Dermatomycosis microbiology. Mycoses caused by molds and yeast-like fungi

Currently, the group of glucan synthesis inhibitors (echinocandins) is represented by three drugs: caspofungin, micafungin and anidulafungin, of which only one is registered in the Russian Federation caspofungin .

Mechanism of action

Echinocandins have a mechanism of action different from other antimycotics associated with the blockade of the synthesis of 1,3-beta-D-glucan, an important structural and functional component of the fungal cell wall.

Activity spectrum

The spectrum of activity of caspofungin includes Aspergillus spp. (including those resistant to amphotoriycin B), Candida spp. (including strains resistant to azoles), Pneumocystis juroveci. The drugs of this group act on some rare mycelial pathogens of mycoses, such as Acremonium, Curvularia, Bipolaris spp. Echinocandins are inactive against Zygomycetes, Cryptococcus, Scedosporium and Fusarium spp. Echinocandins lack cross-resistance with other classes of antimycotics.

Pharmacokinetics

Caspofungin is administered intravenously, oral bioavailability is low due to its high molecular weight. The drug is soluble in water. It has a high degree of binding to plasma proteins (97%). Creates high concentrations in the kidneys, liver, spleen and lungs, low - in the brain. After the introduction of 70 mg, the concentration of the drug in the blood serum is 12 mg / l, after 24 hours - 1-2 mg / l. Caspofungin Metabolized in the liver without the participation of isoenzymes of the cytochrome P-450 system. The half-life is 9-11 hours.

Adverse events

Due to the fact that 1,3-beta-D-glucan is absent in the human body, caspofungin is very well tolerated with a minimum number of adverse events. The most frequent are fever (3-26%), phlebitis (3-18%) and headaches (4-15%). In rare cases, nausea, diarrhea, skin rash and itching (1-9%) are possible. Laboratory adverse events may include increased activity of ACT (3-27%), ALT (2-24%) and alkaline phosphatase (4-24%), as well as a decrease in hematocrit and hemoglobin levels (by 3-12%).

Indications

Invasive candidiasis, esophageal candidiasis, invasive aspergillosis in patients refractory to other antimycotic therapy or with poor tolerance to it, empirical therapy in patients with febrile neutropenia.

Contraindications- hypersensitivity to caspofungin or components of the drug.

The international, trade name, formulations and dosing regimens of caspofunkgin are presented in Table 5.

Table 5

Main characteristics of caspofungin

	Tradename	Release form	Dosing regimen
Caspofungin	Cancidas	lyophilisate for solution for infusion	In / in, by slow IV infusion (≥1 h) 1 time per day. In empirical therapy, adults: on the 1st day, a single loading dose of 70 mg is administered, on the 2nd and subsequent days - 50 mg per day. The duration of use depends on the clinical and microbiological efficacy of the drug. Empiric therapy should continue until complete resolution of neutropenia. If a fungal infection is confirmed, patients should receive the drug for at least 14 days, drug therapy should be continued for at least 7 days after the disappearance of the clinical manifestations of both the fungal infection and neutropenia. It is possible to increase the daily dose to 70 mg if the dose of 50 mg is well tolerated, but does not give the expected clinical effect.

Ø FLUOROPYRIDIMINES

The only representative flucytosine (or 5-fluorocytosine).

Mechanism of action associated with impaired DNA and RNA synthesis due to the conversion of 5-fluorocytosine to 5-fluorouracil, whose metabolites are a competitor of uridylic acid in RNA, and also disrupt the activity of thymidylate synthetase, which leads to a lack of intracellular thymidine.

Activity spectrum includes candida, aspergillus, cryptococci, pathogens of chromoblastomycosis.

Pharmacokinetics

It is well absorbed in the gastrointestinal tract (when taken orally, bioavailability ranges from 76 to 90%). Peak concentrations in plasma and biological fluids are reached within 1-2 hours. It penetrates well into most organs and tissues, including cerebrospinal fluid, vitreous body, peritoneum, joints. The percentage of plasma protein binding is very low. Minimal metabolism in the liver. It is excreted mainly by the kidneys, the concentration of the drug in the urine is high. The half-life is from 3 to 5 hours and increases to 85 hours in patients with renal insufficiency.

Adverse events

It has a fairly high myelotoxicity and hepatotoxicity. In most patients, these adverse events are dose-dependent and reversible. It is possible to develop cardiac arrhythmias, ataxia, paresthesia, neuropathy, etc. Due to its ability to suppress bone marrow function, it is not recommended as a drug for empirical therapy in patients during neutropenia. Serum levels of flucytosine should be monitored whenever possible (especially when combined with amphotericin B), with the most important to determine the residual concentration.

