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

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

Mechanism of action

Echinocandins have a mechanism of action that is 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 cell wall of fungi.

Activity spectrum

The spectrum of activity of caspofungin includes Aspergillus spp. (including those resistant to amphothoriicin B), Candida spp. (including azole-resistant strains), Pneumocystis juroveci. Drugs in 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 do not have cross-resistance with other classes of antimycotics.

Pharmacokinetics

Caspofungin is administered intravenously, and oral bioavailability is low due to its high molecular weight. The drug is soluble in water. It has a high degree of binding to blood plasma proteins (97%). Creates high concentrations in the kidneys, liver, spleen and lungs, low concentrations in the brain. After administration 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 minimal adverse events. The most common are fever (3-26%), phlebitis (3-18%) and headaches (4-15%). In rare cases, nausea, diarrhea, skin rash and itching may occur (1-9%). Laboratory adverse events may include increased AST (3-27%), ALT (2-24%), and alkaline phosphatase (4-24%), as well as decreased hematocrit and hemoglobin levels (3-12%).

Indications

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

Contraindications– hypersensitivity to caspofungin or components of the drug.

The international trade name, release forms and dosage regimens of caspofungin are presented in Table 5.

Table 5

Main characteristics of caspofungin

	Tradename	Release form	Dosage regimen
Caspofungin	Cancidas	lyophilisate for the preparation of solution for infusion	IV, by slow intravenous infusion (≥1 hour) 1 time per day. For 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 effectiveness of the drug. Empirical therapy should be continued until the neutropenia resolves completely. 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 clinical manifestations of both fungal infection and neutropenia. It is possible to increase the daily dose to 70 mg if a dose of 50 mg is well tolerated but does not produce the expected clinical effect.

Ø FLUOROPYRIDIMINES

The only representative is flucytosine (or 5-fluorocytosine).

Mechanism of action associated with disruption of DNA and RNA synthesis due to the conversion of 5-fluorocytosine to 5-fluorouracil, the metabolites of which 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, Aspirgillus, Cryptococcus, causative agents of chromoblastomycosis.

Pharmacokinetics

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

Adverse events

It has fairly high myelototoxicity and hepatotoxicity. In most patients, these adverse events are dose-dependent and reversible. Possible development of 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. It is necessary to monitor serum concentrations of flucytosine whenever possible (especially when combined with amphotericin B), with the most important determination of the residual concentration.

Indications

Monotherapy for 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, aspergillosis resistant to monotherapy, and fungal endocarditis.

Contraindications

Allergic reaction to flucytosine.

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

Table 6

Main characteristics of flucytosine

	Tradename	Release form	Dosage 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 during pregnancy or breastfeeding.

Ø Allylamines

Allylamines, which are synthetic antimycotics, include terbinafine, used internally and topically, and naftifine, intended for local use. The main indications for the use of allylamines are dermatomycosis.

Mechanism of action

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

Activity spectrum

Allylamines have a broad spectrum of antifungal activity. Dermatomycetes (Trichophyton, Microsporum and Epidermophyton spp.), M. furfur, some Candida, Aspergillus spp., C. neoformans, S. schenckii and pathogens of chromomycosis are sensitive to them.

Terbinafine It is also active in vitro against a number of protozoa (some species of Leishmania and Trypanosomes).

Despite the wide range of activity of allylamines, only their effect on dermatomycetes is of clinical significance.

Pharmacokinetics

Terbinafine

It is well absorbed from 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 and nail plates. Metabolized in the liver, excreted by the kidneys. T ½ 11-17 hours, increases with renal and liver failure.

Adverse events

Adverse events occur rarely and usually do not lead to discontinuation of the drug.

Terbinafine orally

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

Terbinafine topically, naftifine

Skin: itching, burning, hyperemia, dryness.

Indications

Skin mycoses caused by dermatomycetes (with limited damage - locally, widespread - inside). Microsporia, trichophytosis of the scalp (inside). Onychomycosis (inside). Chromomycosis (inside). Sporotrichosis cutaneous, cutaneous-lymphatic (internal). Skin candidiasis (local). Pityriasis versicolor (topically).

Contraindications

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

International trade names, release forms and dosage regimens of allylamines are presented in Table 7.

Table 7

Main characteristics of allylamines

	Tradename	Release form	Dosage regimen
Terbinafine		· pills	*Inside* , after meals, 1 time a day in the evening at a dose of 250 mg or 2 times a day 125 mg. *Locally* , the cream is applied in the morning and/or evening to the affected skin, previously cleansed and dried, as well as to the surrounding areas. The average course duration for skin lesions is 1–2 weeks, for nail plates – 3–6 months. For children, the dose is determined depending on body weight.
		cream for external use · pills
		cream for external use · pills
	Lamisil Dermgel
	Lamisil Uno
		· pills
	Lamitel	spray for external use
	Mikonorm	cream for external use
	Mycoterbin
		· pills
	Terbizil	cream for external use · pills
		cream for external use spray for external use
	Terbinafine	cream for external use · pills
	Terbinafine-MFF	ointment for external use
	Terbinafine-Sar	· pills
	Terbinafine hydrochloride	substance-powder
	Terbinox	cream for external use · pills
	Terbifin	cream for external use spray for external use · pills
	Thermikon	cream for external use spray for external use · pills
	Fungoterbin	cream for external use spray for external use · pills
		· pills
		· pills cream for external use
Naftifin	Exoderil	cream for external use solution for external use	*Externally.* Used as a cream (1%) or solution (1%). For dermatomycosis - applied to the affected surface and adjacent areas of the skin, previously cleaned and dried, 1 time per day. The duration of treatment for dermatomycosis is 2–4 weeks; for candidiasis - at least 4 weeks; if necessary, the course is extended to 6–8 weeks. If there is no clinical improvement after 4 weeks of use, it is recommended to clarify the diagnosis. For onychomycosis, the solution is applied to the affected surface, covered with a thick bandage, 2 times a day, course - 6 months; for complicated forms - up to 8 months. To prevent relapses, treatment is continued for another 2 weeks after clinical improvement is achieved.

Ø drugs of other groups

Griseofulvin (fulcine)

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. Ineffective against 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 in tablets is mainly used. The tablets are taken orally during meals with a spoon of vegetable oil, since griseofulvin is a lipophilic substance. Absorption increases with a diet rich in fat.

Mechanism of action.

