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Chronic Eosinophilic Pneumonia Masquerading as Non-resolving Upper Lobe Pneumonia

Source: PubMed Central Open Access, NCBI / U.S. National Library of Medicine

CureusLast synced 8/26/2026Status: syncedPMID: 42639625 pmidDOI: 10.7759/cureus.113372

Chronic eosinophilic pneumonia (CEP) is an uncommon, idiopathic respiratory disorder characterized by the accumulation of eosinophils in the lung parenchyma and alveolar spaces, often accompanied by peripheral blood eosinophilia. Clinically, it frequently presents insidiously with non-specific symptoms such as chronic cough, mimicking infectious pneumonias. In tuberculosis (TB)-endemic regions, upper lobe consolidations routinely anchor clinicians toward mycobacterial workups, resulting in profound diagnostic delays and inappropriate antibiotic use. While bronchoalveolar lavage (BAL) or lung biopsy remains the academic diagnostic gold standard, real-world practice demands clinical flexibility when patients decline invasive interventions. We describe the case of a 65-year-old male non-smoker with a history of diabetes mellitus and hypertension who presented with a one-year history of a waxing and waning chronic cough associated with migratory ("fleeting") pulmonary infiltrates. Due to persistent right upper lobe opacities, he underwent an extensive evaluation at a specialized TB center, which rigorously ruled out activevia negative serial sputum smears, molecular assays, and cultures. Subsequent high-resolution chest imaging revealed peripheral-predominant consolidations. Serial laboratory monitoring captured marked systemic peripheral blood eosinophilia (peak absolute eosinophil count: 3.8×10^9/L) and elevated serum immunoglobulin E (729 IU/mL), while systemic vasculitis, fun

Abstract

Chronic eosinophilic pneumonia (CEP) is an uncommon, idiopathic respiratory disorder characterized by the accumulation of eosinophils in the lung parenchyma and alveolar spaces, often accompanied by peripheral blood eosinophilia. Clinically, it frequently presents insidiously with non-specific symptoms such as chronic cough, mimicking infectious pneumonias. In tuberculosis (TB)-endemic regions, upper lobe consolidations routinely anchor clinicians toward mycobacterial workups, resulting in profound diagnostic delays and inappropriate antibiotic use. While bronchoalveolar lavage (BAL) or lung biopsy remains the academic diagnostic gold standard, real-world practice demands clinical flexibility when patients decline invasive interventions. We describe the case of a 65-year-old male non-smoker with a history of diabetes mellitus and hypertension who presented with a one-year history of a waxing and waning chronic cough associated with migratory ("fleeting") pulmonary infiltrates. Due to persistent right upper lobe opacities, he underwent an extensive evaluation at a specialized TB center, which rigorously ruled out activevia negative serial sputum smears, molecular assays, and cultures. Subsequent high-resolution chest imaging revealed peripheral-predominant consolidations. Serial laboratory monitoring captured marked systemic peripheral blood eosinophilia (peak absolute eosinophil count: 3.8×10^9/L) and elevated serum immunoglobulin E (729 IU/mL), while systemic vasculitis, fungal infections, and parasitic infestations were systematically excluded. Because the patient strongly declined a recommended diagnostic bronchoscopy with BAL, a pragmatic clinical-radiological diagnosis of CEP was established, and empirical oral corticosteroid therapy (prednisolone 30 mg daily) was initiated. The patient demonstrated an immediate, dramatic clinical resolution within 48 hours, followed by swift normalization of eosinophil kinetics and complete radiological regression of the pulmonary infiltrates within four weeks. This case underscores that a secure, definitive diagnosis of CEP can be safely achieved using longitudinal clinical, radiological, and kinetic laboratory surveillance when gold-standard invasive procedures are declined by the patient and that a rapid, robust therapeutic response to corticosteroids further validates this pragmatic approach once mimicking infectious and autoimmune etiologies are thoroughly excluded.

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