Indications

Monotherapy of chromoblastomycosis (drug of choice) and candidiasis of the lower urinary tract. In combination with amphotericin B, it is used to treat severe systemic candidiasis, cryptococcal meningitis, monotherapy-resistant aspergillosis, and fungal endocarditis.

Contraindications

Allergic reaction to flucytosine.

The international, trade name, form of release and dosing regimens of flucytosine are presented in table 6.

Table 6

Main characteristics of flucytosine

	Tradename	Release form	Dosing regimen
flucytosine		solution for infusion	Intravenously adults and children: 37.5 mg/kg body weight 4 times a day. Use only in combination with amphotericin B or fluconazole. Do not use if pregnant or breastfeeding.

Ø Allylamines

Allylamines, which are synthetic antimycotics, include terbinafine applied orally and topically, and naftifin intended for local use. The main indications for the use of allylamines are dermatomycosis.

Mechanism of action

The fungicidal action of allylamines is based on a highly specific inhibition of squalene epoxidase, which catalyzes one of the early processes of the synthesis of ergosterol, which is part of the fungal membrane. Unlike azoles, allylamines block earlier stages of biosynthesis.

Activity spectrum

Allylamines have a wide spectrum of antifungal activity. Dermatomycetes (Trichophyton, Microsporum and Epidermo-phyton spp.), M. furfur, some Candida, Aspergillus spp., C. neoformans, S. schenckii and causative agents of chromomycosis are sensitive to them.

Terbinafine it is also active in vitro against a number of protozoa (some varieties of leishmania and trypanosomes).

Despite the wide spectrum of activity of allylamines, only their effect on dermatomycetes is of clinical importance.

Pharmacokinetics

Terbinafine

It is well absorbed in the gastrointestinal tract (bioavailability 70%) and partially when applied topically. As a result of diffusion through the dermal layer of the skin, as well as secretion by the sebaceous and sweat glands, it creates high concentrations in the stratum corneum of the epidermis, nail plates. Metabolized in the liver, excreted by the kidneys. T ½ 11-17 hours, increases with renal and hepatic insufficiency.

Adverse events

Adverse events are rare and usually do not lead to discontinuation of the drug.

Terbinafine inside

Dyspeptic disorders (abdominal pain, loss of appetite, nausea, vomiting, diarrhea, changes and loss of taste), headache, dizziness, allergic reactions are possible (rash, urticaria, exfoliative dermatitis, Stevens-Johnson syndrome), increased activity of transaminases, cholestatic jaundice , liver failure.

Terbinafine topically, naftifine

Skin: itching, burning, hyperemia, dryness.

Indications

Mycoses of the skin caused by dermatomycetes (with limited damage - locally, widespread - inside). Microsporia, trichophytosis of the scalp (inside). Onychomycosis (inside). Chromomycosis (inside). Sporotrichosis skin, skin-lymphatic (inside). Skin candidiasis (locally). Pityriasis versicolor (locally).

Contraindications

Allergic reaction to drugs of the allylamine group. Pregnancy. Lactation.

International, trade names, formulations and dosing regimens of allylamines are presented in table 7.

Table 7

Main characteristics of allylamines

	Tradename	Release form	Dosing regimen
Terbinafine		· tablets	*inside* , after meals, 1 time per day in the evening at a dose of 250 mg or 2 times a day for 125 mg. *locally* , the cream is applied in the morning and / or in the evening on the affected skin, previously cleansed and dried, as well as on the surrounding areas. The average duration of the course for skin lesions is 1-2 weeks, nail plates - 3-6 months. For children, the dose is set depending on body weight.
		cream for external use · tablets
		cream for external use · tablets
	Lamisil Dermgel
	Lamisil Uno
		· tablets
	Lamitel	spray for external use
	Mikonorm	cream for external use
	Mycoterbin
		· tablets
	Terbizil	cream for external use · tablets
		cream for external use spray for external use
	Terbinafine	cream for external use · tablets
	Terbinafine-MFF	ointment for external use
	Terbinafine-Sar	· tablets
	Terbinafine hydrochloride	Substance-powder
	Terbinox	cream for external use · tablets
	Terbifin	cream for external use spray for external use · tablets
	Thermicon	cream for external use spray for external use · tablets
	Fungoterbin	cream for external use spray for external use · tablets
		· tablets
		· tablets cream for external use
Naftifin	Exoderil	cream for external use solution for external use	*Outwardly.* Used as a cream (1%) or solution (1%). With dermatomycosis - applied to the affected surface and adjacent areas of the skin, previously cleaned and dried, 1 time per day. Duration of treatment for ringworm - 2-4 weeks; with candidiasis - at least 4 weeks; if necessary, the course is extended to 6-8 weeks. In the absence of clinical improvement after 4 weeks of use, it is recommended to clarify the diagnosis. With onychomycosis, the solution is applied to the affected surface, covering with a thick bandage, 2 times a day, the course is 6 months; with complicated forms - up to 8 months. To prevent relapse, treatment is continued for another 2 weeks after clinical improvement is achieved.

