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Table of contents

1. Structure and function of the skin
2. Parasitic dermatoses (Scabies. Lice)
3. Atopic dermatitis
4. Viral dermatoses (Herpes viral infections. Human papillomavirus infection. Molluscum contagiosum)
5. Pustular skin diseases (Staphylococcal pyoderma. Streptococcal and streptostaphylococcal pyoderma. Atypical chronic pyoderma)
6. Diffuse connective tissue diseases (Lupus erythematosus. Scleroderma. Dermatomyositis)
7. Mycosis (Keratomycosis. Dermatomycosis. Candidiasis. Deep mycoses. Pseudomycosis)
8. Psoriasis
9. Lichen planus
10. Syphilis (Routes of infection. Pathogenesis. Course of syphilis. Clinical manifestations. Latent syphilis. Congenital syphilis. Diagnosis of syphilis. Principles of syphilis therapy)
11. Lupus
12. Leprosy
13. Eczema
14. Skin tumors (Epithelial tumors. Tumors of the skin glands and hair follicle. Neuroectodermal tumors. Tumors of mesenchymal tissue. Tumors of blood and lymphatic vessels)
15. Principles of external therapy (External therapy. Forms of external medications)

LECTURE No. 1. The structure and functions of the skin

Dermatovenereology - a branch of medical science that studies skin diseases, which are a manifestation of the pathology of internal organs and systems, a reflection on the skin of only a part of the lesion of the whole organism.

Leather - this is an element of the body's immune system, a protective cover of a person, which has an impact on the functioning of all internal organs and systems. The skin performs a number of vital functions that ensure the normal functioning of all body systems. The main functions of the skin include: protective function (mechanical protection, UV protection, protection against microorganisms, maintaining water balance), thermoregulatory function, metabolic function, receptor function, participation in water-salt metabolism, excretory function (excretion with sweat and sebum metabolic products, medicinal and toxic substances), resorption function (absorption into the systemic circulation of substances that enter the skin by superficial vascular plexuses), immune function (synthesis of interleukins and other cytokines in the epidermis, capture, processing and transport of antigens).

The skin consists of three main layers tightly attached to each other: epidermis, dermis and subcutaneous fat. There are two main types of skin: thick and thin.

Thick skin (more than 5 mm thick) covers the palms and soles, it is characterized by thicker epidermis and its stratum corneum than in other parts of the body, as well as a relatively thin dermis.

Thin skin (1-2 mm thick) covers all other parts of the body, is characterized by the presence of a thin epidermis, as well as a very pronounced dermis. Hair and sebaceous glands are present only in thin skin.

Epidermis is a stratified squamous keratinized epithelium of the epidermal type. The bulk of the cells of the epidermal layer are keratinocytes (epidermocytes), there are also dendritic cells. The epidermis consists of the following layers: basal, spiny, granular, shiny (only present in the skin of the palms and soles), and horny.

The basal layer is located on the basement membrane. The cells of the basal layer (basal keratinocytes) are arranged in one row and have a cubic or prismatic shape and a large light nucleus. The basal layer is called the cambial layer of the epidermis. In the basal layer, stem cells are located, due to which the layer of the epidermis is constantly replenished as a result of their constant division.

The stratum spinosum is represented by 3-15 rows (thick skin contains a larger number of rows) of polygonal cells, which are firmly connected to each other due to interdigitations and desmosomes. A large number of intercellular contacts such as desmosomes around each cell (up to 2000) resemble spines. The cells of the stratum spinosum contain keratinosomes. These are single specific granules. Spicular keratinocytes retain the ability to divide by mitosis, and therefore the basal and spinous layers of the epidermis are collectively called the “germinal layer.”

The granular layer is represented by 1-3 rows of spindle-shaped cells with a dark nucleus and inclusions in the cytoplasm (keratohyaline granules). These inclusions contain a protein that ensures the process of keratinization of keratinocytes - filaggrin. Filaggrin promotes aggregation, resulting in the transformation of the cell into a postcellular structure - a horny scale (horny plate).

The shiny layer is present only in areas of thick skin. It consists of 1-2 rows of oxyphilic cells with unclear boundaries and poorly defined organelles. When examined under an electron microscope, it is clear that this layer represents the lower rows of the stratum corneum.

The stratum corneum is represented by horny scales - postcellular structures, which are sometimes called cornetites. They do not contain nuclei and organelles, but are rich in keratin and constantly exfoliate. The thickness of the stratum corneum of the epidermis depends on the anatomical localization of the skin area. In the epidermis, a dynamic balance is maintained between the number of desquamated horny scales and the proliferation of basal keratinocytes.

The protective function of the skin consists in the constant renewal of the epidermis: due to the rejection of horny scales from the surface of the skin, it is cleansed of external pollution and microorganisms. The rate of renewal of the epithelial layer depends on the localization, on average it is about 28 days.

In the epidermis, in addition to keratinocytes, there are three types of dendritic cells: melanocytes, Langerhans cells (pigmentless dendrocytes), Merkel cells.

Melanocytes (pigmented dendritic cells, pigmented dendrocytes) are localized in the basal layer of the epidermis in white-skinned individuals. In representatives of the Negroid race, as well as in representatives of the Caucasian race, in places of natural pigmentation, these cells are also found in the spinous layer.

Langerhans cells (non-pigmented dendritic cells, intraepidermal macrophages) are elements of monocytic origin responsible for antigen capture, processing, antigen presentation and interaction with T-lymphocytes of the dermis. These cells participate in immune reactions, produce lysozyme and interferon.

Merkel cells (tactile epitheliocytes) are located in the basal layer of the epidermis and in the epithelium of the hair follicles. These cells are of neuroglial origin and are involved in the formation of tactile sensations on the skin.

Dermis. It consists of two layers that are not clearly demarcated from each other: papillary and reticular. The first is adjacent directly to the epidermis and is represented by loose fibrous connective tissue. The papillary dermis defines the pattern of ridges and grooves on the surface of the skin. The pattern of the skin on the palms and soles is strictly individual. The reticular layer of the dermis is formed by dense, irregular fibrous connective tissue. It contains fibrous structures: collagen, elastic and reticular fibers.

Subcutaneous fat. This is a continuation of the dermis, consisting of white adipose tissue and layers of loose fibrous connective tissue. The thickness of the dermis depends on location, gender and nutrition. The distribution of subcutaneous fat is regulated by sex hormones.

Blood vessels. The blood supply to the skin is carried out by two arterial and venous plexuses - superficial and deep.

Lymphatic system of the skin. It is represented by a superficial network, which begins with the papillary sinuses (in the papillae of the dermis), and a deep network (in the hypodermis), between which the efferent vessels are located.

Nerve fibers. Innervation of the skin is provided by afferent and efferent fibers, forming the subepidermal and dermal plexuses.

Appendages of the skin

Sebaceous glands. They belong to simple alveolar glands, consist of terminal sections and excretory ducts and are characterized by a holocrine type of secretion. The vast majority of sebaceous glands are associated with hair follicles, and their ducts open into the mouths of the hair follicles. In the area of ​​the back of the hands, on the red border of the lips, there are few sebaceous glands, and they are small in size. On the skin of the face (on the eyebrows, forehead, nose, chin), scalp, midline of the chest, back, armpits, perianal and perigenital areas, the number of sebaceous glands is large and reaches 400-900 per 1 cm2, and the glands there are large and multilobular . The sebaceous glands secrete a complex secretion called sebum. The composition of sebum includes free and bound (esterified) fatty acids, small amounts of hydrocarbons, polyhydric alcohols, glycerol, cholesterol and its esters, wax esters, squalene, phospholipids, carotene, as well as metabolites of steroid hormones. A special biological role is played by unsaturated fatty acids, which have fungicidal, bactericidal and virusostatic properties.

Sebum secretion is regulated mainly by hormonal and, to a lesser extent, neurogenic mechanisms. Androgens increase the secretion of sebum.

Sweat glands. They are divided into eccrine (simple tubular) and apocrine (simple tubular-alveolar) glands.

Eccrine sweat glands are located on all parts of the skin. They begin to function from the moment of birth and are involved in thermoregulation. They consist of a terminal secretory section and an excretory duct. The terminal section is located in the subcutaneous adipose tissue, contains myoepithelial and secretory (light and dark) cells, the activity of the latter is regulated by cholinergic nerve fibers. The excretory ducts open freely on the surface of the skin and are formed by a two-layer cuboidal epithelium.

Apocrine sweat glands are located only in some parts of the body: in the skin of the armpits, areolas of the nipples of the mammary glands, perianal, perigenital areas. Sometimes they are found on the skin around the navel, in the sacrum. These glands begin to function during puberty.

Hair. They are keratinized thread-like appendages of the skin. Adults have up to 2 million hairs on the surface of the body, of which there are up to 100 thousand on the head. The structure of hair is genetically determined and largely depends on race.

The hair consists of a shaft protruding above the level of the skin, and a root located in the hair follicle, immersed deep in the dermis and subcutaneous fatty tissue.

LECTURE No. 2. Parasitic dermatoses

Infectious parasitic diseases of the skin include scabies and lice.

1. Scabies

Scabies is a very common and contagious parasitic skin disease caused by an external parasite, the scabies mite.

Etiology and pathogenesis. The causative agent of the disease is the scabies mite or, as it is also called, itching. The tick is an obligate parasite of humans (humans are the only host of the tick in nature). The pathogen has a size of about 100 microns.

After individuals or larvae enter human skin, females burrow through the epidermis for 0,5-1 hour, forming scabies burrows in which they lay eggs. After 3-4 days, larvae emerge from the laid eggs and accumulate in the area of ​​the stratum corneum. After 2-3 days, they have their first molt with the formation of nymphs from the larvae, which emerge to the surface of the skin, then after 3-4 days ticks appear from the nymphs. The walls of scabies ducts are covered with excreta of parasites, which can cause an allergic reaction, causing clinical manifestations of scabies.

In the external environment, the tick is unstable: at negative temperatures, as well as at a temperature of +55 ° C, it dies within 10 minutes, at a temperature of +80 ° C and above, the tick dies instantly.

Transmission routes. The source of infection is a person with scabies. Scabies is transmitted by contact. Infection can occur directly through contact with a sick person, as well as indirectly, i.e. through contact with infected household items (bed linen, used clothing, soft toys, upholstered furniture). An epidemic focus is created due to the fact that a sick person infects people with scabies who are in household, professional or sexual contact with him. Animals cannot be carriers of the scabies mite, since the mite can only parasitize human skin.

Clinic. Immediately after infection, an incubation period for the pathogen begins, the duration of which varies. When females begin to lay eggs, morphological changes appear on the skin, which are the result of a proliferative inflammatory response. As the number of parasites living in the skin increases, a person begins to feel itching. The average incubation period is from 3 to 14 days.

The main complaint presented by patients with scabies is skin itching, which bothers them mainly in the evening and at night.

The clinical picture of scabies is due to several factors: the vital activity of the mite and the formation of scabies by it, the degree of allergization of the body to the pathogen and the appearance of allergic rashes on the skin. There are several clinical forms of the disease.

Typical form of scabies. The rashes are localized in the most typical places: on the abdomen, especially around the navel, on the anterior inner thigh, on the buttocks, mammary glands, lateral surfaces of the fingers and toes, in men on the skin of the penis and scrotum. Rashes on the face and scalp are very rare; only isolated rashes may appear on the skin of the palms and soles. Scabies burrows look like a slightly raised whitish or grayish straight or curved line, 5-7 mm long.

More often, it is difficult to visually detect the course, and its endings are visible in the form of miliary papules and vesicles, in which a scabies mite can be detected in a laboratory study. These small papulovesicular elements (0,5 - 0,7 mm) are located at one of the ends of the course and are partially covered with dotted bloody crusts due to scratching.

In addition to paired papulovesicles and scabies, pinpoint and linear excoriations (indicating itching) are found on the patient's skin, as well as various pyococcal complications, which often begin in the extensor zone of the elbows. Ardi's symptom - detection of purulent or purulent-bloody crusts on the elbows.

К atypical forms of scabies include: clean scabies, nodular scabies and crusted (Norwegian) scabies. Differences in the clinical picture are due to the patient's altered reactivity (increased or decreased), which leads to a different reaction of the body to tick infestation.

Cleanliness scabies is an erased, abortive form of the disease that develops in people who carefully follow the rules of personal hygiene and have normal immunoreactivity. Clinical manifestations in this case will be minimal and represent separate small follicular papules or vesicles, single small hemorrhagic crusts located mainly on the front surface of the body (around the navel and on the chest). Single rashes are accompanied by severe itching at night.

Nodular scabies (nodular scabious lymphoplasia) occurs as a result of a delayed-type hyperergic reaction that develops on the waste products of the mite. Papules can form with untreated scabies (typical form or erased), mainly in patients who have been ill for a long time or had scabies as a result of misdiagnosis, reinvasion or relapse.

Itchy, lenticular, reddish-brown nodules occur under the burrows and are always located in areas characteristic of typical scabies. Papules are located mainly on closed areas of the skin. The nodules are resistant to a variety of antiscabiosis therapy.

