Endemic fungi share several key biologic and ecological characteristics that contribute to their pathogenicity in humans. All endemic fungi exhibit temperature-dependent dimorphism, meaning they can propagate as either yeast (single cells that reproduce by budding into daughter cells) or molds (multicellular filamentous fungi that reproduce through production of conidia or spores). At environmental temperatures (25-30°C [77-86°F]), H. capsulatum, B. dermatitidis, and C. immitis grow in the mold form producing 2- to 10-p.m round to oval shaped (Histoplasma and Blastomyces) or barrel-shaped (Coccidioides) conidia that are dispersed throughout the environment and in air currents. At physiologic temperatures, the conidia germinate into yeast (Histoplasma and Blastomyces) or in specialized cell forms called spherules (Coccidioides) that are resistant to killing by resident alveolar macrophages and neutrophils in the lung. Control of infection is mediated by the development of antigen-specific T-lymphocyte response that enhances macrophage fungicidal activity and formation of a granuloma to contain the fungus.5 Not surprisingly, patients with T-cell-mediated immune deficiency (e.g., AIDS patients and transplant recipients) or suppressed cellular immunity due to drug therapy (e.g., chemotherapy, high-dose corticosteroids, or tumor necrosis-a-blockers) are especially prone to severe reactivation of fungal disease.

FIGURE 84-1. Geographic localization of primary (endemic) fungi in the United States.

The most common route of infection for endemic fungi is the respiratory tract, where conidia aerosolized from contaminated soil are inhaled into the lung. Once in the lung, conidia are phagocytosed but not destroyed by resident macrophages and neutrophils in the alveoli and bronchioles. Within 2 to 3 days, conidia germinate into facultative yeast resistant to phagocytosis and killing by macrophages and neutrophils (Fig. 84-2A and B). For C. immitis, germination of the arthroconidia results in the formation of a sac-like structure called a spherule filled with endospores (Fig. 84-2C). Spherules then rupture to release large numbers of endospores, which are the propagating form of the infection. Control of infection in the lungs is typically accomplished through formation of granulomas. However, in patients exposed to an overwhelming inoculum, or lower inocula in the setting of suppressed T-cell-mediated immunity, dissemination outside the lung to the skin and oral mucosa (especially blastomycoses), adrenal glands, bone, spleen, thyroid, GI tract, heart, and CNS is possible and uniformly fatal if left untreated.

FIGURE 84-2. Histopathology of endemic mycoses in tissue. A. Histoplasmosis (yeast). B. Blastomycoses (broad-based budding yeast). C. Coccidioidomycoses (spherules with endospores)
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