Morphology and Staining Properties
Bacteria of the genus Nocardia were first isolated by the researcher Nocard in 1888. They form branching filaments with a diameter of 0.5–1.2 µm and are also capable of forming conidia.
The life cycle of the pathogen exhibits characteristic dynamics. During the first hours of growth, an unseptated mycelium forms. Septa then appear within it, and the filaments gradually fragment into rod-shaped and coccobacillary forms. Bacteria reproduce by binary fission or budding. In older cultures, complete fragmentation is disrupted, leading to the formation of long multicellular filaments.
Under microscopy, Nocardia show variable Gram-staining results. A critical tinctorial feature is their partial acid-fastness; the Kinyoun stain (a modification of the classical Ziehl–Neelsen stain) is used for visualization.
Cultural Characteristics
Several nutrient media are used for laboratory cultivation of Nocardia: Sabouraud agar, nutrient agar, Columbia agar (supplemented with colistin and nalidixic acid), and centrifuged thioglycolate broth for blood cultures. The optimal growth temperature is 25–35 °C.
A distinctive feature of the pathogen is its slow growth. Visible colonies of most species appear only after 7–9 days, and in some cases, cultures are incubated for up to three weeks. Grown colonies may possess aerial hyphae or lack them. Pigment color is species-specific:
- N. asteroides (the most common species) forms bright pink colonies;
- N. brasiliensis forms orange-brown colonies;
- N. otitidiscaviarum forms light brown colonies;
- N. transvalensis varies from pale brown to purple;
- N. farcinica is distinguished by a white chalky dusting.
Epidemiology and Pathogenesis
The natural ecological niche of the pathogen is soil, where Nocardia reside as saprophytes, possessing high environmental persistence. Infection occurs primarily via the aerogenous route (the main mechanism), and less frequently via contact or ingestion.
General susceptibility to the infection is low, and the disease is relatively rare (1.5–2.0 thousand cases per year). Nocardiosis is strictly opportunistic: approximately 50% of patients have immunodeficiencies, with males being statistically affected more often.
The primary portal of entry is the respiratory tract. Upon reaching the alveoli, the bacteria are engulfed by alveolar macrophages. However, Nocardia can survive intracellularly. They block phagosome-lysosome fusion and inhibit the action of lysosomal enzymes. Unimpeded bacterial multiplication within macrophages ultimately leads to suppurative-granulomatous inflammation.
Clinical Forms, Diagnosis, and Treatment
The disease can present in several forms:
- Visceral form. The primary localization is the lungs, where multiple confluent granulomas and abscesses form. Hematogenous dissemination (metastasis) with involvement of the brain, kidneys, and other internal organs is characteristic.
- Subcutaneous tissue involvement. The process begins with superficial pustules that progressively develop into deep abscesses and granulomas. The clinical presentation of this form requires differential diagnosis as it closely resembles cutaneous actinomycosis.
Microbiological diagnostic specimens include sputum, pus, and tissue biopsies. Bacterioscopy (preliminary method) reveals characteristic granules (sulfur granules/mycetoma grains) measuring 25–150 µm. They have a soft consistency, a white or yellow color, a lobulated structure, and consist of a network of branching unseptated hyphae. A definitive diagnosis is established using bacteriological methods after isolating a pure culture.
Etiotropic therapy utilizes sulfonamides and aminoglycosides (gentamicin, amikacin). Treatment is prolonged (spanning several months) due to the slow clinical response. Specific vaccines for the prevention of nocardiosis are currently unavailable.