Book contents
- Frontmatter
- Contents
- Preface
- Contributors
- Part I Clinical Syndromes – General
- Part II Clinical Syndromes – Head and Neck
- Part III Clinical Syndromes – Eye
- Part IV Clinical Syndromes – Skin and Lymph Nodes
- Part V Clinical Syndromes – Respiratory Tract
- Part VI Clinical Syndromes – Heart and Blood Vessels
- Part VII Clinical Syndromes – Gastrointestinal Tract, Liver, and Abdomen
- Part VIII Clinical Syndromes – Genitourinary Tract
- Part IX Clinical Syndromes – Musculoskeletal System
- Part X Clinical Syndromes – Neurologic System
- Part XI The Susceptible Host
- Part XII HIV
- Part XIII Nosocomial Infection
- Part XIV Infections Related to Surgery and Trauma
- Part XV Prevention of Infection
- Part XVI Travel and Recreation
- Part XVII Bioterrorism
- Part XVIII Specific Organisms – Bacteria
- Part XIX Specific Organisms – Spirochetes
- Part XX Specific Organisms – Mycoplasma and Chlamydia
- Part XXI Specific Organisms – Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific Organisms – Fungi
- 170 Candidiasis
- 171 Aspergillosis
- 172 Zygomycosis (Mucormycosis)
- 173 Sporotrichosis
- 174 Cryptococcus
- 175 Histoplasmosis
- 176 Blastomycosis
- 177 Coccidioidomycosis
- 178 Pneumocystis Pneumonia
- 179 Miscellaneous Fungi and Algae
- Part XXIII Specific Organisms – Viruses
- Part XXIV Specific Organisms – Parasites
- Part XXV Antimicrobial Therapy – General Considerations
- Index
175 - Histoplasmosis
from Part XXII - Specific Organisms – Fungi
Published online by Cambridge University Press: 05 March 2013
- Frontmatter
- Contents
- Preface
- Contributors
- Part I Clinical Syndromes – General
- Part II Clinical Syndromes – Head and Neck
- Part III Clinical Syndromes – Eye
- Part IV Clinical Syndromes – Skin and Lymph Nodes
- Part V Clinical Syndromes – Respiratory Tract
- Part VI Clinical Syndromes – Heart and Blood Vessels
- Part VII Clinical Syndromes – Gastrointestinal Tract, Liver, and Abdomen
- Part VIII Clinical Syndromes – Genitourinary Tract
- Part IX Clinical Syndromes – Musculoskeletal System
- Part X Clinical Syndromes – Neurologic System
- Part XI The Susceptible Host
- Part XII HIV
- Part XIII Nosocomial Infection
- Part XIV Infections Related to Surgery and Trauma
- Part XV Prevention of Infection
- Part XVI Travel and Recreation
- Part XVII Bioterrorism
- Part XVIII Specific Organisms – Bacteria
- Part XIX Specific Organisms – Spirochetes
- Part XX Specific Organisms – Mycoplasma and Chlamydia
- Part XXI Specific Organisms – Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific Organisms – Fungi
- 170 Candidiasis
- 171 Aspergillosis
- 172 Zygomycosis (Mucormycosis)
- 173 Sporotrichosis
- 174 Cryptococcus
- 175 Histoplasmosis
- 176 Blastomycosis
- 177 Coccidioidomycosis
- 178 Pneumocystis Pneumonia
- 179 Miscellaneous Fungi and Algae
- Part XXIII Specific Organisms – Viruses
- Part XXIV Specific Organisms – Parasites
- Part XXV Antimicrobial Therapy – General Considerations
- Index
Summary
INTRODUCTION
Histoplasma capsulatum is a thermal dimorphic fungus found most frequently in soil in the midwestern United States. Bird and bat excreta rich in organic nitrogen support the growth of the fungus. Sites associated with blackbird roosts are the most commonly identified sources of outbreaks nowadays, whereas domestic chicken coops were the source of the fungus in the past. When sites are disturbed the spores become airborne, producing the infective aerosol. The lung is considered the portal of entry in almost every case of histoplasmosis. The spores of H. capsulatum are inhaled, and once in the alveoli they convert to a yeast, which is the tissue invasive form. The now multiplying yeasts are phagocytosed by alveolar macrophages that are initially incapable of killing the fungus. The ingested yeasts multiply inside the macrophages and are spread throughout the body via the lymphatics during the preimmune phase of the illness to organs rich in reticuloendothelial cells. Once adequate cell-mediated immunity (CMI) develops, the now “armed” macrophages can either kill or wall off the infecting organisms. When immunity is at a high level, as seen in normal individuals, necrosis occurs, which in time becomes calcified. These calcified granulomas are seen in the lung, hilar lymph nodes, liver, and spleen of individuals who successfully limited the infection.
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- Information
- Clinical Infectious Disease , pp. 1211 - 1214Publisher: Cambridge University PressPrint publication year: 2008