Case Presentation: This patient was a 32 year old male with one week of fevers, coughing, and shortness of breath. On examination, the patient was tachycardic with an oxygen saturation of 85%. He had increased work of breathing with accessory muscle use, but no crackles or wheezing. Complete blood count showed leukocytosis. CT angiogram showed ground glass opacities with subpleural sparing in both lungs and enlarged mediastinal and hilar lymph nodes. Bronchoscopy was unremarkable. Bronchoalveolar lavage (BAL) showed clusters of reactive bronchial cells and alveolar macrophages. The patient was thought to have pneumonia and was started on antibiotics.A few days after the initiation of antibiotics the patient had mild improvement, but continued to desaturate as low as 80% with ambulation. By this time, all BAL studies had come back negative for signs of microorganisms. Other etiologies of the patient’s condition were considered; including hypersensitivity pneumonitis (HP). Upon further questioning, the patient revealed his apartment building had two episodes of flooding in the past year, and was now crowded with rat carcasses and mold. Prednisone was started for suspicion of HP given his living situation and CT findings. He showed considerable improvement and was discharged on a prednisone taper.

Discussion: Diagnosis of HP is made using a combination of diagnostic tests and history of antigen exposure. There is no gold standard test for HP but, the diagnosis can be supported with evidence from other studies. Examples include pulmonary function tests with a restrictive pattern, a CT showing diffuse ground glass opacities, or BAL with a lymphocytic predominance. Serum antibodies to specific antigens known to cause HP can also be obtained. BAL is highly sensitive for HP and will often show a lymphocytosis greater than 20%. Lymphocytosis is seen in up to 83% of patients with HP that undergo BAL. While highly sensitive, this finding is non-specific and may occur in other interstitial lung diseases. BAL can also show increased neutrophils in the acute phase. It is a common misconception that BAL will show eosinophilia, however this finding is more consistent with eosinophilic pneumonia. Ground glass opacities on CT are also commonplace in HP, occurring in 34-68% of cases. The characteristic appearance of HP on CT is diffuse ground glass or nodular opacities in the upper and middle lungs with signs of air trapping.HP is usually associated with occupational exposures, but can also be triggered by home exposures such as mold, rats, or water reservoirs. HP is often first treated as pneumonia or COPD and is refractory to standard therapy for these conditions, prompting further investigation into the patient’s illness. While occupational exposures are often elicited during initial history-taking for patients with respiratory symptoms, domestic exposures are increasingly implicated in HP. Important exposures to ask about include mold, flooding, bird droppings or feathers, saw dust, hot tub or sauna use, electronic cigarette use, and heroin inhalation.

Conclusions: Hypersensitivity pneumonitis is diagnosed using pulmonary function tests, chest CT, bronchoalveolar lavage, and serum antibodies to known HP antigens. Clinical signs of HP can look similar to a number of other lung pathologies, and it is important to consider other diagnoses when a patient has minimal improvement following treatments for pneumonia or COPD. When considering HP it is important to ask about occupational and domestic exposures during initial history-taking.