Dermatomycosis is a condition that belongs to a large group of fungal diseases that affect the skin, nails, body folds, and internal organs.
Occurrence and ways of spread of infection
Fungal infections occur in more than 20% of the adult population. Especially often they affect the elderly, half of whom suffer from ringworm. Older people are a reservoir of infection, spreading it among their family members. So infected with ringworm up to a third of young people and children.
The development of infection in a particular person is facilitated by primary or acquired immunodeficiency (HIV infection, taking glucocorticoids, cytostatics, immunosuppressants), an unfavorable environmental background, and chronic stress, leading to the depletion of the body's defenses.
Mycoses often affect certain occupational groups. These diseases are common among miners, metallurgists, the military, and athletes. This is due to the isolation of industrial premises, the use of common locker rooms and showers, wearing clothes that are impervious to air and moisture, and closed shoes.
The most common disease from this group is ringworm of the feet. It affects at least a fifth of the adult population. Up to a third of patients became infected in common pools, saunas, gyms.
Classification of dermatomycosis
A full-fledged classification that meets all the demands of practice has not yet been created. This is due to the variety of infectious agents and the variety of symptoms they cause. According to the course, acute and chronic dermatomycosis are distinguished, according to the depth of the lesion - superficial and deep, according to limitation - local and widespread forms.
The Russian Federation traditionally uses the classification created in 1976 by N. D. Shcheklakov. She divides the diseases of this group depending on the fungus that caused them, with the corresponding localization of the lesion. According to her, all ringworms belong to one of the following groups:
- keratomycosis (lichen versicolor, nodular microsporia);
- dermatophytosis (inguinal epidermophytosis, rubrophytosis, epidermophytosis of the feet, trichophytosis, favus, microsporia, tiled mycosis);
- candidiasis (superficial, chronic generalized, visceral);
- deep mycoses (histoplasmosis, cryptococcosis, sporotrichosis, aspergillosis and others);
- pseudomycosis (erythrasma, actinomycosis, axillary trichomycosis and others).
The International Classification of Diseases of the 10th revision (ICD-10) proposes to divide dermatomycosis depending on the location of the lesion. This is convenient, but does not always take into account the cause of the disease, on which the treatment depends. This classification distinguishes the following forms of dermatomycosis:
- dermatophytosis;
- a) head and beard (trichophytosis and microsporia of the scalp, beard and mustache);
- b) nails (dermatophytic onychomycosis), hands (rubrophytosis of the palms), feet (epidermophytosis and rubrophytosis of the feet);
- c) torso (dermatophytosis of smooth skin, including the face);
- d) inguinal (groin epidermophytosis and rubrophytosis);
- e) tiled;
- other and unspecified dermatophytosis (including deep forms).
Causes and mechanism of development
The causative agents of dermatomycosis belong to three genera:
- Trichophyton;
- microsporum;
- epidermophyton.
These fungi are widely distributed in nature - in the ground, sand, coastal pebbles, on trees and wood products. They can persist in the environment for more than two years.
Fungi produce aggressive enzymes that destroy keratin, a dense protein that is part of the surface layers of the skin. The infection penetrates much better into the initially damaged areas of the skin.
With a reduced susceptibility of the patient to infection, the fungus does not penetrate the skin for a long time, but spreads to its surface. Such a person is not sick, but is a carrier of ringworm. It has been established that the body produces protective antifungal factors that are released on the surface of the skin and prevent the development of the disease. Any suppression of the immune system causes a weakening of the protective skin barrier, the penetration of the fungus into the tissues.
Varieties of dermatomycosis
Let us briefly describe the main forms according to the ICD-10 classification.
Inguinal dermatophytosis
This infection affects large folds (most often inguinal) and adjacent areas of the skin. Ringworm in the groin accounts for 10% of all fungal infections. The disease affects mainly men with increased body weight, severe sweating, patients with diabetes mellitus. The infection is transmitted by contact with a sick person, but more often by household means - when using common sports equipment (rugs, mats in the gym), bed linen or a vessel in hospitals. The disease first affects the inguinal folds, then spreads to the inner thighs, perineum, the area around the anus, and the intergluteal fold. With self-infection, areas under the mammary glands, elbows and any other areas of the skin may suffer.
The primary foci of ringworm look like small rounded pink spots with clear boundaries. Their surface is smooth, slightly edematous. With an increase and merging of spots, a continuous focus with uneven edges is formed, prone to peripheral growth. Bubbles, scales, crusts form along the edge of the focus. The patient complains of very severe itching. Gradually, peeling appears, inflammation subsides, especially if the increased moisture of the skin is eliminated.
Mycoses of the feet
These diseases are very common. They predominantly affect young men. First, the fungus is localized in the interdigital folds, where there is a slight peeling and cracks. These symptoms do not disturb the patient. Subsequently, one of the more severe clinical forms of ringworm of the feet develops.
The squamous form is accompanied by the appearance of scales and peeling on the lateral surfaces of the feet. The hyperkeratotic form is accompanied by the formation of dry rashes, plaques on the feet. Merging, they form large foci covered with light scales. There is a pronounced skin peeling of the feet, itching, dryness, soreness of the skin.
The intertriginous form resembles diaper rash: cracks, erosion appear in the interdigital folds, the skin swells, becomes wet and reddens. Disturbs itching, burning, soreness. With a dyshidrotic form, numerous bubbles form on the arches of the feet, soles, fingers. After opening the bubbles, erosion appears.
Mycosis of the feet is characterized by a long-term course. In the elderly, “dry” mycoses predominate, exacerbations and inflammation are more characteristic of young people.
In some cases, as a result of a high allergic mood (sensitization) to fungi, acute mycosis occurs: the lesion quickly spreads to the feet and legs with the formation of opening blisters. Fever appears, inguinal lymphadenitis develops. The general well-being of the patient suffers.
Dermatophytosis of the hands
The disease develops slowly. When located on the back of the hands, it resembles dermatophytosis of smooth skin. If the palms are affected, the disease resembles ringworm of the feet. At the same time, and often develops. At the same time, patients in many cases do not notice their illness, believing that thick, flaky skin on the palms is a consequence of physical labor.
Dermatophytosis of smooth skin
Ringworm of smooth skin is more often observed in warm countries. Epidemics were observed among athletes involved in wrestling. In the classical form, an annular focus is formed, containing small vesicles, with peeling along the edges. It gradually spreads over a large area, accompanied by moderate itching.
Dermatophytosis of the scalp
Dermatomycosis of the scalp is manifested mainly by brittle hair in the lesion. The defeat of the beard and mustache area in men is accompanied by the appearance of vesicles, inflammation of the hair follicles, the addition of a secondary infection, edema and bloody crusts. The patient is concerned about soreness and a pronounced cosmetic defect.
Laboratory diagnostics
Recognition of the disease takes into account the symptoms of ringworm, microscopic examination of tissues and the isolation of pathogens from them.
Microbiological diagnosis of dermatomycosis is carried out either by direct examination of the pathogen under a microscope (microsporia), or after cultivation on nutrient media. Even in favorable conditions, fungi grow slowly. After obtaining colonies, they are examined under a microscope and, on the basis of characteristic external signs, the type of pathogen is established.
Treatment of ringworm
For the treatment of these diseases, antimycotic drugs are used. Without their use, it is impossible to achieve a cure for mycosis. How to treat the disease, the dermatologist determines, because there are more than 200 types of antifungal drugs for both local and internal use. Terbinafine (Lamisil) has proven itself most well. It can be used for both treatment and prevention of infection.
Treatment of tinea groin involves the use of creams, ointments, or sprays containing ketoconazole and terbinafine. If there is no effect, fluconazole is prescribed orally for 2 weeks. At the same time, antihistamines and powders that do not contain starch are used.
Mycosis of the feet with abundant weeping is first treated with lotions with potassium permanganate, chlorhexidine or boric acid, and then local antifungal, hormonal and antibacterial agents are prescribed. With significant keratinization, keratolytic drugs are first used, and then fungicidal ones.
Dermatophytosis of the smooth skin of the face is treated with topical antifungal agents. Onychomycosis requires the appointment of systemic drugs.
How to treat ringworm at home?
You should strictly observe the rules of personal hygiene, change linen daily, dry the body after washing, use special talc or powder to prevent sweating. It is recommended to wear loose shoes, use special dilators for the interdigital spaces, use special foot powders.
What can not be eaten with a fungal skin infection?
91. The causative agents of mycoses (candidiasis and dermatomycosis) and protozoal infections (amebiasis, giardiasis, trichomoniasis, leishmaniasis, trypanosomiasis, malaria, toxoplasmosis, balantidiasis). Microbiological diagnosis of candidiasis and dermatomycosis. Diagnostic, prophylactic and therapeutic preparations.
The causative agents of opportunistic mycoses
The causative agents of opportunistic mycoses are opportunistic fungi of the genera Aspergillus, Mucor, Penicillium, Fusarium, Candida etc. They cause diseases in persons with transplants, against the background of reduced immunity, irrational long-term antibiotic therapy, hormone therapy, and the use of invasive research methods. They are found in soil, water, air, on decaying plants; some are part of the facultative human microflora (for example, fungi of the genus candida).
18.5.1. Causative agents of candidiasis Candida
Mushrooms of the genus Candida cause superficial, invasive and other forms of candidiasis (candidomycosis). There are about 200 species of mushrooms of the genus Candida. Taxonomic relationships within the genus are not well understood. Some representatives of the genus are deuteromycetes; sexual reproduction has not been established. Teleomorphic genera have also been identified, including representatives with sexual reproduction: Clavispora, Debaryomyces, Issatchenkia, Kluyveromyces And Pichia.
Clinically significant species are Candida albicans, C. tropicalis, C. catenulata, C. cifferrii, C. guilliermondii, C. haemulonii, C. kefyr(previously C. pseudotropicalis), C. krusei, C. lipolytica, C. lusitaniae, C. norvegensis, C. parapsilosis, C. pulherrima, C. rugosa, C. utilis, C. viswanathii, C. zeylanoides And C. glabrata. The leading role in the development of candidiasis is C. albicans, then follow C. glabrata, C. tropicali And C. parapsilosis.
Morphology and physiology. Mushrooms of the genus Candida consist of oval budding yeast cells (4-8 µm), pseudohyphae and septate hyphae. For C. albicans characteristic is the formation of a growth tube from the blastospore (kidney) when placed in serum. Besides C. albicans forms chlamydospores - thick-walled double-circuit large oval spores. On simple nutrient media at 25–27°C, they form yeast and pseudohyphae cells. Colonies are convex, shiny, creamy, opaque with various shades. Candida grows in tissues in the form of yeast and pseudohyphae.
Epidemiology.Candida are part of the normal microflora of mammals and humans. They live on plants
fruits, being part of the normal microbiota, they can invade tissue (endogenous infection) and cause candidiasis in immunocompromised patients. Less commonly, the pathogen is transmitted to children at birth, while breastfeeding. When transmitted sexually, the development of urogenital candidiasis is possible.
The development of candidiasis is facilitated by improper prescription of antibiotics, metabolic and hormonal disorders, immunodeficiencies, increased skin moisture, damage to the skin and mucous membranes. The most common cause of candidiasis is C. albicans, which produces proteases and integrin-like molecules for adhesion to extracellular matrix proteins and other virulence factors. Candida can cause visceral candidiasis of various organs, systemic (disseminated or candidasepticemia) candidiasis, superficial candidiasis of mucous membranes, skin and nails, chronic (granulomatous) candidiasis, allergy to candida antigens. Visceral candidiasis is accompanied by an inflammatory lesion of certain organs and tissues (esophageal candidiasis, candidal gastritis, respiratory candidiasis, urinary system candidiasis). An important sign of disseminated candidiasis is fungal endophthalmitis (exudative change in the yellow-white color of the choroid).
With oral candidiasis, an acute pseudomembranous form of the disease (the so-called thrush) develops on the mucous membranes with the appearance of a white curdled plaque, atrophy or hypertrophy, hyperkeratosis of the papillae of the tongue may develop. With vaginal candidiasis (vulvovaginitis), white cheesy discharge, swelling and erythema of the mucous membranes appear. Skin lesions are more common in neonates; small nodules, papules and pustules are observed on the trunk and buttocks. Possible candida allergy of the gastrointestinal tract, allergic damage to the organs of vision with the development of itching of the eyelids, blepharoconjunctivitis.
