Classification of the pathogen
The disease is caused by two main varieties of the fungus Histoplasma capsulatum:
- H. capsulatum var. capsulatum — the causative agent of American histoplasmosis. Endemic to South and Central America as well as the USA (tropics and river valleys). It is characterized by higher virulence and a propensity for dissemination to the central nervous system, adrenal glands, and mucous membranes.
- H. capsulatum var. duboisii — the causative agent of African histoplasmosis. Found in Equatorial Africa. It is less virulent, more frequently affecting the skin, bones, and subcutaneous tissue. In addition to humans, baboons serve as a natural reservoir.
Morphology and life cycle forms
Histoplasma capsulatum is a dimorphic fungus, meaning it is capable of changing its form depending on environmental conditions. Notably, despite the species name (capsulatum), the fungus does not form a true capsule.
- Tissue (yeast) form: exists within the organism (inside macrophages) or on blood media at 37 °C. It appears as small, round cells (2–5 µm) that reproduce by budding from a narrow end, sometimes forming chains of buds.
- Mycelial (saprophytic) form: develops in the external environment or on Sabouraud agar at 20–25 °C. It is represented by a branched, septate mycelium with hyphae up to 5 µm in diameter. It forms large macroconidia (8–20 µm) with spiky projections and small teardrop-shaped microconidia.
Epidemiology and pathogenesis
The natural reservoir of histoplasmosis is soil heavily contaminated with bird and bat droppings (often in caves or nesting sites). Rural residents and individuals in contact with such soil and dust are at risk.
Infection occurs via the airborne route when inhaling dust containing fungal spores. The respiratory tract serves as the portal of entry. The primary lesion forms in the lungs. Subsequently (especially with American-type infection), dissemination of the pathogen to other organs and tissues can occur, where specific granulomas develop. The disease elicits both cellular and humoral immunity. The infection is not transmitted from person to person.
Laboratory diagnostics
Fungi of the genus Histoplasma are classified as highly hazardous infections, so diagnostics are strictly performed in specialized laboratories inside laminar flow hoods with double protection.
Sputum, pus, cerebrospinal fluid, urine, ulcer scrapings, and punctates are used for testing.
Main methods:
- Microscopy: Gram, Ziehl-Neelsen, or Romanowsky-Giemsa staining of smears. Small, double-contoured, yeast-like cells with a single bud are found in the preparations (inside histiocytes or extracellularly).
- Rapid diagnostics: PCR and DFA (direct fluorescent antibody assay).
- Culture method: inoculation onto Sabouraud agar or blood agar. Fluffy white-brown colonies develop.
- Immunology: skin test with histoplasmin and detection of antibodies (CFT, precipitin test, DFA).
- Animal inoculation: infection of white mice to observe the transformation of mycelium into yeast in vivo.
Briefly: answers to topical questions
What clinical forms of pulmonary histoplasmosis are distinguished?
Primary, secondary, and disseminated forms of histoplasmosis are distinguished.
- Primary form — formation of a single primary affect, predominantly in the lung apex, with the development of a primary infection complex; it may be latent.
- Secondary forms — involvement of the lung apices and a chronic progressive course.
- Disseminated form — spread of the pathogen to the central nervous system, adrenal glands, skin, mucous membranes, and other tissues.
What radiographic features are characteristic of pulmonary histoplasmosis?
Pulmonary histoplasmosis is characterized by signs of bilateral fibrosis and specific changes in the intrathoracic lymph nodes.
- Bilateral fibrosis — pathological changes are localized predominantly in the upper lobes of the lungs.
- Lymph node necrosis — computed tomography reveals low-density nodes with characteristic peripheral contrast enhancement.
What is the role of cellular immunity and macrophages in the pathogenesis of histoplasmosis?
Cellular immunity and macrophages ensure the destruction of the pathogen and the development of delayed-type hypersensitivity.
- Unactivated macrophages — engulf Histoplasma capsulatum, however, the fungi multiply within phagolysosomes and destroy the cells.
- T-lymphocytes (Th1) — recognize fungal antigens and release interferon-gamma.
- Activated macrophages — acquire the ability to destroy intracellular fungi under the influence of cytokines.
A negative delayed-type hypersensitivity reaction indicates cellular immunodeficiency and serves as a poor prognostic sign.
Histoplasmosis is the "capless chameleon fungus from the bat cave." It changes shape (dimorphic), loves to hide inside macrophages, and the name capsulatum is a misnomer.
Class and exam questions
Why is the fungus called capsulatum if it has no capsule?
This is a historically established name. The discoverers mistook the halo effect around the cell in tissues for a capsule, but it was later found that the fungus has no true capsule.
Is a patient with histoplasmosis contagious to other people?
No, an infected patient is completely non-contagious. Infection occurs exclusively through the inhalation of spores from the external environment.
What is the main difference between African and American histoplasmosis?
The African type (var. duboisii) is less virulent, less frequently affects the lungs, and more often causes skin and bone lesions. The American type (var. capsulatum) more frequently results in severe dissemination.
What else to study on this topic
- Pathomorphology of granulomas in histoplasmosis
- Features of cellular immunity in fungal infections
- Differential diagnosis of dimorphic fungi
- Mechanism of action of amphotericin B
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