Ø drugs of other groups

Griseofulvin (fulcin)

It is an antifungal agent that has a fungistatic effect on trichophytons, microsporums, epidermophytons. In our country, it is used as the main systemic antimycotic for rubrophytosis. Not effective for candidiasis. An important feature of griseofulvin is its effectiveness when taken orally. Available in tablets of 0.125 g, in the form of suspensions and 2.5% liniment for topical use. The activity of griseofulvin to a certain extent depends on the dispersion of its crystals. Currently, a highly dispersed drug is mainly used in tablets. Tablets are taken orally during meals with a spoonful of vegetable oil, since griseofulvin is a lipophilic substance. Absorption is increased with a high-fat diet.

Mechanism of action.

It has a fungistatic effect, which is due to the inhibition of the mitotic activity of fungal cells in the metaphase and the disruption of DNA synthesis. Selectively accumulating in the "prokeratin" cells of the skin, hair, nails, griseofulvin gives the newly formed keratin resistance to fungal infection. The cure occurs after the complete replacement of the infected keratin, so the clinical effect develops slowly.

Pharmacokinetics

When taken orally, it is well absorbed. Reaches the maximum concentration in blood in 4-5 h after appointment. T½ about 20 hours. Absorption from the gastrointestinal tract varies greatly from person to person, mainly due to the insolubility of the substance in the aquatic environment of the upper gastrointestinal tract. It should be noted that in some patients there is a tendency to create low levels of the substance in the blood regardless of time. This may explain the unsatisfactory therapeutic effect in some patients. Bioavailability in most patients increases when taken together with fatty foods. After ingestion, it accumulates in the stratum corneum and its appendages, as well as in the liver, adipose tissue, and skeletal muscles. Minor amounts enter liquid media and other tissues of the body. Biotransformation occurs in the liver, the main metabolites are 6-methylgriseofulvin and a glucuronide derivative.

When applied topically, griseofulvin has a weak effect.

Adverse reactions

On the part of the digestive tract: nausea, vomiting, dry mouth, diarrhea, abdominal pain, candidal stomatitis, increased activity of hepatic transaminases, jaundice, hepatitis. From the nervous system and sensory organs: headache, dizziness, excessive fatigue or weakness, insomnia, peripheral neuropathy, paresthesia of the extremities, impaired coordination of movements, lethargy, disorientation, confusion, depression, impaired taste sensitivity. From the side of the cardiovascular system and blood (hematopoiesis, hemostasis): granulocytopenia, agranulocytosis, leukopenia. Allergic reactions: rash, itching, urticaria, Quincke's edema, photosensitivity, lupus-like syndrome, erythema multiforme exudative, topical epidermal necrolysis (Lyell's syndrome).

Indications

Griseofulvin is one of the main means for the treatment of patients with dermatomycosis, both for resorptive and local action. The drug is prescribed in the treatment of patients suffering from favus, rubrophytia, microsporia, trichophytosis of the scalp and smooth skin, epidermofetiya of smooth skin, onychomycosis.

Contraindications

Hypersensitivity, porphyria, systemic lupus erythematosus, lupus-like syndrome, systemic blood diseases, leukopenia, organic diseases of the liver and kidneys, hepatocellular insufficiency, malignant neoplasms.

Application restrictions

Children's age up to 2 years (efficacy and safety of use have not been determined).

Use during pregnancy and lactation

There are data on the teratogenic and embryotoxic effects of griseofulvin in animals (when administered orally in pregnant rats, the presence of pups with several disorders was reported in the offspring). Contraindicated in pregnancy (griseofulvin crosses the placenta, adequate and well-controlled studies in pregnant women have not been conducted). Use during breastfeeding is not recommended (it is not known whether griseofulvin passes into breast milk). There are no adequate data.

Interaction

Griseofulvin induces liver microsomal enzymes and, as a result, can increase liver metabolism and, therefore, weaken the activity of indirect anticoagulants (PT control is necessary, anticoagulant dose adjustment may be required), oral hypoglycemic agents (blood glucose control, dose adjustment of an antidiabetic agent is possible), oral estrogen-containing contraceptives, theophylline (monitoring of its concentration in the blood with possible dose adjustment). Inducers of microsomal enzymes (including barbiturates, rifampicin) can increase the metabolism of griseofulvin and reduce its fungistatic activity. Enhances the effect of ethanol.