Immunity.Cellular immunity predominates. Mononuclear phagocytes, neutrophils and eosinophils, which capture elements of fungi, are involved in protecting the body from candida. DTH develops, granulomas with epithelioid and giant cells are formed.
In smears from clinical material, pseudomycelium is detected (cells are connected by a constriction
kami), septate mycelium and budding blastospores. Inoculations from the patient are carried out on Sabouraud agar, wort agar, etc. Colonies C. albicans whitish-cream, convex, round. Mushrooms are differentiated according to morphological, biochemical and physiological properties. Candida species differ during growth on potato-glucose agar according to the type of filamentation: the location of glomeruli - clusters of small rounded yeast-like cells around pseudomycelium. For blastospores C. albicans characteristic is the formation of germ tubes during cultivation on liquid media with serum or plasma (2–3 h at 37°C). In addition to this, C. albicans chlamydospores are detected: the sowing area on rice agar is covered with a sterile coverslip and after incubation (at 25 ° C for 2-5 days) is microscoped. Saccharomycetes, unlike Candida spp., are true yeasts and form ascospores located inside the cells, stained with a modified Ziehl-Neelsen method; Saccharomycetes usually do not form pseudomycelia. The presence of candidemia is established with a positive blood culture with isolation from the blood Candida spp. Candidal uroinfection is established when more than 10 5 colonies are found Candida spp. in 1 ml of urine. It is also possible to carry out serological diagnostics (agglutination reaction, RSK, RP, ELISA) and the setting of a skin-allergic test with a candida allergen.
Treatment.Apply nystatin, levorin (for the treatment of local superficial mycoses, such as oropharyngeal), clotrimazole, ketoconazole, caspofungin, itraconazole, fluconazole (does not affect C. krusei, many strains C. glabrata).
Prevention.It is necessary to follow the rules of asepsis, sterility of invasive procedures (catheterization of veins, bladder, bronchoscopy, etc.). Patients with severe neutropenia are prescribed anti-candidiasis drugs to prevent the development of systemic candidiasis.
Causative agents of epidermomycosis (dermatomycosis)
The causative agents of epidermomycosis are anamorphs (structures of asexual reproduction) of 40 closely related species from three genera: Epidermophyton (2 species), Microsporum (16 species), Trichophyton (24 species); their teleomorphs (sexual reproduction structures) are included in one genus, Arthroderma. In 1839, Yu. Shenlein first described favus (scab) as a fungal disease. In 1845, R. Remak named this fungus Achorion schoenleinii. Later, other pathogens of epidermomycosis were discovered. Dermatomycetes are not dimorphic fungi. Their differentiation is based mainly on morphological and cultural features.
Morphological and cultural properties
Dermatomycetes form septate mycelium with spirals, rocket-like swellings, arthrospores, chlamydospores, macro- and microconidia. They undergo pleomorphic changes in the laboratory when they lose their ability to form pigments and form conidia. Species are distinguished by pigmentation and the shape of the colonies. Dermatomycetes grow well on Sabouraud's glucose agar.
Trichophytons are characterized by granular or powdery colonies with abundant microconidia, located in clusters on terminal hyphae.
Microsporums form thick-walled or thin-walled macroconidia, consisting of 8-15 (M. canis) or 4-6 (M. gypseum) cells. Their colonies are colored yellow-orange. When ultraviolet irradiation of hair affected by microsporums, fluorescence is observed in a light green color.
Epidermophytons are characterized by 1-5-cell club-shaped conidia.
Antigens
All dermatomycetes are weak antigens. Glycoproteins of the cell walls of these fungi are allergens, and the carbohydrate part of the allergen causes the development of GNT, and the protein part - DTH.
Pathogenesis and immunity
The causative agents of epidermomycosis affect the epidermis, hair, nails due to direct contact of a healthy person with infected scales or hair of the patient. Fungal hyphae then grow into the stratum corneum, causing a variety of clinical manifestations and localization of the disease. Individual cases of diseases are associated with the contact of people (especially children) with sick dogs and cats. In rare cases, generalized forms of epidermomycosis may develop, affecting large areas of the skin of the trunk and head, with involvement of the lymph nodes.
With epidermomycosis, the development of immediate hypersensitivity (GHT) and delayed types (DTH) is observed. Ecology and epidemiology. Most dermatomycetes are widely distributed in nature. Some species are found in the soil and never cause disease in humans, while others are pathogenic to humans. More than a dozen species of anthropophilic dermatomycetes (T. rubrum, T. tonsurans, etc.) are transmitted from person to person; others - zoophilic dermatomycetes (M. canis, T. verrucocum), pathogenic for domestic and wild animals, are transmitted to humans; the third - geophilic dermatomycetes (M. gypseum, M. fulvum), live in the soil, but are also capable of infecting humans.
Dermatomycetes are quite resistant to environmental factors. Some species are found mainly in certain geographic regions.
Laboratory diagnostics
Pathological material (scales of the skin, nails, hair extracted from the affected areas) is microscoped after softening them in a 10-20% KOH solution. Microsporum forms tight sheets of spores in a mosaic pattern around the hair, while Trichophyton forms parallel rows of spores, outside (ectothrix) and inside (endotrix) of the affected hair.
Dermatomycetes of the ectothrix group include Microsporum audouinii, M.canis, M.gypseum, etc.; to the endotrix group - T. gourvilii, T. tonsurans, etc. Some of them do not form conidia in the hair, others rarely penetrate the hair, and the third hair does not invade. Hair infected with Microsporum fluoresces when exposed to ultraviolet radiation. The final identification of dermatomycetes is carried out on the basis of the study of cultures grown for 1-3 weeks on Sabouraud medium at 20°C, according to the morphological features of the mycelium and spores. To identify dermatomycetes with their release from contaminating fungi and bacteria, a special nutrient medium is used - DTM, which is widely used in clinical laboratories.
No specific prophylaxis
Sarcodidae (amoeba)
Most amoebas (from the Greek. amoibe- change) live in the environment, some species - in humans and animals. Amoebas move with the help of changing cell outgrowths - pseudopodia, and feed on bacteria and small protozoa. They reproduce asexually (by splitting in two). The life cycle includes the trophozoite stage (growing, mobile cell) and the cyst stage. A cyst is formed from the trophozoite, which is resistant to external factors. Once in the intestine, it turns into a trophozoite.
Distinguish between pathogenic and non-pathogenic amoeba. Pathogenic amoeba include dysenteric amoeba (Entamoeba histolytica) and free-living pathogenic amoebae: acanthamoeba (genus Acanthamoeba) and neglerii (genus Naegleria). Naegleria fowleri is a flagellated amoeba. It causes amoebic meningoencephalitis. Non-pathogenic amoebae live in the human colon - intestinal amoeba (Entamoeba coli) amoeba Hartmann (Entamoeba hartmanni), yodameba Büchli (Iodamoeba buetschlii) etc. It turned out that sometimes these amoebas can cause diseases. The oral amoeba is often found in the mouth (Entamoeba gingivalis), especially in diseases of the oral cavity.
19.1.1. The causative agent of amoebiasis (Entamoeba histolytica)
Amoebiasis- anthroponotic disease caused by amoeba Entamoeba histolytica, accompanied (in clinically expressed cases) with ulcerative lesions of the colon, frequent loose stools, tenesmus and dehydration (amebic dysentery), as well as the development of abscesses in various organs. The causative agent was discovered in 1875 by the Russian military doctor F.A. Lesh.
Morphology.There are three forms of dysenteric amoeba: small vegetative, large vegetative and cystic (Fig. 19.1). Small vegetative (translucent) form Entamoeba histolytica forma minuta has a size of 15-20 microns, is inactive, lives in the lumen of the upper colon as a harmless commensal, feeding on bacteria and detritus. Large vegetative form Entamoeba histolytica forma magna(pathogenic, tissue form about 30 microns in size) is formed from a small vegetative form, has pseudopodia, has a jerky forward movement, can phagocytize erythrocytes. Found in fresh feces in amoebiasis. The cystic form (resting stage) is represented by a cyst with a diameter of 9-16 microns. A mature cyst contains 4 nuclei (in a non-pathogenic Entamoeba coli cyst contains 8 nuclei).
resistance.Vegetative forms of the pathogen outside the body quickly die. Cysts persist in faeces and water at 20°C for 2 weeks. In foodstuffs, on vegetables and fruits, cysts persist for several days. When boiled, they die.
Epidemiology.The source of infection is a person, i.e. amoebiasis is an anthroponotic disease. The mechanism of transmission of amoebas is fecal-oral, the routes of transmission are alimentary, water and
Rice. 19.1.Morphology of amoebas: a, b - trophozoites Entamoeba histolitica, one of which absorbs red blood cells; in - Entamoeba hartmani- trophozoite with food vacuole; g - cysts with 1, 2 and 4 nuclei; e - dual-core (left) and single-core (right) precysts Entamoeba hartmani
contact-household. Infection occurs when cysts are introduced with food, especially vegetables and fruits, less often with water, through household items. Flies and cockroaches contribute to the spread of cysts. Children over 5 years of age are more commonly affected. The highest incidence is observed in regions of tropical and subtropical climate.
Pathogenesis and clinical picture. From cysts that have entered the intestine, luminal forms of amoebas are formed that live in the large intestine without causing disease. The luminal forms act as commensals of the intestine, feeding on its contents without adverse effects. Such a person is a healthy carrier E. histolytica, excreting cysts. Asymptomatic carriage is widespread E. histolytica. With a decrease in the body's immunity, luminal forms of amoebas are introduced into the intestinal wall and multiply in the form of tissue forms. Intestinal amebiasis develops, which is facilitated by some representatives of the intestinal microflora. Trophozoites of the tissue form are mobile due to the formation of pseudopodia. They penetrate the colon wall, causing coagulative necrosis, are able to phagocytize erythrocytes (erythrophages, hematophages), and can be found in freshly excreted human feces. With necrosis, crater-shaped ulcers with undermined edges are formed. Clinically, intestinal amebiasis manifests itself in the form of frequent liquid stools with blood ("raspberry jelly"), accompanied by tenesmus, fever and dehydration. Pus and mucus, sometimes with blood, are found in the feces.
Extraintestinal amebiasis develops when amoebae penetrate the bloodstream into the liver, lungs, brain and other organs. Formed single or multiple amoebic abscesses ranging in size from barely visible to the eye to 10 cm in diameter. Perhaps the development of skin amebiasis: on the skin of the perianal region and the perineum, erosions and painless ulcers form.
Immunityunstable in amoebiasis. Antibodies are formed only to tissue forms E. histolytica. The cellular link of immunity is activated mainly.
Microbiological diagnostics. The main method is a microscopic examination of the patient's feces, as well as the contents of abscesses of internal organs. Smears are stained with Lugol's solution or hematoxylin. E. histolytica differentiate by cysts and trophozoites from other intestinal protozoa
charge type E. coli, E. hartmanni, E. polecki, E. gingivalis, Endolimax nana, Iodamoeba buetschlii and etc . Antibodies to the pathogen are detected in RNGA, ELISA, indirect RIF, RSK, etc. The highest titer of antibodies in the blood serum is detected with extraintestinal amoebiasis. Molecular biological method (PCR) makes it possible to determine DNA marker regions in faeces E. histolytica.
Treatment.Metronidazole, tinidazole, mexaform, osarsol, yatren, diyodoquine, delagil, dihydroemitin, etc. are used.
Prevention.Identification and treatment of cystic excretors and amoeba carriers, as well as general sanitary measures.
19.2. Flagellates
Flagellates include Leishmania, Trypanosomes, Giardia, and Trichomonas. They have one or more flagella. A blepharoplast is located at the base of the flagellum, in some protozoa there is a kinetoplast nearby - a DNA-containing organoid of mitochondrial origin that promotes the movement of the flagellum.
19.2.1. Leishmania (genus Leischmania)
Leishmaniasis - protozoan diseases of animals and humans, caused by leishmania and transmitted by mosquitoes; the internal organs (visceral leishmaniasis) or the skin and mucous membranes (cutaneous, mucocutaneous leishmaniasis) are affected.
