Case Presentation:

This is a 28–year–old male with history of Type 1 diabetes, polysubstance abuse and childhood asthma who was admitted for complaints of fatigue, night sweats and bilateral pleuritic chest pain that had been persisting for a few days prior to admission. He denied any cough, high fevers, chills, or shortness of breath that limited his physical activities. He denied any recent travel, sick contacts, new pets or any new medications. He denied any change in his home or work environment. Initial vitals showed low grade fever of 38.2, moderate tachycardia of 130 and physical examination was remarkable for diminished breath sounds on chest ausculation, bilateral chest wall tenderness on palpation of lower ribs in anterior axillary plane, and tenderness to palpation of lower abdomen. Initial labs were significant for moderate leukocytosis with severe eosinophilia. Chest x–ray showed patchy bilateral infiltrates. Blood and urine cultures were sent. Empiric IV antibiotics were started for the initial diagnosis of community acquired pnuemonia. Computed tomography (CT) of chest was performed to evaluate x–ray findings and showed groundglass opacities, predominantly in upper and right middle lobes. All his cultures were negative as were the serologies for aspergilus, histoplasmosis and legionella. Based on the moderate leucocytosis with severe eosinophilia of nearly 50% on the peripheral smear and CT findings, presumed diagnosis of CEP was made. He was placed on 40 mg of oral prednisone daily. His eosinophila and CT chest findings improved dramatically over the next 72 hours. He was discharged on long steroid taper. Discussion: CEP is characterized by idiopathic accumulation of eosinophils in the lung. Patients often present with a subacute illness that have a myriad of symptoms including cough, fever, breathlessness, weight loss, wheezing, and night sweats. Often asthma preceeds or subsequently develops in half of these cases. CT chest findings of bilateral peripheral opacities described as “photographic negative”of pulmonary edema in the setting of peripheral blood eosinophilia >25% are diagnostic. Therapy typically involves long course of steroids until infiltrates resolve on the radiological scans. Although optimal duration of therapy is unknown, most patients require treatment >6 months. Untreated, CEP may lead to chronic pulmonary fibrosis and pulmonary hypertension.

Conclusions:

This case shows that CEP may masquerade as a community acquired pneumonia. Appropriate vigilance for the telltale signs and rapid initiation of steroids may lead to complete cure and prevent long term damage.