Features of application and dosing

Adults: 0.25-0.5 g every 12 hours,

Children: 22 mg / kg / day (no more than 1000 mg / day) in 1-2 doses.

Griseofulvin should be taken orally during or immediately after a meal.

If a low-fat diet is used, griseofulvin should be taken with 1 tablespoon of vegetable oil. Do not drink alcoholic beverages during treatment, be careful with dizziness. Avoid sun exposure.

Do not use griseofulvin during pregnancy and lactation.

During treatment with griseofulvin and within 1 month after the end, do not use only estrogen-containing oral preparations for contraception, be sure to use additional or alternative methods

In the treatment of mycosis of the feet, onychomycosis, it is necessary to carry out antifungal treatment of shoes, socks and stockings.

International, trade names, formulations and dosing regimens of griseofulvin are presented in table 8.

Table 8

Main characteristics of griseofulvin

	Tradename	Release form	Dosing regimen
Griseofulvin	Griseofulvin	standard sample - powder Substance-powder · tablets	Inside (during or immediately after a meal), in one or more doses. The daily dose for adults is 500 mg (in case of severe mycoses, the dose is increased), for children - 10 mg / kg. The highest daily dose is 1 g. The duration of treatment depends on the infection and on the thickness of the keratin at the site of infection and is: in case of damage to the skin of the scalp - 4-6 weeks, body - 2-4 weeks, feet - 4-8 weeks, fingers - not less than 4 months, toes - not less than 6 months.
Griseofulvin tablets 0.125 g	· tablets
	· tablets

Potassium iodide

As an antifungal drug, potassium iodide is used orally as a concentrated solution (1.0 g/ml). The mechanism of action is not exactly known.

Activity spectrum

Active against many fungi, but the main clinical significance is the action on Sschenckii.

Pharmacokinetics

Quickly and almost completely absorbed in the gastrointestinal tract. It is distributed mainly in the thyroid gland. It also accumulates in the salivary glands, gastric mucosa, and mammary glands. Concentrations in saliva, gastric juice and breast milk are 30 times higher than in blood plasma Excreted mainly by the kidneys.

Adverse events

gastrointestinal tract: abdominal pain, nausea, vomiting, diarrhea.

Endocrine system: changes in thyroid function (requires appropriate clinical and laboratory monitoring).

Reactions of iodism: rash, rhinitis, conjunctivitis, stomatitis, laryngitis, bronchitis.

Other: lymphadenopathy, swelling of the submandibular salivary glands.

With the development of severe AEs, the dose should be reduced or the intake should be temporarily discontinued. After 1-2 weeks, treatment can be resumed at lower doses.

Indications

Sporotrichosis skin, skin-lymphatic.

Contraindications

Hypersensitivity to iodine preparations.

Hyperthyroidism.

Tumors of the thyroid gland.

Amorolfine

Synthetic antimycotic agent for topical use (in the form of nail polish), which is a derivative of morpholine. Used to treat onychomycosis.

Mechanism of action

Depending on the concentration, it can have both fungistatic and fungicidal effects due to a violation of the structure of the cytoplasmic membrane of the fungal cell.

Activity spectrum

It is characterized by a wide spectrum of antifungal activity. Dermatomycetes, Candida, Malassezia, Cryptococcus spp. are sensitive to it. and other mushrooms.

Pharmacokinetics

When applied topically, it penetrates well into the nail plate and nail bed. Systemic absorption is insignificant and has no clinical significance.

Adverse reactions

Local: burning, itching or irritation of the skin around the nail, discoloration of the nails (rarely).

Indications

Onychomycosis caused by dermatomycetes, yeasts and molds (if no more than 1/2 of the nail plate is affected). Combined treatment of onychomycosis. Prevention of onychomycosis.

Contraindications

Hypersensitivity to amorolfine. Pregnancy. Lactation.

The trade name, formulations and dosing regimens of amorolfine are presented in Table 9.

Table 9

Main characteristics of amorolfine

	Tradename	Release form	Dosing regimen
Amorolfine		· nail polish	Outwardly. Lacquer is applied to the affected nails 1-2 times a week. Before use, remove the affected areas of the nail with the supplied nail file, clean the surface with the supplied swab moistened with alcohol; before the next application, the procedure is repeated, after removing the remnants of the varnish with a swab with alcohol. Treatment is continued continuously until the growth of a new nail and the disappearance of the affected areas. The duration of therapy depends on the localization and severity of the process and averages 6 months (nails of the fingers) or 9-12 months (nails of the toes).