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

Pharmacokinetics

When taken orally it is well absorbed. Reaches maximum concentration in the blood 4-5 hours after administration. T½ is about 20 hours. Absorption from the gastrointestinal tract varies greatly among different people, mainly due to the insolubility of the substance in the aqueous environment of the upper gastrointestinal tract. It should be noted that some patients tend to develop 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 of the skin and its appendages, as well as in the liver, fatty tissue, and skeletal muscles. Minor amounts enter fluids 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

From the gastrointestinal tract: nausea, vomiting, dry mouth, diarrhea, abdominal pain, candidal stomatitis, increased activity of liver 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 cardiovascular system and blood (hematopoiesis, hemostasis): granulocytopenia, agranulocytosis, leukopenia. Allergic reactions: rash, itching, urticaria, Quincke's edema, photosensitivity, lupus-like syndrome, exudative erythema multiforme, topical epidermal necrolysis (Lyell's syndrome).

Indications

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

Contraindications

Hypersensitivity, porphyria, systemic lupus erythematosus, lupus-like syndrome, systemic blood diseases, leukopenia, organic liver and kidney diseases, hepatocellular failure, malignant neoplasms.

Restrictions on use

Children under 2 years of age (efficacy and safety of use have not been determined).

Use during pregnancy and breastfeeding

There is evidence of the teratogenic and embryotoxic effects of griseofulvin in animals (with oral administration in pregnant rats, pups with several disorders have been reported). Contraindicated during pregnancy (griseofulvin crosses the placenta; adequate and strictly controlled studies have not been conducted in pregnant women). Use during breastfeeding is not recommended (it is unknown whether griseofulvin passes into breast milk). No adequate data available.

Interaction

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

Features of application and dosage

Adults: 0.25-0.5 g every 12 hours,

Children: 22 mg/kg/day (not more than 1000 mg/day) in 1-2 doses.

Griseofulvin should be taken orally during or immediately after meals.

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 if you feel dizzy. Avoid sun exposure.

Do not use griseofulvin if you are pregnant or breastfeeding.

During treatment with griseofulvin and for 1 month after termination, do not use only estrogen-containing oral medications for contraception; be sure to use additional or alternative methods

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

International, trade names, release forms and dosage regimens of griseofulvin are presented in Table 8.

Table 8

Main characteristics of griseofulvin

	Tradename	Release form	Dosage regimen
Griseofulvin	Griseofulvin	· standard sample – powder substance-powder · pills	Orally (during or immediately after meals), in one or more doses. The daily dose for adults is 500 mg (for 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 the thickness of the keratin at the site of infection and is: for the scalp - 4-6 weeks, body - 2-4 weeks, feet - 4-8 weeks, fingers - at least 4 months, toes - at least 6 months.
Griseofulvin tablets 0.125 g	· pills
	· pills

Potassium iodide

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

Activity spectrum

Active against many fungi, but its main clinical significance is against Sschenckii.

Pharmacokinetics

Quickly and almost completely absorbed into the gastrointestinal tract. Distributed predominantly into 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 (appropriate clinical and laboratory monitoring is required).

Iodism reactions: rash, rhinitis, conjunctivitis, stomatitis, laryngitis, bronchitis.

Other: lymphadenopathy, swelling of the submandibular salivary glands.

If severe adverse events develop, the dose should be reduced or temporarily discontinued. After 1-2 weeks, treatment can be resumed at lower doses.

Indications

Sporotrichosis cutaneous, skin-lymphatic.

Contraindications

Hypersensitivity to iodine preparations.

Hyperfunction of the thyroid gland.

Tumors of the thyroid gland.

Amorolfine

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

Mechanism of action

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

Activity spectrum

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 negligible 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, yeast and mold fungi (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, release forms and dosage regimens of amorolfine are presented in Table 9.

Table 9

Main characteristics of amorolfine

	Tradename	Release form	Dosage regimen
Amorolfine		· nail polish	Externally. The varnish is applied to the affected nails 1-2 times a week. Before use, remove the affected areas of the nail using 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 remaining varnish with a swab with alcohol. Treatment is continued continuously until a new nail grows and the affected areas disappear. The duration of therapy depends on the location and severity of the process and averages 6 months (fingernails) or 9–12 months (toenails).

Ciclopirox ( trade names Batrafen, Dafnedzhin, Fongial)

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

Activity spectrum

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 (damage only surface of the nail plate), and follow-up treatment of onychomycosis after systemic therapy to prevent relapses. With multicolored lichen, clinical and mycological improvement is observed after 2 weeks of treatment (not earlier). In the form of nail polish, it quickly (within the first hours from the moment of application) and deeply penetrates the nail and is deposited for a long time at the site of infection; The 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 T1/2 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 around the diseased nail; allergic phenomena

Indications

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

Contraindications

Hypersensitivity, pregnancy, breastfeeding, children (up to 10 years).

Trade names, release forms and dosage regimens of ciclopirox are presented in Table 10.

Table 10

Main characteristics of ciclopirox

	Tradename	Release form	Dosage regimen
Ciclopirox	Batrafen	gel for external use · vaginal cream cream for external use · nail polish solution for external use	*Externally.* The varnish is applied to the affected nail in a thin layer using a special brush on the lid of the bottle every other day for the first month, 2 times a week for the second month, 1 time per week for the third month. To increase effectiveness, before starting treatment, it is recommended to remove as much of the affected nail as possible and file the remaining part to create an uneven surface. Once a week, all varnish is removed using a regular solvent, or after a warm bath, the surface layer is scraped off. The cream or solution is applied to the skin 2 times a day and rubbed in (for at least 2 weeks). After the disappearance of clinical manifestations, the drug is used for another 1–2 weeks to prevent relapse. Vaginal cream is inserted deep into the vagina using an applicator once a day for 6 days; The cream can be used to treat the peri-vaginal and perianal areas. Powder: pour a sufficient amount into socks or shoes (for prevention). Vaginal suppositories: 1 suppository 1 time per day for 3–6 days.
Dafnedjin	· vaginal cream · vaginal suppositories
Fongial	cream for external use · nail polish

Chlornitrophenol (Nitrofungin)

pharmachologic effect- antifungal.

Causes the growth and development of certain types of fungi to stop.

Indications

Ringworm (athlete's foot, trichophytosis, candidiasis, mycotic eczema), mycosis of the external auditory canal.

Contraindications

Hypersensitivity.

Side effects of the drug

Local irritation, photosensitivity.

Directions for use and doses

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

Precautionary measures

Areas treated with the drug should not be exposed to sunlight. For dermatomycosis, accompanied by severe local inflammation, and when irritation occurs, you can use a solution diluted with water in a 1:1 ratio.

