following 2 months. He was seen at an outpatient follow up visit and was notably asymptomatic with repeat CT thorax demonstrating complete resolution of prior infiltrates. DISCUSSION: Acute eosinophilic pneumonia (AEP) causes diffuse alveolar damage with accumulation of eosinophils within interstitial and alveolar spaces typically leading to rapid hypoxic respiratory failure. It is hypothesized that AEP is an immune mediated reaction to antigens, leading to eosinophilic infiltration. There is a strong association with cigarette smoking and the development of AEP. Case reports following smoke inhalation from camp fires, burning buildings, and exposure to cigarette smoke after cessation have been described. There is a paucity of cases with regard to AEP and marijuana inhalation. P. betae is a mold which naturally grows on plants, including sugar beet leaves. It has also been shown to stimulate an IgE mediated reaction in susceptible individuals. Our patient tested positive for P. betae and had smoked marijuana from a new dealer prior to developing respiratory failure. CONCLUSIONS: It is probable the marijuana was grown or transported in an area with Phoma betae exposure with subsequent trigger of AEP. Reference #1: Allen JN, Pacht ER, Gadek JE, Davis WB. Acute Eosinophilic Pneumonia as a Reversible Cause of Noninfectious Respiratory Failure. New England Journal of Medicine. 1989;321(9):569-574. doi:10.1056/nejm198908313210903. DISCLOSURE: The following authors have nothing to disclose: Maureen McElligott, Joseph Carrington, Candace Huebert No Product/Research Disclosure Information