The causative agent of cutaneous leishmaniasis was discovered in 1897 by the Russian doctor P.F. Borovsky in Tashkent, and the causative agent of visceral leishmaniasis in 1900 by W. Leishman and in 1903 by Sh. Donovan independently of each other.
The disease in humans is caused by over 20 species of Leishmania that infect mammals: L. donovani-complex with 3 types (L. donovani, L. infantum, L. chagasi); L. mexicana-complex with 3 main species (L. mexicana, L. amazonensis, L. venesuelensis); L. tropica; L. major; L. aethiopica; subgenus Viannia with 4 main views. All species of Leishmania are morphologically indistinguishable. They are differentiated using monoclonal antibodies or molecular genetic methods.
prethelial system. They reproduce by simple division. They have flagellated (promastigous) and non-flagellated (amastigote) cycles of asexual development.
Rice. 19.2.Leishmania donovani:a - a large reticuloendothelial cell of the spleen with amastigotes; b - promastigotes observed in mosquitoes and when cultivated on a nutrient medium; c - fissile forms
Cultivation. Leishmania cultivated on the medium NNN(authors - Nicole, Novi, Neil), containing agar with defibrinated rabbit blood. They can be grown on chick chorioallantoic membranes, in cell cultures, or on white mice, hamsters, and monkeys.
Epidemiology.Leishmaniasis is common in warm and tropical climates. The mechanism of transmission of pathogens is transmissible through the bite of mosquitoes.
The main sources of infection are: in cutaneous anthroponotic leishmaniasis, people; with cutaneous zoonotic leishmaniasis of gerbils and other rodents; with visceral leishmaniasis people (with Indian visceral leishmaniasis) or dogs, jackals, foxes, rodents (with Mediterranean-Central Asian visceral leishmaniasis); with mucocutaneous leishmaniasis rodents, wild and domestic animals.
Pathogenesis and clinical picture. Anthroponotic cutaneous leishmaniasis causes L. tropica. The disease had various names: late ulcerative leishmaniasis, urban form, Ashgabat ulcer, "year-old". The disease is more common in cities and is characterized by a long incubation period - from 2-4 months to 1-2 years. At the site of a mosquito bite, a tubercle appears, which increases and ulcerates after 3-4 months. Ulcers are more often located on the face and upper limbs, scarring by the end of the year (hence the popular term "year-old").
Zoonotic cutaneous leishmaniasis (early ulcerating leishmaniasis, penda ulcer, rural form) causes L. major. The disease is more acute. The incubation period is 2-4 weeks. Weeping ulcers are more often localized on the lower extremities. The duration of the disease is 2-6 months.
Indian visceral leishmaniasis (anthroponotic visceral leishmaniasis (kala-azar, black disease)) is caused by leishmania complex L. donovani; found mainly in Europe, Asia and South America. Average incubation period
5-9 months In patients, the spleen, liver, lymph nodes, bone marrow and digestive tract are affected. Hypergammaglobulinemia, dystrophy and necrosis of organs develop. Due to the defeat of the adrenal glands, the skin darkens, rashes appear on it - leishmanoids.
Mediterranean-Central Asian visceral leishmaniasis (pathogen L. infantum) has a similar clinical picture, except for changes in the skin, which turns pale. The incubation period is from 1 month to 1 year. Children get sick more often.
Brazilian mucocutaneous leishmaniasis (espundia) causes L. braziliensis; develops granulomatous and ulcerative lesions of the skin of the nose, mucous membranes of the mouth and larynx. The incubation period is from 2 weeks to 3 months. Changes in the shape of the nose (tapir nose). It occurs mainly in Central and South America, as well as similar diseases caused by L. mexicana(Mexican leishmaniasis), L. peruviana(Peruvian leishmaniasis), L. panamensis(Panamanian leishmaniasis), etc.
Immunity.People who have been ill still have lifelong immunity.
Microbiological diagnostics. Smears from tubercles, contents of ulcers or punctates from organs are stained according to Romanovsky-Giemsa. Microscopic examination reveals intracellularly located amastigotes. A pure culture of the pathogen is isolated on the medium NNN: incubation for 3 weeks at room temperature. They also infect white mice and hamsters. From serological methods, RIF, ELISA are used. The skin allergy test (Montenegro test) for HRT to leishmanin (a preparation made from killed promastigotes) is used in epidemiological studies of leishmaniasis. It is positive after 4-6 weeks of illness.
Treatment.In systemic treatment, injections of preparations of oxide of 5-valent antimony - stibogluconate (pentostam) are prescribed. For cutaneous leishmaniasis, chlorpromazine, paromomycin, or clotrimazole ointments are topically applied.
Trypanosomes (genus trypanosoma)
Trypanosomes cause vector-borne diseases - trypanosomiasis. Trypanosoma brucei gambiense And Trypanosoma brucei rhodesiense(varieties T.brucei) cause African trypanosomiasis, or sleeping sickness, and Trypanosoma cruzi- American trypanosomiasis (Chagas disease). Pathogens were discovered in 1902 by D. Daton (T. gambiense), in 1909 by Sh. Chagas (T. cruzi) and in 1910 G. Fantenem (T. rhodesiense).
characteristics of pathogens. Trypanosomes are larger in size (1.5-3x15-30 microns) than Leishmania. They have a narrow oblong shape, a flagellum and an undulating membrane (Fig. 19.3). They reproduce asexually (longitudinal fission). The source of infection are domestic and wild animals, an infected person. African trypanosomiasis is transmitted by blood-sucking tsetse flies, while Chagas disease is carried by triatomine bugs. Pathogens have different stages of development: amastigotes, epimastigotes, trypomastigotes. amastigotes are oval in shape and do not have a flagellum. This stage is typical for T. cruzi, living in muscles and other human tissue cells. Epimastigotes grow in the intestines of carriers and on nutrient media. The flagellum extends from the middle of the elongated cell (near the nucleus). Trypomastigote found in the blood of animals and humans. The flagellum extends from the back of the elongated cell. The undulating membrane is pronounced.
Pathogenesis and clinical picture. Gambian form African trypanosomiasis, called T. gambiense, is chronic, and the Rhodesian form, caused by T. rhodesiense, is a more acute and severe form of the disease. At the site of a bite by a carrier - a tsetse fly - by the end of the week an ulcerative
Rice. 19.3.Morphology of trypanosomes: a, b - trypomastigotes in the blood; c - epimastigote in the intestines of carriers
Patients develop lymphadenitis, myocarditis, fever. The gastrointestinal tract, liver, spleen, and brain are affected. It has a long latent period, up to several decades.
Immunity.In response to invasion, IgM antibodies are formed in large quantities. In the chronic phase, IgG antibodies predominate. Trypanosomes are able to form new antigenic variants that change the immune response. Autoimmune processes develop.
Microbiological diagnostics. Smears from blood, punctate of cervical lymph nodes, cerebrospinal fluid are stained according to Romanovsky-Giemsa or Wright. To isolate the pathogen, you can infect white mice or rats, as well as inoculate on nutrient media with blood. With the serological method, IgM antibodies are determined using ELISA, RSK or indirect RIF.
Treatment.For the treatment of African trypanosomiasis, suramin or pentamidine is prescribed, and for CNS damage, melarsoprol.
Treatment of American trypanosomiasis is possible only in the acute phase with benznidazole or nifurtimox.
Preventionnonspecific. Eliminate breeding sites of carriers of the pathogen, destroy infected animals. Identify and treat infected individuals. Apply repellents and protective clothing.
Giardia, or Giardia (genus Lamblia, or Giardia)
Giardiasis (giardiasis) is a disease caused by Lamblia intestinalis (Giardia lamblia), proceeding in a latent or manifest form in the form of intestinal dysfunction with enteritis phenomena. The causative agent was discovered by D.F. Lamblem in 1859. In 1915, he was assigned to the genus Giardia in honor of Giard.
Characteristics of the pathogen. The vegetative cell of lamblia is flat, pear-shaped (5-10x9-20 microns), contains two nuclei (Fig. 19.4) and 4 pairs of flagella. Giardia reproduce by longitudinal division. They are attached to intestinal epitheliocytes with the help of a suction disk and due to the adhesion of microoutgrowths of the trophozoite plasmolemma. Giardia lives in the upper sections of the intestine, and in the less favorable lower sections of the intestine they form oval four-core cysts (6-10x12-14 microns), surrounded by a thick double-circuit membrane.
Rice. 19.4.Giardia lamblia.Vegetative forms: a - in front; b - on the side; c, d - cysts
resistance.Giardia cysts are resistant to low temperatures and chlorinated water. They die instantly when boiled. They remain in soil and water for more than 2 months.
Epidemiology.The source of infection with cysts are people, less often dogs, cattle, beavers, muskrats, deer. The mechanism of infection is fecal-oral: through contaminated water, food, hands and household items. Waterborne outbreaks of diarrhea are possible.
Pathogenesis and clinical picture. Giardia live in the duodenum and jejunum. Propagating in large numbers, they block the mucous membrane, disrupting parietal digestion and intestinal motility. The development of giardiasis depends on the degree of resistance of the organism. Giardia can cause diarrhea, enterocolitis, and metabolic disorders. Perhaps the development of gastroenterocolitic, cholecystopancreatic and asthenic syndromes.
Microbiological diagnostics. In smears from feces, cysts are detected (stained with Lugol's solution). With diarrhea and duodenal sounding, vegetative forms (trophozoites) are found in native preparations. Typical is their movement in the form of a falling leaf. The serological method can determine the increase in antibody titer in ELISA and indirect RIF.
Treatment.Apply metronidazole, tinidazole, furazolidone.
Preventionsimilar to that of amoebiasis. It is important to follow the rules of personal hygiene.
Trichomonas (genus Trichomonas)
Trichomoniasis is an anthroponotic disease caused by Trichomonas urogenital (Trichomonas vaginalis); accompanied by damage to the genitourinary system. Another Trichomonas - intestinal - is called Pentatrichomonas (Trichomonas) hominis. It causes intestinal trichomoniasis in weakened individuals - anthroponosis in the form of colitis and enteritis. There are also oral Trichomonas (T. tenax), which is the commensal of the mouth.
Characteristics of the pathogen. Trichomonas vaginalisexists only as a trophozoite, reproduces by division. Cyst does not form. It has a pear shape, size 8-40x3-14 microns. Five flagella are located at the anterior end of the cell. One of them is connected to
Rice. 19.5.Trichomonas vaginalis:a - normal trophozoite; b - rounded shape after division; c - the form observed after staining the preparation
cell with an undulating membrane reaching to the middle of the cell. An axial thread (hyaline axostyle) passes through the cell, emerging from the posterior end of the cell in the form of a spike (Fig. 19.5). The cytostome (cell mouth) looks like a small gap on the front of the body. Reproduces by longitudinal division.
resistance.It quickly dies in the environment, remains on sponges and washcloths for 10-15 minutes, and in mucus, semen and urine -
24 hours
Epidemiology.Humans are the source of the invasion. The disease is transmitted sexually, through the birth canal (infant), rarely through personal hygiene items. The incubation period is 7-10 days, sometimes 1 month.
Pathogenesis and clinical picture. Trichomonas vaginalis,attaching to the mucous membrane, causes vaginitis, urethritis, prostatitis. The inflammatory process is accompanied by pain, itching, purulent-serous discharge. The pathogen can phagocytize gonococci, chlamydia and other microbes, which complicates the pathological process. Trichomonas often causes an asymptomatic infection.
Microbiological diagnostics. Trichomonas are detected microscopically in native and stained smears from a fresh drop of vaginal discharge, urethral discharge, prostate secretion or urine sediment. Smears are stained with methylene blue or Romanovsky-Giemsa. With phase-contrast or dark-field microscopy of native
ny drugs, the mobility of trichomonads is observed. The native preparation is prepared on a glass slide by mixing the discharge with a drop of warm isotonic sodium chloride solution. The smears are covered with a coverslip and microscoped (x400 magnification). Trichomonas have characteristic jerky movements of the undulating membrane and flagella. They are smaller in size than epithelial cells, but larger than leukocytes. There may be large atypical amoeboid forms of Trichomonas. The leading method for diagnosing chronic forms of the disease is the cultivation of Trichomonas on nutrient media, such as SKDS (saline solution with casein, yeast and maltose hydrolysates). The serological method using ELISA or indirect RIF helps in the diagnosis. They also do PCR.