Cyclopirox ( trade names Batrafen, Dafnedzhin, Fongial)

Synthetic antifungal drug for topical use with a wide spectrum of activity.

Activity spectrum

It is active against the main pathogens of onychomycosis, individual strains of bacteria (both gram-positive and gram-negative). Most effective (local application) in the early stages of onychomycosis caused by dermatophytes, yeast-like and mold fungi, with a distal type of nail lesion (no more than half or one third of the nail), without matrix involvement, with white superficial onychomycosis caused by T. mentagrophytes (lesion only surface of the nail plate), and post-treatment of onychomycosis after systemic therapy in order to prevent relapses. With multi-colored lichen, clinical and mycological improvement is noted after 2 weeks of treatment (not earlier). In the form of nail polish, it quickly (during the first hours after application) and deeply penetrates into the nail and is deposited for a long time at the site of infection; varnish forms a physical barrier that prevents reinfection.

Pharmacokinetics

Quickly penetrates the skin and mucous membranes, creating concentration levels. When applied to large surfaces (750 cm2) and for a long time (6 hours), it can be detected in the blood (1.3% of the dose), while T 1/2 is about 1.7 hours and excretion is carried out by the kidneys.

Adverse reactions

Local reactions: itching, burning sensation, redness and peeling of the skin near the diseased nail; allergic phenomena

Indications

Onychomycosis, fungal lesions of the skin and mucous membranes (especially vaginal candidiasis).

Contraindications

Hypersensitivity, pregnancy, breast-feeding, children's age (up to 10 years).

Trade names, formulations and dosing regimens of ciclopirox are presented in Table 10.

Table 10

The main characteristics of ciclopirox

	Tradename	Release form	Dosing regimen
Cyclopirox	Batrafen	gel for external use vaginal cream cream for external use · nail polish solution for external use	*Outwardly.* The varnish is applied to the affected nail with a thin layer using a special brush on the lid of the bottle during the first month every other day, the second - 2 times a week, the third - 1 time per week. In order to increase efficiency, before starting treatment, it is recommended to remove as much of the affected nail as possible and process the rest with a nail file to create an uneven surface. Once a week, all varnish is removed with a conventional solvent, or after a warm bath, its surface layer is scraped off. Cream or solution is applied to the skin 2 times a day and rubbed (at least 2 weeks). After the disappearance of clinical manifestations, the drug is used for another 1-2 weeks to prevent relapse. Vaginal cream with an applicator is inserted deep into the vagina 1 time per day for 6 days; the cream can be used to treat the perivaginal and perianal areas. Powder: pour enough into socks or shoes (for prevention). Vaginal suppositories: 1 suppository 1 time per day for 3-6 days.
Dafnedgin	vaginal cream vaginal suppositories
Fongial	cream for external use · nail polish

Chlornitrophenol (Nitrofungin)

pharmachologic effect- antifungal.

Causes a halt in the growth and development of some types of fungi.

Indications

Dermatomycosis (epidermophytosis, trichophytosis, candidiasis, mycotic eczema), mycosis of the external auditory canal.

Contraindications

Hypersensitivity.

Side effects of the drug

Local irritation, photosensitivity.

Dosage and administration

Outwardly, the affected areas are treated 2-3 times a day until the disappearance of clinical signs, then for at least 4 weeks, using the drug 1-2 times a week. For prevention - 1-2 times a week.

Precautionary measures

Places treated with the drug should not be exposed to sunlight. With dermatomycosis, accompanied by severe local inflammatory phenomena, and with the appearance of irritation, a solution diluted with water in a ratio of 1: 1 can be used.

Despite the fact that many different effective medicines have appeared in mycology over the past decade, the fungus is not treated in 2 days. Of course, all the sick people want to take a pill, and even better - to anoint themselves with ointment, and so that after that the fungus goes away instantly and forever. However, miracles do not happen! The recovery process is long, and therapy is selected individually depending on the type of disease, its severity and the characteristics of the patient. Unfortunately, it is mycosis that is famous for its secondary appeals: more than 70% of the sick are primary.