The most rare atypical form of scabies is crusted or Norwegian scabies. This type of scabies occurs in patients who have a sharply weakened immunoreactivity. Crusted scabies is manifested by the formation of crusts on the surface of the skin and is the most contagious form of scabies. Most often, Norwegian scabies develops in patients who suffer from immunodeficiency conditions (AIDS, long-term treatment with cytostatic and glucocorticoid drugs for systemic diseases, alcoholism, exhaustion).

The manifestation can be limited and widespread, up to the development of erythroderma. This form of scabies is characterized by grayish-dirty crusts, which tend to layer on top of each other, having a different area and thickness. The crusts are tightly soldered to the underlying tissues, they are removed with difficulty and painfully. After removing the crusts, yellow erosions are exposed under them.

The extensor surfaces of the limbs (rear of the hands, fingers, elbows, knees), buttocks, scalp, face, ears are affected mainly. When the palms and soles are affected, thick hyperkeratosis develops, which limits movement and simulates flexion contractures. In addition, nail plates can also be affected: they are deformed, thickened, their color changes, they easily crumble and resemble onychomycosis.

Complications. Clinical manifestations of scabies can be masked by its complications, leading to errors in diagnosis. Dermatitis (simple or allergic), pyoderma, less common - microbial eczema and nodular lymphoplasia are more common.

Diagnostics. The diagnosis of scabies can be made taking into account the following criteria:

1) clinical data (evening-night itching, characteristic rashes in typical places, as well as the symptom of Ardi and Gorchakov, the presence of papules on the glans penis, foreskin or skin of the mammary glands);

2) epidemiological information (examination of contact persons and detection of clinical signs of scabies in them, information about the patient's stay in the epidemiological site);

3) laboratory diagnostics (detection of a tick and its eggs in scrapings of rash elements).

Treatment. To treat patients with scabies, it is necessary to use agents that have a detrimental effect on scabies mites and their larvae parasitizing in the stratum corneum. Regardless of the drug chosen and the method of its use, for successful treatment, a patient with scabies must follow the following rules:

1) treat the entire skin with a proto-scab preparation, and not just the areas affected by the scabies mite, the only exception is the scalp;

2) strictly observe the method of treatment recommended by the doctor;

3) wash only immediately before treatment and after its final completion;

4) carry out a change of underwear and bed linen before and after treatment.

In recent years, due to high efficiency and low toxicity, benzyl benzoate (benzyl ester of benzoic acid) has become widespread.

This drug is made in the form of an official emulsion ointment (20% ointment), which is carefully rubbed into the skin. In children, a 10% ointment is used. First, it is necessary to treat the upper limbs (2 minutes each), the trunk (excluding the scalp, face and neck), and then the lower limbs (also 2 minutes each). Particular attention should be paid to the interdigital spaces, free nail edge, large skin folds, perianal and genital areas.

The sequence of protoparasitic treatment of the skin is the same for all methods of treatment. After each treatment of the surface of the body, the patient needs to change underwear and bedding; dirty bed linen and underwear must be subjected to heat treatment after washing. Re-treatment of the skin is carried out on the second (or fourth) day. This method of processing is due to the fact that the larvae of scabies that hatched within 2 days are more accessible to the effects of anti-scabies therapy. 3 days after the end of treatment, the patient should be advised to re-change underwear and bed linen, as well as thorough washing. It is necessary to disinfect outerwear and upholstered furniture.

The use of drugs containing sulfur for scabies is common; sulfur ointment is more often used (20%, for children 6-10%), and the method of M. P. Demyanovich is also used. Sulfur ointment is rubbed daily at night for 5 days onto the entire skin (except for the scalp, face and neck). A day after completion of treatment, the patient washes in the shower with soap and changes his underwear and bed linen, and thermally treats outer clothing (iron).

Modern treatments for scabies such as spregal (aerosol of esdepalletrin in combination with piperonyl butoxide in a balloon, produced in France) and lindane are highly effective and safe. In the evening, without prior washing, the patient sprays the entire skin (except the head and face) with spregal from a distance of 20-30 cm from the surface of the skin, leaving no area of ​​the body untreated. After 12 hours, you need to wash yourself thoroughly with soap; usually, a single use of the drug is sufficient. If the disease lasts for a long time, the skin is treated twice (once a day).

Undesirable effects such as tingling of the skin and irritation of the larynx are rare. Usually one cylinder is enough to treat 2-3 people. Spregal can be used to treat children.

Lindane is an organochlorine insecticide (hexachlorocyclohexane). It is highly effective, colorless and odorless. Rub 1% cream (emulsion) in the evening for 3 days in a row over the entire skin (from the neck to the tips of the toes). Before treatment and every day 12-24 hours after treatment, you should take a warm shower or bath. Lindane treatment is not recommended for pregnant women and children.

Features of the treatment of crusted scabies. After the removal of massive crusts (as a result of the use of keratolytic ointments and general baths), courses of treatment of scabies with conventional anti-scabiosis drugs are carried out until a complete cure. It is important to express the pathogenesis of the immunodeficiency state, i.e., to establish the disease (condition) that led to a sharp weakening of the patient's reactivity, and, if possible, to correct it.

Prevention. For prevention, active early identification of patients with scabies and their timely treatment are important. It is necessary to identify foci of scabies and organize work to eliminate them (examination and treatment of family members, people living in the same room with the patient, members of organized groups). It is very important to carry out simultaneous treatment of all patients identified in one outbreak (to prevent reinvasion).

2. Nice

Lice is a parasitic lesion of the skin by obligate human parasites - lice.

Etiology. Three types of lice can infest human skin: head, body and pubic lice.

head lice - mobile parasites of dark gray color, size from 2-3 mm (male) to 3,5 mm (female). After the female settles on the scalp, she lays whitish eggs (nits) 0,7 - 0,8 mm long, tightly gluing them to the surface of the hair. Nits are most noticeable on dark hair.

body lice - mobile insects of whitish-gray color, ranging in size from 3-4 mm (male) to 3-5 mm (female) - lay eggs (nits) in the folds of the skin, gluing them to the fibers of the fabric.

Pubic lice, or flatheads, - sedentary small (1-2 mm) insects, yellowish-brown in color, reminiscent of a crab in shape. The intensity of the color depends on the content of the host’s blood in the lice’s intestines (after the insect bites, the insect becomes darker). Nits stick to the hair on the pubic area, thighs, and abdomen. In advanced cases, nits can be found on the hair in the armpits, chest, eyebrows, and eyelashes. In persons with pronounced hair growth, insects and nits can be located in any area of ​​hair growth (except for the scalp).

Infection with all types of lice is carried out through direct bodily contact with a sick person (household and sexual contact), as well as through indirect contact (through household items, bedding, underwear, clothes, sports equipment).

Clinic.

Head lice. Head lice settle on the scalp mainly in the occipital and temporal regions. Head lice are blood-sucking insects, so inflammatory spherical papules form at the site of their bites. Bites cause unbearable itching, as a result of which the patient excoriates papules, which are complicated by a pyogenic infection in the form of impetigo vulgaris. Purulent crusts glue the hair into a single continuous glomerate, and cervical and occipital lymph nodes can also increase. Upon careful examination of the patient, whitish nits can be found on the hair, mobile head lice are not always visible. Detection of nits and especially lice confirms the diagnosis.

Clothes lice. By contact with a sick person, body lice get on the clothes and skin of people around them. Body lice settle in the folds of clothing and bite the skin adjacent to them. The reaction of the skin to bites can be in the form of inflammatory spots and edematous serous papules. The localization of the bites coincides with the areas where the clothing is as close as possible to the surface of the skin (these are the lower back, interscapular and axillary zones, the skin of the neck, legs). Bites cause intense itching, which can result in scratching and pyogenic complications in the form of streptostaphylococcal pyodermatitis. With prolonged existence of lice and chronic scratching, the skin becomes pigmented and lichenified. Body lice is a great epidemiological danger, since these insects are carriers of the causative agent of typhus.

Pubic lice. Infection occurs mainly through sexual contact. Pubic lice (ploshchitsy) settle in areas of body hair (mainly in the pubic region and perineum, less often in the armpits, on the chest). In advanced cases, lice are found on the eyebrows and eyelashes, where they stick their nits. Ploshchitsy are inactive, attached to the skin and hair bases; sometimes in these places an inflammatory reaction develops in the form of small (up to 1 cm) cyanotic spots with a hemorrhagic tint (the so-called lousy spots) that do not disappear during diascopy. If the eyelashes are damaged, swelling occurs and the eyelids become inflamed.

Diagnostics. It is the same for all types of lice and is based on the detection of parasites, nits and traces of their bites. However, with the development of extensive purulent complications on the scalp and skin of the body, the clinical picture of lice can be masked. In such cases, you should pay attention to the patient’s complaints (itching of the skin in the appropriate locations), as well as information about itching from family members and other contact persons.

Anti-epidemic measures should include:

1) antiparasitic treatment in a sick person of hair and skin in the affected areas;

2) medical examination and mandatory antiparasitic treatment of contact persons (sexual and household contacts);

3) sanitization of clothes, hats, bedding, upholstery of upholstered furniture, towels, washcloths, soft toys for children (washing at temperatures above 80 ° C, ironing with steam, treatment with chemical acaricidal agents).

Treatment. Therapeutic measures are aimed primarily at the destruction of adult insects and nits (the biological characteristics of their habitat on human skin are taken into account).

Most antiparasitic agents are derivatives of permethrin. Permethrin (nittifor) is available in the form of a 0,5% aqueous-alcoholic solution. When applied externally, nits, larvae and mature individuals of head and pubic lice are destroyed. Para-plus - an aerosol for external use - contains permethrin, malathion, piperonyl butoxide. It is used for the treatment of pubic and head lice, destroys adult insects and nits, the required exposure time is 10 minutes. After 7 days, it is recommended to repeat the antiparasitic treatment in order to destroy the lice larvae that may hatch from the remaining viable nits.

When dealing with body lice, one should take into account the fact that lice parasitize in clothes where nits are also located. Therefore, the main activities should be aimed at thermal processing of clothing, bedding (including boiling, washing in hot water, ironing, autoclaving).

LECTURE No. 3. Atopic dermatitis

Atopic dermatitis (or diffuse neurodermatitis, endogenous eczema, constitutional eczema, diathetic prurigo) is a hereditary chronic disease of the whole body with a predominant skin lesion, which is characterized by polyvalent hypersensitivity and eosinophilia in the peripheral blood.

Etiology and pathogenesis. Atopic dermatitis is a multifactorial disease. The model of multifactorial inheritance in the form of a polygenic system with a threshold defect is currently considered the most accurate. Thus, hereditary predisposition to atopic diseases is realized under the influence of provoking environmental factors.

The inferiority of the immune response contributes to increased susceptibility to various skin infections (viral, bacterial and mycotic). Superantigens of bacterial origin are of great importance.

An important role in the pathogenesis of atopic dermatitis is played by the inferiority of the skin barrier associated with a violation of the synthesis of ceramides: the skin of patients loses water, becoming dry and more permeable to various allergens or irritants that fall on it.

The peculiarities of the psycho-emotional status of patients are of great importance. Characteristic features of introversion, depressiveness, tension and anxiety. Changes in the reactivity of the autonomic nervous system. There is a pronounced change in the reactivity of the vessels and the pilomotor apparatus, which is dynamic in nature in accordance with the severity of the disease.

Children who had manifestations of atopic dermatitis at an early age represent a risk group for the development of atopic bronchial asthma and allergic rhinitis.

Diagnostics. To make the correct diagnosis, basic and additional diagnostic criteria are used. The criteria proposed at the First International Symposium on Atopic Dermatitis are used as a basis.

Main criteria.

1. Itching. The severity and perception of itching can be different. As a rule, itching is more disturbing in the evening and at night. This is due to the natural biological rhythm.

2. Typical morphology and localization of lesions:

1) in childhood: damage to the face, extensor surface of the limbs, torso;

2) in adults: rough skin with an accentuated pattern (lichenification) on the flexion surfaces of the limbs.

3. Family or individual history of atopy: bronchial asthma, allergic rhinoconjunctivitis, urticaria, atopic dermatitis, eczema, allergic dermatitis.

4. The onset of the disease in childhood. In most cases, the first manifestation of atopic dermatitis occurs in infancy. Often this is due to the introduction of complementary foods, the appointment of antibiotics for some reason, climate change.

5. Chronic relapsing course with exacerbations in the spring and autumn-winter seasons. This characteristic feature of the disease usually appears no earlier than 3-4 years of age. A continuous off-season course of the disease is possible.

Additional criteria.

