Histoplasm capsulatum

Dimorphic fungus, which in its parasitic form apparently grows temperature-dependent (Shen Q et al. 2017) as a yeast in its saprophytic form as a filamentous fungus and causes life-threatening lung infections in humans (histoplasmosis of the lung) (Mittal J et al. 2019). The genus Histoplasma consists of at least four genetically differentiable species, which also differ in their virulence (Sepúlveda VE et al. 2017).

The natural habitat of Histoplasma capsulatum is the earth in dry-hot regions of Latin America, the mid-west of the USA, India and Africa, after the spores were transferred by bird and bat droppings. Saprophytically, the fungus lives as mycelium on which macro- and microconidia are formed. The microconidia are then transferred to humans with dust. Since they are highly contagious, they are classified in risk group III. In the USA > 60% of the population is exposed to Histoplasma capsulatum at some point in their lives (Sepúlveda VE et al. 2017).

After inhalation, the microconidia are phagocyted by the alveolar macrophages, but are not inactivated with certainty. In these cells they multiply as shoot fungi! A transmission from person to person is not possible. In most cases, the infection proceeds clinically as a local infection. In individual cases, however, especially in cases of immune deficiency, the fungi continue to multiply and haematogenic seeding occurs (Mittal J et al. 2019).

(see histoplasmosis below)

Acute pulmonary histoplasmosis is usually clinically diagnosed as a rule of exclusion, since the pathogen can rarely be culturally detected from sputum or bronchial secretion.

The granulomas in the lung or bone are round foci which are misinterpreted as carcinoma metastases. In chronic or disseminated forms, direct microscopic detection from suitable material (sputum, bronchial secretion, pus, urine, biopsy material - Fig.)

Much more common are the atypical microconidia.

The fungi can be more easily identified in histological sections with PAS or with silver staining according to Grocott-Gomori (Fig.). In the blood smear the intracellular fungi are visible in granulocytes as a notch.

Using molecular biological methods (e.g. PCR) histoplasm can be detected in biopsies, blood or pus.

If haematogenous systematization is not treated early, a high mortality rate must be expected.

1. Darling STA (1906) A protozoon general infection producing pseudotubercels in the lungs and focal necroses in the liver, spleen and lymph nodes. JAMA 46: 1283-1285
2. Jackson A et al (1994) Oral azole drugs as systemic antifungal therapy. N Engl J Med 330: 263-272
3. LeMonte AM (2000) Amphotericin B combined with itraconazole or fluconazole for treatment of histoplasmosis. J Infect Dis 182: 545-550
4. Mittal J et al (2019) Histoplasma Capsulatum: Mechanisms for Pathogenesis. Curr Top Microbiol Immunol 422:157-191.
5. Norris S et al (1994) Prevention of relapse of histoplasmosis with fluconazole in patients with the acquired immunodeficiency syndrome. At J Med 96: 504-508
6. Sepúlveda VE et al (2017) Genome Sequences Reveal Cryptic Speciation in the Human Pathogen Histoplasma capsulatum. mBio 8:e01339-17.
7. Shen Q et al (2017) Differentiation of the fungus Histoplasma capsulatum into a pathogen of phagocytes. Curr Opin Microbiol 40:1-7.
8. Wheat J et al (1993) Prevention of relapse of histoplasmosis with itraconazole in patients with the acquired immunodeficiency syndrome. The national institute of allergy and infectious disease clinical trials and mycosis study group collaborators. Ann Inter Med 118: 610-616
9. Vathesatogkit P et al (2003) A 27-year-old HIV-infected woman with severe sepsis and pulmonary infiltrates. Disseminated histoplasmosis with severe sepsis and acute respiratory failure. Chest 123: 272-273, 274-276