Choose multiple correct answers

01 Amphotericin B is used for

1) systemic and deep mycoses

2) ringworm

3) disseminated forms of candidiasis

02 Used as antifungal agents

1) streptomycin

2) amphotericin B

3) tetracycline

4) nystatin

5) griseofulvin

03 Causative agents of dermatomycosis are sensitive to

1) griseofulvin

2) ketoconazole

3) nystatin

4) terbinafine

04 The causative agents of systemic mycoses are sensitive to

1) amphotericin in

2) griseofulvin

3) ketoconazole

4) nystatin

05 Amphotericin B sensitive

1) causative agents of dermatomycosis

3) the causative agent of candidiasis

06 Ketoconazole sensitive

1) causative agents of dermatomycosis

2) pathogens of systemic mycoses (histoplasmosis, blastomycosis)

07 antifungals that are antibiotics

1) amphotericin B

2) ketoconazole

3) griseofulvin

4) nystatin

5) terbinafine

08 Violation of the permeability of the cytoplasmic membranes of fungi causes

1) amphotericin B

2) nystatin

3) griseofulvin

4) ketoconazole

09 is used to treat candidiasis

1) nystatin

2) griseofulvin

3) fluconazole

10 Effective for ringworm

1) griseofulvin

2) nystatin

3) terbinafine

11 When resorptive, amphotericin B causes

1) neurotoxic effects

2) nephrotoxic effects

3) increased blood pressure

4) lowering blood pressure

5) hyperkalemia

6) hypokalemia

12 For systemic and deep mycoses, apply

1) amphotericin B

2) griseofulvin

3) fluconazole

4) nystatin

Choose one correct answer

13 cross-allergy with penicillins causes

1) ketoconazole

2) griseofulvin

3) amphotericin B

4) terbinafine

5) clotrimazole

14 Side effects of nystatin are manifested mainly

1) dyspeptic disorders

2) hearing loss

3) inhibition of kidney function

15 antiandrogenic action has

1) nystatin

2) levorin

3) teribinafine

4) naftifine

5) ketoconazole

16 fungicidal and fungistatic action has

1) nystatin

2) amphotericin B

3) ketoconazole

4) terbinafine

5) naftifine

17 inducer of microsomal liver enzymes is

1) amphotericin B

2) griseofulvin

3) naftifine

4) teribinafine

5) ketoconazole

18 Ketoconazole causes

1) violation of the synthesis of the cell membrane of fungi

2) inhibition of nucleic acid synthesis

3) violation of the permeability of the cytoplasmic membranes of fungi

19 The mechanism of the fungicidal action of amphotericin B is due to

1) a violation of the synthesis of the cell membrane of fungi

2) inhibition of nucleic acid synthesis

3) violation of the permeability of the cytoplasmic membranes of fungi

20 The highest toxicity has

1) nystatin

2) amphotericin B

3) griseofulvin

1. Clinical pharmacology: national guidelines / ed. , . - M.: GEOTAR-Media, 2009. - 976 p. - (Series "National Guidelines").

2. Mycoses: diagnosis and treatment / - M .: Wee G Group, 2008. - 336 p.

3. Fundamentals of clinical pharmacology and pharmacotherapy /, -Yaroshevsky - M.: Alliance-V, 2002. - P.668-672.

4. The market of antifungal drugs // Remedium, 2011. - No. 10. - P.39-41.

5. Antifungal agents for external use in pharmacy sales / // New Pharmacy, 2010. - No. 7. – P.8-9.

6. Mycosis and onychomycosis / // New pharmacy, 2010. - No. 6. - P.52-56.

Introduction.. 3

Ø The main groups of fungal diseases.. 4

Ø Classification of antifungal drugs.. 7

Ø Polyena... 8

Ø Azole derivatives.. 15

Ø GLUCAN SYNTHESIS INHIBITORS.. 26

Ø FLUOROPYRIDIMINES... 28

Ø Allylamines... 30

Ø drugs of other groups.. 33

test tasks for self-control.. 42

Answers to the questions of the test task.. 46

The causative agents of epidermomycosis are anamorphs (asexual reproduction structures) 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.

Trichophyton

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 light. 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

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. Mushrooms are more sensitive to the effects of quaternary ammonium compounds (QAC), compositions based on cationic surfactants (STS), SSs 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 hairdressers, beauty salons - hair clippers, combs, curlers, shaving brushes, negligees, 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-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.

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)

Morphological and cultural properties

Trichophytons are characterized by granular or powdery colonies with abundant microconidia, located in clusters on terminal hyphae.

Epidermophytons are characterized by 1-5-cell club-shaped conidia.

Antigens

Pathogenesis and immunity

Dermatomycetes are quite resistant to environmental factors. Some species are found mainly in certain geographic regions.

Laboratory diagnostics

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 contributes to 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.