1. Xeroderma.

2. Ichthyosis.

3. Palmar hyperlinearity.

4. Follicular keratosis.

5. Increased level of immunoglobulin E in blood serum.

6. Tendency to staphyloderma.

7. Tendency to nonspecific dermatitis of the hands and feet.

8. Dermatitis of the breast nipples.

9. Cheilitis.

10. Keratoconus.

11. Anterior subcapsular cataract.

12. Recurrent conjunctivitis.

13. Darkening of the skin of the periorbital region.

14. Denny-Morgan infraorbital fold.

15. Paleness or erythema of the face.

16. White pityriasis.

17. Itching when sweating.

18. Perifollicular seals.

19. Food hypersensitivity.

20. White dermographism.

Clinic. Age periodization. Atopic dermatitis usually manifests itself quite early - in the first year of life, although its later manifestation is possible. The duration of the course and the timing of remissions vary significantly. The disease can continue into old age, but more often its activity subsides significantly with age. There are three types of atopic dermatitis:

1) recovery up to 2 years (most common);

2) pronounced manifestation up to 2 years with subsequent remissions;

3) continuous flow.

Currently, there is an increase in the third type of flow. At an early age, due to the imperfection of various regulatory systems of the child, various age-related dysfunctions, the effect of external provoking factors is much stronger. This may explain the decrease in the number of patients in older age groups.

In a deteriorating environmental situation, the role of external factors is increasingly increasing. These include exposure to atmospheric pollution and professional aggressive factors, increased contact with allergens. Psychological stress is also significant.

Atopic dermatitis proceeds, chronically recurring. Clinical manifestations of the disease change with the age of patients. During the course of the disease, long-term remissions are possible.

The clinical picture of atopic dermatitis in children aged 2 months to 2 years has its own characteristics. Therefore, the infant stage of the disease is distinguished, which is characterized by an acute and subacute inflammatory nature of lesions with a tendency to exudative changes and a certain localization - on the face, and with a widespread lesion - on the extensor surfaces of the extremities, less often on the skin of the body.

In the vast majority of cases, there is a clear connection with alimentary irritants. Initial changes usually appear on the cheeks, less often on the outer surfaces of the legs and other areas. Possible disseminated skin lesions. The lesions are located primarily on the cheeks, in addition to the nasolabial triangle, the unaffected skin of which is sharply demarcated from the lesions on the cheeks. The presence of rashes on the skin of the nasolabial triangle in a patient with atopic dermatitis at this age indicates a very severe course of the disease.

Primary are erythematooedema and erythematosquamous foci. With a more acute course, papulovesicles, cracks, weeping, and crusts develop. Severe pruritus is characteristic (uncontrolled scratching during the day and during sleep, multiple excoriations). An early sign of atopic dermatitis may be milky crusts (the appearance on the skin of the scalp of oily brownish crusts, relatively tightly soldered to the reddened skin underlying them).

By the end of the first - the beginning of the second year of life, exudative phenomena usually decrease. Infiltration and peeling of the foci are intensifying. Lichenoid papules and mild lichenification appear. Perhaps the appearance of follicular or pruriginous papules, rarely - urticaria elements. In the future, complete involution of rashes or a gradual change in morphology and localization with the development of a clinical picture characteristic of the second age period is possible.

The second age period (childhood stage) covers the age from 3 years to puberty. It is characterized by a chronically relapsing course that often depends on the season (exacerbation of the disease in spring and autumn). Periods of severe relapse may be followed by prolonged remissions, during which children feel practically healthy. Exudative phenomena decrease, pruriginous papules, excoriations predominate, and a tendency to lichenification, which increases with age. Eczema-like manifestations tend to be clustered, most often appearing on the forearms and lower legs, resembling plaque eczema or eczematids. Often there are difficult-to-treat erythematosquamous rashes around the eyes and mouth. At this stage, typical lichenified plaques can also be present in the elbows, popliteal fossae, and on the back of the neck. The characteristic manifestations of this period also include dyschromia, which is especially noticeable in the upper back.

With the development of vegetovascular dystonia, a grayish pallor of the skin appears.

By the end of the second period, the formation of changes typical of atopic dermatitis on the face is already possible: pigmentation on the eyelids (especially the lower ones), a deep crease on the lower eyelid (Denny-Morgan symptom, especially characteristic of the exacerbation phase), in some patients thinning of the outer third of the eyebrows. In most cases, atopic cheilitis is formed, which is characterized by damage to the red border of the lips and skin. The process is most intense in the region of the corners of the mouth. Part of the red border adjacent to the oral mucosa remains unaffected. The process never passes to the oral mucosa. Erythema is typical with fairly clear boundaries, slight swelling of the skin and the red border of the lips is possible.

After subsiding of acute inflammatory phenomena, lichenification of the lips is formed. The red border is infiltrated, flaky, on its surface there are multiple thin radial grooves. After the exacerbation of the disease subsides, infiltration and small cracks in the corners of the mouth may persist for a long time.

The third age period (adult stage) is characterized by a lesser tendency to acute inflammatory reactions and a less noticeable reaction to allergic stimuli. Patients mainly complain of pruritus. Clinically, lichenified lesions, excoriations, and lichenoid papules are most characteristic.

Eczema-like reactions are observed mainly during periods of exacerbation of the disease. Severe dryness of the skin, persistent white dermographism, and a sharply enhanced pilomotor reflex are characteristic.

Age periodization of the disease is not observed in all patients. Atopic dermatitis is characterized by a polymorphic clinical picture, including eczematous, lichenoid and pruriginous manifestations. Based on the predominance of certain rashes, a number of such clinical forms of the disease in adults can be distinguished, such as:

1) lichenoid (diffuse) form: dryness and dyschromia of the skin, biopsy pruritus, severe lichenification, a large number of lichenoid papules (hypertrophied triangular and rhombic skin fields);

2) eczema-like (exudative) form: most characteristic of the initial manifestations of the disease, but in adults, the clinical picture of the disease may have a predominance of skin changes such as plaque eczema, eczematis and eczema of the hands;

3) prurigo-like form: characterized by a large number of pruriginous papules, hemorrhagic crusts, excoriations.

Among the dermatological complications of atopic dermatitis, the first place is occupied by the addition of a secondary bacterial infection. In cases where staphylococcal infection predominates, they speak of pustulization. If the complication of the disease is due mainly to streptococci, impetiginization develops. Often develops sensitization to streptococci and eczematization of foci of streptoderma.

With prolonged existence of inflammatory changes in the skin, dermatogenic lymphadenopathy develops. Lymph nodes can be significantly enlarged and of a dense consistency, which leads to diagnostic errors.

Treatment. Therapeutic measures for atopic dermatitis include active treatment in the acute phase, as well as constant strict adherence to the regimen and diet, general and external treatment, and climatic therapy.

Before starting therapy, it is necessary to conduct a clinical and laboratory examination, to identify factors that provoke an exacerbation of the disease.

For the successful treatment of atopic dermatitis, the detection and control of risk factors that cause an exacerbation of the disease (triggers - alimentary, psychogenic, meteorological, infectious and other factors) are very important. The exclusion of such factors greatly facilitates the course of the disease (sometimes to complete remission), prevents the need for hospitalization and reduces the need for drug therapy.

In the infantile phase, nutritional factors usually come to the fore. Identification of such factors is possible with sufficient activity of the child's parents (careful keeping of a food diary). In the future, the role of food allergens is somewhat reduced.

Patients with atopic dermatitis should avoid foods rich in histamine (fermented cheeses, dried sausages, sauerkraut, tomatoes).

Among non-food allergens and irritants, dermatophagoid mites, animal hair, and pollen occupy a significant place.

Colds and respiratory viral infections can exacerbate atopic dermatitis. At the first symptoms of a cold, it is necessary to start taking hyposensitizing drugs.

In young children, such nutritional factors as enzymatic deficiency and functional disorders are of great importance. It is advisable for such patients to prescribe enzymatic preparations, to recommend treatment at gastrointestinal resorts. With dysbacteriosis, intestinal infections, a targeted correction is also carried out.

With mild exacerbations of the disease, you can limit yourself to the appointment of antihistamines. Most often, blockers of the H1-receptors of histamine of the new generation (cetirizine, loratadine) are used, which do not have a sedative side effect. Preparations of this group reduce the body's response to histamine, reducing spasms of smooth muscles caused by histamine, reduce capillary permeability, and prevent the development of tissue edema caused by histamine.

Under the influence of these drugs, the toxicity of histamine decreases. Along with the antihistamine action, the drugs of this group also have other pharmacological properties.

For moderate exacerbations of the disease, in most cases it is advisable to begin therapy with intravenous infusions of solutions of aminophylline (2,4% solution - 10 ml) and magnesium sulfate (25% solution - 10 ml) in 200-400 ml of isotonic sodium chloride solution ( daily, 6-10 infusions per course). In the lichenoid form of the disease, it is advisable to include atarax or antihistamines with a sedative effect in therapy. For an eczema-like form of the disease, atarax or cinnarizine is added to therapy (2 tablets 3 times a day for 7-10 days, then 1 tablet 3 times a day). It is also possible to prescribe antihistamines that have a sedative effect.

External therapy is carried out according to the usual rules - taking into account the severity and characteristics of inflammation in the skin. The most commonly used creams and pastes containing antipruritic and anti-inflammatory substances. Naftalan oil, ASD, wood tar are often used. To enhance the antipruritic action, phenol, trimecaine, diphenhydramine are added.

In the presence of an acute inflammatory reaction of the skin with weeping, lotions and wet-drying dressings with astringent antimicrobial agents are used.

With the complication of the disease by the addition of a secondary infection, stronger antimicrobial agents are added to the external agents.

Externally, for mild to moderate exacerbations of atopic dermatitis, short courses of topical steroids and topical calcineurin inhibitors are used.

External use of drugs containing glucocorticosteroids in atopic dermatitis is based on their anti-inflammatory, epidermostatic, coreostatic, anti-allergic, local anesthetic actions.

In case of severe exacerbation of the process, it is advisable to carry out a short course of treatment with glucocorticosteroid hormones. The drug betamethasone is used. The maximum daily dose of the drug is 3-5 mg with gradual withdrawal after achieving a clinical effect. The maximum duration of therapy is 14 days.

For severe exacerbations of atopic dermatitis, it is also possible to use cyclosporine A (daily dose 3-5 mg per 1 kg of patient body weight).

Most patients in the acute phase require psychotropic medications. A long course of itchy dermatosis often provokes the appearance of significant general neurotic symptoms. The first indication for prescribing drugs that inhibit the function of cortico-subcortical centers is persistent night sleep disorders and general irritability of patients. For persistent sleep disturbances, sleeping pills are prescribed. To relieve excitability and tension, small doses of atarax are recommended (25-75 mg per day in separate dosages during the day and at night), a drug that has a pronounced sedative, as well as antihistamine and antipruritic effect.

The use of physical factors in therapy should be strictly individual. It is necessary to take into account the forms of the disease, the severity of the condition, the phase of the disease, the presence of complications and concomitant diseases. In the phase of stabilization and regression, as well as as a prophylactic, general ultraviolet irradiation is used.

Prevention. Preventive measures should be aimed at preventing relapses and severe complicated course of atopic dermatitis, as well as preventing the occurrence of the disease in risk groups.

LECTURE No. 4. Viral dermatoses

1. Herpes virus infections

Herpes virus infections are epidemically widespread in the human population, with a variety of clinical forms, and a persistent course. These diseases are chronic, recur and are accompanied by depression of the immune system. Severe course and frequent relapses of herpes virus infections may be markers of increasing immunodeficiency.

Typical shapes

Herpes simplex, or herpes simplex. Herpes simplex virus (HSV) is a DNA-containing filterable virus. There are HSV-1, the causative agent of predominantly non-genital forms, and HSV-2, the causative agent of genital forms of the disease. Viruses differ in their set of antigen proteins, some biological properties, as well as in the preferred route of transmission of the virus in natural conditions.

The source of infection is an infected person, both during the period of clinical manifestations and during the latent course of the infection.

The virus can be isolated from various biological secretions (saliva, tears, vesicle contents). HSV-1 infection often occurs in the first 3 years of a child's life, HSV-2 is associated with the onset of sexual activity. However, HSV-1 can cause damage in the anogenital region, and HSV-2 clinically manifests itself in other areas of the skin and mucous membranes.

The routes of transmission of HSV are as follows:

1) direct contact (household, sexual);

2) indirect contact (through household items, dishes, toys, medical instruments);

3) airborne;

4) parenteral (transplantation of organs and tissues, artificial insemination with infected donor sperm);

5) from mother to fetus (transplacental and when passing through the birth canal).

During primary infection, virions are adsorbed on epitheliocytes and attached to cell receptors. After a series of transformations in the nucleus of epithelial cells, immature capsids are formed, which are transported to the cytoplasm and, acquiring a membrane, leave the cell. Inflammatory phenomena are noted on the skin or mucosa in case of damage: chemotaxis of cellular elements, release of biologically active substances into the tissues, reactive changes in blood vessels, degradation of epitheliocytes. Clinically, this is manifested by limited edema, hyperemia, microvesicles, as well as a sensation of itching, burning.

During primary infection, the virus enters the sensory spinal or cerebral ganglia from the entrance gate of infection (spread along the endo- and perineural pathways, intraaxonally or along Schwann cells). In addition, HSV spreads hematogenously. Primary infection is always accompanied by a period of viremia, as a result of which HSV penetrates not only into the sensory ganglia, but also into many cells of the body.