Treatment.Ornidazole, nimorazole, metronidazole, tinidazole are used.
Preventionas in venereal diseases. Prevention in women can be carried out with the Solkotrivak vaccine, which is prepared from lactobacillus acidophilus.
19.3. spores
19.3.1. Plasmodium malaria (genus Plasmodium)
Malaria is an anthroponotic disease caused by protozoa of the genus Plasmodium accompanied by bouts of fever, anemia, enlargement of the liver and spleen. There are four types of malaria that cause malaria in humans: Plasmodium vivax, Plasmodium ovale, Plasmodium malariae And Plasmodium falciparum. The first malaria pathogen (P. malariae) was discovered in 1880 by the French physician A. Laveran.
characteristics of pathogens. The life cycle of plasmodia occurs with a change of hosts: in a mosquito of the genus Anopheles(the final host) sexual reproduction occurs, or sporogony (the formation of elongated cells - sporozoites), and in the human body (intermediate host) asexual reproduction occurs - schizogony, or rather merogony, in which small cells are formed, called merozoites.
The duration of the development cycle in erythrocytes in P. vivax, P. ovale, P. falciparum is 48 hours, R. malariae- 72 hours. In some erythrocytes, merozoites also give rise to the formation of sexual immature forms - male and female gametes (gamonts, gametocytes). Gametes are oval, except for banana-shaped gametes P. falciparum. With the onset of erythrocyte schizogony, the reproduction of pathogens in the liver stops, except P. vivax And R. ovale, in which part of the sporozoites (dormant, the so-called hypnozoites, or bradyzoites) remain in hepatocytes for weeks or months, which leads to the appearance of late, distant relapses of the disease. When a female mosquito bites a malaria patient, immature sexual forms of the pathogen enter her stomach along with blood. Gametogony begins in the mosquito. Gamonts mature and fertilize, forming a zygote, which turns into an elongated mobile form - an ookinete. The ookinete penetrates the wall of the stomach and forms an oocyst on the outer surface of the stomach, in which sporogony is completed with the formation of up to 10,000 sporozoites. Part of the sporozoites (2%) then enters the salivary glands of the carrier with the hemolymph current. Different types of pathogen cause disease with different clinical presentation and morphological changes in blood smears.
Tropical malaria is the most severe, in which Plasmodium P. falciparum multiply in erythrocytes (of any age) of small vessels of internal organs, causing intravascular hemolysis, blockage of capillaries, hemoglobinuric fever. This process is enhanced as a result of immunopathological hemolysis of uninfected erythrocytes. Violation of blood microcirculation and hemolysis lead to brain damage (malarial coma), the development of acute renal failure. Lethality is about 1%.
Treatment.The main antimalarial drugs include: quinine, mefloquine, chloroquine, quinacrine, primaquine, bigumal, pyrimethamine, etc. Antimalarial drugs have different effects on the asexual and sexual stages of Plasmodium. There are preparations of schizontocidal (histo- and hematoschisontotropic), gamontotropic and sporozoitotropic action.
Toxoplasma (genus Toxoplasma)
Tachyzoites(trophozoites) are formed during the reproduction of sporozoites in epithelial cells. They have a characteristic shape
cultivation .Toxoplasma is cultivated in chicken embryos and tissue cultures, as well as by infecting white mice and other animals.
resistance.Oocysts can remain viable in the environment for a year. Toxoplasma quickly die at 55? C, highly sensitive to 50% alcohol, 5% NH 4 OH solution.
Epidemiology.The disease is ubiquitous, but is more common in warm, humid climates, with a high prevalence of cats. Humans become infected through the alimentary route through food and water containing oocysts excreted by cats, or by ingestion of undercooked meat, milk, eggs containing pseudocysts and cysts. Animals and humans can also become infected through food and water containing oocysts excreted by cats. Less commonly, Toxoplasma enters by contact (through damaged skin and mucous membranes) or by airborne dust. With congenital toxoplasmosis, the pathogen enters the fetus through the placenta. Sometimes infection occurs as a result of blood transfusion, organ transplantation.
Pathogenesis and clinical picture. Toxoplasma enters the small intestine, reaches regional lymph nodes with lymph flow,
Immunitynon-sterile. When the disease develops cellular and humoral immunity. Allergy develops (HRT). With congenital toxoplasmosis, a high level of specific antibodies is detected in the blood of the mother and child.
Microbiological diagnostics. Smears are microscopically taken from biopsy specimens, biological fluids (blood, cerebrospinal fluid, punctates of lymph nodes, fetal membranes, etc.), stained according to Romanovsky-Giemsa or Wright.
The serological method is the main one in the diagnosis of toxoplasmosis: the appearance of IgM antibodies indicates the early stages of the disease; the level of IgG-antibody reaches a maximum at the 4-8th week of illness. ELISA, RIF, RNGA, RSK, as well as the Sabin-Feldman reaction, or a coloring test are used (with this method, the pathogen, depending on the properties of the antibodies of the blood serum under study, stains differently with methylene blue). They also use the allergological method - intradermal pro-
bu with toxoplasmin, which is positive from 4 weeks of illness and then for many years. The biological method is used less frequently; after parenteral injection of infected material (blood, cerebrospinal fluid, biopsies of organs and tissues) to mice, they die in 7-10 days. Toxoplasma can be cultured on cells HeLa or on 7-8 day old chick embryos. It is possible to use PCR.
Treatment.The most effective combination of pyrimethamine with sulfonamides. During pregnancy, it is recommended to use spiramycin instead of pyrimethamine, which does not pass through the placenta.
Prevention.To prevent congenital toxoplasmosis, women who are planning a pregnancy should be screened for antibodies. Non-specific prevention of toxoplasmosis is carried out, including personal hygiene, in particular hand washing before eating; careful heat treatment of meat is necessary. Contact with felines should be avoided. The extermination of rodents, flies and cockroaches - potential mechanical carriers of oocysts - is also important.
ciliated
Ciliated are represented by balantidia, which affect the human large intestine (balantidiasis dysentery). They have cilia - organelles of movement that cover the cell and cell mouth (cytostome), two nuclei (macro- and micronucleus).
19.4.1. Balantidia (genus Balantidium)
Balantidiasis (infusor dysentery) is a zoonotic disease caused by Balantidium coli, characterized by general intoxication and ulcerative lesions of the colon. The causative agent was discovered in 1856 by the Swedish physician P. Malmsten.
swallow microbes and other cells, including blood cells.
Microbiological diagnostics. For microscopy, a drop of fresh liquid feces is placed in an isotonic sodium chloride solution and the “crushed drop” preparation is repeatedly examined under a low magnification microscope, observing the active movement of large balantidia. Cysts in human feces are rare.
Treatment.Apply metronidazole, oxytetracycline and other drugs prescribed for amoebiasis.
Prevention.Compliance with the rules of personal hygiene, especially for pig workers. Prevention of environmental pollution by feces of pigs and other animals.
Dermatomycoses include trichophytosis, microsporia, school desk (favus), epidermophytosis. The causative agents are dermatomycetes, related to imperfect fungi.
Trichophytosis. The causative agents belong to the genus Trychophyton. Depending on the type of pathogen, superficial trichophytosis (ringworm) or deep (infiltrative suppurative) develops. With ringworm, the hair breaks at the very surface of the skin, hence the name of the disease. Mostly children are ill.
Microsporia. The causative agent is a fungus of the genus Microsnoron. Around the affected hair, a kind of sheath of small spores is formed, which is why the hair seems to be sprinkled with flour. Only affects children.
Scab (favus). The causative agent is fungi of the genus Aehorion. Affects skin, hair, nails. Possible damage to the lymph nodes and internal organs. Mostly children get sick.
Epidermophthia. Pathogens from the genus Bpidermophyton affect the horny elephant of the epidermis, less often the nails, do not affect the hair. Distinguish between inguinal epidermophytosis and epidermophytosis of the feet. It affects mostly adults, sometimes teenagers.
The source of infection in ringworm are sick people or animals. Infection occurs through direct contact and through objects.
Laboratory diagnostics carried out by microscopy of the affected hair, scales of the skin and nails. In the preparation of a "crushed" drop, the hair treated with a hot 15% alkali solution to dissolve the horny substance is microscoped. Segments of hyphae of the fungus are found under a microscope (Fig. 48).
In cases where microscopic examination does not give results, seeding is done on Sabouraud's medium. The growth of characteristic colonies appears after 6-8 days.
Allergic intradermal tests are also used.
candidiasis
The causative agents are yeast-like fungi of the genus Candida, most often Candida albicans.
Yeast-like fungi are similar to yeast in the morphology of round and oval cells - blastospores. They differ from true yeasts in the ability to form pseudomycelium and the absence of sexual reproduction (Fig. 49).
On a dense Sabouraud medium, white creamy colonies form, which grow into the thickness of the agar during aging.
Candidiasis can result from exogenous infection by contact with a sick person, through infected objects, or from carriers, for example, by contact of a newborn and infant with an adult, but endogenous infection is often observed, since Candida albicans is a representative of the normal microflora of the body. Endogenous candidiasis develops with dysbacteriosis or as a concomitant disease with another chronic and severe process. In the occurrence of candidiasis, a large role is played by the long-term use of broad-spectrum antibiotics, which suppress the normal microflora of the body, which leads to dysbacteriosis and increased reproduction of Candida fungi, which are naturally resistant to antibiotics.
Candidiasis is an occupational disease of persons whose work is related to vegetables, fruits, fruit confectionery, as well as dishwashers and bath workers.
With superficial candidiasis, white plaques (thrush) appear on the mucous membranes of the oral cavity, tongue, in the corners of the mouth, and on the vaginal mucosa. Small red spots, vesicles appear on the skin, which turn into erosion.
With deep candidiasis, the lungs, intestines, renal pelvis and bladder are affected, and sepsis may develop.
Laboratory diagnostics. The greatest importance is attached to the microscopic, serological and somewhat less - to the cultural method.
Microscopically native unstained preparations or stained by conventional methods. Single yeast cells can be found in sputum, feces, and urine of healthy individuals. The pathological picture corresponds to the presence of a large number of budding cells and especially mycelial filaments.
Serological studies are of great importance in the defeat of internal organs. Put RSK and other reactions.
Growing a culture from the test material is of limited importance, since in healthy individuals, when sowing sputum, urine, and scrapings from the mucous membranes, Candida growth can be obtained. Obtaining a culture is certainly demonstrative when sowing blood, cerebrospinal fluid, punctate lymph nodes, closed abscesses. Sowing material produced on Sabouraud medium and grown at 30°C. After 2-3 days, the growth of white creamy colonies is noted, with microscopy - budding cells, mycelial filaments, the presence of which is necessary to distinguish from true yeast. For treatment, decampn, nystatin, levorin, clotrimazole, fluconazole are used.
Deep mycoses
Deep mycoses: coccidioidomycosis, histoplasmosis, cryptococcosis, blastomycosis. The disease is characterized by damage to internal organs, often with dissemination of the process.
Pneumocystosis refers to opportunistic mycoses. Opportunistic infections are infections caused by opportunistic pathogens.
The causative agent of pneumocystosis or pneumocystis pneumonia is Pneumocystis carinii, which belongs to blastomycetes (yeast microorganisms). It is found in lung tissue; it was not obtained in pure culture on nutrient media.
In people with normal immune systems, P. carinii does not cause disease. Pneumocystosis develops with immunodeficiencies. Among people with AIDS, pneumocystis pneumonia develops in 80% of cases. The disease is also observed in patients receiving immunosuppressants for therapeutic purposes.
Laboratory diagnostics is carried out by microscopy of pathological material. For staining, the Romanovsky-Giemsa method is used. Serological diagnostics - with the help of RIF and ELISA.
For treatment, trimethoprim is used in combination with sulfamethoxazole or diaminodiphenyl sulfone.
PATHOGENIC PROTOZA
The simplest microorganisms are widely distributed in nature, among them there are saprophytes and pathogenic species that cause diseases in humans and animals. These include dysenteric amoeba, Giardia, Trichomonas, Leishmania, Plasmodium malaria, Toxoplasma and others.
dysenteric amoeba
Dysenteric amoeba (Entamoeba histolytica) was discovered by the Russian doctor F.A. Lesh in 1875 in a patient with chronic colitis.