Dermatomycosis is a fungal skin disease caused by a certain pathogenic microflora. This form of epidermal lesion is characterized by a high degree of contagiousness and requires timely treatment. Ringworm can affect any part of the body and is equally common in people of all age groups.

Dermatomycosis of smooth skin is a lesion of the epidermis of the body by a fungal infection. A feature of the disease is a high degree of contagiousness. Pathology is caused by dermatophyte fungi that enter the skin from the outside, but are not part of the normal microflora.

Ringworm can affect only one area, but in the absence of timely treatment, it quickly spreads to healthy areas of the epidermis. Fungal spores can remain viable in the environment for a long time, which greatly complicates the treatment of this disease.

Often, patients experience a relapse of the disease just a few weeks after the end of the therapeutic course. This is due to the fact that the fungi remained on clothes and other household items and again got on the skin, causing damage to the epidermis.

Dermatomycosis is classified according to localization, causative agent and degree of damage. This disease refers to superficial mycoses, as dermatophytes feed on keratin. Not a single person is immune from the disease. Various ringworms are found in both children and adults.

Dermatomycosis are highly contagious diseases

Classification of dermatomycosis

The disease is caused by dermatophyte fungi. This type includes:

microsporum;
Trichophyton;
epidermophyton.

Depending on the pathogen, there are three types of dermatomycosis:

microsporia;
trichophytosis;
epidermophytosis.

Microsporia is ringworm. It affects the upper layer of the epidermis and hair follicles, causing alopecia in the zone of activity of the fungus. Trichophytosis is also a lichen, manifested by small lesions on the body. Both of these diseases are highly contagious. Epidermophytosis is a type of dermatomycosis in which only the stratum corneum of the epidermis is affected. All three diseases have a similar mechanism of development and are treated with the same drugs.

According to localization, they distinguish:

inguinal ringworm;
onychomycosis;
tinea pedis;
damage to the scalp;
damage to the smooth skin of the body.

All these diseases are caused by the same pathogens of dermatomycosis. The symptoms of these diseases are almost the same. The exceptions are microsporia and onychomycosis. In the first case, there is abundant hair loss in the affected area and severe itching, in the second case, the nail plates are affected. Dermatophytes feed on keratin, which is the building block of nails. Onychomycosis leads to deformation, delamination and exfoliation of the nail plates. Due to the peculiarities of localization, this form of the disease is quite difficult to treat, compared with other types of dermatomycosis.

Reasons for the development of the disease

Children often become infected with mycosis from animals.

Unlike other forms of fungal skin lesions, ringworm is a contagious disease. The pathogen is transmitted from person to person and from animal to person. However, ringworm does not always develop after contact with an infected person. Immunity plays an important role in the development of the disease. With strong immune protection, even if the fungus enters the body, ringworm will not occur, since the immune system will independently defeat the pathogenic microflora.

Factors that increase the risk of developing dermatomycosis:

non-compliance with personal hygiene;
weak immune system;
endocrine disorders;
excess weight;
profuse sweating;
stress;
taking antibiotics and glucocorticosteroids.

Fungal flora can enter the body through any damage to the skin. With weak immunity, it is enough for the spores of the fungus to get on the epidermis so that this disease develops after a while.

Dermatophytes, like other pathogenic fungi, prefer a humid environment with high temperatures. An acidic environment is detrimental to them. You can get infected with ringworm when you visit public showers, pools and saunas with an average air temperature.

Children most often suffer from microsporia. Ringworm is the result of excessive contact with stray animals, which are so fond of stroking small children.

The risk of developing dermatomycosis increases with non-compliance with personal hygiene and profuse sweating. This reduces the local immunity of the skin and creates favorable conditions for the active reproduction of fungi.

Symptoms of ringworm

Common symptoms of dermatomycosis are reddening of the skin, peeling, severe itching. Specific symptoms depend on the exact location of the lesion.

Any ringworm in the photo can be recognized at a glance. The skin looks unhealthy, flaky, inflamed. The severity of symptoms depends on various factors.

Microsporia and trichophytosis are a small spot of regular shape. In this case, the spot has clearly defined boundaries, the skin in the affected area becomes inflamed. The surface of the affected epidermis becomes gray, itchy and flaky. When separating scales that look like dandruff, no discomfort is felt. In the affected area, first break off, and then all the hair falls out. Ringworm on the head is especially dangerous, as it can lead to alopecia areata. After treating the fungus, the hair will grow back, but this will take a long time.