The virus has a tropism for blood cells, immunocytes. Penetrating into the genetic apparatus of the cell, HSV causes cell degradation and death or a significant decrease in functional activity and a state of secondary immunodeficiency, which makes it impossible to completely eliminate HSV.

The presence of HSV in the human body leads to a decrease in the tension of both cellular and humoral immunity. The functional activity of nonspecific protective factors is impaired. The interferonogenic ability of leukocytes, the activity of natural killers, and the antibody-dependent cellular cytotoxicity of peripheral blood leukocytes are reduced. The absolute number and functional activity of T-lymphocytes may decrease.

With a decrease in immunity, secondary relapses of herpes simplex occur, since the virus can spread from the sensory ganglia through the perineural spaces and re-reach the skin or mucous membranes. The weakening of immune control makes it impossible to completely eliminate the virus from the body; in addition, HSV may be involved in the development of neoplastic processes, such as cervical cancer, prostate cancer, and induction of atherosclerosis.

Diseases caused by HSV are divided into primary and secondary or recurrent herpes infection. Allocate the usual course of herpetic infection (localized forms) and forms of severe course against the background of immunodeficiency (common and generalized forms).

Primary infection occurs when a person first comes into contact with HSV (usually in children). With a primary infection, the incubation period lasts 2-14 days and in 80% of cases the infection occurs in a subclinical, latent form. Only in 20% of cases are clinical manifestations observed, either in the form of an acute respiratory viral disease of unspecified origin, or in the form of acute aphthous herpetic stomatitis. It is the most common clinical form of primary infection, but can occur as gingivitis, glossitis, or herpetic sore throat. In some cases, during a primary infection, rashes may appear on the skin in various locations.

The manifest form of primary infection is accompanied by pronounced signs of intoxication. After the end of the incubation period, a rise in temperature to 39-40 ° C, weakness, headache, and loss of appetite are noted. On the oral mucosa (most often on the mucous membrane of the cheeks, gums, tongue, less often on the soft and hard palate, tonsils) foci of pronounced edema and hyperemia appear, against which grouped vesicles appear after a few hours. Then the vesicles are opened, and in their place point erosive or superficial ulcerative defects are formed. Sometimes erosions merge, forming a defect with a polycyclic contour. Damage to the oral mucosa is always accompanied by severe pain, burning, and salivation. The submandibular, lingual, and cervical lymph nodes are moderately enlarged and more painful on the side of the rash. Clinical recovery occurs after 2-3 weeks.

Secondary, or recurrent, herpes simplex occurs when the virus is activated in an infected organism. The number of relapses, the severity of the course, localization, prevalence depend on the type of virus and the immune status of the person. Relapses often occur with a moderate intoxication syndrome or without it.

Both primary infection and relapse are characterized by typical rashes on the skin and mucous membranes. Rashes do not migrate, have a fixed character and a tendency to recur on the same areas of the skin and mucous membranes. Any areas on the skin and mucous membranes can be affected, but most often rashes occur on the face, oral mucosa, conjunctiva, skin and mucous membranes of the anogenital region.

In typical cases, the lesion is represented by an area of ​​limited edema and hyperemia, against which a group of vesicles with clear, serous content appears. After a few hours, the contents of the vesicles become cloudy due to the chemotaxis of cellular elements and the development of inflammation. The vesicles then break open to form small, closely grouped erosions, or they coalesce into a larger defect with a polycyclic outline. Sometimes the exudate of the vesicles shrinks, forming serous crusts. The addition of secondary coccal flora is possible, and then the crusts take on the appearance of honey. Often, simultaneously with the rash, there is a reaction from the regional lymph nodes in the form of enlargement and moderate pain. After 7-10 days, the crusts are removed, the erosions are epithelialized. A stain remains at the site of the former rash. Blistering rashes are preceded by subjective sensations at the site of future rashes, such as pain, itching, burning, the so-called precursor symptoms. Some patients experience prodromal phenomena in the form of low-grade fever, malaise, weakness, and headache. Relapses often occur during the cold season; they can be provoked by foci of chronic infection.

According to the localization of herpetic eruptions, there are:

1) herpetic skin lesions. Typical rashes are most often localized in the region of the red border of the lips, periorally, in the region of the wings of the nose, in other places on the face, as well as on the hands, in the buttocks;

2) herpetic lesions of the mucous membranes. Typical rashes can be localized on any part of the oral mucosa. In place of bubble eruptions, surface erosions with polycyclic edges, aphthae, are formed. The expressed morbidity in the centers of defeat, intensive salivation are typical;

3) herpetic eye lesions (ophthalmoherpes). It is more often observed in children aged 6 months to 5-6 years with a primary infection and in adults 16-25 years old with reduced immune reactivity. A poor prognostic sign is eye damage during a primary infection, as this may be a precursor to the generalization of the process. Ophthalmoherpes is prone to frequent relapses and can manifest itself in the form of vesicular and dendritic keratitis, recurrent corneal erosion, and iridocyclitis. Optic neuritis is rarely observed. The result of ophthalmoherpes may be a decrease in visual acuity;

4) damage to the anogenital area (genital herpes). One of the most common clinical forms of herpes infection. Primary infection occurs with the onset of sexual activity.

The disease is often asymptomatic, but such a person is a source of infection for a sexual partner. In some cases, primary infection can be severe, with pronounced signs of intoxication. The clinical picture develops after an incubation period, which lasts on average 7 days. Typical vesicular rashes occur against a background of significant swelling and hyperemia. Having existed for a short time, the vesicles open and leave behind weeping, painful erosions, which epithelialize after 10-14 days.

In men, the glans penis, the coronal sulcus, the inner leaf of the foreskin, and the body of the penis are affected. In women, rashes are localized on the skin and mucous membranes of the labia majora and labia minora, in the perineum. Localization of rashes is often determined by the nature of sexual contacts. Rashes are accompanied by regional lymphadenitis, severe pain syndrome; pains are sometimes wired, can be shooting, pulling. Patients feel a burning sensation or itching at the site of the rash. In the future, in more than half of the cases, relapses of the disease are noted, clinically proceeding in the same way as the primary infection, but with a less pronounced intoxication syndrome.

Herpes simplex therapy is complex and includes the use of antiviral drugs, immunocorrective agents, and symptomatic treatment. The duration, intensity and volume of the course of therapy is determined by the clinical form of the disease and the severity of its course, the frequency of relapses.

If relapses occur once every 1 months or less, localized damage to the skin or mucous membranes and the absence of general symptoms, the following methods are indicated: local and general therapy using antiherpetic drugs. External etiotropic therapy - acyclovir in the form of 6% cream, tebrofen 5-2% ointment. At the same time, the use of aqueous and alcoholic solutions of aniline dyes is indicated.

In the event of relapses 1 time in 3 months or more, widespread lesions of the skin and mucous membranes, expressed general phenomena, staged therapy is indicated.

Stage I - treatment in the acute period of the disease (relapse). The etiotropic link in therapy is antiherpetic drugs (intravenously, orally, topically). Use acyclovir, famciclovir, alpizarin, flacoside. In persons with immunodeficiencies of various origins, it is necessary to increase the dose of the chemotherapy drug and the duration of administration (the course can be extended for several months, the dose is increased by 2 times). Antiviral chemotherapy drugs can be combined with interferon preparations or its inducers. Immunomodulatory agents, natural antioxidants and herbal adaptogens are recommended. In the case of a pronounced exudative component, prostaglandin inhibitors are prescribed. In case of damage to the oral mucosa, along with external antiviral agents, solutions of aniline dyes and other disinfectants are used.

Stage II - therapy in remission, after the subsidence of the main clinical manifestations. The goal is to consolidate the positive effect of the therapy carried out in the acute stage and prepare the patient for vaccination. It is necessary to continue or repeat the course of etiotropic therapy. Sanitation of foci of chronic infection is carried out.

Stage III - specific prevention of recurrence of herpes infection using herpes vaccines. Live, inactivated or recombinant antiherpetic vaccines are used if stable remission is achieved.

Stage IV - clinical observation. They conduct routine clinical and laboratory examinations of patients (once every 1-3 months), treatment of chronic processes, and correction of immunological disorders.

Herpes zoster, or shingles. Unlike simple herpes, shingles affects middle-aged and older people who have previously had chickenpox.

Caused by the herpes simplex virus type III. In the case of infection with the herpes virus type III, the source of infection is a person with chickenpox or shingles. A person is contagious at the end of the incubation period until the crusts fall off, especially in the first 7 days from the onset of the rash.

The main routes of transmission are airborne, contact and parenteral. Transmission of infection from mother to fetus is possible.

The clinical picture of herpes zoster has a number of features. The disease begins acutely or with a prodromal period. Then intense burning pain occurs along the sensory nerve. The pain intensifies with movement, cooling, touching the skin and is monolateral in nature. They can simulate myocardial infarction, renal and hepatic colic. Soon, typical herpetic eruptions appear on the skin along the nerve: grouped vesicles filled with serous contents. After the skin manifestations resolve (after 1-3 weeks), neuralgic pain may persist for several months.

There are localized, widespread and generalized forms of herpes zoster.

Of the localized forms of herpes zoster, the form that occurs with damage to the intervertebral ganglia of the thoracic and lumbar regions is more common, less often - damage to the ganglion of the trigeminal nerve, the so-called ophthalmic form of herpes zoster, and damage to the geniculate node of the facial nerve. Typical for the ophthalmic form is a monolateral lesion of the skin and mucous membranes. The patient is concerned about photophobia, lacrimation, blepharospasm, severe neuralgic pain, which can spread to the entire face, neck, and scalp. In this case, the danger is vesicular rashes on the cornea, resulting in keratitis, followed by scarring and decreased visual acuity.

Rashes, which are localized not only along the affected nerve, but also in other areas of the skin and mucous membranes, determine the common form that is noted in immunosuppression.

Therapy for herpes zoster depends on the form of the disease and the general condition of the patient. In severe forms of herpetic infection, accompanied by widespread rashes, ulcerative necrotic lesions, generalization of the process, inpatient treatment in the clinic of infectious diseases is necessary.

Etiotropic therapy - general and external treatment with antiviral agents. Use the same drugs as for herpes simplex. General therapy with antiviral drugs is started as early as possible and continued until the rash ceases.

Pathogenetic therapy includes interferon preparations, immunomodulators.

Symptomatic therapy is aimed at eliminating the pain syndrome, secondary purulent complications.

Drug therapy can be combined with novocaine blockade, sessions of diathermy of the perivertebral areas. Apply B vitamins, vitamin C, phytoadaptogens. Outwardly, alcohol and aqueous solutions of aniline dyes are used.

Atypical forms

There are atypical forms of herpes simplex and herpes zoster.

1. Abortive form. It is characterized by slight hyperemia, edema, barely noticeable papular elements, subjective sensations are usually absent, there may be slight itching. Localization - skin areas with a thickened stratum corneum (skin of the palms and soles). The abortive form of herpes zoster proceeds without typical rashes and is characterized by pain syndrome.

2. Edema form. In this case, the rashes are localized in areas of the skin with loose subcutaneous tissue. The leading symptoms are pronounced edema, hyperemia, against which the vesicles remain invisible or absent.

3. Bullous form. In this form, along with typical vesicles, larger cavity formations (confluent vesicles) are noted, which clinically resemble blisters.

4. Hemorrhagic form. It differs in that the contents of the vesicles are hemorrhagic in nature.

5. Ulcerative necrotic form. Occurs with severe immunodeficiency. In place of the opened vesicles, ulcers are formed, which can increase in size, merge into extensive ulcerative surfaces. May be accompanied by severe signs of intoxication.

Generalized forms

Children and adults suffering from atopic dermatitis and eczematous reactions may develop a generalized form of herpes simplex - Kaposi's varicelliform pustulosis. It is characterized by an acute onset, a rise in body temperature. On the first day, sometimes a little later, against the background of a general severe condition, multiple vesicles appear on the skin with a depression in the center. Mucous membranes may also be affected. The secondary bacterial flora quickly joins, an admixture of blood appears in the serous contents of the vesicles. As a result of the evolution of elements on the skin, extensive foci covered with hemorrhagic crusts appear, pustular elements and erosions are noted. Characterized by enlarged lymph nodes.

There are also generalized clinical forms in which the internal organs are affected. Most often the nervous system suffers: serous meningitis, meningoencephalitis, encephalitis develops. Herpetic encephalitis is a serious condition, which is accompanied by pronounced signs of intoxication, proceeds with cerebral and focal symptoms.

For the diagnosis of herpes infection, virological, immunological and serological methods are used (for example, isolation of the virus from the lesion using cell cultures and detection of the viral antigen in biosubstrates using the direct immunofluorescence reaction).

Measures for the prevention of herpetic infection are similar to the control measures used for other infections transmitted by contact (including sexual) and airborne droplets. Prevention of herpes zoster is reduced to the exclusion of factors that provoke a decrease in the tension of antiviral immunity.

