Morphology and staining properties
Bacteria of the genus Nocardia were first isolated by the researcher Nocard in 1888. They are microorganisms that form branching filaments 0.5–1.2 µm in diameter and are also capable of forming conidia.
The life cycle of the causative agent features a characteristic dynamic. In the first hours of growth, a non-septate mycelium is formed. Then, septa appear within it, and the filaments gradually fragment, forming rod-shaped and coccobacillary forms. The bacteria reproduce by binary fission or budding. In old cultures, the process of complete separation of fragments is disrupted, resulting in long multicellular filaments.
Upon microscopy, Nocardia exhibit variable Gram staining. The most important tinctorial feature is their relative acid-fastness — Kinyoun staining (a modification of the classic Ziehl–Neelsen method) is used for visualization.
Cultural properties
A number of nutrient media are used to grow Nocardia in the laboratory: Sabouraud agar, meat peptone agar (MPA), Columbia agar (enriched with colistin and nalidixic acid), and centrifuged thioglycolate broth is used for blood inoculation. The optimal growth temperature is 25–35 °C.
A distinctive feature of the pathogen is its prolonged 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 have aerial hyphae or lack them. Pigment color is species-specific:
- N. asteroides (the most common species) forms bright pink colonies;
- N. brasiliensis — orange-brown;
- N. otitidiscaviarum — light brown;
- N. transvalensis — ranging from pale brown to violet;
- N. farcinica — distinguished by a white chalky coating.
Epidemiology and pathogenesis
The natural ecological niche for the pathogen is soil, where Nocardia live as saprophytes while possessing high resistance in the external environment. Infection occurs predominantly via the aerogenic route (the main mechanism), and less frequently via contact or alimentary routes.
General susceptibility to infection is low, and the disease is relatively rare (1.5–2.0 thousand cases per year). Nocardiosis has a pronounced opportunistic character: about 50% of patients are individuals with immunodeficiencies, with males statistically affected more often.
The primary portal of entry for the infection is the respiratory tract. Upon reaching the alveoli, the bacteria are engulfed by alveolar macrophages. However, Nocardia are able to survive inside cells. They block the fusion of the phagosome with the lysosome and inhibit the action of lysosomal enzymes. Unimpeded multiplication of the bacteria inside macrophages ultimately leads to the development of suppurative-granulomatous inflammation.
Clinical forms, diagnosis, and treatment
The disease can occur in several forms:
- Visceral form. The main localization is the lungs, where multiple coalescing 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 the formation of shallow pustules, which gradually progress into deep abscesses and granulomas. The clinical presentation of this form requires differential diagnosis, as it strongly resembles cutaneous actinomycosis.
Material for microbiological diagnosis includes sputum, pus, and tissue biopsies. Bacterioscopy (preliminary method) reveals characteristic granules (sulfur granules) 25–150 µm in size. They have a soft consistency, white or yellow color, lobular structure, and consist of a network of branching non-septate hyphae. The definitive diagnosis is established using the bacteriological method after isolating a pure culture.
As etiotropic therapy, sulfonamides and aminoglycosides (gentamicin, amikacin) are used. Treatment is prolonged (taking several months) due to the slow clinical effect. Specific vaccines for the prevention of nocardiosis have not been developed at present.
Briefly: answers to topical questions
What specific virulence factors ensure the survival of Nocardia inside macrophages?
The survival of Nocardia inside macrophages is ensured by mechanisms that prevent their intracellular digestion. These include:
- Fusion blockage — preventing the merger of the phagosome with the lysosome.
- Enzyme inhibition — suppressing the activity of lysosomal enzymes.
As a result of these processes, the bacteria persist in the cytoplasm of alveolar macrophages, which subsequently leads to the multiplication of the pathogen and the development of suppurative-granulomatous inflammation.
With which infections must the cutaneous form of nocardiosis be differentiated?
The cutaneous form of nocardiosis must be differentiated from cutaneous actinomycosis. Subcutaneous tissue involvement begins with shallow pustules that progress into abscesses and granulomas. The clinical picture resembles cutaneous actinomycosis.
Which antibacterial drugs are the drugs of choice for etiotropic therapy of nocardiosis?
The drugs of choice for etiotropic therapy of nocardiosis are sulfonamides and aminoglycosides. Among aminoglycosides, amikacin and gentamicin are used. The clinical effect develops slowly, so the course of treatment lasts for several months.
Which species of Nocardia are the main causative agents of human disease?
The main species of the genus Nocardia are N. asteroides — the most common species, N. brasiliensis, N. otitidiscaviarum, and N. farcinica. N. brasiliensis is characterized by orange-brown colonies, N. otitidiscaviarum by light brown colonies, and N. farcinica by a white chalky coating.
To remember the pigment colors of the main species: Aster (asteroides) — bright pink, Brazil (brasiliensis) — orange-brown (tan color), Porcelain (farcinica) — white (chalky coating).
Class and exam questions
How do Nocardia survive after phagocytosis by macrophages?
They prevent the fusion of the phagosome with the lysosome and simultaneously suppress the activity of lysosomal enzymes, which gives them the ability to multiply freely within the macrophage cytoplasm.
What can be seen upon microscopy of pus from a patient with nocardiosis?
Specific granules (sulfur granules) 25–150 µm in size are found in the pathological material. These are soft white or yellow formations with a lobular structure, consisting of branching non-septate hyphae.
What else to study on this topic
- Mechanisms of formation and microscopic structure of granules in nocardiosis
- Differential diagnosis of cutaneous nocardiosis and actinomycosis
- Virulence factors of Nocardia at the molecular level
- Features of the body's immune response during Nocardia infection
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