Two stages are distinguished in the development cycle of the dysenteric amoeba: 1) the vegetative stage, which includes the large vegetative, projet, and precystic forms; 2) resting stage - cyst.
Amoebic dysentery - anthroponosis. The source of invasion is a person with a chronic form of the disease, or a carrier. The main mechanism of infection transmission is fecal-oral. The main role in human infection belongs to cysts, which persist for a long time in the external environment.
When it enters the small intestine, the cyst shell is destroyed, amoebas come out of it, which
multiply in the large intestine, are introduced into its wall. Ulcers form in the intestines. Amoebas can be carried with the bloodstream to the liver, lepsy, and brain.
Laboratory diagnostics is carried out by microscopic examination of preparations from feces (Fig. 50).
Metronidazole and furamid are used for treatment.
lamblia
The causative agent of giardiasis Lamblia intestinalis was discovered by the Russian scientist D.F. Lamblem in 1859. It belongs to the flagellar protozoa. It lives in the upper intestines, in the lower sections it forms cysts. The source of invasion are sick people and carriers. Infection occurs by the fecal-oral route. Infection with Giardia does not always lead to disease. With a large accumulation of Giardia, they can cause chronic cholecystitis.
Laboratory diagnostics is carried out by microscopic examination of native and stained with Lugol's solution preparations prepared from duodenal contents (Fig. 51). Giardia are cultivated on nutrient media with an extract of yeast-like fungi.
For treatment, quinacrine and aminocholine are used.
Trichomonas
The causative agent of urogenital trichomoniasis is Trichomonas vaginalis. It belongs to the flagellated protozoa. Cyst does not form. In the environment, it quickly dies. Trichomonas grow well on nutrient media in the presence of bacteria that serve to feed them.
For treatment, osarsol, aminarson, furazolidone, etc. are used.
Leishmania
The causative agents of leishmaniasis Leishraania tropica, L. donovani, L. braziliensis are flagellated protozoa.
In laboratory conditions, Leishmania are cultivated on special nutrient media.
The main reservoir and source of cutaneous leishmaniasis are ground squirrels, gerbils and other rodents, visceral leishmaniasis - dogs. The infection is transmitted by the bite of mosquitoes.
Cutaneous leishmaniasis cause two types of leishmania.
L. tropica minor is the causative agent of urban cutaneous leishmaniasis, in which sick people and dogs are the source of infection. The incubation period is long - 3-6 months. At the site of the mosquito bite, a tubercle appears, which slowly increases and ulcerates. The disease lasts 1-2 years.
L. tropica major is the causative agent of rural cutaneous leishmaniasis, in which ground squirrels, gerbils, and other rodents are the source of infection. The incubation period is short, 2-4 weeks, the formation of a tubercle at the site of implementation, ulceration and scarring occur faster.
Visceral leishmaniasis caused by L. donovani, found in countries with a tropical climate.
L. braziliensis causes leishmaniasis that affects the skin of the nose and the mucous membranes of the mouth and larynx.
After the transfer of leishmaniasis, strong immunity remains.
For the treatment of visceral leishmaniasis, solyusurmin, neostibosan are used. In cutaneous leishmaniasis, quinacrine, amphotericin B.
For prevention, vaccinations with a live culture of L. tropica major are practiced.
Plasmodium malaria
Pathogens belong to the class of sporozoans. Malaria in humans is caused by 4 types of malarial plasmodia: Plasmodium vivax - the causative agent of three-day malaria, Plasmodium malariae - the causative agent of four-day malaria, Plasmodium falciparum - the causative agent of tropical malaria, Plasmodium ovale causes three-day malaria (color insert Fig. 53).
In the human body (the intermediate host of malarial plasmodia), the asexual phase of the life cycle (schizogony) of parasites occurs. The sexual phase of their life cycle (sporogony) takes place in the body of the final host - a blood-sucking mosquito of the genus Anopheles. As a result, long thin cells - sporozoites - are formed in the body of the mosquito. They accumulate in large quantities in the salivary glands of the mosquito. When a mosquito bites, the sporozoites, along with the saliva of the mosquito, enter the human bloodstream, then penetrate the liver.
The development of plasmodium in the human body takes place in two cycles: tissue or extra-erythrocyte schizogony occurs in liver cells; erythrocyte schizogony - in erythrocytes.
The tissue cycle of schizogony occurs in liver cells and ends with the formation of tissue merozoites, which destroy liver cells, enter the bloodstream and infect erythrocytes.
Erythrocyte cycle of schizogony. The tissue merozoite, having penetrated into the erythrocyte, takes the form of a ring, since there is a vacuole in its center. Its cytoplasm is stained blue according to Romanovsky-Giemsa, the nucleus is red. The merozoite grows and becomes a schizont. The schizont divides to form merozoites. Erythrocytes are destroyed, merozoites enter the bloodstream and infect other red blood cells. Some merozoites, penetrating into an erythrocyte, turn into sexual forms, which enter the stomach of a female mosquito with blood when she bites a sick person.
The duration of the erythrocyte development cycle in P. vivax, P. falciparum and P. ovale is 48 hours, P. malariae is 72 hours. Accordingly, febrile attacks are repeated: with three-day and tropical malaria - after a day, with four-day - after two days.
Laboratory diagnostics is carried out by microscopic examination of a thick drop and a blood smear stained according to Romanovsky-Giemsa. Serological diagnostics is used.
For treatment, drugs are used that act on asexual forms of plasmodium (chloroquine, amodaquine) and on sexual forms (pyrimethamine, proguanil, quinocide, primaquine).
For the specific prevention of malaria, a vaccine is being developed that contains antigens obtained by genetic engineering.
Toxoplasma.
The causative agent of toxoplasmosis, Toxoplasma gondii, belongs to the class of sporozoans. First discovered by Nicol and Manso in 1908 in gondii rodents in North Africa.
Intermediate hosts are, in addition to humans, many species of animals and birds. In the body of intermediate hosts, Toxoplasma go through an asexual development cycle.
The clinical manifestations of toxoplasmosis are varied. Acquired toxoplasmosis is expressed in the defeat of the lymph nodes, eyes, heart, lungs, intestines, nervous system. Often, toxoplasmosis occurs in an asymptomatic form, in which, however, antibodies are formed. In the cells of the reticulo-macrophage and central nervous system, cysts are formed that persist for a long time without clinical manifestations. A person infected with toxoplasma does not release them into the external environment.
Congenital toxoplasmosis is a serious disease. The child has lesions of the central nervous system, eyes, developmental defects.
Infection of the fetus in early pregnancy leads to its death.
Laboratory diagnostics is carried out by microscopy of a smear from a pathological material stained according to Romanovsky-Giemsa. It is possible to obtain a culture of Toxoplasma by intraperitoneal infection of mice, followed by a study of peritoneal exudate. In laboratory practice, serological methods are usually used: RSK, RIF, RIGA, as well as the Sebin-Feldman reaction, the principle of which is that live Toxoplasma in the presence of antibodies in the patient's blood serum lose their ability to stain with methylene blue. An allergic test with toxoplasmin is put.
For treatment, chloridine (tsaraprim), sulfa drugs are used.
Introduction 5
Brief outline of the history of the development of microbiology 5
Part one
GENERAL MICROBIOLOGY
Chapter 1 The place of microorganisms among other living beings 13
Classification and systematics 13
Chapter 2 Morphology of microorganisms 15
Bacteria 15
Mycoplasmas 21
Rickettsia 21
Chlamydia 22
Actin o midets 22
Spirochetes 23
Protozoa 25
Chapter 3 Methods of microscopic examination of microbes 26
Microscopy in a light optical microscope 26
Dark field microscopy 28
Phase contrast microscopy 29
Fluorescence microscopy 29
Electron microscopy 30
Chapter 4 Physiology of Microorganisms 30
Chemical cociaB microorganisms 30
Metabolism (substance exchange) of microorganisms 32
Nutrition of microbes (constructive metabolism) 32
Enzymes 33
Biological oxidation (energy storage) 34
Growth and reproduction of microorganisms 36
Formation of pigments, aromatic substances by microbes
Luminous microorganisms 37
Chapter 5 Microorganism Cultivation Methods
Study of cultural and biochemical properties 38
Culture media 38
Cultivation and isolation of pure cultures of aerobic bacteria 39 Cultivation and isolation of pure cultures of anaerobic bacteria 41 Cultivation of other microorganisms of mycoplasmas, rickettsia, chlamydia, spirochetes, fungi, protozoa 42 Methods for studying the enzymatic activity (biochemical properties) of microorganisms 42 Chapter 6 General virology 44 General characteristics of viruses ,
morphology and structure of virions 44 Reproduction of viruses 46 Methods of cultivation of viruses 48 Chapter? Bacteriophages and bacteriophage 49 Structure of bacteriophages 50 Interaction of a bacteriophage with a bacterial cell 50 Practical significance of bacteriophages 52 Chapter 8 Ecological microbiology (microecology) 53 Soil microflora 54 Water microflora 55 Microflora in the air 55 Food microorganism 56 Microflora of various objects 56 The role of microorganisms in the circulation of substances in nature, in the emergence and existence of the biosphere 57 Chapter 9 Influence of environmental factors on microorganisms 60 Influence of physical factors 61 Influence of chemical factors 62 Influence of biological factors 64 Antiseptic asepsis, disinfection, sterilization 64 Chapter 10 Genetics of microorganisms 68 Organization of genetic material in bacteria Genotype and phenotype 68 Variability of microorganisms 69 Genetic recombinations 70 Practical significance of the doctrine of the genetics of microorganisms 73 Genetic engineering 73 Chapter 11 Antibiotics 74 Natural and semi-synthetic antibiotics 75 Chemotherapeutic agents (si synthetic antibiotics) 76
Side effects of antibiotic therapy...............................................................79
Drug resistance of microbes ........................................................:.... .......80
Chapter 12. Microflora of the human body .............................................. ......................83
The relationship of microbes and the macroorganism .............................................. 83
Characteristics of the microflora of the human body .............................................. 84
The value of the microflora of the human body. Dysbacteriosis...................86
Chapter 13 ................................................. ..........88
Properties of a pathogenic microorganism .............................................................. ......88
The value of the state of the macroorganism and the conditions of external
environment in the infectious process .............................................................. ....................91
f Characteristic features of an infectious disease....................................................92
Forms of manifestation of the infectious process .............................................. 92
Peculiarities of viral infections .............................................................. .................94
Congenital infections .................................................................. .................................94
Opportunistic pathogens .................................................................. .........95
Nosocomial infections .................................................................. ......................95
Glaven. Immunity................................................. ................................................. ....96
Types of immunity. Non-specific protective factors ..........................................97
Acquired immunity .................................................................. .........................102
Types and forms of acquired immunity.........................................102
Antigens...................................................................................................104
The immune system of the body..................................................................106
Immune response (immunogenesis)............................................................108
Antibodies (immunoglobulins)...................................................................110
Allergy......................................................................................................................... 115
Peculiarities of antiviral immunity....................................................... 118
Immunodeficiency states .................................................................. ...................119
Assessment of the body's immune status .............................................................. ...........120
Immunopharmacological agents .................................................................. .......120
Formation and development of the immune system in ontogeny .............................. 121
Immune reactions .................................................................. ...................................123
Toxin neutralization reaction with antitoxin..................................123
Agglutination reaction.............................................................................124
Indirect or passive hemagglutination reaction..............................125
Coombs reaction (antiglobulin test)............................................................125
Precipitation reaction .................................................................................... „125
Immune lysis reaction........................................................................ 126
Complement fixation reaction............................................................127
Reactions Involving Labeled Antigens or Antipel..........................127
Medical biological preparations for diagnostics, .
prevention and treatment of infectious diseases ..............................................130
, Diagnostic drugs............................................................. 130
Therapeutic and prophylactic drugs. Vaccines......................133
Immune sera and immunoglobulins................................L 36
gi U Part two.
