Abstract In coccidioidomycosis-endemic regions, eosinophilic pneumonia (EP) may closely mimic pulmonary coccidioidomycosis, both clinically and radiographically. We report a case of coccidioidomycosis masquerading as EP. A 47-year-old male was admitted with a four-week history of cough, fever, and pleuritic chest pain. Imaging revealed multifocal ground-glass opacities and a predominant right upper lobe consolidation. Initial testing showed the following: WBC of 13.6 K/uL H with neutrophils 9.51 K/uL H, lymphocytes 2.18 K/uL, monocytes 1.17 K/uL H, eosinophils 0.64 K/uL H, basophils 0.05 K/uL, and immature granulocytes 0.08 K/u, negative coccidioidomycosis EIA IgM, indeterminate IgG, CF 1:2, and negative β-D-glucan. Despite broad-spectrum antibiotics and fluconazole, fevers persisted. BAL demonstrated 42% eosinophils, raising concern for acute eosinophilic pneumonia; corticosteroids were deferred due to high clinical suspicion for coccidioidomycosis based on imaging. The patient was discharged on fluconazole with pending BAL Cocci EIA, sputum fungal culture, and serum IgE, with pulmonary and ID follow-up. BAL Cocci EIA was not detected, serum IgE was elevated at 639 IU/mL, but sputum fungal culture grew coccidioidomycosis. Chronic EP and coccidioidomycosis can both manifest with weeks to months of cough, pleuritic pain, fatigue, night sweats, and weight loss. The key distinction between chronic EP and coccidioidomycosis lies in their underlying causes—coccidioidomycosis spore inhalation in endemic regions versus elevated IgE levels and eosinophilia in serum or BAL for EP.1,2 Radiographically, EP shows diffuse bilateral ground-glass opacities with interlobular septal thickening—such as a batwing pattern—predominantly involving the peripheral and middle-to-upper lobes.3 In contrast, coccidioidomycosis often demonstrates focal lobar consolidation, nodules, cysts, or cavitation. Hilar lymphadenopathy or pleural effusion may occur in either condition but tends to be more frequent in coccidioidomycosis.4 Diagnostic differentiation relies on identifying eosinophilia (25%) in bronchoalveolar lavage fluid without detectable pathogens in EP versus positive serology, culture, or histopathology confirming Coccidioides infection in CM, along with a thorough history of environmental exposures and travel. Given the patient’s imaging findings and history of residence in an endemic region, deferring corticosteroid therapy was appropriate despite negative laboratory results, as corticosteroid use could have exacerbated underlying coccidioidomycosis. In conclusion, distinguishing between EP and coccidioidomycosis requires a thorough clinical evaluation, including travel history, laboratory tests, and imaging studies, given that the first-line treatment for EP is steroids, which may further exacerbate coccidioidomycosis. This abstract is funded by: none
Brown et al. (Fri,) studied this question.