Chronic eosinophilic pneumonia, or CEP, occupies a distinctive niche in pulmonary medicine. The disease is characterized by dense infiltration of the lung parenchyma by eosinophils, the white blood cells best known for fighting parasites and driving allergic reactions. It typically strikes middle-aged adults, shows a marked female predominance, and is strongly linked to asthma and atopic disease, with up to two-thirds of patients carrying a history of asthma before the lung disease declares itself. Clinically, CEP follows a subacute to chronic course, unfolding over weeks to months with cough, progressive shortness of breath on exertion, and constitutional symptoms such as weight loss and fatigue. The classic radiological picture is equally recognizable: bilateral consolidations and ground-glass opacities clustered at the periphery of the lungs, hugging the pleural surface in a pattern that experienced radiologists can spot from across the reading room.

The diagnostic architecture of CEP rests on a tripod of findings. Because no universally accepted diagnostic criteria exist, clinicians generally require a compatible subacute clinical course, characteristic peripheral-predominant pulmonary infiltrates on imaging, and evidence of eosinophilic inflammation, either in the blood or in bronchoalveolar lavage fluid, while systematically excluding secondary causes of pulmonary eosinophilia such as drugs, parasites, and systemic autoimmune disease. In typical cases, the lavage findings are dramatic. BAL eosinophilia is usually marked, often reaching 40 percent or more of the recovered cells, and peripheral blood eosinophil counts commonly exceed 1,000 cells per microliter. When the clinical picture, the imaging, and the cellular evidence all align, lung biopsy is generally considered unnecessary, reserved for the minority of cases in which features are atypical or inconclusive. That reserve clause, as this case demonstrates, is where diagnostic danger lives.

The patient at the center of the report was a 61-year-old ex-smoker who arrived with two months of progressively worsening breathlessness on exertion and two weeks of a productive cough that would not relent, accompanied by weight loss. His medical history included asthma, managed with inhaled fluticasone furoate and vilanterol, along with type 2 diabetes treated with empagliflozin and metformin and hyperlipidaemia controlled with simvastatin for more than a decade. He reported no recent travel abroad and no consumption of raw or undercooked food, closing off the most common routes to parasitic lung infection. On examination, doctors heard bilateral fine inspiratory crackles but no wheezing, and they found none of the peripheral stigmata, purpura, mechanic’s hands, Gottron papules, Raynaud phenomenon, synovitis, or neurological deficits, that would suggest a connective tissue disease or vasculitis masquerading as lung disease.

Laboratory testing initially seemed to confirm the suspicion of CEP. The patient’s peripheral blood showed eosinophilia of 15 percent, corresponding to 1,314 cells per microliter, comfortably above the threshold commonly associated with eosinophilic lung disease. Chest radiography revealed bilateral peripheral patchy opacities with an upper-lobe predominance, and high-resolution computed tomography went further, demonstrating multifocal peripheral consolidations and ground-glass opacities with a subpleural predilection, along with traction bronchiectasis indicating that the process had been smoldering long enough to begin remodeling the lung’s architecture. Taken together, the subacute course, the blood eosinophilia, and the textbook peripheral distribution of disease made CEP the leading diagnosis on admission, and a reasonable one by any standard.

Then the bronchoscope told a different story. Bronchoalveolar lavage of the patient’s lung returned a cellular differential that was 85 percent neutrophils and only 6 percent eosinophils, a profile that belongs to bacterial pneumonia, not to eosinophilic lung disease. Autoimmune serology, including antinuclear antibody, proteinase 3-antineutrophil cytoplasmic antibody, and myeloperoxidase-antineutrophil cytoplasmic antibody, came back negative, and the total IgE level of 289 kU/L offered no signal of an allergic driver. Urinalysis showed neither haematuria nor proteinuria, and renal function was normal, further arguing against a systemic vasculitis. Confronted with neutrophil-predominant lavage fluid, the clinical team reasonably pivoted to an infectious explanation and initiated empirical treatment with amoxicillin and clavulanate. The antibiotics failed. Symptoms persisted, radiographic abnormalities did not budge, follow-up lavage microbiological cultures were negative, cytological examination identified no parasitic organisms, and stool examination for parasites was also unrevealing.

