Case Presentation: A 41-year-old healthy male presented to emergency department with cough and shortness of breath. Shortness of breath and cough was gradually progressive over one week, worsening with exertion. Cough is dry with no known aggravating factor. He denied fever or wheezing. No history of active or passive cigarette smoking, sick contact, recent travel, personal or family history of asthma or atopy. He has been working in a hay farm for more than a year. At presentation he was tachycardic (HR 110/min), tachypneic (RR 24/min), his oxygen saturation was 82% on room air and he required high-flow nasal cannula to maintain oxygen saturation > 92%. He was afebrile and blood pressure was normal. On examination of lungs there was decreased breath sounds at lung bases bilaterally; cardiac, abdominal and neurological examinations were normal. Laboratory tests showed leukocytosis (WBC-13,700/uL) with neutrophilic predominance, CRP elevated to 11, basic metabolic panel, liver function tests were normal. X-ray of chest showed diffuse bilateral ground-glass opacities, CT scan without contrast showed extensive areas of ground-glass opacities with diffuse interstitial thickening and air containing cysts within both lung fields. Differential diagnosis including hypersensitivity pneumonitis, multifocal community acquired pneumonia, atypical pneumonia was considered. Hypersensitivity pneumonitis panels including Micropolyspora faeni antibody and aspergillus antibody were sent. He was started on ceftriaxone and azithromycin and intravenous steroids (methylprednisolone 40 mg). S. pneumoniae antigen, legionella antigen, sputum culture was unrevealing. On the 3rd day Micropolyspora faeni antibody was positive which strongly suggested hypersensitivity pneumonitis. Antibiotics were discontinued and he was continued on steroids. Oxygen requirement subsequently improved and he was discharged with short term tapering dose of oral steroid.
Discussion: Hypersensitivity pneumonitis is an immune mediated granulomatous interstitial lung disease which develops after exposure to an antigen in susceptible individuals. It is a very rare condition with incidence between 0.3 to 0.9 per 100,000 individuals. Based on radiological and/or histopathological evidence of fibrosis it is classified as fibrotic and non-fibrotic. Prognosis is worse in those with fibrotic type. Diagnosis is confirmed with clinical features, CT finding, serum IgG antibody testing against potential antigens and bronchoalveolar lavage. In some cases, lung biopsy may be needed. Management is typically steroid for non-fibrotic and immunosuppressants like mycophenolate or azathioprine for fibrotic. In our patient we did not perform BAL as clinical suspicion was very high and the patient improved significantly with steroid.
Conclusions: This case highlights the importance of careful and thorough history to reveal the possibility of a temporal relationship between environmental exposure and onset of symptoms. Many patients should proceed to BAL but strong clinical suspicion, suggestive CT scan of lungs and positive serum IgG testing against potential antigens are sufficient to initiate the treatment for hypersensitivity pneumonitis.