PRIVATE MICROBIOLOGY
- f J t
Methods of laboratory diagnostics h >. infectious diseases .................................................................. .........................139
PATHOGENIC COCCI.................................................................. ......................................141
Staphylococcus.................................................................. ................................................. .....141 ,
Streptococcus.................................................................. ................................................. ......146
Meningococcus.................................................................. ................................................. .....150
Gonococcus.................................................................. ................................................. .......152
FAMILY OF INTESTINAL BACTERIA.................................................................. ...........153 1
Escherichia ............................................................ ................................................. ........155
Salmonella .............................................................. ................................................. .158
Salmonella is the causative agent of typhoid fever and paratyphoid fever............158
Salmonella - causative agents of acute gastroenterocolitis...........161
" Shigella .................................................. ................................................. ......163
Klebsiella ............................................................ ................................................. .....165
J Protea .................................................. ................................................. ...............166
Yersinia ............................................................ ................................................. ........ 167
VIBRIO CHOLERA .............................................................. ......................................... |?2
CAMPYLOBACTER ...............................^
HEMOPHILIC BACTERIA .................................................................. ......................175
Pseudomonas aeruginosa .............................................................. .................................178
LEGAONELLA.;....................................................... ...............................,.............. ..............179
BRUCELLA......................,............................. ................................................. .............,..181
TULAREMIA BACTERIA.................................................................. ......................................^!
BACILLA OF ANTHRAX.................................................................. .........................L83
CORINEBACTERIIDIPHTERIA .................................................................. ............185
MYCOBACTERIA.................................................................. ................................................. 188
Mycobacterium tuberculosis .................................................................. ...............................188
f Mycobacterium leprosy .................................................................. ................................................191
"ACTINOMYCETS.................................................................. ...............................................192
PATHOGENIC ANAEROBES OF THE GENUS CLOSTRIDIUM..................................................193
Clostridia tetanus 193
Clostridia anaerobic gas infection 195
Clostridia bot\lisma 197
ANTI-POORING ANAEROYS 199
PATHOGENIC SPIROCHETES 200
Treponema Excite syphilis 200
Borrelia 203
Leigospira 205
MYCOPLASMS 206
RICKEGSII 208
The causative agent of epidemic typhus 208
Pathogen K> Ashkhoradka 209
CHLAMYDIA 210 VIRAL DISEASE CAUSES 212
flu virus 214
measles virus 217
Viru with mumps 218
Virus with human immunodeficiency (HIV) 219
Rabies virus 222
Polio virus 224 Coxsackie ECHO viruses and other enteroviruses 225
Rotaviruses 226
Viru with rubella 228
Arboviruses 229
Variola virus 231
Herpesviruses 232
Hepatitis viruses 235
Causative agents of slow viral infections 239
Oncogenic viruses 240
PATHOGENIC!? MUSHROOMS 24 2
PATHOGENIC PROTOZES 246
Characteristics of pathogens of dermatomycosis
Dermatomycosis (dermatophytosis) - superficial diseases of the skin and its appendages (hair, nails) caused by microscopic fungi - dermatomycetes (dermatophytes). Among them, anthropophilic (causing diseases in humans), zooanthropophilic (causing diseases in animals and humans) are distinguished.
Currently, more than 400 species of pathogenic fungi are known to be the causative agents of fungal diseases. With superficial mycoses (dermatomycosis), the skin and its appendages are affected: hair and nails.
The causative agents of dermatomycosis are dermatomycetes, which include fungi of the genera Trichophyton, Microsporum and Epidermophyton. According to different authors, these diseases affect from 10 to 40% of the world's population. More than 40 species of dermatomycetes are known, but Trichophytonrubrum, Trichophytonmentagrophytesvar are more common in our country. interdigitale, Trichophytonmentagrophytesvar.gypseum, Trichophytontonsurans, Trichophytonverrucosum, Trichophytonviolaceum, Microsporumcanis, less often Epidermophytonfloccosum.
Mycosis of nails (onychomycosis)
The main causative agents of nail mycosis are dermatomycetes (more than 90%). The leading place is occupied by mushrooms: Trichophytonrubrum (75%), then Trichophytonmentagrophytesvar. interdigitale (15%), molds (13.6%), Epidermophytonfloccosum (5%), Trichophytonviolaceum and Trichophytontonsurans (together about 1%).
Mycosis of hands and feet
The main causative agent of mycosis of the feet is Trichophyton rubrum, the 2nd most common is Trichophytonmentagrophytesvar. interdigitale, on the 3rd - Epidermophyton floccosum. Fungi Microsporumcanis, Trichophytonmentagrophytesvar.gypseum and Trichophytonverrucosum can affect the skin of the hands on both the dorsal and palmar surfaces.
Mycosis of the smooth skin of the trunk, limbs
The causative agents of mycosis of smooth skin are dermatomycetes Microsporumcanis, Trichophytonrubrum, Trichophytonmentagrophytesvar.gypseum, Trichophytonverrucosum, Epidermophytonfloccosum, Trichophytonviolaceum and Trichophytontonsurans are less common.
Mycosis of the inguinal folds. Epidermophytosis inguinal (true), (epidermomycos inguinal)
The main causative agent of mycosis of the inguinal folds is Trichophyton rubrum. Less common pathogens may be T. mentagrophytesvar.gypseum or Microsporum. A favorite localization of this area is epidermophytosis inguinal (true, epidermomycosopahivy), caused by Epidermophytonfloccosum.
Fungal diseases of the scalp (dermatomycosis of the scalp)
Microsporia (microsporosis) is a fungal disease of the skin and hair, which is caused by various types of fungi of the genus Microsporum.
There are anthropophilic, zoophilic and geophilic species of fungi of the genus Microsporum. Microsporum ferrugineum is an anthropophilic fungus. Infection occurs through contact with patients or objects contaminated with the pathogen. The disease is highly contagious.
The zoophilic fungus is Microsporumcanis. Infection occurs from animals: cats, more often kittens (80-85%), less often dogs as a result of direct contact with a sick animal (or carrier) or in contact with objects contaminated with the hair of sick animals.
Trichophytosis is a fungal disease of the skin, hair, less often nails, caused by various types of fungi of the genus Trichophyton (Trichophyton). There are anthropophilic and zoophilic trichophytons. Superficial trichophytosis is caused by anthropophilic fungi, which include Trichophytonviolaceum and Trichophytontonsurans.
Infection with superficial trichophytosis occurs through close contact with a sick person (from hair, skin flakes from lesions, pieces of nails) or through infected objects (hats, clothes, bedding, combs, furniture, hairdresser's tools, etc.). Often, infection occurs within the family or children's groups.
Since infiltrative-suppurative trichophytosis is caused by zooanthropophilic fungi, which include Trichophytonmentagrophytesvar. gypseum and Trichophytonverrucosum, which are carried by animals, infection with infiltrative-suppurative trichophytosis can also occur through direct contact with mouse-like rodents (carriers of this pathogen) or through hay, straw, contaminated with the hair of mice with trichophytosis. Recently, cases of infiltrative-suppurative trichophytosis have become more frequent after exercising in the gym (at school), through gymnastic mats infected with the hair of mice with trichophytosis. The main carrier of the pathogen Trichophytonverrucosum is cattle (calves, cows). Infection occurs through direct contact with a sick animal or through objects infected with the fungus.
Microsporia is contracted by contact with pets - cats, dogs (sick or carriers) or sick people.
The causative agents of fungal diseases are resistant to chemical and physical factors: ultraviolet radiation, atmospheric and osmotic pressure, freezing, disinfectants, etc. Chlorine-active (chloramine, hypochlorites), oxygen-containing compounds, aldehydes, tertiary amines, polymeric derivatives of guanidine are effective against fungi in high concentrations for long periods of exposure. Alcohols are ineffective against these microorganisms. Fungi are more sensitive to the effects of quaternary ammonium compounds (QAC), compositions based on cationic surfactants (SAS), SS and aldehydes, alcohols; phenolic preparations, anolytes, preparations based on chlorine derivatives of hydantoin, sodium chlorisocyanurate and trichloroichocyanuric acid.
The causative agents of fungal diseases survive being in the pathological material in the external environment from 1.5 to 10 years.
Ways and factors of transmission of dermatomycosis
The main way of distribution of dermatomycosis is contact-household (direct and indirect contact). The disease is transmitted by direct contact with a sick person, sick animal or carrier, or by contact with various environmental objects contaminated with dermatophytes.
Skin scales, hair fragments, nails, which contain elements of a viable fungus in abundance, falling off from the lesions, infect the patient's things - clothes, headgear, bed linen, towels, household items (toys, books, carpets, upholstered furniture, etc.), toilet items (combs, combs, washcloths), shoes, gloves, cleaning equipment, bedding for animals and pet care items.
Transmission factors are:
In infectious foci - sanitary equipment, floors, upholstered furniture, carpets, rugs, underwear and bedding, stockings, socks, clothes, hats, shoes, toilet items (combs, brushes, washcloths, etc.), bedding, books, indoor surfaces, patient care items, toys, pet bedding and care items;
In medical institutions - sanitary equipment, incl. baths for medical procedures (except for salt and hydrogen sulfide baths), furnishings, underwear and bed linen, clothes for medical personnel, shoes, toilet items (combs, brushes, washcloths, etc.), medical products (tools), dressings, liners oilcloths (napkins), medical waste, surfaces of devices, devices;
In hairdressing and beauty salons - hair clippers, combs, curlers, shaving brushes, peignoirs, manicure and pedicure accessories, tools, waste;
In sports complexes (fitness clubs, swimming pools, saunas, baths, gyms) - sanitary equipment, showers, rubber mats, wooden gratings, pool paths, stairs and ladder handrails, the surface of the pool bowl, sports equipment, gymnastic mats, wrestling carpets, wardrobes, floors, especially wood;
In children's institutions - bed linen, towels, toys, books, carpets, upholstered furniture, pet care items in zoo corners;
In baths, saunas, showers - sanitary equipment, showers, rubber mats, wooden grates, floors, washcloths, sponges, scissors, foot basins, bath and shower mats, etc.;
In the environment - sand of children's sandboxes, platforms for garbage collectors, dust of stairwells, backfill material of attics and basements, water from shallow reservoirs.
Types of disinfection for dermatomycosis
In the prevention of dermatomycosis, an important role is played not only by early detection of patients, isolation, timely specific treatment, strict adherence to personal hygiene rules, but also by a set of sanitary and anti-epidemic measures, incl. disinfection of objects involved in the transmission of fungal diseases.
Preventive measures for dermatomycosis include sanitary and hygienic and disinfection (preventive and focal disinfection).
Focal (current and final) disinfection is carried out in the places of detection and treatment of the patient: foci of the disease at home, in children's institutions, in mycological complexes, medical institutions, etc.
Preventive sanitary-hygienic and disinfection measures are carried out in hairdressing salons, beauty salons, beauty parlors, baths, saunas, sanitary checkpoints, swimming pools, sports complexes, hotels, hostels, etc.
The purpose of the lesson. To acquaint students with the properties of pathogens, methods of mycological examination and stages of laboratory diagnosis of trichophytosis, microsporia, aspergillosis, penicilliosis, mucormycosis, candidiasis, epizootic lymphangitis, coccidioidomycosis.
Equipment and materials. Material from animals affected by trichophytosis and microsporia, cultures of fungi of the genus Mysog, Aspergillus, Candida on a dense nutrient medium Sabouraud or others, dissecting needles, mycological hooks, slides and coverslips, a mixture of water, alcohol, glycerol (equally), 20% sodium hydroxide or potassium hydroxide solution, 50% aqueous glycerol solution, posters , tables, biological products.
METHODOLOGICAL INSTRUCTIONS
Mycoses are a group of animal and human diseases caused by pathogenic microscopic fungi. The main methods of laboratory diagnosis of these diseases: microscopy, isolation and identification of pathogenic fungi.
Dermatomycosis. Diseases of the skin and its derivatives. Susceptible farm animals of all kinds (mainly young animals), fur and predatory animals. In humans, children are more susceptible to infection. An important factor in infection is maceration of the skin.
Trichophytosis. Infection. It is characterized by the appearance on the skin of rounded or oval bald lesions with soft, sometimes dry crusts in the head area. Lesions can spread over the surface of the animal's body (Fig. 117, 118).