With the non-invasive pathway exhausted, the team turned to video-assisted thoracoscopic surgery, resecting a wedge of the left lower lobe for histopathological examination. What the pathologist found rewrote the case entirely. The tissue demonstrated an organizing pneumonia pattern, defined by intra-alveolar proliferation of fibroblastic foci, the plug-like clusters of immature connective tissue known as Masson bodies, accompanied by active immature fibrosis. Critically, woven through the interstitial and peribronchiolar regions was a prominent eosinophilic inflammatory infiltrate, with plasma cells and scattered lymphocytes in attendance. The alveolar architecture was relatively preserved, and, importantly, a blood vessel examined in the specimen showed an intact wall with no histological evidence of vasculitis, excluding one of the most dangerous mimics. Integrating the clinical course, the peripheral eosinophilia, the radiological findings, the histopathological features, and a thorough assessment for secondary causes, the physicians made the diagnosis of chronic eosinophilic pneumonia.

Treatment followed the established playbook for CEP. Intravenous methylprednisolone was commenced at 40 milligrams daily, a dose equivalent to prednisolone at 1 milligram per kilogram of body weight per day, then converted to oral methylprednisolone before discharge and gradually tapered over approximately two months. The response was swift and convincing. Symptoms improved progressively, and a chest radiograph obtained after roughly one month of corticosteroid therapy showed resolution of the bilateral peripheral opacities that had dominated the initial films. The trajectory underscores why making the correct diagnosis matters so much: corticosteroids, which are useless against bacterial pneumonia and potentially harmful, are precisely the right weapon against CEP, and delays in reaching the diagnosis translate directly into prolonged symptoms and unnecessary exposure to antibiotics.

The case’s most instructive twist lies in what the lavage fluid did and did not reveal. Although BAL eosinophilia is usually prominent in CEP, the authors note that considerable variability has been reported across published series, with eosinophil proportions ranging from as low as 12 percent to as high as 95 percent. There is a technical reason for this scatter: bronchoalveolar lavage samples only a limited portion of the distal airways and alveolar compartment, a tiny and possibly unrepresentative window onto a patchy disease process. A normal or atypical BAL differential, the authors emphasize, does not exclude microscopic abnormalities elsewhere in the lung tissue. The cellular profile of lavage fluid should therefore be interpreted in conjunction with the clinical and radiological findings rather than wielded in isolation, and when the lavage results clash with the broader picture, surgical lung biopsy may be justified in selected patients to establish the diagnosis definitively.

The report also untangles a second source of confusion, the relationship between CEP and cryptogenic organizing pneumonia. The two conditions share several clinical and radiological features, including subacute respiratory symptoms, pulmonary consolidation, and ground-glass opacities, which can complicate their distinction even for experienced clinicians. Histologically, however, organizing pneumonia is a non-specific pattern of lung injury that may occur in a variety of pulmonary disorders, CEP among them. Although eosinophilic infiltration of the alveolar spaces and interstitium is the characteristic histopathological hallmark of CEP, foci of organizing pneumonia with intra-alveolar fibroblastic plugs may also be present within it. The presence of an organizing pneumonia pattern on biopsy, in other words, does not automatically signify cryptogenic organizing pneumonia. In this patient, the combination of that pattern with prominent eosinophilic infiltration, alongside compatible clinical, radiological, and peripheral blood findings, anchored the diagnosis firmly in eosinophilic territory. For clinicians navigating the eosinophilic lung diseases, the message is blunt: lavage fluid is a supporting witness, not the judge, and when the evidence conflicts, the tissue still holds the final word.

Subject of Research: Diagnosis of chronic eosinophilic pneumonia with atypical bronchoalveolar lavage findings and an organizing pneumonia pattern on lung biopsy

Article Title: Chronic Eosinophilic Pneumonia: A Diagnostic Challenge With Atypical Bronchoalveolar Lavage Findings and an Organizing Pneumonia Pattern

Article References: Chronic Eosinophilic Pneumonia: A Diagnostic Challenge With Atypical Bronchoalveolar Lavage Findings and an Organizing Pneumonia Pattern. (n.d.). https://doi.org/10.1002/rcr2.70780

Image Credits: AI Generated

DOI: 10.1002/rcr2.70780

Keywords: chronic eosinophilic pneumonia, bronchoalveolar lavage, organizing pneumonia, lung biopsy, eosinophilia, interstitial lung disease, corticosteroids, high-resolution computed tomography, cryptogenic organizing pneumonia, respiratory medicine, case report, differential diagnosis