A Disorganized Case of Eosinophilic Pneumonia

Abstract Introduction: Chronic eosinophilic pneumonia (CEP) is a significant cause of lung disease characterized by peripheral eosinophilia, lung infiltrates, eosinophilia in bronchoalveolar lavage fluid (BAL), and eosinophilic infiltration in histology. These key features define CEP, but the condition can also present with varied manifestations, complicating diagnosis in atypical cases. We describe a case of CEP with atypical imaging and histological findings. Case Presentation: An 86-year-old man presented to the emergency department with weeks of worsening hypoxemic respiratory failure, dry cough, dyspnea, and fatigue following recent hospitalization for community-acquired pneumonia that had been unresponsive to antibiotics. Laboratory tests revealed peripheral eosinophilia at 1.9 K/uL, higher than previous admissions, with no signs of sepsis or active infection. Chest computed tomography (CT) showed progression of bilateral, upper-lobe-predominant alveolar opacities that were airway-oriented with pleural sparing and effusions (Figure 1A). Bronchoscopy revealed a normal tracheobronchial tree, and BAL cell count showed a total of 223/uL with 33% eosinophils. Cultures for bacteria, fungi, and parasites were negative, as were tests for serum strongyloides IgG, Fungitell, and Galactomannan. A transbronchial biopsy indicated an organizing pneumonia (OP) pattern without tissue eosinophils.Due to the combination of peripheral and BAL eosinophilia, progressive pulmonary infiltrates unresponsive to antibiotics, and a negative infectious workup, systemic steroids were initiated for presumed CEP. Prednisone was started at 1 mg/kg and tapered over two months. Follow-up imaging after six weeks demonstrated near-complete resolution of the pulmonary opacities and effusions (Figure 1B), along with improvement in symptoms and respiratory function. Discussion: CEP and OP can present similarly with subacute respiratory failure and pneumonia unresponsive to antibiotics. One distinguishing feature of CEP is the presence of serum and BAL eosinophilia. Histopathology often helps to differentiate these diseases; OP classically shows granulation tissue in alveoli and terminal bronchioles, whereas CEP is marked by eosinophilic infiltration of the alveolar spaces. However, eosinophils are not present in the tissue in up to 36% of CEP cases with BAL eosinophilia. In this case, the combination of peripheral and BAL eosinophilia with radiographic findings suggests CEP, despite OP-like histology. Pleural effusions are common in acute eosinophilic pneumonia but may be rare in CEP, which underscores the importance of considering CEP in pneumonia cases with peripheral eosinophilia. Conclusion: CEP can present with diverse clinical features, including OP-like findings. A high index of suspicion is necessary for accurate diagnosis in cases with peripheral eosinophilia and non-resolving pneumonia.