Despite the fact that many different effective medicines have appeared in mycology over the past decade, the fungus cannot be cured in 2 days. Of course, all sick people want to take a pill, or even better, to anoint themselves with ointment, and then the fungus will go 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 cases: more than 70% of cases are primary.

Choose multiple correct answers

01 Amphotericin B is used for

1) systemic and deep mycoses

2) dermatomycosis

3) disseminated forms of candidiasis

02 Used as antifungal agents

1) streptomycin

2) amphotericin B

3) tetracycline

4) nystatin

5) griseofulvin

03 Pathogens of dermatomycosis are sensitive to

1) griseofulvin

2) ketoconazole

3) nystatin

4) terbinafine

04 Pathogens of systemic mycoses are sensitive to

1) amphotericin b

2) griseofulvin

3) ketoconazole

4) nystatin

05 Sensitive to amphotericin B

1) pathogens of dermatomycosis

3) causative agent of candidiasis

06 Sensitive to ketoconazole

1) pathogens of dermatomycosis

2) pathogens of systemic mycoses (histoplasmosis, blastomycosis)

07 antifungal agents that are antibiotics

1) amphotericin B

2) ketoconazole

3) griseofulvin

4) nystatin

5) terbinafine

08 Violation of the permeability of cytoplasmic membranes of fungi is caused by

1) amphotericin B

2) nystatin

3) griseofulvin

4) ketoconazole

09 is used for the treatment of candidiasis

1) nystatin

2) griseofulvin

3) fluconazole

10 Effective for dermatomycosis

1) griseofulvin

2) nystatin

3) terbinafine

11 With its resorptive effect, 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 it is used

1) amphotericin B

2) griseofulvin

3) fluconazole

4) nystatin

Choose one correct answer

13 causes cross-allergy with penicillins

1) ketoconazole

2) griseofulvin

3) amphotericin B

4) terbinafine

5) clotrimazole

14 Side effects of nystatin occur predominantly

1) dyspeptic disorders

2) hearing loss

3) depression of renal function

15 has an antiandrogenic effect

1) nystatin

2) levorin

3) teribinafine

4) naftifine

5) ketoconazole

16 has fungicidal and fungistatic effects

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) disruption of the synthesis of the cell membrane of fungi

2) inhibition of nucleic acid synthesis

3) disruption of the permeability of cytoplasmic membranes of fungi

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

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

2) inhibition of nucleic acid synthesis

3) impaired permeability of the cytoplasmic membranes of fungi

20 Has the highest toxicity

1) nystatin

2) amphotericin B

3) griseofulvin

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

2. Mycoses: diagnosis and treatment / – M.: VG Group, 2008. – 336 p.

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

4. 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. Mycoses and onychomycosis // New Pharmacy, 2010. – No. 6. – P.52-56.

Introduction.. 3

Ø Main groups of fungal diseases.. 4

Ø Classification of antifungal drugs.. 7

Ø Polyenes... 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 test questions.. 46

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 reproductive structures) are included in the same genus Arthroderma. In 1839, Yu. Schönlein first described favus (scab) as a fungal disease. In 1845, R. Remak named this mushroom Achorion schoenleinii. Later, other pathogens of epidermomycosis were discovered. Dermatomycetes are not dimorphic fungi. Their differentiation is based primarily on morphological and cultural characteristics.

Trichophyton

Morphological and cultural properties

Dermatomycetes form septate mycelium with spirals, rocket-shaped swellings, arthrospores, chlamydospores, macro- and microconidia. They undergo pleomorphic changes in laboratory conditions, when they lose the ability to form pigment and form conidia. Species are distinguished by pigmentation and colony shape. Dermatomycetes grow well on Sabouraud glucose agar.

Trichophytons are characterized by granular or mealy colonies with abundant microconidia located in clusters on the 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 yellow-orange. Upon ultraviolet irradiation of hair affected by microsporum, fluorescence in a light green color is observed.

Epidermophytons are characterized by 1-5-celled 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 hyperthyroidism, and the protein part causes hyperthyroidism.

Pathogenesis and immunity

The causative agents of epidermomycosis affect the epidermis, hair, and nails due to direct contact of a healthy person with infected scales or hair of a patient. Fungal hyphae then grow into the stratum corneum, causing diseases of varying clinical manifestations and localization. Some cases of disease are associated with 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 torso and head, involving the lymph nodes.

With epidermomycosis, the development of immediate (IHT) and delayed type hypersensitivity (DHT) is observed. Ecology and epidemiology. Most dermatomycetes are widespread in nature. Some species are found in 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 are zoophilic dermatomycetes (M. canis, T. verrucocum), pathogenic for domestic and wild animals, transmitted to humans; 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 primarily in certain geographic regions.

Laboratory diagnostics

Pathological material (skin flakes, nails, hair extracted from affected areas) is examined microscopically, having previously softened them in a 10-20% KOH solution. Microsporum forms close layers of spores in a mosaic pattern around the hair, while Trichophyton forms parallel rows of spores, outside (ectothrix) and inside (endothrix) the affected hair.

Dermatomycetes of the ectothrix group include Microsporum audouinii, M.canis, M.gypseum, etc.; to the endothrix group - T. gourvilii, T. tonsurans, etc. Some of them do not form conidia in the hair, others rarely penetrate the hair, and others do not invade the hair. Hair infected with Microsporum fluoresces when exposed to ultraviolet light. The final identification of dermatomycetes is carried out based on the study of cultures grown for 1-3 weeks on Sabouraud's medium at 20°C, based on the morphological characteristics of the mycelium and spores. To identify dermatomycetes and free them from contaminating fungi and bacteria, a special nutrient medium, DTM, is used, which is widely used in clinical laboratories.

There is no specific prevention

Characteristics of pathogens of dermatomycosis

Dermatomycosis (dermatophytosis) is a superficial disease of the skin and its appendages (hair, nails) caused by microscopic fungi - dermatomycetes (dermatophytes). Among them there are anthropophilic (causing diseases in humans), zooanthropophilic (causing diseases in animals and humans).

Currently, more than 400 species of pathogenic fungi are known that are 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 various authors, these diseases affect from 10 to 40% of the world's population. More than 40 species of dermatomycetes are known, but in our country Trichophytonrubrum and Trichophytonmentagrophytesvar are more common. interdigitale, Trichophytonmentagrophytesvar.gypseum, Trichophytontonsurans, Trichophytonverrucosum, Trichophytonviolaceum, Microsporumcanis, less commonly Epidermophytonfloccosum.

Nail mycosis (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 Trichophyton tonsurans (together about 1%).

