Nocardia

Nocardia was first singled out by Nokar in 1888; Eppinger described lung lesions and brain abscesses in humans caused by nocardia.

[1], [2], [3], [4], [5], [6], [7]

Nocardial morphology

In the early stages of growth, a relatively developed mycelium forms on the surface and penetrates into the interior of the medium. The cells are straight or curved with frequent branching. In the first hours of growth, the mycelium is unsepted and the entire plexus is unicellular. The diameter of the filaments is 0.3-1.3 μm. With age, septa form in them, and the mycelium is fragmented into individual pointlike or coccoid elements that reproduce by binary fission or budding. In old cultures, multicellular filaments formed as a result of incomplete separation of the fragmenting mycelium can be detected. Conidia formation. Gram staining is variable: in the pathological material are represented by gram-positive short branching strands and lifteroid elements, in old cultures it is possible to find gram-negative dissociated shems. Nocardia are relatively acid resistant, stained according to Tsil-Nelson. In the form of the mycelium and the time of its dissociation are divided into three groups:

• 1st - mycelium limited, does not form conidia, dissociates after 12-14 hours of incubation; in the old cultures short sticks and coccoid forms are common;
• 2nd - mycelium limited, does not form conidia, dissociates after 20 hours of incubation; in older cultures, long fragments of mycelium predominate;
• 3rd - a mycelium abundant with sparse conidia; In older cultures, long branching threads predominate.

The cultural properties of nocardia

Nocardia grow well on simple nutrient media (MPA, MPB, Saburo environment, etc.). The temperature optimum of growth is 28-37 ° C. On liquid media form a thin transparent film, reminiscent of a growing droplet of fat; gradually acquire a cream yellow color. Benthic growth is possible in the form of cotton balls or dense grains. On dense media, after 45-72 h, small smooth moist colonies of a testic consistency form. After 72 hours the surface of the colonies changes, they take the form of a raised and twisted center and scalloped edges on the 10-14th day. Pigments from cream to red are produced, which diffuse into the nutrient medium. Bacteria of the 1 st group form soft, pasty and mucous colonies, the second - pasty or oily, 3rd - dry leathery colonies.

Biochemical activity is quite high.

Ecological niche of the nocardi

Nocardia are ubiquitous in the soil and in organic substrates. They are not representative of the normal microflora of the human body, although they are sometimes isolated from clinically healthy people. Resistance to the environment is high.

[8], [9], [10], [11]

Sensitivity to antimicrobial agents

Nocardia are sensitive to gentamicin and levomycetin. Commonly used antiseptics and disinfectants.

Pathogenesis of nocardiosis

Nocardia cause an opportunistic infection. The causative agent is captured by alveolar macrophages, in the cytoplasm of which it remains viable, blocking the fusion of phagosome with dysosomes and inhibiting the synthesis of lysosomal enzymes. Persistence of the pathogen leads to the development of inflammation with the formation of multiple discharge abscesses and granulomas. Infection of the subcutaneous tissue develops when the wound enters the wound and is characterized by the development of purulent inflammation. Immunodeficient individuals may develop disseminated infection.

Epidemiology of nocardiosis

The source of infection is the soil. The transmission mechanism is contact, the transmission path is wounded. Aerogenous transmission of the pathogen by airborne or airborne dust and by alimentary transmission from the ischa through damaged mucous membranes of the gastrointestinal tract are also possible. The susceptibility to nocardia, as to all conditionally pathogenic microbes, is low in individuals with normal immune status and is elevated in immunodeficient hosts.

[12], [13], [14], [15], [16], [17], [18], [19], [20]

Symptoms of nocardiosis

Nocardiosis - opportunistic infections of the person, caused by nocardia, which are characterized by a predominant lesion of the lungs and subcutaneous tissue with the development of purulent-granulomatous inflammation.

Relate to rare infectious diseases. Annually, in the world, 1.5-2 thousand cases are registered, more than half of them in individuals with immunodeficiencies. The main forms of damage are pulmonary and subcutaneous nocardiosis. The most common lung damage caused by Nocardia aateroides, and subcutaneous damage caused by Nocardia brasiliensis.

With pulmonary lesions in the lung parenchyma, multiple discharge abscesses and granulomas are formed. The mediastinal organs, soft tissues of the chest, etc. Are often involved in the inflammatory process. The disease is especially dangerous for people with immunodeficiencies, which often develop disseminated infections accompanied by central nervous system damage, meningeal phenomena and paralysis. With disseminated forms, it is possible to damage the skin, lymph nodes, liver and kidneys.

Infections of the subcutaneous tissue are characterized by the development of pustules at the site of penetration of the pathogen. With the progression of the disease, abscesses and granulomas are formed, which resemble cutaneous actinomycosis.

Immunity has not been studied enough.

Laboratory diagnosis of nocardiosis

The material for the study is sputum, pus, biopsy tissue. For diagnosis use microscopic and bacteriological methods. Usually diamine is placed bacterioscopically by the detection of unseptivated hyphae in the material under study. The final diagnosis is established on the basis of excretory excretion.

Treatment of nocardiosis

Satisfactory results can be achieved using sulfonamides or a combination of them with gentamycin or levomycetin.

Prophylaxis of nocardiosis

Specific prevention of nocardiosis is not developed, nonspecific prophylaxis is aimed at increasing the immune status.