With a superficial form, the size of the lesions is 1 ... 5 cm in diameter, sometimes more extensive foci develop. The crusts are easily separated together with glued hair, broken hair sticks out under them on a slightly damp surface of the skin, in some places there are papules and vesicles.
With a deep form of the disease, several lesions with pronounced exudative and inflammatory processes, infiltration, and a large number of follicular pustules are observed. There are multiple exudative lesions. All foci are covered with dried serous-purulent exudate. Erosions are found when the crusts are removed. Complications of secondary infection are often noted.
The main causative agents of trichophytosis: in cattle, buffaloes, zebu, deer - T. verrucosum(syn. T. faviforme), less often T. mentagrophytes; in horses - T. equinum And T. mentagrophytes; in sheep and goats T. verrucosum, T. mentagrophytes; in pigs T. mentagrophytes; camels - T. verrucosum, T. sarkisovi; in dogs and cats T. mentagrophytes(cats rarely get trichophytosis); in fur animals and rabbits - T. mentagrophytes, seldom T. verrucosum; in laboratory animals (mice, rats, hamsters, guinea pigs) - T. mentagrophytes; in birds - T. gallinae. This pathogen has long been known as the causative agent of scab (favus), mainly in the chicken genus. Previously, the disease was called "white comb".
Microsporia. Infectious disease of the skin and its derivatives. The appearance of lesions is accompanied by an inflammatory process, breaking off and hair loss, sometimes damage to the claws is observed.
The main causative agents of microsporia: in cats and dogs - M. canis(syn. M. lanosum); in horses - M. equinum, seldom M. distorum And M. gypseum; in pigs M. canis; in fur animals, rabbits - M. canis; in laboratory animals M. canis; in cattle and sheep M. canis And M. gypseum. Microsporia affects wild animals, as well as animals of zoos and circuses.
Laboratory diagnosis of trichophytosis and microsporia based on the results of mycological research.
Mycological research includes the detection of the pathogen in the source material by light microscopy and luminescent analysis, the isolation of a pure culture by inoculation on special nutrient media and the identification of the pathogen by cultural and morphological properties.
Research material. Scrapings are sent to the laboratory from the affected parts of the animal's body along with crusts and scales, affected hair from areas bordering healthy skin.
More often, unstained (native) preparations are prepared. The test material is placed in Petri dishes, crushed with scissors and split with a scalpel. Then pieces of hair, scales, crusts are transferred to a glass slide, a drop of a 20% solution of sodium hydroxide or potassium hydroxide is applied and slightly heated over a burner flame until the vapors escape. After that add a drop of 50% aqueous solution of glycerin. A cover slip is applied to the prepared preparation and viewed first under a low magnification of a dry lens (x 8), then with a x 40 lens or using an immersion system.
In order to differentiate fungi of the genus Trichophyton And microsporum take into account the nature of the location of the spores in the affected hair (Fig. 119, 120) (chains or mosaic), using the following criteria:
Luminescent analysis is as follows. The test material is placed in Petri dishes at a distance of 20 cm from a PRK-2 or PRK-4 mercury-quartz lamp with a Wood filter and viewed under ultraviolet rays in a darkened room. The hair affected by the microsporia pathogen gives a bright greenish glow. Crusts, scales do not glow. In addition, with the help of luminescent analysis, an early diagnosis of atypical and latent forms of microsporia is carried out.
The detection of mycelium of the fungus and various spores in the material is a sufficient basis for making a diagnosis of ringworm.
Isolation and identification of cultures of pathogens of trichophytosis and microsporia. Cultures are isolated in doubtful cases to confirm the diagnosis. To obtain a pure culture of fungi, individual hairs or skin fragments, crusts are sown on special nutrient media - Sabouraud agar, wort agar, MPA containing 2% glucose, Chapek agar and some others. To free the test material from accompanying microflora, before sowing on nutrient media, it is treated with 60% ethanol for 5–7 min, and then washed twice with distilled water and dried in a thermostat at 37 ° C, or added to nutrient media antibiotics (penicillin, streptomycin, etc.) at the rate of 100 ... 200 IU / ml. Crops are incubated at a temperature of 26 ... 28 ° C for 20 ... 30 days or more. In grown mushroom cultures, cultural and morphological properties are studied. Crushed drop preparations are prepared (see Topic 5) and microscoped. When identifying fungal species, they are guided by the signs set forth in Table 35.
Biologicals. Preparation TF-130 (VIEV) and dry vaccine LTF-130 (VIEV) against trichophytosis in cattle contain an attenuated strain Trichophyton verrucosum (faviforme).
SP-I vaccine against trichophytosis of horses from a strain of Trichophyton equinum.
Vaccine Trichovis (VIEV) dry against trichophytosis of sheep from a strain Trichophyton verrucosum(variant autotrophicum).
The MENTAVAK vaccine against trichophytosis of fur-bearing animals and rabbits is prepared from a culture Trichophyton mentagrophytes.
Camelvac-TS vaccine against trichophytosis of camels contains an attenuated strain of the fungus Trichophyton sarkisovi.
MIKOLAM vaccine against trichophytosis and microsporia of carnivores, nutria and rabbits.
Polivak-TM is an inactivated vaccine against dermatophytosis in dogs, including 8 species and varieties of fungi of the genus Trichophyton And microsporum.
The VAKDERM vaccine against animal dermatophytosis is intended to combat microsporia and trichophytosis in dogs, cats, fur animals and rabbits. Prepared from highly immunogenic strains Microsporum canis, Microsporum gypseum And Trichophyton mentagrophytes.
Aspergillosis. Disease of domestic and wild birds, bees, rare mammals (cattle, sheep, goats, pigs, horses); receptive person. It is characterized by granulomatous lesions of the respiratory organs, mainly the lungs, often by abortion. Aspergilloma is formed in the lungs during the reproduction of the pathogen. Aspergilloma (Aspergillus mycetoma) - a spherical mass of mycelium up to 2 cm in diameter (usually Aspergillus fumigatus) and cellular detritus that fills the lung cavities formed as a result of tissue destruction. In domestic practice, this term refers to any infectious granuloma caused by species Aspergillus.
The causative agents of aspergillosis belong to the highest imperfect fungi of the class Deuteromycetes, kind Aspergillus group of capitate molds. The main causative agents of aspergillosis in animals - A. fumigatus, A. flavus, A. niger.
Laboratory diagnosis of aspergillosis based on the results of mycological research.
Mycological research includes the detection of the pathogen in the source material by light microscopy, the isolation of a pure culture by inoculation on nutrient media and the identification of the pathogen by cultural-morphological and pathogenic properties.
Research material. Fresh corpses of small animals, overlays, nodules, affected organs or their pieces, sputum, eggs are sent to the laboratory.
. Direct detection of the fungus in an unstained or stained preparation is only important for a preliminary diagnosis. At the same time, the identification of fruiting organs characteristic of Aspergillus is especially valuable and significantly speeds up laboratory diagnostics. The test material is placed in a mixture of ethanol with glycerol and water equally or in saline. The preparations are microscoped as described in topic 5, focusing on the detection of fruiting organs (Fig. 121) - the head, sterigmata with spores (see topic 5).
For inoculation, Czapek agar, Sabouraud, blood, brain, corn agars, MPA (pH 5.5 ... 6.5) are used. Granulomatous tissue is burned over a flame, sterile pieces are cut out from the middle and laid out on a dense medium in Petri dishes, and the exudate is inoculated into test tubes with the medium, incubated at 25 and 37 °C. On the 3rd...5th day colonies characteristic of Aspergillus are formed on solid media (Fig. 122...124).
A.fumigatus on Čapek's agar forms proliferating colonies - even or rough. The developed aerial mycelium gives them a felted appearance of white or, later, green. Mature cultures in the stage of sporulation are black. On the reverse side, the colonies are colorless or yellowish-brown in color. Interspecific differential diagnosis is based on differences in the structure of sterigmas and conidia.
In culture preparations, smooth, short, green conidiophores can be found. Aerial hyphae are septate and without partitions. Flask-shaped swellings containing spores are found only in the upper part of the hyphae. Sterigmata have a single-tiered structure. Conidia are dark green in color, rounded, prickly or hemispherical in shape.
A. flavus, A. niger on Čapek's agar, they form widely growing colonies with abundant sporulation. The color of the colony depends on the mass of conidia developing on the conidiophores. Microscopy of cultures reveals colorless or light-colored septate mycelium. Often formed sclerotia spherical shape, represented by thick-walled cells.
Bioassay. The method is used to confirm the pathogenicity of isolated aspergillus cultures. Rabbits, guinea pigs or white mice are injected intravenously with a suspension of fungal spores (0.5 ... 1) 10 6, which causes the development of a generalized process with a typical lesion of the respiratory organs, kidneys, and heart. At autopsy, many small nodules with intensive development of the fungus are found in these organs.
Birds are fed food contaminated with aspergillus spores, or the spores are inhaled into the respiratory apparatus.
With the help of mycological studies, aspergillosis is differentiated from mycoses caused by other mold fungi.
Penicilliomycosis. A disease of many animal species that occurs against the background of a decrease in the overall resistance of the body and is characterized by damage to the skin and mucous membranes.
The main causative agents of penicilliomycosis are fungi of the genus Penicillium: P. crustosum, P. glaucum, P. mycetomagenum.
Laboratory diagnosis of penicilliomycosis based on the results of mycological research. Diagnosis of this mycosis is difficult due to the fact that fungi of the genus Penicillium often isolated from the lungs and other tissues in tuberculosis and other infections. An important sign for confirming the diagnosis is the detection of fungal elements phagocytosed by macrophages in the lesion.
Mycological research includes the detection of the pathogen in the source material by light microscopy, the isolation of a pure culture by inoculation on nutrient media and the identification of the pathogen by cultural, morphological and pathogenic properties.
Material for research. The affected areas of the skin, mucous membranes, affected organs and tissues from corpses are sent to the laboratory.
Microscopy of preparations from the starting material. The "crushed drop" preparations are examined under a microscope in stained (according to the methods of Gram, Ziehl-Neelsen, etc.) and unstained.
An important diagnostic sign is the detection in native preparations of septate mycelium and conidiophores branching at the top one or more times in the form of a brush.
Isolation and identification of the pathogen culture. The material is sown on wort-agar, Czapek's, Saburo's and other agars and cultivated in the same way as the pathogens of aspergillosis and mucormycosis. In the isolated cultures of fungi, the morphology of the colonies and the internal structure are studied (Table 36).
Bioassay. Infect rabbits, guinea pigs, rats, white mice subcutaneously. An abscess develops at the injection site of the fungal culture and granulation tissue is formed. With intraperitoneal and intravenous administration, a generalized process develops.
Mucormycosis (mucormycoses). Chronic diseases caused by fungi. They are characterized by the development of a granulomatous process similar to tuberculosis in the lymph nodes and lungs, less often in other organs and tissues (skin, nails, mucous membranes, digestive tract, central nervous system, brain). Pigs, horses, cattle, sheep, fur-bearing animals are susceptible to the causative agent of mucorosis; from laboratory animals - guinea pigs, mice; monkeys, seals get sick. Mucorosis in humans occurs as sporadic cases.
The main causative agents of mucormycosis are fungi species Mysog mucedo, M. racemosus, Rhisopus nigricans and etc.
Laboratory diagnosis of mucormycosis
Mycological research includes the detection of the pathogen in the source material by light microscopy, the isolation of a pure culture by inoculation on nutrient media and the identification of the pathogen by cultural, morphological and pathogenic properties.
Research material. The object of the study are necrotic tissues, pus, exudate, granulomatous tissues, etc.
Microscopy of preparations from the starting material. In preparations from the test material, in positive cases, unsepted mycelium is found. In round sporangia, endospores are visible on the sporangiophore (Fig. 125). The presence of chlamydospores is characteristic of the old mycelium.
Rice. 125. Four day culture Mysog racemosus on Čapek's agar:
1 - mycelium;
2- sporangia;
3- sporangiospores inside and outside the sporangium;
4- sporangiophore
Isolation and identification of the pathogen culture. Granulomatous tissue is burned over the flame of a burner and pieces are sterilely cut out from the middle, which are laid out on the surface of Czapek's medium (in Petri dishes) or other media. Crops are incubated at 25...30ºС. Mushroom cultures are quite large and actively develop on artificial nutrient media. On the third day, they take the form of felted ragged grayish-white colonies (Fig. 126), subsequently the color may change to brown or brown.