Mycosis of hands and feet

The main causative agent of mycosis of the feet is Trichophytonrubrum, with Trichophytonmentagrophytesvar in second place in terms of prevalence. interdigitale, on the 3rd - Epidermophytonfloccosum. The fungi Microsporumcanis, Trichophytonmentagrophytesvar.gypseum and Trichophytonverrucosum can infect the skin of the hands on both the dorsal and palmar surfaces.

Mycosis of smooth skin of the trunk, limbs

The causative agents of mycosis of smooth skin are dermatomycetes Microsporumcanis, Trichophytonrubrum, Trichophytonmentagrophytesvar.gypseum, Trichophytonverrucosum, Epidermophytonfloccosum, less common are Trichophytonviolaceum and Trichophytontonsurans.

Mycosis of the inguinal folds. Athlete's foot (true), (athlete's foot)

The main causative agent of mycosis of the inguinal folds is Trichophytonrubrum. Less commonly, the causative agents may be T. mentagrophytesvar.gypseum or Microsporum. The favorite localization of this area is epidermophyton inguinal (true, epidermomycosis inguinal), 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 through contact with objects contaminated with the hair of sick animals.

Trichophytosis is a fungal disease of the skin, hair, and, less commonly, nails, caused by various types of fungi of the genus Trichophyton. There are anthropophilic and zoophilic trichophytons. Superficial trichophytosis is caused by anthropophilic fungi, which include Trichophyton violaceum and Trichophyton tonsurans.

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 families or children's groups.

Since infiltrative-suppurative trichophytosis is caused by zooanthropophilic fungi, which include Trichophytonmentagrophytesvar. gypseum and Trichophytonverrucosum, the carriers of which are 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 classes 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 occurs through contact with domestic animals - 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. Chloractive agents (chloramine, hypochlorites), oxygen-containing compounds, aldehydes, tertiary amines, polymer 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 (QACs), compositions based on cationic surfactants (CSAS), CSAS and aldehydes, alcohols; phenolic preparations, anolytes, preparations based on chlorinated derivatives of hydantoin, sodium chloroisocyanurate and trichloroichocyanuric acid.

The causative agents of fungal diseases survive in pathological material in the external environment for 1.5 to 10 years.

Pathways and factors of transmission of dermatomycosis

The main route of spread of dermatomycosis is through household contact (direct and indirect contact). The disease is transmitted through direct contact with a sick person, sick animal or carrier, or through contact with various environmental objects contaminated with dermatophytes.

Skin scales, fragments of hair, nails containing abundant elements of a viable fungus, falling off from the lesions, infect the patient’s things - clothes, hats, bed linen, towels, household items (toys, books, carpets, upholstered furniture, etc.), toiletries (combs, combs, washcloths), shoes, gloves, cleaning equipment, bedding for animals and care items.

Factors of transmission of infection are:

In infectious foci - sanitary equipment, floors, upholstered furniture, carpets, rugs, underwear and bed linen, stockings, socks, clothing, hats, shoes, toiletries (combs, brushes, washcloths, etc.), bedding, books, indoor surfaces, patient care items, toys, animal bedding and pet care items;

In medical institutions - sanitary equipment, incl. baths for medical procedures (except for saline and hydrogen sulfide), furnishings, underwear and bed linen, clothing of medical personnel, shoes, toiletries (combs, brushes, washcloths, etc.), medical products (instruments), dressings, bed linen oilcloths (napkins), medical waste, surfaces of apparatus, devices;

In hairdressing salons 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, shower cabins, rubber mats, wooden gratings, pool paths, steps and handrails of ladders, the surface of the pool bowl, sports equipment, gymnastic mats, wrestling mats carpets, wardrobes, floors, especially wooden ones;

In children's institutions - bed linen, towels, toys, books, carpets, upholstered furniture, animal care items in zoo corners;

In baths, saunas, showers - sanitary equipment, shower cabins, rubber mats, wooden grates, floors, washcloths, sponges, scissors, basins for washing feet, bath and shower mats, etc.;

In the environment - sand from children's sandboxes, waste disposal areas, dust from staircases, backfill material from attics and basements, water from small reservoirs.

Types of disinfection for dermatomycosis

In the prevention of dermatomycosis, an important role is played not only by the early identification of patients, isolation, timely specific treatment, strict adherence to the rules of personal hygiene, but also by carrying out 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 measures (preventive and focal disinfection).

Focal (current and final) disinfection is carried out in places where the patient is identified and treated: 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. Causative agents of mycoses (candidiasis and dermatomycosis) and protozoal infections (amoebiasis, giardiasis, trichomoniasis, leishmaniasis, trypanosomiasis, malaria, toxoplasmosis, balantidiasis). Microbiological diagnosis of candidiasis and dermatomycosis. Diagnostic, preventive and therapeutic drugs.

Pathogens 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 people with transplants, against the background of reduced immunity, irrational long-term antibiotic therapy, hormone therapy, and the use of invasive research methods. Found in soil, water, air, and on rotting plants; some are part of the facultative microflora of humans (for example, fungi of the genus Candida).

18.5.1. Causative agents of candidiasis (genus 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; whose 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 S. 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 blastospores (buds) when they are placed in serum. Besides C. albicans forms chlamydospores - thick-walled, double-circuited, large oval spores. On simple nutrient media at 25-27°C they form yeast and pseudohyphal cells. Colonies are convex, shiny, creamy, opaque with various shades. In tissues, Candida grows in the form of yeasts and pseudohyphae.

Epidemiology.Candida is part of the normal microflora of mammals and humans. They live on plants

In fruits, being part of the normal microflora, they can invade the tissue (endogenous infection) and cause candidiasis in patients with weakened immune defenses. Less commonly, the pathogen is transmitted to children at birth or during 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. Most often candidiasis is caused by 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 the mucous membranes, skin and nails, chronic (granulomatous) candidiasis, allergy to candida antigens. Visceral candidiasis is accompanied by inflammatory damage to certain organs and tissues (esophageal candidiasis, gastritis candidiasis, 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 cheesy coating, and the development of atrophy or hypertrophy, hyperkeratosis of the papillae of the tongue is possible. With vaginal candidiasis (vulvovaginitis), white cheesy discharge, swelling and erythema of the mucous membranes appear. Skin lesions most often develop in newborns; Small nodules, papules and pustules are observed on the torso and buttocks. Candida allergy of the gastrointestinal tract, allergic damage to the organs of vision with the development of itching of the eyelids, blepharoconjunctivitis are possible.

