Cryptococcosis pathophysiology

Cryptococcosis Microchapters
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian M.D.; Yazan Daaboul, M.D.

Pathophysiology

• Infective cryptococcal species are ubiquitous and natural exposure is very common.
• Infection occurs by inhalation of aerosolized, dessicated basidiospores.
• Once these spores reach the alveoli, they are phagocytosed by the alveolar macrophages without prior opsonization (usually required for yeast forms).
• Cryptococci are intracellular pathogens. Once they are phagocytosed, they germinate and multiply within the macrophages.
• Activated macrophages are capable of destroying the yeast forms that develop; however, non-activated macrophages act as germination centers for cryptococci.
• Cryptococci have the ability of forming giant cells that resist phagocytosis and have been hypothesized to play a role in latent infections and reactivation.
• Cryptococci also have the ability of changing the number of sets of chromosomes during infection, this has been associated with heteroresistance to certain antifungal agents.
• After exposure to desiccated yeast cells or spores, patients may clear infection or contain it within granulomata as a latent infection, or it may disseminate depending on host immune status or other less well understood mechanisms.
• Disseminated disease occurs among patients with compromised cell-mediated immunity.
• The immune response to cryptococcal infection is highly dependent on host T-cell function, and interferon-γ and TNF-α signaling.
• Granuloma formation can also be seen and may also be responsible for reactivation in patients with immunocompromised states.

Microscopic Pathology

Cryptococcosis of the lung in patient with AIDS (Mucicarmine stain)

Multimedia

Cryptococcosis (PAS stain)

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