Coccidia - causative agents of coccidioidosis

Coccidioidosis is an endemic systemic mycosis with a predominant airway disease.

[1], [2], [3], [4]

Morphology of coccidia

Coccidioides immitis is a dimorphic fungus. At room temperature (20-22 X) and in natural conditions it grows to the mycelial form. Mycelium septate, 2-4 microns wide, without microconidia. As the cytoplasm of the fungus grows, the mycelial tube in the septum region becomes empty, then the cell wall of the mycelium breaks and the mycelium breaks down into arthrospores 1.5-2.3 μm wide and 1.5-15 μm long. Fragmentation is observed on a 10-L2-C culture day.

The cultural properties of coccidia

It is undemanding to nutrient media. In Sabur's environment, at room temperature, forms a variety of colonies of white, gray or brown color. Biochemical activity is low.

Antigenic structure of coccidia

When growing on a liquid medium for 3 days. The mycelial form produces exoantigens HS, F (chitinase), HL, which can be determined by immunodiffusion in the gel.

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Factors of pathogenicity of coccidia

Reduction of arthrospore formation in museum strains is accompanied by a fall in their virulence.

Ecological niche - the soil of endemic zones. Endemic zones are located in the Western Hemisphere between 40 ° North and South latitude, and 65 ° and 120 ° W longitude in the United States (western and southwestern states), as well as Central (Mexico, Guatemala, Honduras) and South (Venezuela, Paraguay, Argentina) of America. The fungus is mainly found in the zone of deserts and semi-deserts, sometimes found in tropical zones and coastal forests (Northern California). Soil is a natural habitat for the fungus.

Sustainability in the environment. Arthrospores are highly resistant to drying.

Sensitivity to antibiotics. Sensitive to amphotericin B, ketoconazole, miconazole, fluconazole, intraconazole. Sensitivity to antiseptics and disinfectants. Sensitive to the action of commonly used antiseptics and disinfectants, especially to salts of heavy metals.

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The pathogenesis of coccidioidosis

After infection, arthrospores in the host's body are transformed into a tissue form - the spherule. Spherules are rounded formations with a size of 20-90 μm, less often 2 (H) μm with a two-cell mosnetic cell wall with a width of up to 5 μm. With the rupture of the cell wall of the spheres, the spores contained in them spread throughout the body, which ensures the dissemination of the pathogen and the formation of secondary foci.

Secondary coccidioidosis develops in persons with impaired cellular immunity. T-cell immunodeficiency is the cause of the development of severe pneumonia followed by the spread of the fungus to the body from the primary focus of inflammation.

Immunity cellular

The main role is played by T-effectors, including T-effectors of HRT, which accumulate on the 2-3 nd week of the disease. Phagocytosis is incomplete, phagocytes are not able to protect the body at the stage of penetration of the pathogen. Antibodies and complement do not provide protection of the body against the pathogen. The presence of antibodies in patients with negative HRT on antigens of the fungus is a poor prognostic sign.

Epidemiology of coccidioidosis

Coccidioidosis is a sapronosis. The source of the infectious agent is the soil of endemic zones, during which the intensive growth of the fib occurs during the wet season, and with the onset of the dry season, the mycelium splits into arthrospores, which are the only infectious element. A sick person is not at odds with others.

The transmission mechanism is aerogenic and contact, the transmission path is air-dust. Any contact with contaminated soil in endemic areas can lead to infection.

The susceptibility is high. For infection, enough aspiration of 10 arthrospores. The greatest risk of infection is susceptible to lya with various immunodeficiencies.

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Symptoms of coccidioidosis

Symptoms of coccidioidosis are nonspecific and are determined by the nature of the organs affected by fungi. The secondary generalized coccidioidosis is characterized by a chronic course - remissions are replaced by exacerbations for decades; the presence of fistulous movements opening on the surface of the body, often removed from the focus of purulent inflammation; presence of the spheres in the pathological material.

Laboratory diagnosis of coccidioidosis

The investigated material is urine, sputum, blood, liquor, biopsy material,

Microscopic examination of native and Manus or Gram-Welsh-stained preparations allows detection of a spherule (spherical with a two-contour envelope of formation, filled with small rounded endospores). Despite the characteristic morphology of the spherules, artifacts are possible: macrophages containing phagocytized mineral particles (dust cells), as well as granulocyte detritus accumulations, can simulate spherical structures that are hardly distinguishable from the tissue phase of the pathogen. Diagnosis, based only on the search for spheres, leads to false positive results. A simple way to exclude artifacts is to germinate the spheres: the pathological material is mixed in equal volumes with distilled water, the preparation is prepared using the "differentiated drop" method, the cover glass is sealed with paraffin and incubated at 37 ° C. The true sphere sprouts in 4-6 hrs by the filaments of the mycelium emanating from the endospores.

Mycological examination is carried out in compliance with a special regime. On dense nutrient media, coccidiococci form at 37 ° C colony of a leathery consistency, growing into a substrate, at 25 ° C the mycelial form of the fungus develops. Mycelium septated, chlamydospores large, located at the ends and sides of the mycelium. Typical arthrospores are formed on the 10th-12th laziness of incubation.

Biological research is conducted on hamsters and guinea pigs (males). Infection of experimental animals with intrastestic and intraperitoneal leads to the development of tissue forms of the fungus - the sphere.

For serological diagnosis use RA, RP, DSC. RNGA. REEF. RP becomes positive in 53% of patients at the first week and in 91% for the 2-3 nd week of the disease. Clear diagnostic titers of RSK are absent, therefore, for the purposes of diagnosis, a 4-fold seroconversion is determined. The increase in the titer of the DSC testifies to the generalization of the process.

Intradermal allergic test with coccidioidin has diagnostic value only in persons with whom it was negative at the onset of the disease; in other cases, this sample can serve as an indicator of the infected and used to determine the boundaries of the endemic zone.

Treatment of coccidioidosis

In primary infection, fluconazole, intraconazole, amphotericin B, secondary generalized ketoconazole, miconazole are used.

How to prevent coccidioidosis?

Specific prophylaxis of coccidioidosis is not developed. To prevent the disease, endemic areas should be avoided for persons who lack cellular immunity to the pathogen antigens, as well as patients with T-lymphocyte deficiency. To prevent intralaboratory infections, all manipulations with suspicious cultures are performed after they are filled with a sterile saline solution, which eliminates the spraying of arthrospores.