Immunity.Cellular immunity predominates. Mononuclear cell phagocytes, neutrophils and eosinophils, which capture fungal elements, participate in protecting the body from candida. HRT develops, granulomas with epithelioid and giant cells are formed.

In smears from clinical material, pseudomycelium is detected (cells are connected by constrictions

kami), mycelium with septa and budding blastospores. Cultures from the patient are carried out on Sabouraud agar, wort agar, etc. Colonies C. albicans whitish-cream, convex, round. Fungi are differentiated by morphological, biochemical and physiological properties. Candida species differ when growing on glucose-potato agar by the type of filamentation: the location of the glomeruli - clusters of small round yeast-like cells around the pseudomycelium. For blastospores C. albicans The formation of germ tubes is typical when cultivated in liquid media with serum or plasma (2-3 hours at 37°C). In addition to this, C. albicans chlamydospores are detected: the inoculated area on rice agar is covered with a sterile coverslip and after incubation (at 25°C for 2-5 days) it is examined under a microscope. Saccharomycetes, unlike Candida spp. are true yeasts and form ascospores located inside cells, stained by the modified Ziehl-Neelsen method; Saccharomyces usually do not form pseudomycelia. The presence of candidemia is established by a positive blood culture with isolation from the blood Candida spp. Candidiasis urinary infection is established when more than 10 5 colonies are detected Candida spp. in 1 ml of urine. It is also possible to carry out serological diagnostics (agglutination reaction, RSK, RP, ELISA) and a skin allergy test with candida allergen.

Treatment.Nystatin, levorin (for the treatment of local superficial mycoses, such as oropharyngeal), clotrimazole, ketoconazole, caspofungin, itraconazole, fluconazole (does not affect S. krusei, many strains C. glabrata).

Prevention.It is necessary to observe the rules of asepsis and sterility of invasive procedures (catheterization of veins, bladder, bronchoscopy, etc.). Patients with severe neutropenia are prescribed anticandidal drugs to prevent the development of systemic candidiasis.

Pathogens of epidermomycosis (dermatomycosis)

Morphological and cultural properties

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

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

Antigens

Pathogenesis and immunity

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

Laboratory diagnostics

There is no specific prevention

Sarcodaceae (amoebas)

Most amoebas (from Greek. amoibe- change) live in the environment, some species - in the body of humans and animals. Amoebas move with the help of changing cell outgrowths - pseudopodia, and feed on bacteria and small protozoa. They reproduce asexually (by division in two). The life cycle includes a trophozoite stage (a growing, motile cell) and a cyst stage. The trophozoite forms a cyst that is resistant to external factors. Once in the intestine, it turns into a trophozoite.

There are pathogenic and non-pathogenic amoebas. Pathogenic amoebas include dysenteric amoeba (Entamoeba histolytica) and free-living pathogenic amoebas: Acanthamoeba (genus Acanthamoeba) and Naegleria (genus Naegleria). Naegleria fowleri is a flagellated amoeba. It causes amoebic meningoencephalitis. The human colon is inhabited by non-pathogenic amoebas - intestinal amoeba. (Entamoeba coli), Hartmann's amoeba (Entamoeba hartmanni), Yodamoeba Bütschli (Iodamoeba buetschlii) etc. It turned out that sometimes these amoebas can cause diseases. An oral amoeba is often found in the mouth (Entamoeba gingivalis), especially for 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 pronounced cases) by ulcerative lesions of the colon, frequent loose stools, tenesmus and dehydration (amebic dysentery), as well as the development of abscesses in various organs. The pathogen was discovered in 1875 by Russian military doctor F.A. Leshem.

Morphology.There are three forms of dysenteric amoeba: small vegetative, large vegetative and cystic (Fig. 19.1). Small vegetative (luminal) form Entamoeba histolytica forma minuta has a size of 15-20 microns, is inactive, lives in the lumen of the upper part of the 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, and can phagocytose red blood cells. Found in fresh feces during 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 non-pathogenic Entamoeba coli cyst contains 8 nuclei).

Resistance.Vegetative forms of the pathogen outside the body quickly die. Cysts persist in feces and water at a temperature of 20°C for 2 weeks. In food, vegetables and fruits, cysts persist for several days. When boiled they die.

Epidemiology.The source of infection is humans, i.e. amoebiasis is an anthroponotic disease. The mechanism of transmission of amoebas is fecal-oral, transmission routes are alimentary, water and

Rice. 19.1.Morphology of amoebas: a, b - trophozoites Entamoeba histolitica, one of which absorbs red blood cells; V - Entamoeba hartmani- trophozoite with food vacuole; d - cysts with 1, 2 and 4 nuclei; d - binuclear (left) and mononuclear (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. The spread of cysts is facilitated by flies and cockroaches. Children over 5 years of age are most often affected. The highest incidence is observed in regions of tropical and subtropical climates.

Pathogenesis and clinical picture. From cysts that enter the intestine, luminal forms of amoebas are formed, which live in the large intestine without causing disease. Luminal forms behave as commensals of the intestine, feeding on its contents without causing harmful effects. Such a person is a healthy carrier E. histolytica, secreting cysts. Asymptomatic carriage is widespread E. histolytica. When the body's immunity decreases, luminal forms of amoebas penetrate the intestinal wall and multiply in the form of tissue forms. Intestinal amebiasis develops, which is facilitated by some representatives of the intestinal microflora. Tissue form trophozoites are motile due to the formation of pseudopodia. They penetrate the wall of the colon, causing coagulative necrosis, are able to phagocytose 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 loose 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 through the bloodstream into the liver, lungs, brain and other organs. Single or multiple amoebic abscesses form, ranging in size from barely visible to the eye to 10 cm in diameter. The development of cutaneous amebiasis is possible: erosions and mildly painful ulcers form on the skin of the perianal area and perineum.

ImmunityUnstable in case of amoebiasis. Antibodies are formed only to tissue forms E. histolytica. The cellular component of immunity is activated predominantly.

Microbiological diagnostics. The main method is a microscopic examination of the patient’s stool, 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-

chemical 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 amebiasis. The molecular biological method (PCR) makes it possible to determine DNA marker regions in feces E. histolytica.

Treatment.Metronidazole, tinidazole, mexaform, osarsol, yatren, diiodoquine, delagil, dihydroemitin, etc. are used.

Prevention.Identification and treatment of cyst excretors and amoeba carriers, as well as carrying out general sanitary measures.

19.2. Flagellates

Flagellates include Leishmania, Trypanosomes, Giardia and Trichomonas. They have one or more flagella. At the base of the flagellum there is a blepharoplast; some protozoa have a kinetoplast nearby, a DNA-containing organelle of mitochondrial origin that facilitates the movement of the flagellum.

