Morphology and Cultural Characteristics
Pathogens of aspergillosis are septate mold fungi. They possess branching mycelium and reproduce asexually by forming spores called conidia.
- Microscopic structure: The spore-bearing hypha ends in a characteristic swelling (the conidiophore), upon which sterigmata (phialides, metulae) are arranged in one or two rows. Chains of conidia extend from them. Under the microscope, this complex structure strongly resembles a watering can.
- Pigmentation: Colony color directly depends on the color of the formed conidia. They can be black, green, white, or yellow.
- Cultivation: Aspergilli are obligate aerobes. They grow exceptionally well on standard nutrient media (wort agar, Czapek-Dox agar, Sabouraud agar) with an optimal temperature of 24–37 °C. Initially, fluffy white colonies grow, which acquire a species-specific color within 2–4 days.
Epidemiology and Pathogenicity Factors
Fungi of the genus Aspergillus are ubiquitous: their conidia are constantly present in soil, water, ambient air, and decaying plant matter. Out of approximately 200 known species, about 20 are considered pathogenic to humans, with A. fumigatus, A. niger, A. flavus, A. terreus, and A. nidulans playing the leading roles.
The primary route of infection is airborne (inhalation of conidia). Contact transmission is less common. Risk groups include individuals in specific occupations (working with dust or moldy paper — the so-called 'ragpicker's disease'). Iatrogenic factors are of paramount importance, including invasive medical procedures such as bronchoscopy, punctures, or vascular catheterization.
Key pathogenicity factors of Aspergillus:
- Aggressive enzymes: the pathogen synthesizes protease, elastase, collagenase, and acid phosphatase, which destroy host tissues.
- Toxins: certain species (especially A. flavus and A. parasiticus) produce potent aflatoxins. When these accumulate in food products, alimentary aflatoxicoses develop, characterized by pronounced carcinogenic effects and the potential to cause severe liver cirrhosis.
Pathogenesis and Clinical Forms
The development of severe forms of aspergillosis is closely linked to immunodeficiency. Normally, cellular defense factors (macrophages and granulocytes simply phagocytose and digest them) successfully handle fungal conidia, and the patient develops delayed-type hypersensitivity (DTH). However, when the immune system fails, the pathogen can disseminate, affecting the central nervous system, endocardium, and paranasal sinuses.
Main clinical variants:
- Invasive pulmonary aspergillosis. The most severe form, most commonly caused by A. fumigatus. It is characterized by rapid invasive fungal growth, invasion into blood vessels, and subsequent thrombosis.
- Allergic bronchopulmonary aspergillosis (ABPA). The disease mimics bronchial asthma. It is characterized by allergic alveolitis and persistent blood eosinophilia.
- Aspergilloma (aspergillus mycetoma). A specific form of granuloma, most commonly localized in lung tissue. It represents a dense ball of mycelium surrounded by a thick fibrous wall.
- Cutaneous aspergillosis. Develops either from direct contamination of an open wound by spores or via hematogenous dissemination. Hyperemic plaques appear on the skin and subsequently ulcerate.
Diagnosis, Treatment, and Prevention
The fundamental and primary method of laboratory diagnosis is microscopy. Smears of pus, sputum, or affected tissues (using Gram staining) are examined for septate mycelium and characteristic conidial chains. Wet mounts using 10% KOH are widely used. Additionally, culture isolation of a pure strain, serological tests (ELISA, precipitation reactions), and skin-allergy tests are employed.
- Treatment: Based on the administration of antifungals (amphotericin B, itraconazole, caspofungin). Crucially, the species A. terreus exhibits intrinsic resistance to amphotericin B! For localized forms (e.g., aspergilloma), surgical excision of affected tissue areas is often necessary.
- Prevention: Relies on strict sanitary and hygienic measures. To prevent nosocomial (iatrogenic) infection, absolute sterility control of medical equipment and maximum indoor air purity are required.