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Updated: May 25, 2026
Passive Administration of Monoclonal Antibodies Against H. capsulatum and Others Fungal Pathogens
Published on: February 14, 2011
Invasive models of histoplasmosis
1Infectious Disease Division, Cincinnati VA Medical Center, University of Cincinnati, Cincinnati, OH, USA. Alan.Smulian@uc.edu
Abstract:
Histoplasmosis results from infection with the fungal organism Histoplasma capsulatum. Most Histoplasma research today uses models based on primary pulmonary infection. Following inhalation, conidia are rapidly ingested and intracellularly convert to the yeast form. After initial pulmonary infection, organisms are carried throughout the body giving rise to disseminated infection. Three murine infection models have been developed which mimic human disease. These comprise models of primary infection following initial exposure to the organism, secondary exposure to Histoplasma following spontaneous recovery from primary disease and a model of reactivated infection following spontaneous clearance of primary disease. This chapter describes these models and explores variability introduced with the use of mice of varied genetic backgrounds and different H. capsulatum strains.
Insights
This study details three mouse models for Histoplasmosis research, mimicking primary, secondary, and reactivated infections. These models help understand Histoplasma capsulatum
Area of Science:
- Mycology
- Immunology
- Infectious Diseases
Background:
- Histoplasmosis is caused by the fungus Histoplasma capsulatum.
- Current research primarily uses models of primary pulmonary infection.
- Disseminated infection can occur after initial pulmonary disease.
Purpose of the Study:
- To describe three murine models of Histoplasmosis.
- To mimic primary, secondary, and reactivated infection in humans.
- To explore variability in Histoplasma research models.
Main Methods:
- Development of three distinct murine infection models.
- Models simulate primary, secondary, and reactivated Histoplasma infections.
- Investigation of host genetic background and fungal strain variability.
Main Results:
- Established models accurately reflect different stages of human Histoplasmosis.
- Variability in mouse genetics and H. capsulatum strains impacts infection outcomes.
- Models provide a framework for studying fungal pathogenesis and immune response.
Conclusions:
- Murine models are crucial for understanding Histoplasmosis.
- Host-pathogen interactions are key in disease development.
- Further research should consider genetic and strain variability for accurate modeling.