19.2.1. Leishmania (genus Leischmania)

Leishmaniasis is a protozoal disease of animals and humans caused by Leishmania and transmitted by mosquitoes; internal organs (visceral leishmaniasis) or 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 S. 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. venezuelensis); L. tropica; L. major; L. aethiopica; subgenus Viannia with 4 main types. All Leishmania species are morphologically indistinguishable. They are differentiated using monoclonal antibodies or molecular genetic methods.

prethelial system. They reproduce by simple division. They have flagellar (promastigote) and flagellate (amastigote) cycles of asexual development.

Rice. 19.2.Leishmania donovani: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 is cultivated on medium NNN(authors - Nicole, Novi, Neil), containing agar with defibrinated rabbit blood. They can be grown on the chorioallantoic membrane of the chick embryo, in cell cultures or on white mice, hamsters and monkeys.

Epidemiology.Leishmaniasis is common in countries with warm and tropical climates. The mechanism of transmission of pathogens is transmissible through the bite of mosquitoes.

The main sources of infection are: for cutaneous anthroponotic leishmaniasis, people; for cutaneous zoonotic leishmaniasis in gerbils and other rodents; with visceral leishmaniasis, people (with Indian visceral leishmaniasis) or dogs, jackals, foxes, rodents (with Mediterranean-Central Asian visceral leishmaniasis); for mucocutaneous leishmaniasis in rodents, wild and domestic animals.

Pathogenesis and clinical picture. Anthroponotic cutaneous leishmaniasis causes L. tropica. The disease had different names: late ulcerating leishmaniasis, urban form, Ashgabat ulcer, “yearling”. 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 the mosquito bite, a tubercle appears, which enlarges and ulcerates after 3-4 months. Ulcers are most often located on the face and upper extremities, scarring by the end of the year (hence the popular term “yearling”).

Zoonotic cutaneous leishmaniasis (early ulcerating leishmaniasis, Pendinsky ulcer, rural form) causes L. major. The disease is more acute. The incubation period is 2-4 weeks. Weeping ulcers are most 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 damage to the adrenal glands, the skin darkens and 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; granulomatous and ulcerative lesions of the skin of the nose, mucous membranes of the mouth and larynx develop. The incubation period is from 2 weeks to 3 months. The shape of the nose changes (tapir nose). Found mainly in Central and South America, like similar diseases caused by L. mexicana(Mexican leishmaniasis), L. peruviana(Peruvian leishmaniasis), L. panamensis(Panamanian leishmaniasis), etc.

Immunity.People who have recovered from the disease remain immune for life.

Microbiological diagnostics. Smears from tubercles, contents of ulcers or punctures from organs are stained according to Romanovsky-Giemsa. Microscopy reveals intracellularly located amastigotes. A pure culture of the pathogen is isolated on the medium NNN: incubation of the crop for 3 weeks at room temperature. White mice and hamsters are also infected. Serological methods include RIF and ELISA. The allergic skin test (Montenegro test) for HRT to leishmanin (a drug made from killed promastigotes) is used in epidemiological studies of leishmaniasis. It is positive after 4-6 weeks of illness.

Treatment.For systemic treatment, injections of 5-valent antimony oxide preparations - stibogluconate (Pentostam) - are prescribed. For cutaneous leishmaniasis, ointments of chlorpromazine, paromomycin or clotrimazole are used topically.

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). The pathogens were discovered in 1902 by D. Daton (T. gambiense), in 1909 by Ch. Chagas (T. cruzi) and in 1910 G. Fantenham (T. rhodesiense).

Characteristics of pathogens. Trypanosomes are larger in size (1.5-3x15-30 µm) than Leishmania. They have a narrow oblong shape, a flagellum and an undulating membrane (Fig. 19.3). They reproduce asexually (longitudinal division). The source of infection is domestic and wild animals, and infected humans. African trypanosomiasis is transmitted by blood-sucking tsetse flies, and Chagas disease is transmitted by triatomine bugs. Pathogens have different stages of development: amastigotes, epimastigotes, trypomastigotes. Amastigotes They 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). Trypomastigotes found in the blood of animals and humans. The flagellum extends from the back of the elongated cell. The undulating membrane is sharply expressed.

Pathogenesis and clinical picture. Gambian uniform African trypanosomiasis, called T. gambiense, occurs chronically, and the Rhodesian form, caused T. rhodesiense, is a more acute and severe form of the disease. At the site of the bite by the vector, the tsetse fly, an ulceration develops by the end of the week.

Rice. 19.3.Morphology of trypanosomes: a, b - trypomastigotes in the blood; c - epimastigote in the intestines of carriers

Patients develop lymphadenitis, myocarditis, and fever. The gastrointestinal tract, liver, spleen, and brain are affected. A long latent period is characteristic, up to several decades.

Immunity.In response to invasion, large quantities of IgM antibodies are formed. In the chronic phase, IgG antibodies predominate. Trypanosomes are capable of producing new antigenic variants that alter the immune response. Autoimmune processes develop.

Microbiological diagnostics. Smears from blood, punctate cervical lymph nodes, cerebrospinal fluid are stained according to Romanovsky-Giemsa or Wright. To isolate the pathogen, you can infect white mice or rats, and also inoculate it 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 in case of damage to the central nervous system, melarsoprol is prescribed.

Treatment of American trypanosomiasis is possible only in the acute phase with benznidazole or nifurtimox.

Preventionnonspecific. Eliminate breeding sites of pathogen carriers and destroy infected animals. Infected individuals are identified and treated. Use repellents and protective clothing.

Giardia, or Giardia (genus Lamblia, or Giardia)

Giardiasis (giardiasis) is a disease caused by Lamblia intestinalis (Giardia lamblia), occurring in latent or manifest form in the form of intestinal dysfunction with symptoms of enteritis. The pathogen 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 Giardia is flat, pear-shaped (5-10x9-20 µm), contains two nuclei (Fig. 19.4) and 4 pairs of flagella. Giardia reproduces by longitudinal division. They attach to intestinal epithelial cells using a suction disk and due to the adhesion of microprotrusions of the trophozoite plasmalemma. Giardia lives in the upper sections of the intestine, and in the less favorable lower sections of the intestine they form oval quadruple cysts (6-10x12-14 microns), surrounded by a thick double-circuit membrane.