2. Papillomavirus infection

Etiology. Papillomaviruses are the cause of various warts. Belongs to the papovavirus family, which includes a group of DNA-containing viruses. The papillomavirus genus is represented by a very large group of human and animal viruses. Several types of human papillomaviruses (HPV) are pathogenic for humans. HPV-1 causes plantar warts, HPV-2 - vulgar warts, HPV-3 - flat warts, HPV-4 - verruciform dysplasia, HPV-5, 6, 11 - genital warts. All papillomaviruses can play the role of oncogenes. Transmission of HPV infection occurs by contact directly from person to person and indirectly through household items, as well as by autoinoculation. The incubation period can range from several months to several years. The activity of the immune system, especially its cellular component, is of great importance in the development of all types of warts.

Clinic. Common warts are localized mainly on the back of the hands, fingers, in the periungual area, and rarely on the face. They are round, dense, non-inflammatory nodules of a grayish-yellow color, rising above the surface of the skin, with an uneven, rough surface.

Warts are flat, or youthful, localized on the face and back of the hands. They have the appearance of flat, small rounded papules, normal skin color or yellowish brown. Slightly rise above the level of the skin, have a smooth surface.

Plantar warts are localized on the plantar surface of the feet. They resemble a dense grayish callus with a central core, which consists of filiform dermal papillae surrounded by a powerful roller of horny layers. Often painful when walking.

Genital warts are localized in the area of ​​the external genital organs, inguinal-femoral, intergluteal fold, perianally, they are small papillary papules on a thin stalk of normal skin color.

Papillomas of the mucous membranes and skin are localized on the mucous membranes of the oral cavity, pharynx, larynx, paranasal sinuses, on the mucous membranes of the urinary tract, on the skin of the neck, in the axillary regions. These are single or multiple papillary growths on a thin stalk, having a soft texture.

On the mucous membranes, the color is pink or whitish. On the skin, the color varies from flesh to red-brown.

Verruciform epidermodysplasia Lewandowski-Lutz is a rare chronic disease that develops in childhood due to a congenital defect of the immune system. The rashes are localized on the skin of the hands, forearms, legs, and less often in other places. They are flat, round papules up to 2 cm in diameter, prone to fusion, without a tendency to regress, covered with grayish-black horny masses soaked in sebum. With this variant of warts, malignant transformation often occurs.

Treatment. General therapy:

1) antiviral or etiological therapy;

2) pathogenetic therapy aimed at increasing the body's immune defenses (immunomodulatory therapy).

Local Therapy:

1) antiviral external therapy;

2) external destructive methods (cryolysis, electrothermocaustics, laser destruction, exposure to acid solutions), curettage;

3) cytotoxic drugs: condilin, podophyllotoxin, phyllotoxin, 5-fluorouracil.

3. Molluscum contagiosum

Molluscum contagiosum is a viral disease characterized by the appearance on the skin of white hemispherical nodules with a central depression, visually resembling a mollusk shell.

Etiology. Molluscum contagiosum virus belongs to the smallpox group of viruses. The disease occurs in people everywhere. The infection is transmitted through direct contact with a sick person, or indirectly through household items.

Children under 1 year of age rarely get sick, possibly due to immunity acquired from the mother and a long incubation period. The disease is most common in underdeveloped countries with a hot climate. Possible sexual transmission. More often, molluscum contagiosum occurs in patients suffering from atopic dermatitis and eczema. This is due to both a decrease in skin reactivity and prolonged use of topical steroids. Unusually widespread rashes have been noted in patients with sarcoidosis, in patients receiving immunosuppressive therapy, and in HIV-infected subjects.

Pathogenesis. The virus invades the keratinocytes of the basal layer of the epidermis and significantly increases the rate of cell division. Then the active accumulation of viral DNA occurs in the spinous layer. As a result, a nodule is formed, in the center of which destruction occurs and the cells of the epidermis are destroyed, while the cells of the basal layer are not affected. The central part of the nodule is represented by detritus containing hyaline bodies with a diameter of 25 microns, which contain viral material.

Inflammatory changes in the dermis are insignificant or absent, however, in the case of long-term elements, they can be represented by a chronic granulomatous infiltrate.

Clinic. The incubation period ranges from 14 days to 6 months. The rashes are represented by shiny pearly white hemispherical papules with an umbilical depression in the center. Slowly increasing in size, the papule can reach a diameter of 5-10 mm in 6-12 weeks. With a single lesion, the diameter of the papule reaches significant sizes. Plaques consisting of multiple fused nodules are rare. After an injury or spontaneously after a few months, papules can fester and ulcerate. Usually, after existing for 6-9 months, the rash resolves spontaneously, but some persist for up to 3-4 years.

Rashes are more often localized on the neck, trunk, especially in the armpits, with the exception of a sexually transmitted infection, when the anogenital region is usually affected.

There are single rashes in the face, especially on the eyelids. Molluscum contagiosum elements can also be localized on any part of the skin, including atypical localization - the skin of the soles and the mucous membrane of the cheeks.

In HIV-infected subjects, rashes are multiple, localized mainly on the face and resistant to conventional therapy.

Diagnostics. Diagnosis is based on the characteristic clinical picture. Microscopic examination of the contents of the nodule clarifies the diagnosis. Electron microscopy and histological examination can be used.

Treatment. Patients should avoid visiting swimming pools, public baths, and carefully observe the rules of personal hygiene.

Treatment consists of cryotherapy every 2-3 weeks until the lesions completely disappear. Diathermocoagulation, squeezing with tweezers, superficial scraping, followed by lubrication of the elements with a solution of silver nitride, phenol or 5-10% iodine solution are used.

LECTURE No. 5. Pustular skin diseases

Pustular skin diseases (pyoderma) are infectious skin lesions that are caused by the introduction of staphylococci or streptococci.

Less commonly, the cause of pyoderma can be other pathogens - Pseudomonas aeruginosa, Proteus vulgaris, Escherichia coli, pneumococci. Pyodermas are very common diseases.

Etiology. The causative agents of pyoderma are most often staphylococci and streptococci, which belong to the gram-positive microbial flora. The most pathogenic of all types of staphylococci are species such as Staphylococcus aureus (the most pathogenic), epidermal and saprophytic staphylococcus (residents of the normal skin flora).

Staphylococci are facultative anaerobes and colonize the upper layers of the epidermis, more in the region of the mouths of hair follicles, sebaceous and sweat glands, i.e. most often affect the skin appendages.

Streptococci (saprophytic and epidermal) are present on the surface of smooth human skin without connection with skin appendages, more often on the face and in the area of ​​natural folds.

Under conditions of normal homeostasis of the human body, normal sweating and sebum secretion with a slightly acidic pH of the environment, the resident microflora of the skin surface is a constantly acting "biological brake", which, due to microbial antagonism, prevents the reproduction of pathogenic microflora, displacing it from the microbial population. Systemic immune and endocrine disorders of the macroorganism, changing the chemistry of skin sweat and sebum, can lead to biological changes in the resident flora and the transition of pathogenic strains of staphylococci and streptococci into pathogenic ones, which can also be associated with gram-negative flora.

Pathogenesis. There are exogenous and endogenous factors that contribute to the penetration of pyococci into the skin and the development of pyodermatitis.

Exogenous factors include microtrauma and macrotrauma (scratches, abrasions, cuts, insect bites); maceration of the stratum corneum as a result of excessive sweating, exposure to moisture; skin contamination, both domestic (violation of hygiene standards) and professional (lubricating oils, flammable liquids, coarse dust particles of coal, cement, earth, lime); general and local hypothermia and overheating.

All of these exogenous factors violate the protective barrier function of the skin and contribute to the penetration of microflora.

Endogenous factors include:

1) the presence in the body of foci of chronic infection (ENT pathology, odontogenic, urogenital chronic pathology);

2) endocrine diseases (diabetes mellitus, hypercortisolism, hyperandrogenism);

3) chronic intoxication (alcoholism, drug addiction);

4) malnutrition (hypovitaminosis, protein deficiency);

5) immunodeficiency states (treatment with glucocorticoid drugs, immunosuppressants, HIV infection, radiation therapy).

Both endogenous and exogenous factors ultimately lead to a decrease in humoral and cellular immunity, resulting in a decrease in the protective function of the skin. This leads to a change in the amount and composition of the microbial flora on the surface of the skin towards the predominance of pathogenic species and strains of cocci.

Classification. Pyoderma is classified according to etiological principle. According to this classification, staphylococcal, streptococcal and mixed (streptostaphylococcal) skin lesions are distinguished. Each group includes superficial and deep pyoderma, which can occur acutely or chronically.

Superficial pustular skin lesions include those nosological forms in which the epidermis and the upper layer of the dermis are affected.

With deep pyoderma, the lesion can capture not only the dermis, but also the hypodermis.

Staphylococcal pyoderma

Staphylococcal pyoderma, occurring acutely:

1) superficial (ostiofolliculitis, superficial folliculitis, staphylococcal bullous impetigo (in children), staphylococcal pemphigoid of newborns);

2) deep (deep folliculitis, furuncle, acute furunculosis, carbuncle, hydradenitis, multiple abscesses of infants).

Staphylococcal pyoderma, occurring chronically:

1) superficial (sycosis vulgaris);

2) deep (chronic furunculosis (localized and general), decalving folliculitis).

Streptococcal pyoderma

Streptococcal pyoderma, occurring acutely:

1) superficial (streptococcal impetigo, diaper rash);

2) deep (streptococcal ecthyma, erysipelas).

Streptococcal pyoderma, occurring chronically - chronic diffuse streptoderma.

Streptostaphylococcal pyoderma

Streptostaphylococcal pyoderma, occurring acutely:

1) superficial (impetigo vulgaris);

2) deep (ecthyma vulgaris).

Streptostaphylococcal pyoderma, occurring chronically (chronic atypical pyoderma):

1) ulcerative chronic pyoderma and its varieties (chancriform pyoderma);

2) ulcerative-vegetative pyoderma;

3) abscessing chronic pyoderma and its varieties (inverse conglobate acne).

Various pyodermas can occur primarily on previously unaltered skin, as well as secondarily against the background of existing skin lesions. Most often, these are itchy dermatoses (scabies, lice, atopic dermatitis, eczema), predisposing to the development of pustular pathology.

Clinic. Skin rashes with pyoderma are polymorphic. The type of primary elements of the rash depends on the type of pathogen and the depth of skin damage.

Staphylococcal skin lesions are usually associated with sebaceous hair follicles and sweat glands (apocrine and eccrine), and the inflammatory reaction they cause is purulent or purulent-necrotic in nature.

Different nosological forms of pustular skin lesions can manifest themselves with the same element of the rash. For example, follicular abscess manifests ostiofolliculitis, superficial folliculitis and vulgar sycosis, and an inflammatory follicular nodule occurs with folliculitis (superficial and deep), folliculitis decalvans, sometimes with a small boil.

The inflammatory node is found at the debut of a furuncle, carbuncle, multiple abscesses of infants (pseudofurunculosis).

Streptococcal skin lesions, unlike staphyloderma, do not affect the sebaceous hair follicle and sweat glands. They are characterized by a predominantly superficial inflammatory lesion of smooth skin with the release of serous exudate.

The main primary eruptive element in superficial streptoderma is the superficial bladder. In those localizations of the skin, where the stratum corneum is relatively thin, the streptococcal bladder looks sluggish, flabby, it is called conflict. In those areas where there is hyperkeratosis (palms, soles, periungual zones), streptococcal blisters may have a tense appearance, a fairly dense cover, serous or cloudy contents.

With deep streptococcal skin lesions, the primary eruptive element may be a deep epidermal pustule with limited necrosis of the underlying dermis (ecthyma) or edematous erythema with clear, rapidly increasing borders (erysipelas).

1. Staphylococcal pyoderma

Ostiofolliculitis

This is an inflammation of the mouth of the hair follicle. It manifests itself as a small (up to 2-3 mm in diameter) cone-shaped or hemispherical abscess containing whitish or yellowish cloudy pus. The pustule is located at the mouth of the hair follicle, permeated with hair in the center and surrounded by a narrow rim of hyperemia. Ostiofolliculitis most often occurs on open areas of the body exposed to friction, shaving, scratching, and exposure to lubricating oils (face, neck, extensor surfaces of the extremities, scalp). The process is superficial, resolution is observed after 2-3 days. The pustule dries to a yellowish-brownish crust, the halo of hyperemia disappears, and after the crust is rejected, slight hyperpigmentation may remain.

In unfavorable situations (friction, maceration), ostiofolliculitis can deepen (turn into folliculitis and even furuncle), or individual ostiofolliculitis can increase in area and form the so-called staphylococcal impetigo.

Folliculitis

This is a purulent inflammation of the hair follicle with a lesion of its upper part or the entire hair follicle. Depending on the depth of the lesion, there are superficial and deep folliculitis.