Ringworm in the groin

Fungal infection loves a warm and humid environment, so it often settles in the inguinal folds

Inguinal ringworm develops due to profuse sweating in this area. In this case, the pathogen can get on the skin in any way, since the spores of the fungus remain viable in the air for a long time. Symptoms of inguinal ringworm - redness of the inguinal folds, peeling of the skin, severe itching. This form of the disease is dangerous by the risk of infection. This is due to rubbing of the inguinal folds with clothing. In the hot season, diaper rash may appear. Since sweat acts as a favorable environment for the reproduction of various bacteria, inguinal ringworm is often accompanied by the addition of a secondary infection, which is manifested by the formation of a small pustular rash.

The main causes of this disease are overweight, wearing synthetic underwear, poor personal hygiene and excessive sweating. Ringworm in the groin is more common in men.

Smooth skin lesions

The spots are itchy and swollen

Smooth skin dermatophytosis is a common disease that most often occurs in people living in hot climates. It is high air temperature and profuse sweating that increase the risk of infection with dermatophytosis.

Dermatomycosis of smooth skin is also called epidermophytosis. This fungus infects the stratum corneum of the epidermis, but does not affect the hair follicles. The disease is characterized by the formation of red spots on the skin of the body. Spots can be localized in any area. Mycosis of smooth skin is a lesion of the back, abdomen, area under the mammary glands in women and the chest area in men.

Typical symptoms:

large areas of reddening of the epidermis;
swelling of the skin;
severe itching and peeling;
the appearance of cracks and erosion;
small rash on the border of the affected skin.

When large areas of the skin are affected by ringworm, the symptoms and treatment are complicated, since it is necessary to comprehensively influence the causative agent of the disease. Due to severe itching, a person becomes irritable and nervous, the quality of sleep and working capacity suffer, so we can say that ringworm of smooth skin negatively affects the weight of the body.

Dermatophytosis or mycosis of smooth skin must be treated in a timely manner, as the disease quickly affects healthy areas of the epidermis. Such dermatomycosis in humans is easily recognizable from the photo due to the characteristic symptoms, so there are no problems with diagnosis.

Scalp injury

Cutaneous ringworm can spread to the scalp. In this case, two types of the disease are distinguished - ringworm or epidermophytosis. In the first case, a focal skin lesion appears on the head with severe peeling and hair loss. Alopecia develops at the site of the lesion.

In the second case, red scaly spots are observed on the scalp and on the border of the scalp with the neck or forehead skin. The earlier therapy of epidermophytosis is started, which should be treated immediately, the less the risk of spreading ringworm to the neck and skin on the face.

Onychomycosis and ringworm of the feet

Dermatomycosis of the feet progresses rapidly

The most common types of dermatomycosis are lesions of the skin of the feet and toenails. This is accompanied by:

thickening of the skin of the feet;
the formation of cracks;
redness between the toes;
severe itching and peeling;
destruction of the nail plates.

Treatment of ringworm on the legs in humans is complicated by the specifics of this part of the body. Feet are always covered with shoes, sweat a lot, so the disease progresses rapidly. Having noticed the first signs and symptoms of tinea pedis or onychomycosis of the nails, treatment should be started immediately, otherwise therapy may take several months.

The fungus usually affects one nail first.

Diagnostics

The diagnosis is made on the basis of an external examination and microscopic examination of the scraping of the affected skin. Detection of the mycelium of the fungus is the basis for the diagnosis. Additionally, bacterial culture is carried out to determine the type of fungus and analysis for the sensitivity of pathogenic microflora to various antibiotics.

Principle of treatment

With dermatomycosis, treatment includes the appointment of topical agents and systemic antimycotics in tablets.

Topical preparations based on terbinafine are effective against dermatophytes:

Lamisil;
Lamiderm;
Mycofin;
Terbinox.

These drugs are available in the form of a cream, ointment, gel or spray. They are suitable for the treatment of skin lesions of the body, groin and feet. In case of damage to the nails, the same drugs are used, as well as Exoderil solution.

With ringworm, an antiseptic is additionally used, most often an iodine solution. This is necessary in order to prevent the spread of infection.

When the scalp is affected, shampoos and solutions based on terbinafine are used. In this case, the administration of systemic antimycotics in tablets, in particular Terbinafine and Itraconazole, is also indicated.

The exact treatment regimen is selected by a specialist. The main thing to remember is that mycosis must be treated for a long time. On average, therapy takes about two weeks, but it is recommended to continue using the remedy prescribed by the doctor for another week after the symptoms disappear.

To prevent the development of dermatomycosis, it is necessary:

observe the rules of personal hygiene;
maintain immunity;
do not contact with stray animals;
use personal hygiene items in public places.

When the first symptoms of the disease appear, you should consult a dermatologist. The sooner treatment is started, the sooner it will be possible to get rid of the fungus.