BIRD FANCIER'S DISEASE: A CASE OF HYPERSENSITIVITY PNEUMONITIS

Abstract

TOPIC: Occupational and Environmental Lung Diseases TYPE: Medical Student/Resident Case Reports INTRODUCTION: The immunologic lung disease through inhalation and sensitization of an aerosolized antigen is termed hypersensitivity pneumonitis (HP). Here we describe a case of HP from exposure to avian antigen. CASE PRESENTATION: A 42 y/o F presented with progressively worsening dyspnea at rest & exertion, pleuritic chest pain, dry cough for past 2 months. She denied sick contacts or recent travel. On exam BP: 122/76mmHg, HR 107bpm, RR 30bpm, SpO2 82% on room air. Physical exam, significant for b/l crackles. Labs: WBC 16.33 k/mm3, ABG PaO2 of 45mmHg. CXR showed b/l airspace opacities & CT-thorax showed b/l diffuse GGO. ECHO showed LVEF 55% with normal global systolic function with mildly elevated PASP. Treatment was initiated with hi-flo oxygen and her SpO2 improved to 97%. QuantiFERON Gold, urine legionella, Mycoplasma IgM, and respiratory multiplex viral panel were negative. Cardiac CT revealed patent coronaries. Spirometry revealed severe restrictive ventilatory defect. Further questioning revealed that patient got parakeets a few months prior to onset of symptoms. She was then started on methylprednisolone for possible HP. Bronchoscopy with BAL and transbronchial biopsies showed no bacterial/fungal/viral growth. Cytology was unremarkable and biopsies revealed mild inflammatory changes with lymphocytes and aggregates of intralaveolar foamy macrophages. The CD4:CD8 ratio was 0.89. Patient clinically improved with steroid therapy and gradually weaned from supplemental oxygen. She was discharged on oral prednisone with close follow up where she continued to improve after removal of her parakeets DISCUSSION: HP an immune-mediated response from repeated inhalation, sensitization, & hyperresponsiveness to various organic particles which can be mammalian or avian proteins, fungi, bacterial, or chemicals. Based on duration of exposure & symptoms onset, HP can be divided into acute, subacute, or chronic. Acute HP presents as flu-like illness, subacute HP has insidious onset of symptoms, dyspnea on exertion or reduced exercise capacity. Physical exam reveals inspiratory crackles. Imaging usually demonstrates GGO, mosaic attenuation and centrilobular nodules. BAL reveals lymphocytic predominant cells with CD8 alveolitis. Histopathology usually demonstrates cellular bronchiolitis with predominant lymphocytic or plasmocytic infiltrates. It can also present as interstitial mononuclear infiltrates or loosely-formed granulomas. Treatment for HP is avoidance of antigen exposure. Role of steroids in treating HP is not well known, however general practice is slow tapering steroid regimen for about 3-6 months duration. Prognosis is usually good with complete recovery in most patients; a few may progress to chronic fibrosing HP. CONCLUSIONS: A high level of suspicion should be present in diagnosing HP with a thorough history and prompt management must be initiated to prevent progression of disease. REFERENCE #1: Selman M, Pardo A, King TE Jr. Hypersensitivity pneumonitis: insights in diagnosis and pathobiology. Is J Respir Crit Care Med. 2012; 186:314-24. REFERENCE #2: Costabel U, Bonella F, Guzman J. Chronic hypersensitivity pneumonitis. Clin Chest Med. 012; 33:15163. REFERENCE #3: Camarena A, Juárez A, Mejía M, Estrada A, Carrillo G, Falfán R, Zuñiga J, Navarro C, Granados J, Selman M. Major histocompatibility complex and tumor necrosis factor-alpha polymorphisms in pigeon breeder's disease. Am J Respir Crit Care Med. 2001;163:1528-33. DISCLOSURES: no disclosure on file for Jagadish Akella; No relevant relationships by Alex Diaz, source=Web Response no disclosure on file for Iqbal Javed; No relevant relationships by Raghavendra Sanivarapu, source=Web Response