Rice. 126. Felt-tufted grayish-white colony of a two-day culture M. racemosus on Čapek's agar
Bioassay. The method is used to study the pathogenicity of fungal cultures isolated from the source material. Rabbits, guinea pigs and white mice are injected intravenously, intramuscularly or intraperitoneally with a wash of spores and mycelium of pure cultures. The fungus develops in all internal organs and tissues. Rabbits die 15...20 days after intravenous infection, mice - after 5...15 days. The kidneys are more often affected, less often the liver, heart, spleen (abscesses, necrosis of the epithelium of the tubules, proliferation of granulation tissue).
Candidiasis (candidiasis, thrush, etc.). Disease of animals and humans. It is characterized by superficial lesions of the skin, mucous membranes of the oral cavity, external genitourinary organs. The pathogen also causes visceral mycosis with damage to the respiratory tract, gastrointestinal tract, genitourinary system, mammary gland, muscle, bone and cardiovascular systems, organs of vision. With the generalization of the candidiasis process, many organs can be affected simultaneously (Fig. 127). The consequence of candidiasis in cows may be mastitis, endometritis and abortion.
Rice. 127. Grayish-white small nodules on the mucous membrane of the goiter of a guinea fowl, which fell from candidiasis
The main causative agents of candidiasis are C. albicans And C. tropicalis, less often C. krusei, genus Candida, Class Deuteromycetes. They are widely distributed in nature. Most often they are isolated from the surface of various fruits, berries, vegetables. candida albicans and others are part of the normal microflora of the human body and animals. Any violation of the functions of immunocompetent cells or normal microbial cenosis leads to the onset of the disease. C. albicans mainly affects birds, chickens, geese, ducks, guinea fowls, turkeys, pigeons, pheasants, etc. Piglets, calves, lambs, puppies are more seriously ill.
Laboratory diagnosis of candidiasis based on the results of mycological research.
Mycological research includes the detection of the pathogen in the source material by light microscopy, the isolation of a pure culture by inoculation on nutrient media and the identification of the pathogen by cultural-morphological and enzymatic properties.
Research material. The object of the study are films, overlays, scrapings from the mucous membrane, the contents of ulcers and erosions, pieces of internal organs.
Microscopy of preparations from the starting material. in animal tissue C. albicans can form yeast cells and hyphae, the detection of which is of diagnostic value (Fig. 128). The cell wall of the mycelium in this case consists of three layers and is significantly inferior in thickness to the five-seven-layer structure of yeast cells.
Isolation and identification of the pathogen culture. The material (except internal organs) is taken with a sterile bacteriological loop and thoroughly rubbed with a loop or a glass spatula over the surface of the medium. Pieces of the liver, spleen or kidneys are immersed in alcohol, burned over the flame of an alcohol lamp, and then a piece of tissue is cut out from the depths of the organs and passed over the surface of a dense medium. Blood from the heart, the contents of the stomach and intestines, the renal pelvis are sown on Sabouraud agar in Petri dishes. Crops are incubated at 37 ° C for 24 ... 48 hours until colonies appear on the nutrient medium (Fig. 129, 130).
Identification of cultures of fungi is carried out in two stages.
At the first stage, the cultural and morphological characteristics of the isolated culture are studied in the primary inoculation on a dense nutrient medium (Sabouraud agar, MPA with glucose) (Table 37).
At the second stage, for the final identification of fungi of the genus Candida the selected culture is sown on liquid nutrient media (Sabouraud broth, potato, corn agars or similar liquid media - corn or potato broth) and cultural characteristics and cytomorphological features are determined. Sowing on potato and corn agars is done by a stroke into the thickness of the medium, cutting the surface of the agar with a loop. Microscopy takes into account the presence of pseudomycelium, the type of growth on these media; the presence of chlamydospores on corn agar in Petri dishes is examined at low magnification (Fig. 131).
Rice. 131. Five day culture C. albicans on corn agar:
1 - spherical chlamydospores; 2-contour shell of chlamydospore
Mushrooms on liquid nutrient media C. albicans after 24...48 hours cause cloudiness of the medium and the formation of a loose precipitate at the bottom of the tube. For mushrooms C. tropicalis And C. krusei characterized by deep growth and the formation of a film and a near-wall ring.
To differentiate species of fungi of the genus Candida enzymatic activity is determined on liquid Hiss media containing 3% of various carbohydrates and the Andrede indicator. Crops are observed for 10 ... 15 days, acid and gas formation are taken into account. Enzymatic properties are shown in table 38.
Epizootic lymphangitis (blastomycosis, African glanders). Chronic disease in animals. It is characterized by damage to the lymph nodes, lymphatic vessels and subcutaneous tissue with the formation of ulcers, abscesses and nodules. Unlike dermatomycosis, the deeper layers of the skin are affected. Single-hoofed animals are ill: horses, mules, donkeys, cases of artiodactyls - camels and cattle (Fig. 132) have been registered with this mycosis.
The causative agent of epizootic lymphangitis - Histoplasma farciminosus(syn. Criptococcus farciminosus). The classification of cryptococcus is unclear: some researchers classify it as a blastomycete, while others, based on some biological data, consider it to be an imperfect fungus.
Laboratory diagnosis of epizootic lymphangitis based on the results of mycological and serological studies.
Mycological research includes the detection of the pathogen by microscopy of preparations-prints from the source material, the isolation of a pure culture by inoculation on nutrient media and the identification of the pathogen by cultural, morphological and serological properties.
Research material. The contents of abscesses, purulent exudate of ulcers are sent to the laboratory.
Microscopy of preparations from the starting material. Prepare the drug "crushed drop". More often, an unstained preparation is microscoped or stained according to Gram or Romanovsky-Giemsa. Due to the coloring, the granules in the cytoplasm are clearly distinguishable. The causative agent of epizootic lymphangitis is classified as a yeast-like fungus. In the test material, cryptococci are found - cells of an ovoid or mono-shaped form with a clearly defined double-circuit membrane, the cells are pointed at one or both ends. The size of cryptococci is 3...5 µm in length and 2...3.5 µm in width. In pus, 2 ... 3 cryptococci are found, connected by their poles and sometimes forming chains (Fig. 133). Some cryptococci can be found in leukocytes (neutrophils and macrophages). The central part of cryptococci is a homogeneous, semi-liquid substance containing one or more (2...4) shiny grains that are in continuous and brisk movement.
It must be taken into account that for N. farciminosus dimorphism is characteristic, i.e., the morphology of the fungus in pathological material and in culture is different.
Isolation and identification of the pathogen culture. In doubtful cases of microscopy, the material is sown on nutrient media. Primary isolation of the fungus is difficult, but the isolated culture can be maintained relatively easily. The fungus is grown on MPPA, glucose-glycerol MPA (carbohydrate content 2...2.5%), Sabouraud agar at a temperature of 25...30°C.
After 10 ... 12 days, colonies are formed on dense nutrient media, first small, later larger, towering above the surface of the medium. Colonies are folded, dry, cream, and later brown. Yeast cells are not detected in culture smears. Outside a living organism, the fungus develops in a mycelial form. Mycelium septate, branching, multicellular.
Serological diagnosis based on the results of RSK with glanders antigen.
Allergic diagnosis. For allergic diagnosis of lymphangitis, histoplasmin (Koroleva) is used - a filtrate of a 3 ... 4-month-old culture of cryptococcus. With a doubtful result of a laboratory study, differential diagnosis of lymphangitis and glanders is used, using an eye test with mallein and a subcutaneous test with histoplasmin.
Coccidioidomycosis (desert rheumatism, valley fever, etc.). A chronic disease of animals and humans, characterized by granulomatous lesions of the lymph nodes, sometimes lungs in cattle and a disseminated form of the process with a malignant course in dogs.
Cattle, horses, donkeys, sheep, pigs, rodents (mice, rats, etc.) are susceptible to the disease. Diseases of coyotes, llamas, kangaroos, monkeys, tigers and other animals are described. Birds don't get sick. Human coccidioidomycosis is classified as a particularly dangerous mycosis.
The causative agent of coccidioidomycosis is a yeast-like soil fungus Coccidioides immitis.
Laboratory diagnosis of coccidioidomycosis based on the results of mycological and serological studies.
Mycological research includes the detection of the pathogen in the source material by light microscopy and bioassay, the isolation of a pure culture by inoculation on nutrient media and the identification of the pathogen by cultural, morphological and pathogenic properties.
Research material. The object of the study is pus, blood, the contents of the lesions and pieces of the affected organs.
Microscopy of preparations from the starting material. Preparations "crushed drop" are prepared from the material. When working with such drugs, extreme caution must be exercised, since the fungi remain alive. It is possible to microscope preparations in a 10% alkali solution when heated: in this case, the fungus dies quickly, but the spherules are deformed. To avoid contamination of the researcher with the fungus C. immitis, before microscopy, the pathological material is recommended to be filled with a 10% formalin solution for 10 ... 15 minutes. Such treatment kills the fungus, but does not affect its morphological features. A positive result is the detection of spherules (for example, in pus and sputum) of mycelium (Fig. 134, 135). Spherules - formations of the correct round shape with a double-circuit shell and with numerous endospores. The protoplasm is granular. The spherule diameter is from 20 to 120 µm. Endospores are small. Sometimes spherules are found with a ruptured membrane and released endospores. Sprouting of spherules into mycelium can be observed directly in the pathological material. To do this, a few drops are applied to a glass slide in a mixture with saline, covered with a coverslip and sealed with paraffin around the edges to prevent drying. The absence of spherules in preparations under microscopic examination does not give grounds to deny coccidioidomycosis.
Isolation and identification of the pathogen culture. For inoculation, the test material is pre-treated with antibiotics for 30...60 minutes to suppress bacterial growth. Penicillin is added at the rate of 20 units/ml of medium, streptomycin - 40 units/ml. To obtain the mycelial form of the fungus, Litman agar, Sabouraud agar, wort agar are used as a nutrient medium; to obtain a yeast-like form - blood agar, liver agar with glucose, open-hearth broth (Table 39). Cultivated at 25...27 and 35...37 °C.
Bioassay. Infect with native material and saline suspension from a pure culture of the fungus. Mice, guinea pigs, rabbits, dogs, chicken embryos are susceptible to coccidioidomycosis. With the development of the pathological process, depending on the method of introduction of the test material, various lesions are noted.
With intravenous injection of a culture of the fungus, abscesses develop in the internal organs, the death of animals occurs after 20 ... 30 days.
With intratracheal infection, damage to the lungs and tracheobronchial lymph nodes is detected.
With intraperitoneal infection, after 7 ... 10 days, the process spreads through the peritoneum with damage to internal organs.
With subcutaneous and intracerebral methods of infection, a local process occurs with damage to the lymph nodes.
With intratesticular - purulent orchitis develops. In pus, spherules of various sizes and at different stages of maturation are found, less often mycelium.
Two-three-day-old chicken embryos die 3-6 days after infection. The materials and tools used in the work are subject to immediate sterilization in an autoclave.
Serological diagnosis based on the results of the following reactions: RA with an antigen from a killed culture, CSC with coccidioidin, RP with a polysaccharide antigen.
When working with C. immitis safety precautions must be followed, in particular, wearing gauze masks. It is better to inoculate in test tubes with Litman's medium, meat-peptone broth or other liquid media, since they are more convenient to use for microscopic work and infection of animals. On these media, the fungus forms more compact, dust-free colonies. Reseeding from solid media is recommended before sporulation begins.
TASKS FOR INDEPENDENT WORK
1. Prepare and microscopy preparations from the material from animals with dermatomycosis.
2. To study the cultural properties of the pathogens of trichophytosis and microsporia.
3. To study the cultural and morphological characteristics of fungi of the genera Mucor, Aspergillus, Candida.
4. Familiarize yourself with biological products.
test questions
1. What microorganisms cause ringworm?
2. What is the scheme of laboratory testing for dermatomycosis?
3. By what criteria are fungi of genera differentiated microsporum And
Trichophyton?
4. What molds and yeast-like fungi cause mycoses?
5. What vaccines are used against agricultural dermatomycosis
animals?
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