Rice. 19.4.Giardia lamblia.Vegetative forms: a - front; b - side; c, d - cysts

Resistance.Giardia cysts are resistant to low temperatures and chlorinated water. They die instantly when boiled. They persist in soil and water for more than 2 months.

Epidemiology.The source of infection with cysts are people, less often dogs, cattle, beavers, muskrats, and deer. The mechanism of infection is fecal-oral: through contaminated water, food, hands and household items. Watery outbreaks of diarrhea are possible.

Pathogenesis and clinical picture. Giardia lives in the duodenum and jejunum. Reproducing 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. The development of gastroenterocolitic, cholecystopancreatic and asthenic syndromes is possible.

Microbiological diagnostics. Cysts are detected in fecal smears (stained with Lugol's solution). With diarrhea and duodenal intubation, vegetative forms (trophozoites) are found in native preparations. Their typical movement is like a falling leaf. Using the serological method, it is possible to determine the increase in antibody titer in ELISA and indirect RIF.

Treatment.Metronidazole, tinidazole, furazolidone are used.

Preventionsimilar to that of amoebiasis. It is important to observe the rules of personal hygiene.

Trichomonas (genus Trichomonas)

Trichomoniasis is an anthroponotic disease caused by genitourinary Trichomonas (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), being a commensal of the mouth.

Characteristics of the pathogen. Trichomonas vaginalisexists only as a trophozoite and reproduces by division. Does not form cysts. 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 - form observed after staining the preparation

cell undulating membrane reaching to the middle of the cell. An axial filament (hyaline axostyle) passes through the cell, emerging from the posterior end of the cell in the form of a spine (Fig. 19.5). The cytostome (cell mouth) looks like a small slit on the front of the body. Reproduces by longitudinal division.

Resistance.It dies quickly in the environment, persists for 10-15 minutes on sponges and washcloths, and in mucus, sperm and urine -

24 hours

Epidemiology.The source of infection is humans. The disease is transmitted sexually, through the birth canal (to the baby), and 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, causing vaginitis, urethritis, prostatitis. The inflammatory process is accompanied by pain, itching, and purulent-serous discharge. The pathogen can phagocytose 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

With these drugs, the mobility of Trichomonas 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 examined microscopically (magnification x400). Trichomonas have characteristic jerky movements of the undulating membrane and flagella. They are smaller in size than epithelial cells, but larger than leukocytes. Large atypical amoeboid forms of Trichomonas may occur. The leading method for diagnosing chronic forms of the disease is the cultivation of trichomonas on nutrient media, for example SKDS (saline solution with hydrolysates of casein, yeast and maltose). The serological method using ELISA or indirect RIF helps in diagnosis. They also do PCR.

Treatment.Ornidazole, nimorazole, metronidazole, tinidazole are used.

Prevention,as with venereal diseases. Prevention in women can be carried out with the Solcotrivak vaccine, which is prepared from Lactobacillus acidophilus.

19.3. Sporozoans

19.3.1. Plasmodium malaria (genus Plasmodium)

Malaria is an anthroponotic disease caused by protozoa of the genus Plasmodium; accompanied by attacks of fever, anemia, enlarged liver and spleen. In humans, malaria is caused by 4 types: Plasmodium vivax, Plasmodium ovale, Plasmodium malariae And Plasmodium falciparum. The first malaria pathogen (P. malariae) was discovered in 1880 by the French doctor A. Laveran.

Characteristics of pathogens. The life cycle of Plasmodium occurs with a change of hosts: in mosquitoes of the genus Anopheles(definitive host) sexual reproduction occurs, or sporogony (formation of elongated cells - sporozoites), and in the human body (intermediate host) asexual reproduction occurs - schizogony, or more precisely merogony, in which small cells called merozoites are formed.

Duration of the development cycle in erythrocytes 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 in shape, except 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 some of the sporozoites (dormant, so-called hypnozoites, or bradyzoites) remain in hepatocytes for weeks or months, which causes the appearance of late, distant relapses of the disease. When a female mosquito bites a patient with malaria, the immature sexual forms of the pathogen enter her stomach along with the blood. Gametogony begins in the mosquito. The gamonts mature and are fertilized, forming a zygote, which turns into an elongated, mobile form - an ookinete. The ookinete penetrates the stomach wall 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. Some sporozoites (2%) then enter the salivary glands of the carrier with the hemolymph flow. Different types of pathogen cause a disease with different clinical pictures and morphological changes in blood smears.

Tropical malaria is the most severe, in which plasmodia P. falciparum multiply in red blood cells (of any age) of small vessels of internal organs, causing intravascular hemolysis, capillary blockage, and hemoglobinuric fever. This process is enhanced as a result of immunopathological hemolysis of uninfected red blood cells. Impaired blood microcirculation and hemolysis lead to brain damage (malarial coma) and the development of acute renal failure. Mortality is about 1%.

Treatment.The main antimalarial drugs include: quinine, mefloquine, chloroquine, quinine, primaquine, bigumal, pyrimethamine, etc. Antimalarial drugs have different effects on the asexual and sexual stages of plasmodia. There are drugs with schizontocidal (histo- and hematoschizontotropic), hamontotropic and sporozoitotropic action.

Toxoplasma (genus Toxoplasma)

Tachyzoites(trophozoites) are formed when sporozoites multiply 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 dies at 55°C and is highly sensitive to 50% alcohol and 5% NH 4 OH solution.

Epidemiology.The disease is widespread, but is more common in warm regions with a humid climate, with a high prevalence of cats. People become infected through the nutritional route through food and water containing oocysts excreted by cats, or by consuming insufficiently heat-treated 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 through airborne dust. In congenital toxoplasmosis, the pathogen enters the fetus through the placenta. Sometimes infection occurs as a result of blood transfusion or organ transplantation.

Pathogenesis and clinical picture. Toxoplasma enters the small intestine, reaches regional lymph nodes with the lymph flow,

Immunityunsterile. During the disease, cellular and humoral immunity develops. Allergy develops (HRT). With congenital toxoplasmosis, a high level of specific antibodies is detected in the blood of the mother and child.

Microbiological diagnostics. Microscopy smears 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 antibodies reaches a maximum at 4-8 weeks of illness. ELISA, RIF, RNGA, RSK, as well as the Seibin-Feldman reaction, or staining test are used (with this method, the pathogen, depending on the properties of the antibodies in the blood serum being studied, is stained differently with methylene blue). They also use an allergological method - intradermal pro-

boo with toxoplasmin, which is positive from 4 weeks of illness and further for many years. The biological method is used less frequently; after parenteral administration of infected material to mice (blood, cerebrospinal fluid, biopsies of organs and tissues), they die within 7-10 days. Toxoplasma can be cultured on cells HeLa or on 7-8 day old chick embryos. PCR can be used.

