Introduction: Bird fancier’s lung is a form of hypersensitivity pneumonitis caused by a non-atopic immunologic response to the inhalation of avian antigens. Although it is the most common type of hypersensitivity pneumonitis in adults, it is rarely diagnosed in the pediatric population. Case Report: A 17-year-old male with intermittent asthma presented with chronic cough, progressively worsening shortness of breath, joint pain and swelling in his wrists and knees, and night sweats. Eight months prior to presentation he had been diagnosed with pneumonia and had lost 24 pounds since that time. His family, including his mother, sister, and several dogs, cats, goats, and parrots, had moved into a mobile home shortly after he was treated for pneumonia. Significant findings on examination included 82% oxygen saturation in room air, cachectic appearance, diaphoresis, shortness of breath at rest, crackles in the bilateral lung bases, right knee edema and tenderness with active/passive motion, and bilateral clubbing of all fingers and toes. He was placed on 4 liters nasal cannula and his saturation increased to 93%. Labs were significant for elevated ESR, LDH, ANA, anti- CCP, and serum IgG. T-spot, induced sputum for TB, HIV, cryptosporidium, legionella, and uric acid were negative. A hypersensitivity pneumonitis panel (including Chlamydophila psittaci) was negative. Chest x-ray was unremarkable, but CT chest showed a diffuse centrilobular pattern of interstitial lung disease. Spirometry showed severely low FEV1 and FVC with normal FEV1/FVC ratio and moderately decreased DLCO. He was treated empirically with IV pulse steroids and was quickly able to wean off supplemental oxygen. Following a 6-week steroid taper his PFT results improved significantly but he continued to have evidence of restrictive lung disease. Discussion: Given chronic cough, weight loss, night sweats, and hypoxemia, there was initial concern for HIV, tuberculosis, or malignancy. His knee and wrist pain/edema as well as elevated ANA and anti-CCP raised concern for autoimmune processes. However, further laboratory testing for these conditions was negative. Chest CT showed evidence of interstitial lung disease, and pulmonary function testing confirmed restrictive lung disease, likely hypersensitivity pneumonitis or avian-related illnesses. Upon further discussion, the patient revealed that his parrots had been in a cage next to the AC unit, which blew directly into his bedroom. Due to his improvement after steroid administration and his significant bird exposure, he was diagnosed with bird fancier’s lung. Conclusion: This patient’s broad constellation of nonspecific symptoms made establishing an initial diagnosis challenging. In fact, his exposure to parrots was not initially identified upon admission, highlighting the importance of taking patient exposures into consideration. Further, this case demonstrates the difficulty of establishing a diagnosis of hypersensitivity pneumonitis through laboratory testing alone, as specific antigens were not identified with serum testing.

Diffuse centrilobular pattern of interstitial lung disease with some sparing at the lower lobes.

Lungs with increased perihilar interstitial markings and peribronchial thickening bilaterally.