In most cases, superficial folliculitis begins, like ostiofolliculitis, with a small pustule at the mouth of the follicle. The process quickly spreads deep into the follicle, which is clinically manifested by an increase in the area of ​​hyperemia, the appearance of a painful dense inflammatory papule at the base of the abscess with a diameter of more than 5-7 mm. In cases where superficial folliculitis develops without previous ostiofolliculitis, a follicularly located inflammatory papule with a diameter of about 5 mm immediately forms. It has a conical or hemispherical shape, permeated with hair in the center. After 2-3 days, a follicular tense pustule forms around the hair. After 4-7 days, the pustule dries to a yellowish crust, after which stagnant hyperemia may remain and pigmentation may persist.

Deep folliculitis is characterized by a total lesion of the entire hair follicle, accompanied by severe pain, hyperemia, swelling, tissue infiltration around the follicle, i.e., an inflammatory node is formed that clinically resembles a boil. It is distinguished from the latter by the absence of a necrotic rod in the center of the infiltrate.

Impetigo staphylococcus

This form of the disease occurs mainly in newborns with their unhygienic content. Pathogenic staphylococci that have penetrated the skin secrete a powerful exotoxin - exfoliatin, which destroys the desmosomes of epidermal cells at the level of the granular layer. This leads to the formation of separate blisters filled with yellow pus. Such a lesion is called epidemic staphylococcal pemphigus of the newborn, or staphylococcal pemphigoid. The disease proceeds severely with an increase in body temperature, the development of intoxication syndrome up to septicemia. Babies suck badly at the breast, lose weight, and septic complications are possible.

Staphylococcal pemphigoid usually occurs 3-5 days after the baby is born, but it can develop during the first month of life. Superficial flaccid blisters (phlycten) appear, ranging in size from a pea to a hazelnut. Their contents are first serous, then serous-purulent. The blisters are surrounded by a mild inflammatory rim and are located on normal skin.

After the rupture of the bubble, weeping erosion remains, surrounded on the periphery by the remnants of the tire. Unlike ordinary impetigo, a crust does not form. Rashes are most often located on the chest, back, in skin folds. Rashes almost never occur on the skin of the palms and soles.

The malignant course of staphylococcal pemphigoid leads to a universal skin lesion. This condition is called exfoliative dermatitis of Ritter von Rittershain, or staphylococcal "burnt" skin syndrome. The clinical picture of this syndrome is characterized by an acute onset, high body temperature and intoxication, an increase in diffuse skin erythema, first around the navel and mouth, then in the skin folds. There is a superficial detachment of the epidermis at the level of the granular layer, fragments of the stratum corneum hang from the affected skin. The clinical picture may resemble toxic epidermal necrolysis (Lyell's syndrome), in which epidermal detachment occurs at the basement membrane level.

Without adequate antibacterial and detoxifying treatment, newborns can die.

Sycosis staphylococcal, or vulgar

This is a chronic superficial skin lesion, manifested by numerous recurrent ostiofolliculitis and superficial folliculitis, followed by infiltration of the surrounding skin.

The disease, as a rule, is observed in adult men and is localized on the face (the area of ​​growth of the mustache and beard), much less often spreads to the pubis, the edges of the eyelids, eyebrows, scalp, axillary zones. In the pathogenesis of vulgar sycosis on the face, chronic foci of infection in the head area and re-traumatization of the skin during wet shaving are important.

The disease begins with small follicular pustules, which repeatedly recur many times in the same place. Gradually, the process expands due to the involvement of more and more new follicles and the formation of new follicular pustules along the periphery of the focus. The skin in the affected area becomes cyanotic and diffusely infiltrated. After the opening of the pustules, accumulations of purulent crusts of different thickness are formed, in the places of their discharge - diffuse weeping. Hair removal in the affected area is painless and easy. In the root zones of epilated hair, a vitreous clutch is clearly visible.

Vulgar sycosis proceeds for a long time, recurring for many years. Subjective sensations are insignificant, patients may feel slight itching, burning, tightening of the skin in the lesion.

In its natural course, the process resolves on its own within 2-3 months, leaving cicatricial baldness in its place.

Folliculitis decalvans, or sycosis lupoid

This is a rare form of staphylococcal lesions of the hair follicle, in which chronic folliculitis without pronounced pustulization and ulceration leads to skin atrophy and persistent baldness. The etiology and pathogenesis are not well understood. The causative agent is Staphylococcus aureus; additional colonization of gram-negative microbial flora in the hair follicles is also possible. This can be caused by altered immunological reactivity of the body against the background of seborrheic status, chronic focal infection, and diabetes mellitus. The microbial factor, apparently, is only one of the pathogenetic links in the development of this disease.

Men of average and advanced age are ill more often. The pathological process can be located in the area of ​​the beard and mustache, in the temporal and parietal areas of the scalp.

The disease is characterized by a chronic course. Against the background of congestive erythema, grouped follicular nodules and pustules appear, as well as follicularly located light yellow crusts and grayish scales, which are easily removed by scraping. These elements merge and form a clearly demarcated round or oval infiltrated plaque with a diameter of 2-3 cm, wine-red in color, with a flat, painless infiltrate at the base. Gradually, in its central part, the skin turns pale, thins, becomes smooth, devoid of hair and slightly sinks - characteristic central atrophy of the skin develops. Within its boundaries, new follicles do not appear and single hairs or tufts of hair may still remain. The peripheral zone of the lesion, about 1 cm wide, is slightly elevated, more hyperemic, and moderately infiltrated. In this zone there are numerous follicular papules with rare pustules in the center. The lesion slowly progressively increases in area due to the appearance of new folliculitis along the periphery. Sometimes the growth of the lesion prevails at one of its poles, which leads to the formation of an irregular, asymmetrical shape of the lesion. During diascopy of the edge of the lesion, the apple jelly symptom is not detected.

The course of the process is chronic, lasting for many months and years with periods of incomplete remission and spontaneous exacerbations. The general condition of patients is not disturbed, subjective sensations are usually absent. When the lesions are located on the scalp, patients may experience pain, which, apparently, is due to the anatomical features of the skin in this area (the proximity of the aponeurosis).

Furuncle

This is an acute purulent-necrotic inflammation of the hair follicle and perifollicular connective tissue. Furuncle refers to the deep form of staphyloderma. The primary eruptive element of the boil is an inflammatory node that forms around the hair follicle infected with staphylococci.

The onset of the disease is associated with the formation of an inflammatory purulent infiltrate around the hair follicle, which in the early stages can be small in size (like folliculitis), however, the process quickly captures the entire depth of the hair follicle, the surrounding connective tissue and the adjacent sebaceous gland and is an inflammatory stagnant-hyperemic node , conically rising above the surface of the skin. Soreness increases, jerking, throbbing pains are possible.

When the boil is localized in the face area, especially on the upper lip, there is extensive swelling around the infiltrate. After 3-4 days, a fluctuation begins to be detected in the center of the infiltrate; a purulent fistula is formed around the hair; when opened, a small amount of thick pus is released and a small ulcer is formed. At the bottom of this ulcer a greenish necrotic core is revealed. After another 2-3 days, the necrotic rod is rejected with a small amount of blood and pus, after which pain and inflammation are significantly reduced. In place of the rejected necrotic core, a deep crater-shaped ulcer is formed, which, after being cleared of pus and remnants of necrotic masses, is filled with granulations, a retracted scar is gradually formed, the size and depth of which depends on the size of the necrosis in the center of the boil.

A furuncle can occur in any part of the skin where there are hair follicles. Single boils are usually localized on the forearms, face, back of the neck, lower back, buttocks, thighs.

Usually, single boils are not accompanied by a violation of general well-being and an increase in body temperature. The exception is the furuncle of the face.

Particular attention should be paid to patients in whom the furuncle is located in the area of ​​the lips, on the nose, in the nasolabial triangle and in the area of ​​the external auditory canal. Mimic movements of the face, traumatization of boils during shaving or an attempt to squeeze them out can lead to serious complications (thrombophlebitis of the veins of the face).

The process is accompanied by the appearance of diffuse hyperemia of facial tissues, their tension and soreness.

Pain and signs of general intoxication increase: body temperature can reach 40 ° C, patients complain of chills, weakness, headache. There may be confusion. The hemogram changes: leukocytosis, accelerated ESR, shift of the leukocyte formula to the left.

The anatomical features of the venous outflow on the face, the presence of anastomoses with the cavernous sinus of the brain can lead to more severe complications - the spread of staphylococcal infection and the development of meningitis, meningoencephalitis, septicopyemia and sepsis with the formation of multiple abscesses in various organs and tissues. Thus, with untimely and irrational treatment of a facial boil, the process can proceed malignantly and lead to death.

Furuncles of the extremities, especially those located near the joints and easily injured, can be complicated by regional lymphadenitis and lymphangitis. Sometimes acute glomerulonephritis develops.

Furunculosis

This is the presence of multiple boils on the skin or sequential recurrence of boils. There are acute furunculosis, in which many boils are present on the skin at the same time, and chronic furunculosis, when boils (single or multiple) recur sequentially at short intervals for months and even years. According to the prevalence, localized (limited) furunculosis and widespread (disseminated) are distinguished.

Acute furunculosis develops, as a rule, with short-term exposure to exogenous and less often endogenous predisposing factors, while chronic furunculosis develops with the long-term presence of endogenous predisposing factors. These include the presence of foci of chronic infection, diabetes mellitus, unbalanced nutrition, hypovitaminosis, chronic intoxication, hypercortisolism, immunodeficiency states.

Localized furunculosis (acute and chronic) develops as a result of the introduction of staphylococci into several adjacent follicles. This is facilitated by a number of factors: pronounced staphylococcus virulence, traumatization, skin contamination with lubricating oils, local hypothermia of the skin.

Carbuncle, or charcoal

This is a very severe and deep form of staphyloderma, which is a purulent-necrotic inflammation of the deep layers of the dermis and hypodermis with the involvement of many hair follicles in the process. It is most often caused by the most pathogenic Staphylococcus aureus. In the pathogenesis of carbuncle development, the weakening of the body's defenses, diabetes mellitus, and immunosuppressive states are of great importance.

More often, the carbuncle is solitary and develops in places that are most susceptible to friction of clothing (this is the back of the neck, lower back, buttocks, upper and lower limbs).

The disease begins with the formation of an extensive inflammatory node in the deep layers of the dermis and hypodermis. A dense painful inflammatory node is not clearly defined, quickly increases in depth and width and can reach a fairly large size. Within a few days, the infiltrate acquires a purple-red color and protrudes significantly above the surface of the skin. Growing perifocal edema and throbbing pain in the node area.

The general condition of the patient is sharply disturbed: high temperature, chills, and headache are noted. After 5-7 days, a fluctuation appears in the center of the infiltrate, indicating purulent melting. The skin in the center of the infiltrate becomes black due to necrosis. The cavity is opened to the surface by multiple fistulous openings, corresponding to the mouths of the hair follicles, from which thick yellow-greenish pus mixed with blood is released. In the resulting holes, deep-lying greenish necrotic masses are visible.

Melting of the edges of individual fistulous passages leads to the formation of a single extensive ulcer with uneven edges and a necrotic bottom.

During the natural course of the process, necrotic masses can persist for a long time, up to 2-3 weeks, gradually being rejected. This is accompanied by a gradual improvement in the patient’s general condition, a decrease in body temperature to normal, and a significant reduction in local swelling and pain. After rejection, a deep, sometimes extensive ulcer with undermined edges forms, sometimes reaching the fascia and muscles, the bottom of which is gradually filled with granulations, and the defect is scarred within 2-3 weeks. A rough, irregularly shaped scar remains.

The most malignant course has an anthrax of the facial zone, since it can be complicated by thrombophlebitis of the facial veins, thrombosis of the sinuses of the brain, embolism, septicemia, and sepsis.

Hydradenite

This is a purulent inflammation of the apocrine sweat glands. The disease is inherent in mature people who have actively functioning apocrine sweat glands. The most common form of localization is hydradenitis in the axillary zone. But hydradenitis can also occur in all anatomical locations where apocrine sweat glands are located: the area around the nipples, perianally, on the skin of the scrotum, labia majora, around the navel.

Factors contributing to the introduction of pathogenic staphylococci into the mouths of the hair follicles and excretory ducts of the glands are skin trauma, the irrational use of antiperspirant deodorants, as well as all pathogenetic factors leading to immunosuppression.

The disease begins with the appearance of a dense node or several nodes in the deep layers of the skin, which are initially determined only by palpation. Gradually, their size increases, the skin over them turns red. As the inflammatory reaction increases, the nodes become soldered to the skin, it acquires a bluish-red color, pain intensifies.

In cases where several nodes are located side by side, a continuous tuberous infiltrate may form, consisting of hemispherical nodes. The process can be two-way. Within a few days, the nodes undergo central softening due to the development of an abscess and gradually open with purulent fistulas with the release of thick yellow-green pus. Gradually, the cavity of abscesses is emptied, the severity of inflammation subsides, and the process of scarring begins. In place of hidradenitis, an inverted scar or scars are formed (depending on the number of fistulous passages).

In the case of timely treatment at the stage of infiltration, the process may not abscess, but gradually dissolve without a trace.

