Histoplasmosis

Question 1

pathology of disseminated histoplasmosis

Answer 1

A-Gross Findings:

1-Liver & spleen: Enlarged (hepatosplenomegaly)
2-Adrenals: May show necrosis and hemorrhage
3-GI tract: Ulcers, nodules, or strictures
4-Lymph nodes: Enlarged and caseating or non-caseating granulomas
B-Microscopic Findings:
1-Yeast forms (2–4 µm) seen within macrophages (PAS, GMS, or H&E stain)
2-Granulomatous inflammation, may be:
-Non-caseating (in early/controlled disease)
-Caseating or necrotizing in severe cases
3-In severe immunosuppression, granulomas may be absent, and there’s diffuse macrophage infiltration packed with yeast

Question 2

pathogenesis of disseminated histoplasmosis

Answer 2

Causative agent: Histoplasma capsulatum – a dimorphic fungus (mold in environment, yeast in tissues)

Question 3

pathogenesis of disseminated histoplasmosis

Answer 3

1. Inhalation of Microconidia
   Spores (microconidia) from bird/bat droppings or contaminated soil are inhaled.

Convert into yeast form in the lungs at body temperature.

2. Intracellular Survival and Dissemination

Yeast cells are phagocytosed by alveolar macrophages.

They survive and replicate inside macrophages by inhibiting phagolysosomal fusion.

Hematogenous dissemination occurs via infected macrophages to:

Liver

Spleen

Bone marrow

Lymph nodes

Adrenal glands

GI tract

3. Impaired Immunity

In immunocompetent hosts, cell-mediated immunity (Th1 response, TNF-α, IFN-γ) usually contains infection.

In immunocompromised (e.g., AIDS, transplant, extremes of age), this control fails, leading to:

Progressive disseminated disease with multiorgan involvement.