Silent Siege: Histoplasmosis-induced Fibrosing Mediastinitis in an Adolescent: A Case Report and Literature Review

To the Editors: A 16-year-old previously healthy male was readmitted with recurrent fevers, weight loss, night sweats and pleuritic chest pain 1 month after treatment for presumed pneumonia. Initial imaging showed right lower lobe consolidation and bulky calcified hilar lymphadenopathy. Serology was positive for Histoplasma capsulatum immunoglobulin G and elevated yeast complement fixation titers (1:64), consistent with prior infection. Despite outpatient antibiotics, he continued to decline, additionally developing oropharyngeal thrush and erythematous patches on his palms and soles. Repeat chest computed tomography (CT) revealed right mediastinal lymphadenopathy encasing the right intermediate bronchus, a large loculated pleural effusion, and a right mediastinal abscess. Biopsy showed dense fibrosis with necrosis and yeast forms consistent with H. capsulatum, suggestive of fibrosing mediastinitis (FM) (Fig. 1). Culture of the mediastinal mass grew Eikenella corrodens and Fusobacterium nucleatum, raising concern for fistula formation. However, this was ruled out by esophagram and bronchoscopy, which confirmed extrinsic compression of the bronchus intermedius.FIGURE 1.: Histopathologic findings. (A) Low power view of dense fibrotic tissue with chronic lymphocytic inflammation. (B) High power view of lymphocytic infiltration with fibrosis. (C) Acellular necrotic debris with microcalcifications. (D) Biopsy of mediastinal mass after GMS staining. The arrow is highlighting rare yeast-like structures, with a morphology suggestive of Histoplasma. GMS indicates Grocott–Gömöri’s methenamine silver stain.Despite nonsteroidal anti-inflammatory drug therapy, his respiratory status worsened, requiring corticosteroids. Pulmonary function tests revealed a restrictive pattern (forced expiratory volume1 58%, forced vital capacity 61%), attributed to pleuritic pain. He also developed bilateral lower extremity edema requiring daily furosemide. Concern for pulmonary hypertension and secondary right heart failure led to a CT angiogram, which revealed narrowing of the right pulmonary vein due to calcified lymph node compression. He was treated with prednisone and a 12-week course of itraconazole. At follow-up, he reported symptom improvement, and imaging noted a decrease, but persistent, calcified mediastinal mass size. FM is a rare and potentially debilitating sequela of histoplasmosis, resulting from an exaggerated immune response that causes invasive fibrosis of mediastinal structures.1,2 Although H. capsulatum infection is common in the central and eastern United States, FM occurs in only about 1 in 100,000 cases, with most reported in adults3,4 Pediatric presentations are exceedingly rare with a paucity of examples documented in the literature. This condition often mimics other thoracic diseases, leading to diagnostic delays.5 FM may involve vital structures such as the airways, pulmonary vessels, and esophagus1,3,4 Contrast-enhanced CT is the modality of choice, typically revealing calcified mediastinal masses.1,5 In our case, serologies supported the diagnosis, and biopsy-confirmed fibrosis further strengthened it. The patient’s empyema with oral flora raised suspicion for fistulization, though further testing ruled it out. Instead, microabrasions from the mass may have allowed bacterial translocation into the thoracic cavity. Currently, no standard treatment guidelines exist for FM. Most literature concludes that corticosteroids and antifungals do not alter the disease course and are not indicated.1,2,4 However, the choice to administer corticosteroids was aimed at addressing the hyperinflammatory state, while antifungal therapy was given due to his positive serologies. While it is unclear if the steroid taper was the nidus for clinical improvement, our patient’s clinical and radiographic improvement after treatment suggests that these therapies may have therapeutic value in acute FM presentations. Given FM’s potential for life-threatening complications, clinicians in endemic areas should maintain a high index of suspicion in pediatric patients with persistent pulmonary symptoms and a history of histoplasmosis.