2. Streptococcal and streptostaphylococcal pyoderma

Streptococcal impetigo

This common superficial form of streptoderma predominantly affects children and young women. Skin lesions usually affect open areas: face (around the nose and mouth), parotid areas, extremities.

The disease becomes more frequent in the warm season. In conditions of close bodily contact, streptococcal infection is easily transmitted from a sick person to a healthy one. Epidemic outbreaks are possible in children's groups.

In the occurrence of streptococcal impetigo, micro- and macrotrauma of the skin, maceration are of great importance.

Pathogenic streptococci that secrete proteolytic enzymes, having penetrated into the skin lesions, lyse the intercellular bonds of the surface layers of the epidermis, leading to the formation of a primary eruptive element - conflicts, which dries up with the formation of a grayish-yellowish crust. Around conflicts and crusts, a small corolla of hyperemia is noticeable. Conflicts and crusts rapidly increase in size and may merge. The serous exudate of the revealed conflicts infects the surrounding skin, and the process spreads rapidly.

Under favorable conditions, erosion epithelialize, the crusts fall off, in their place there is a slight hyperemia, then light pigmentation. There are no permanent marks. The average duration of the development of conflicts in the crust and the completion of epithelialization does not exceed a week. However, with constant dissemination and the emergence of new and fresh conflicts, the process can be delayed. With single rashes of a small area, subjective sensations are insignificant (slight itching). With extensive areas of damage, patients may complain of burning, itching.

Complications of streptococcal impetigo can be lymphangitis and regional lymphadenitis, eczematization (especially in people prone to atopy), in children - the development of infectious-toxic glomerulonephritis.

There are several varieties of impetigo: slit-like, annular, vesicular (bullous) and its variety - periungual impetigo.

Infection with streptococcus of the skin of the wings of the nose and under the nose can lead to the development of superficial impetiginous rhinitis, which is manifested by superficial inflammation of the skin of the wings of the nose and the formation of conflicts there, drying out with confluent crusts.

Angular impetigo, or streptococcal zaeda, affects the corners of the mouth on one or both sides. The primary eruptive element is the superficial conflict, which opens very quickly and forms a slit-like erosion surrounded by a narrow corolla of the macerated stratum corneum of the epidermis. Periodically in the morning after sleep, erosion can be covered with a loose yellowish crust, which is quickly rejected, again exposing a weeping slit-like erosion. Palpation of the base of erosion does not reveal a significant infiltrate.

Impetigo vulgaris or contagious

The disease is caused by pathogenic streptococci, which cause the primary eruptive element - subcorneal conflict. However, the staphylococcal flora joins very quickly, leading to pronounced suppuration and the formation of purulent cavity elements that dry out with honey-yellow or greenish crusts.

Like streptococcal, impetigo vulgaris is most common in children in open areas of the body. With close bodily contact, especially in children's groups, mass outbreaks of impetigo vulgaris are possible.

Streptococcal diaper rash

Streptococcal lesion, accompanied by inflammation of the contacting surfaces in the skin folds and characterized by a long course with frequent relapses.

The development of this lesion is initially based on intertriginous dermatitis (diaper rash), which develops as a result of friction of the skin surfaces in the fold, maceration of the stratum corneum due to intense sweating, discharge from natural openings and other causes, in the absence of proper hygienic skin care (fermentation and decomposition occurs sebum and sweat). These factors lead to the development of an inflammatory reaction of the skin folds and the addition of streptococcal flora, often in association with yeast-like fungi.

A number of diseases predispose to the development of diaper rash: obesity, type XNUMX diabetes, gout, severe forms of seborrheic dermatitis, hypercortisolism.

Manifestations of streptococcal diaper rash are quite typical: the contacting skin surfaces in the folds (especially in obese people) are hyperemic, edematous, maceration of the stratum corneum and its erosion are noted. Due to the constant exposure to friction, the resulting streptococcal conflicts instantly open up, leaving behind confluent surface erosions with a border of a macerated stratum corneum exfoliated along the edge. The eroded zones become wet, cracks are determined in the depth of the fold. The edges of the foci are scalloped. Subjectively, patients complain of burning, itching, and if cracks occur, pain. With regression of diaper rash, persistent pigmentation may remain.

Streptoderma diffuse chronic

This is a chronic diffuse inflammation of the skin of the lower extremities as a result of vascular disorders, prolonged repeated hypothermia or skin maceration.

The skin of the legs is usually affected. The first spill element is multiple conflicts, which quickly dry up to crusts, under which surface erosions remain on a stagnant-hyperemic base. The lesion is asymmetric, the contours are clear, the outlines are large-scalloped. The surface of the focus is covered with lamellar and stratified crusts or cortical scales of a yellowish-greenish color, when removed, an erosive surface with serous-purulent exudate is revealed.

Due to the peripheral growth of the foci, their area gradually increases, fresh conflicts can be found along the edges, which merge with the main focus, dry out in crusts and create scalloped contours of the affected area. The process can be complicated by lymphangitis and lymphadenitis, eczematization may develop. Without adequate treatment, this form of pyoderma is chronic and can recur. In some cases, chronic diffuse streptoderma develops around infected wounds, purulent fistulas, and trophic ulcers. In such cases, it is commonly called paratraumatic streptoderma.

Ecthyma vulgaris, or streptococcal ulcer

This is a deep form of streptoderma.

In addition to streptococci, staphylococci and gram-negative flora (Proteus vulgaris, Escherichia and Pseudomonas aeruginosa) can participate in the development of ecthyma. The development of the disease is promoted by skin injuries, insufficient skin hygiene, circulatory disorders of the lower extremities, immunodeficiency states, and chronic intoxication.

Ecthyma is most often localized on the skin of the legs, but can occur on the skin of the thighs, buttocks, lower back. The disease begins with the appearance of a large conflict with cloudy (sometimes hemorrhagic) contents or a deep epidermal-dermal pustule. On the periphery of these elements there is a bright hyperemic border. Rapidly developing necrosis leads to the formation of a deep ulcer covered with a brown crust. The elements are large, with a diameter of 2 cm or more. The crust is deeply immersed in the skin tissue, a soft infiltrate gradually forms around.

If the crust is removed, a deep, round ulcer with steep or undermined edges and an uneven necrotic bottom is exposed. Self-regression of ecthyma is slow. Over the course of 2-4 weeks, it gradually scars, leaving behind an atrophic scar with surrounding hyperpigmentation. Ecthymas can be multiple, but are always located separately. If no complications arise, the general health of the patients remains satisfactory.

Ecthyma can be complicated by regional lymphadenitis, lymphangitis, and sometimes phlebitis. Perhaps the development of glomerulonephritis. With prolonged existence of ecthyma on the legs, transformation into chronic ulcerative pyoderma is possible.

Erysipelas

It is an acute deep streptococcal inflammation of the skin, accompanied by fever and intoxication.

The source of infection can be both bacteria carriers and patients with tonsillitis, chronic rhinitis, tonsillitis, streptoderma, i.e. those diseases that are caused by streptococci.

The cause of the disease is group A hemolytic streptococcus, which penetrates through damaged skin and affects the lymphatic vessels of the skin, leading to acute inflammation. Chronic traumatization of the skin, the presence of cracks, scratching can lead to recurrence of erysipelas and persistence of infection in the lymph nodes. Repeated inflammatory processes lead to cicatricial changes in the tissues around the lymphocapillaries, their obliteration and the development of elephantiasis of the limb.

The incubation period of infection ranges from several hours to several days. The disease begins acutely, in some patients prodromal phenomena are observed in the form of malaise, chilling, headache. At the site of penetration of the pathogen into the skin, a red edematous spot appears, which quickly increases in size, acquiring a scalloped character. The boundaries are clear, the skin in the focus is edematous, tense, shiny, hot to the touch.

At the site of the lesion, patients are concerned about pain (especially in the marginal zones of the focus), burning sensations, and fullness. This is accompanied by a sharp rise in temperature and other symptoms of intoxication (chills, headache, severe weakness, in the most severe cases, confusion).

According to the severity of intoxication, mild, moderate and severe forms of erysipelas are distinguished. According to the clinical manifestations in the focus, there are the usual form (erythema and edema), bullous-hemorrhagic (against the background of erythema, blisters with serous-hemorrhagic contents are formed), phlegmonous form (suppuration of subcutaneous fatty tissue) and the most severe - gangrenous form (necrotizing fasciitis), flowing with gangrene of subcutaneous tissue, fascia and underlying muscles.

Erysipelatous inflammation of the face can be complicated by dire consequences up to thrombosis of the sinuses of the brain and the development of sepsis. In all forms of the disease, regional lymph nodes are enlarged and painful.

The main complications of erysipelas include the development of persistent lymphostasis (elephantiasis), the formation of abscesses, phlegmon, phlebitis, gangrene. Sensitization to streptococcal toxins can provoke the formation of glomerulonephritis, myocarditis, rheumatism, dermatomyositis.

Due to the high contagiousness of the disease and the possibility of developing severe complications, patients should be hospitalized in a purulent or infectious department in order to maximize isolation from other patients.

3. Atypical chronic pyoderma

A special group of rare chronic (atypical) pyoderma has been isolated from purulent skin diseases. It included ulcerative atypical pyoderma (chronic pyococcal ulcer) and its variety - chancriform pyoderma; chronic abscessed pyoderma and its variety - inverse acne conglobata.

All these rare nosological forms of atypical pyoderma have different etiology and pathogenesis. Monocultures or associations of microorganisms (staphylococci, streptococci, enterococci, Escherichia coli and Pseudomonas aeruginosa, Proteus vulgaris) can be sown from the lesions.

There is no connection between the type of pathogen and the form of pyoderma. The development of these forms of chronic pyoderma is due not so much to an infectious factor as to an unusual, altered reactivity of the macroorganism, the type and severity of immunodeficiency.

In all patients with chronic atypical pyoderma, a variety of immune disorders are detected, as well as a decrease in nonspecific resistance of the body.

In some cases, patients with chronic atypical pyoderma are diagnosed with ulcerative colitis, Crohn's disease, chronic myeloid leukemia, lymphoma, diabetes mellitus, alcoholism and other severe concomitant diseases leading to immunodeficiency.

All forms of chronic atypical pyoderma have common features:

1) the presence of immunodeficiency;

2) chronic course;

3) granulomatous structure of the infiltrate in the dermis and hypodermis;

4) resistance to treatment with antibacterial drugs while maintaining the sensitivity of the microbial flora isolated from the foci to these antibacterial agents;

5) high sensitivity of the skin to various irritants.

Chronic atypical pyoderma may begin with ordinary pyoderma or with skin injuries secondary to pyococcal infection. Gradually, they turn into an ulcerative and ulcerative-vegetative atypical form of pyoderma, clinically resembling skin tuberculosis or deep mycoses.

Diagnosis is based on the clinical picture and the results of microbiological, histological and immunological studies.

There are no standard schemes that could quickly provide a positive clinical effect. Treatment of patients with chronic atypical pyoderma is a difficult task, which often cannot be solved during the first standard treatment.

If immune disorders are detected, they are corrected, after which it is advisable to carry out a combined antibacterial therapy of the patient, taking into account the sensitivity of the microbial flora.

However, it should be noted that antibiotic therapy alone does not give a significant effect. It should be combined with short courses of glucocorticosteroids, anti-inflammatory drugs, sometimes with cytostatics, immune replacement therapy.

For abscessing acne inversus, in addition to antibiotics, treatment with isotretinoin is prescribed at a dose of 0,5-1 mg per 1 kg of body weight per day for 12-16 weeks. This treatment has a positive effect, as well as in severe forms of acne. Patients suffering from chronic pyoderma need to undergo repeated courses of well-founded, individually selected therapy.

Principles of therapy for pyoderma. In the treatment of pyoderma, it is necessary to follow the main principles.

1. Influence the cause of pyoderma, i.e., carry out etiotropic (antimicrobial) treatment.

2. Eliminate predisposing factors (pathogenetic therapy): carry out correction of carbohydrate metabolism, elimination of vitamin deficiency, sanitation of foci of chronic infection, immunostimulating therapy.

3. Prevent the spread of infection to undamaged areas of the skin (temporary prohibition of washing and visiting pools, prohibition of compresses, skin massage in the pyoderma area, treatment of unaffected skin around pyoderma foci with antiseptics).

Etiotropic therapy of pyoderma is aimed at suppressing the vital activity of the pyococcal flora that caused a purulent disease of the human skin. This therapy can be general (systemic) or external, local (topical).

Indications for general antibiotic therapy:

1) multiple pyoderma, their rapid spread over the skin, lack of effect from external therapy;

2) the appearance of lymphangitis, enlarged and painful lymph nodes;

3) the presence of a general reaction of the body to purulent inflammation: fever, chills, malaise, weakness;

4) deep uncomplicated and especially complicated pyoderma of the face (the threat of lymphogenous and hematogenous dissemination of infection up to thrombosis of the venous sinuses of the brain and the development of purulent meningitis).

A relative indication (the issue is decided in each case based on the totality of clinical data) is the presence of even mild forms of pyoderma in debilitated patients on the background of immunosuppressive, radiation therapy, HIV-infected patients, patients with exocrine or hematological pathology.

