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Rev Argent Microbiol. 2006 Oct-Dec;38(4):235-42.

[Dimorphism and pathogenesis of Histoplasma capsulatum].

[Article in Spanish]

Author information

1
Centro de Referencia de Micologia, Facultad de Ciencias Bioquimicas y Farmacdutica, Universidad Nacional de Rosario, Suipacha 531 (2000) Rosario, Argentina. clopez@fbioyf.unr.edu.ar

Abstract

Dimorphism and pathogenesis of Hisdistoplasma capsulatum is a dimorphic fungal pathogen with worldwide significance, which causes a broad spectrum of disease. In the saprophytic stage, it lives as a mycelial form consisting of hyphae bearing both macro and microconidia. Infection with H. capsulatum occurs by inhalation of microconidia (1-4 x 2-6 microm) or small mycelia fragments (5-8 microm) in the terminal bronchioles and alveoli of the lung. Inhaled conidia then convert into the yeast form that is responsible for the pathogenesis of histoplasmosis. As a soil fungus with no known requirements for interacting with a mammalian host as a necessary stage of its life cycle, the number of its strategies for successful pathogenesis is particularly remarkable. They include dimorphic mould-yeast transition, entry into host macrophages, subcellular localization, intracellular survival and proliferation during clinically unapparent infection with capacity for reactivation. H. capsulatum became the subject of increasing studies concurrently with the rising prevalence of human immunodeficiency. This paper presents an overall view of advances in the investigation of H. capsulatum dimorphic transition and pathogenesis.

PMID:
17370580
[Indexed for MEDLINE]
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