Abstract
Glucocorticoids have potent, pleiotropic effects on the immune system that can predispose patients to developing life-threatening invasive aspergillosis (IA). While the exact prevalence and attributable mortality of IA in glucocorticoid-treated patients is difficult to estimate, Aspergillus species are significant pathogens in patients that require prolonged high-dose glucocorticoid therapy including multiple myeloma, collagen vascular diseases, or recipients of solid organ/hematopoietic transplantation. Experimental animal models and autopsy series have revealed important differences in the pathology of aspergillosis between glucocorticoid-treated and neutropenic patients. Although neutropenic hosts develop infection characterized by extensive angioinvasion, hemorrhagic thrombosis and necrosis with a high fungal burden, glucocorticoid-immunosuppressed hosts present with infection dominated by extensive necrosis, less angioinvasion, and a lower fungal burden suggestive of an inflammation-driven pathology. These pathobiological differences may have important implications for the diagnosis and treatment approaches of IA in glucocorticoid-treated patients.