Pulmonary adiaspiromycosis is a rare fungal infection caused by Emmonsia crescens or E. parva, saprophytic soil fungi that, upon inhalation, form non-replicating adiaspores within the lung parenchyma. These structures elicit a granulomatous response, leading to a clinical spectrum that ranges from subclinical presentations to acute respiratory failure [1].

In their landmark review, Anstead et al. [2] compiled 22 well-documented cases of human adiaspiromycosis worldwide, highlighting its occurrence in both immunocompetent and immunocompromised hosts. Diagnosis was most commonly based on lung biopsy, with histopathological identification of characteristic adiaspores. Fungal cultures were negative in most cases, and treatment strategies varied, including conservative management, corticosteroids, and antifungal therapy with heterogeneous outcomes.

Since that publication, no additional human cases with definitive histological findings have been reported. However, experimental murine models have demonstrated adiaspores up to 50μm in diameter with trilaminar walls, reinforcing their diagnostic value [3]. Moreover, adiaspores have been identified in road-killed armadillos in Brazil, supporting the hypothesis of wild animal reservoirs with potential zoonotic implications [4].

We report the case of a 62-year-old woman evaluated for progressive respiratory insufficiency. Chest imaging revealed a bilateral reticulonodular interstitial pattern with mediastinal and hilar lymphadenopathy (Fig. 1A). A surgical lung biopsy demonstrated non-necrotizing granulomas containing spherical thick-walled structures that stained positive with PAS and Grocott, consistent with adiaspores, without evidence of necrosis or fibrosis (Fig. 1B and C). Both microbiological work-up and fungal cultures were negative – a frequent finding in this entity, where diagnosis often relies solely on histology [2]. The patient had no history of immunosuppression or exposure to known reservoirs, such as wild rodents or rural environments.

Fig. 1.

(A) Chest CT showing bilateral reticulonodular interstitial infiltrates with mediastinal and hilar lymphadenopathy. (B) Non-necrotizing pulmonary granuloma with thick-walled spherical structures (he matoxylin–eosin, 20×). (C) Grocott stain showing adiaspores with thickened walls, without endosporulation (10×).

Initial treatment consisted of combined corticosteroids and itraconazole. Due to clinical persistence, infliximab was added but later discontinued following suspected drug-associated myocarditis. The patient's clinical course subsequently improved with tapering doses of corticosteroids alone.

Although rare, adiaspiromycosis should be considered in the differential diagnosis of granulomatous interstitial lung diseases when large spherical structures without endosporulation are identified. Diagnostic confirmation typically relies on histological examination, as cultures are seldom positive [2]. Treatment recommendations remain undefined, with literature supporting an individualized approach using corticosteroids and antifungals (amphotericin B, azoles) according to clinical severity and response.