Treatment.The most effective combination of pyrimethamine with sulfonamides. During pregnancy, it is recommended to use spiramycin instead of pyrimethamine, which does not cross the placenta.

Prevention.To prevent congenital toxoplasmosis, women planning pregnancy should be tested for antibodies. Nonspecific prevention of toxoplasmosis is carried out, including compliance with the rules of personal hygiene, in particular washing hands before eating; Careful heat treatment of meat is necessary. You should avoid contact with felines. It is also important to destroy rodents, flies and cockroaches - potential mechanical carriers of oocysts.

Ciliated

The ciliated ones are represented by balantidia, which affect the human colon (balantidiasis dysentery). They have cilia - organelles of movement covering the cell and cell mouth (cytostome), two nuclei (macro- and micronucleus).

19.4.1. Balantidia (genus Balantidium)

Balantidiasis (ciliate dysentery) is a zoonotic disease caused by Balantidium coli characterized by general intoxication and ulcerative lesions of the colon. The pathogen was discovered in 1856 by the Swedish physician P. Malmsten.

ingest 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 are rarely detected in human stool.

Treatment.Metronidazole, oxytetracycline and other drugs prescribed for amoebiasis are used.

Prevention.Compliance with personal hygiene rules, 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 damage is highly contagious and requires timely treatment. Ringworm can affect any part of the body and is equally common in people of different age groups.

Dermatomycosis of smooth skin is a lesion of the epidermis of the body by a fungal infection. The peculiarity of the disease is its high degree of contagiousness. The pathology is caused by dermatophyte fungi, which enter the skin from the outside, but are not part of the normal microflora.

Dermatomycosis 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 literally a few weeks after the end of the therapeutic course. This is explained by the fact that the fungi remained on clothing and other household items and again entered the skin, causing damage to the epidermis.

Dermatomycoses are classified according to location, pathogen and degree of damage. This disease belongs to superficial mycoses, since dermatophytes feed on keratin. No person is immune from the disease. Various dermatomycosis occurs in both children and adults.

Dermatomycosis is a highly contagious disease

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;
Athlete's foot.

Microsporia is ringworm. It affects the upper layer of the epidermis and hair follicles, causing alopecia in the area of fungal activity. Trichophytosis is also a lichen, manifested by small areas of lesions on the body. Both of these diseases are highly contagious. Athlete's foot 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 dermatomycosis;
onychomycosis;
dermatomycosis of the feet;
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 profuse 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 material for nails. Onychomycosis leads to deformation, delamination and detachment of the nail plates. Due to the peculiarities of localization, this form of the disease is quite difficult to treat, compared to 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 infections, dermatomycosis 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 defense, even if the fungus enters the body, dermatomycosis will not occur, since the immune system will independently defeat the pathogenic microflora.

Factors that increase the risk of developing dermatomycosis:

lack of 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 fungal spores to get on the epidermis for this disease to develop after some time.

Dermatophytes, like other pathogenic fungi, prefer a moist environment with high temperatures. An acidic environment is harmful to them. You can become infected with dermatomycosis by visiting public showers, swimming pools and saunas with average air temperatures.

Children most often suffer from microsporia. Ringworm is the result of excessive contact with stray animals that small children love to pet.

The risk of developing dermatomycosis increases with poor personal hygiene and excessive sweating. At the same time, the local immunity of the skin is reduced and favorable conditions are created for the active proliferation of fungi.

Symptoms of ringworm

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

Any dermatomycosis can be recognized from a photo at first 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, very itchy and flaky. When separating flakes similar to dandruff, no discomfort is felt. In the affected area, all the hair first breaks off and then 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 it will take a long time.

Ringworm in the groin

Fungal infection loves a warm and moist environment, so it often settles in the groin folds

Inguinal dermatomycosis develops due to profuse sweating in this area. In this case, the pathogen can get on the skin in any way, since the fungal spores remain viable in the air for a long time. Symptoms of inguinal dermatomycosis are redness of the inguinal folds, peeling of the skin, severe itching. This form of the disease is dangerous due to the risk of infection. This is due to rubbing of the groin folds by clothing. During the hot season, diaper rash may appear. Since sweat acts as a favorable environment for the proliferation of various bacteria, inguinal dermatomycosis 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 excess body weight, wearing synthetic underwear, poor personal hygiene and excessive sweating. Ringworm in the groin is more common in men.

Damage to smooth skin

The spots are itchy and swollen

Dermatophytosis smooth skin 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.

Ringworm of smooth skin is also called athlete's foot. This fungus affects 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.

Characteristic symptoms:

large areas of redness of the epidermis;
swelling of the skin;
severe itching and peeling;
the appearance of cracks and erosions;
small rash at the border of the affected skin.

When large areas of skin are affected by dermatomycosis, symptoms and treatment become more 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 ability to work suffer, so we can say that dermatomycosis of smooth skin negatively affects the body’s weight.

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

Scalp damage

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

In the second case, red flaky spots are observed on the scalp and at the border of the scalp with the neck or forehead skin. The earlier treatment for athlete's foot is started, which should be treated immediately, the lower the risk of dermatomycosis spreading to the neck and skin on the face.

Onychomycosis and dermatomycosis of the feet

Tinea pedis 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;
formation of cracks;
redness between the toes;
severe itching and peeling;
destruction of the nail plates.

Treatment of dermatomycosis on the legs in humans is complicated by the specifics of this part of the body. The feet are always covered with shoes and sweat a lot, so the disease progresses quickly. Having noticed the first signs and symptoms of dermatomycosis of the feet 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 scrapings of the affected skin. Detection of fungal mycelium is the basis for diagnosis. Additionally, bacterial culture is performed to determine the type of fungus and an analysis of the sensitivity of pathogenic microflora to various antibiotics.

Treatment principle

For dermatomycosis, treatment includes the prescription of agents for external use and systemic antimycotics in tablets.

Terbinafine-based drugs for external use are effective against dermatophytes:

Lamisil;
Lamiderm;
Mycofin;
Terbinox.

The listed drugs are available in the form of cream, ointment, gel or spray. They are suitable for treating skin lesions on the body, groin area and feet. When nails are damaged, the same drugs are used, as well as Exoderil solution.

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

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

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 your doctor for another week after the symptoms disappear.

To prevent the development of dermatomycosis, it is necessary:

observe the rules of personal hygiene;
support immunity;
do not contact 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 faster you can get rid of the fungus.