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A5210 - Invasive Aspergillosis in a Seemingly Immunocompetent Host
Author Block: J. L. Miely1, A. Doyle2, A. J. Gamino2; 1Pulmonary and Critical Care, Rush University Medical Center, Chicago, IL, United States, 2Pulmonary Critical Care, Rush University Medical Center, Chicago, IL, United States.
Introduction:
Aspergillus is a ubiquitous mold, with airborne spores regularly inhaled into the lower respiratory tract. In an immunocompetent host, Aspergillus is most often a benign pathogen, eliminated from the airway by mucociliary clearance and humoral immunity. When spores become pathogenic, patients can develop pulmonary aspergillosis, manifesting as a spectrum of diseases depending on the host’s immune response and underlying lung disease. Classically, invasive aspergillosis is found in immunocompromised patients, especially those with solid organ or stem cell transplants, or profound neutropenia, but may manifest in an immunocompetent patient with other risk factors for local immunosuppression, including use of inhaled corticosteroids (ICS).
Case:
A 69-year-old male with history of asthma presented with a productive cough and dyspnea. He denied fever, weight loss or hemoptysis. Social history was notable for employment in the coal ash industry, with exposure to arsenic and silica. The patient was started on fluticasone intranasal spray, oral antihistamine, oral omeprazole and high-dose fluticasone/salmeterol inhaler. On follow-up, he had pulmonary function testing (PFTs) showing a mild obstructive defect, without bronchodilator response. Given persistent symptoms and history of environmental exposure, CT chest was obtained and demonstrated irregular wall thickening of the right upper lobe (RUL) bronchus with moderate stenosis and complete obstruction in the right anterior segmental bronchus with post-obstructive changes. He underwent bronchoscopy showing significant stenosis at the takeoff of the right upper lobe bronchus with extensive mucous plugging. Balloon dilation was performed, allowing RUL endobronchial biopsies, brushings and BAL to be obtained. Histologic specimen showed rare fungal hyphae, endobronchial cultures grew rare Aspergillus, and BAL galactomannan antigen was elevated at 7.85. The patient was started on oral voriconazole, and at the time of follow up, had significant clinical and radiographic improvement. He subsequently completed a 6-month course.
Discussion:
This case highlights the importance of a thorough diagnostic workup. Although the patient was not classically immunocompromised, his PFT and CT findings were concerning for a severe lung pathology, confirmed to be Aspergillus on culture and biopsy. His use of an ICS made him locally and possibly systemically immunosuppressed, inhibiting the clearance of Aspergillus spores, leading to local inflammation and predisposing him to infection. In a small cohort of patients, ICS have been shown to act as potential risk factors for pulmonary aspergillosis. Fluticasone especially carries this risk due to its potency and prolonged tissue concentrations. Uncommon infectious etiologies in an immunocompetent host on chronic ICS must be considered.