Systemic antibiotic therapy can be carried out with antibiotics or sulfonamides. The choice of these agents is desirable to be carried out in accordance with the results of a microbiological study of purulent discharge from the foci of pyoderma (inoculation, isolation of a pure culture of the pathogen and determination of its sensitivity to antibiotics).

Preparations of the penicillin group have the greatest sensitizing activity, more often than other antibiotics cause toxicoderma. It is undesirable to prescribe them to patients with purulent complications of eczematous rashes, suffering from atopy, since penicillins exacerbate the course of the underlying disease (it is better to replace them with macrolides, fluoroquinolones). In patients with psoriasis, penicillin therapy can lead to an exacerbation of the skin process, the development of psoriatic arthritis.

The volume of external therapy for pyoderma is determined by the depth and severity of skin lesions. So, in acute superficial pyoderma, accompanied by the formation of superficial pustules on the skin, they should be opened, followed by immediate treatment with external antiseptics.

With deep pyoderma in the stage of infiltration, a resolving therapy should be prescribed, aimed at increasing hyperemia in the focus and thereby contributing to either the rapid self-resolution of the infiltrate, or rapid abscess formation. For this, ichthyol applications are used on the emerging infiltrate, physiotherapeutic effects: UHF, low-energy laser radiation, dry thermal procedures . Of particular note is the undesirability of compresses, applications of paraffin or ozocerite, since these procedures are accompanied by skin maceration and can cause aggravation of the purulent process.

If there are signs of an abscess of deep pyoderma, they should be surgically opened, followed by drainage of the purulent cavity with the help of turundas moistened with hypertonic sodium chloride solution, antiseptic solutions.

After the appearance of active granulations, it is advisable to apply dressings with ointments containing antiseptics and biostimulants.

When pyoderma occurs subacutely or chronically, the surface of the foci is covered with purulent crusts, they must be removed by softening with antiseptic ointment, followed by mechanical action with swabs moistened with a 3% aqueous solution of hydrogen peroxide. After removal of purulent crusts, the focus is treated with an aqueous or alcoholic solution of an antiseptic.

LECTURE No. 6. Diffuse connective tissue diseases

1. Lupus erythematosus

Lupus erythematosus is a group of connective tissue diseases that have an autoimmune pathogenesis and affect mainly exposed areas of the skin and internal organs.

Etiology and pathogenesis. The leading role in the etiology of lupus erythematosus is hereditary predisposition and, apparently, viral infection, which contribute to the development of autoimmune processes. Patients with lupus have birth defects in complement genes. Decisive factors in pathogenesis are the acceleration of the synthesis of autoantibodies and increased lymphocyte activity. Most manifestations of the disease are associated with the formation of immune complexes. In cutaneous forms of lupus erythematosus, cellular reactions are of fundamental importance. The development of the disease is facilitated by increased estrogen production, ultraviolet radiation, chronic bacterial infection, and the action of certain medications.

Clinic. There are mainly cutaneous and systemic forms of lupus erythematosus. Among the cutaneous forms, discoid, disseminated and deep forms of the disease are distinguished.

Discoid lupus erythematosus affects women 3 times more often than men. The skin of the face is mainly affected: nose, cheeks (especially the zygomatic region), auricles and adjacent skin, forehead, chin, lips (usually lower), scalp. Single well-defined round or oval foci of infiltrated erythema are typical. The center of the focus sinks somewhat and is covered with scales tightly attached to the surface. Removal of scales is difficult due to follicular hyperkeratosis and is accompanied by soreness.

On the reverse side of the scales there are spines. In the peripheral zone of the plaque, telangiectasias and dyschromia can be expressed. Plaques are characterized by pronounced infiltration, peripheral growth and the formation of gross atrophy in the center. After the resolution of the foci on the scalp, foci of cicatricial alopecia remain.

The red border of the lips is often affected: erythematous foci appear with a tendency to erode and atrophy, extending beyond the immediate red border of the lips.

It is characterized by a long relapsing course with exacerbations mainly in spring and summer. Signs of a systemic lesion are extremely rare.

Disseminated lupus erythematosus is characterized by erythema, infiltration, follicular hyperkeratosis, and atrophy. However, with this variant of lupus erythematosus, the severity of these symptoms is much less. For the disseminated form, the defining feature is the formation of small, poorly infiltrated erythematous plaques with a slight tendency to peripheral growth, covered with densely set scales. When scraping, soreness is revealed. There is usually a significant number of lesions. Typical localization is the skin of the face, scalp, auricles, upper chest and back, rear of the hands.

After resolution of the foci, mild atrophy usually remains. With disseminated lupus erythematosus, it is necessary to conduct examinations in dynamics to exclude systemic damage.

In addition to disseminated lupus erythematosus, there is a special form - the so-called subacute cutaneous form of lupus erythematosus. This form is characterized by widespread annular lesions on the skin, which, when merged, form polycyclic scaly patches along the edges on the chest, back, and extremities with hypopigmentation and telangiectasias in the central part. This variant of lupus erythematosus occupies an intermediate place between cutaneous and systemic forms: there are signs of systemic damage, but they are moderately expressed (artalgia, changes in the kidneys, polyserositis, anemia, leukopenia, thrombocytopenia). Immunological changes are characteristic of systemic lupus erythematosus (LE cells, antinuclear factor, antibodies to DNA). However, unlike systemic lupus erythematosus, the prognosis of the disease is relatively favorable.

The deep form of lupus erythematosus (lupus-panniculitis) is manifested by the formation of one or two asymmetrically located subcutaneous nodes. The nodes are dense, mobile, flat, little protrude above the surrounding skin and are better detected by palpation. The face (cheek, chin, forehead) is more often affected, but other localization of the rash is also possible (on the buttocks, thighs). The skin over the knot is smooth, cherry red or normal in color. Often in patients, manifestations of a deep form of lupus erythematosus are combined with skin changes typical of discoid or disseminated forms.

Systemic lupus erythematosus can develop acutely, often without skin manifestations, or subacute and chronically, when there is skin involvement.

In systemic lupus erythematosus, the following manifestations are most common: fever, skin rashes, arthralgia, arthritis, damage to the serous membranes (pleurisy, much less often pericarditis), lymphadenopathy, carditis, Raynaud's syndrome, nephropathy, psychosis, anemia, leukopenia, thrombocytopenia, detection of autoantibodies is characteristic to DNA.

A typical skin lesion is an edematous erythema on the face, resembling a butterfly, gradually spreading to the neck and chest. On the skin of the body and extremities - polymorphic nonspecific rashes (erythematous and hemorrhagic spots, urticarial elements, papules, sometimes vesicles and blisters with hemorrhagic contents). A characteristic manifestation of the disease are capillaritis - bluish spots on the fingertips and paronychia.

The oral mucosa is frequently affected. The most typical sign is whitish grouping papules on a bright erythematous background. Often, in patients with systemic lupus erythematosus, blisters with hemorrhagic contents form on the oral mucosa.

Diagnostics. The basis for diagnosing cutaneous forms of lupus erythematosus is to identify the main clinical symptoms of skin damage: erythema, infiltration, follicular hyperkeratosis and skin atrophy. In difficult cases, histological examination is recommended.

Suspicion of systemic lupus erythematosus arises already in the presence of a characteristic skin lesion, which is observed in 85% of patients. However, skin changes as the first signs of the disease appear in 40% of cases. In addition to the clinical picture, the results of laboratory tests are important for establishing the diagnosis. A significant increase in ESR, hypochromic anemia, leukopenia, thrombocytopenia, dysproteinemia, the presence of LE cells, the detection of antinuclear factor and antinuclear autoantibodies are characteristic.

Treatment. For all forms of lupus erythematosus, protection from insolation and cold should be used. For cutaneous forms of the disease, aminoquinoline drugs (plaquenil, chloroquine diphosphate) are used in 5-10-day cycles with breaks of 3-5 days. The course dose is about 90 tablets. Topical steroids allow you to more quickly achieve a clinical effect and reduce the severity of cicatricial atrophy in the discoid form of lupus erythematosus. At the onset of the disease and to prevent exacerbations in early spring and autumn, courses of aminoquinoline derivatives, calcium supplements and nicotinic acid derivatives are administered. The use of photoprotective products is mandatory. All patients must be registered at the dispensary. For systemic lupus erythematosus, the main therapeutic agent is systemic glucocorticosteroids. Typically, treatment begins with a loading dose of prednisolone with a gradual reduction in the daily dose after achieving a clinical effect to a maintenance dose.

2. Scleroderma

Scleroderma is a polysyndromic disease manifested by progressive sclerosis of the skin, internal organs, and vascular pathology.

Currently, there are limited (skin) and systemic forms of the disease. In the first case, skin sclerosis is the only manifestation of the disease.

Etiology and pathogenesis. Scleroderma is a multifactorial disease, which is based on dysregulation in the synthesis of connective tissue. Hereditary predisposition to the disease is not very clearly identified.

The main pathogenetic link is a violation of the function of fibroblasts, which is genetically predetermined. In this disease, fibroblasts synthesize large amounts of immature collagen. The life span of such collagen is relatively short, but the rate of its synthesis exceeds the rate of decay. The action of cytotoxic factors (exogenous and endogenous) on the endothelium leads to damage to small vessels and impaired permeability, tissue hypoxia, thickening of the vascular wall with an infiltrate consisting mainly of macrophages, and pericapillary fibrosis.

Scleroderma is also characterized by autoimmune pathogenetic factors. Antibodies to various nuclear components are detected - non-histone nuclear proteins associated with chromosomes, centromeres, fibroblasts, collagen.

Factors of various origin act as provoking factors. In patients with scleroderma, the regulatory effect of estradiol on metabolic processes in the connective tissue is reduced. Often scleroderma develops after abortion, pregnancy, in menopause. There is evidence of a violation of the reception to some hormones and a decrease in the regulatory effect on the connective tissue of steroids and catecholamines.

Classification. There are limited (cutaneous) and systemic forms of scleroderma.

Limited scleroderma is subdivided into plaque (morphea), linear and small-focal scleroderma. Systemic scleroderma is divided into acrosclerotic form (Raynaud's phenomenon, calcification, esophageal lesion, sclerodactyly, telangiectasia) and diffuse (progressive systemic sclerosis).

Clinic. Limited scleroderma occurs more often in women aged 40-60 years. Skin rashes can be either single or multiple.

The most common is plaque scleroderma. Scleroderma plaque is formed from a lilac spot. Such a spot, often not noticed by the patient, may exist for several months, but later its central part thickens and becomes ivory. Along the periphery of the focus, a lilac corolla remains, indicating the activity of the skin process. In this state (or slowly increasing in size), the scleroderma plaque can exist for months or even years. In the future, atrophy is formed in this area (the skin becomes dry, smooth, there is no pattern), dyschromia, telangiectasia, and hair loss are possible. In places of resolved scleroderma plaques, especially in the lumbar region, the formation of atrophoderma (areas of skin retraction due to the death of subcutaneous tissue) is possible.

Linear scleroderma is a variant of plaque scleroderma. With this form of the disease, the rashes are located linearly along the length of the limb, usually monolaterally, along the neurovascular bundle or in the form of a scar from a saber strike. This form of scleroderma is characterized by a fairly deep atrophy of the skin and underlying tissues. In this case, there is a violation of microcirculation in the affected limb, which over the years leads to its hypotrophy, stunting. Scleroderma of the "saber strike" type can be combined with facial hemiatrophy.

Small-focal scleroderma is more common in women who are in menopausal and post-menopausal periods, who often have a history of indications of gynecological diseases or operations. In addition to skin lesions, lesions of the vulva and perianal region are often recorded in women.

Men can also develop this clinical form of scleroderma. In this case, localization of rashes on the foreskin and glans penis is typical (may lead to cicatricial phimosis and urethral stricture). The small-focal form of the disease is characterized by the appearance of white or lilac papules, which quickly transform into foci of white skin atrophy. Moderate hyperkeratosis, horny plugs in the mouths of hair follicles are often noted. Sometimes closely spaced foci merge to form shiny dry plaques, on the surface of which manifestations of follicular keratosis are visible. A sharp and shallow disorganization of the connective tissue can lead to disruption of the connection between the epidermis and the dermis, resulting in the appearance of obvious and hidden blisters. Unlike other clinical forms of localized scleroderma, small focal scleroderma is often accompanied by itching or a burning sensation of the skin.

With deep plaque scleroderma, fibrosis develops around the fatty lobules in the subcutaneous adipose tissue. Clinically, this form of the disease is manifested by dense, small-tuberous nodes located deep in the skin. The skin over these nodes is not changed.

In one patient, it is possible to identify a combination of various clinical forms of scleroderma.

Systemic scleroderma affects women about 10 times more often than men. Diffuse scleroderma is characterized by an acute or subacute course of the disease with rapidly progressive damage to internal organs. Skin lesions are diffuse and rapidly progressive. The rapid development of edema of all or almost all of the skin is characteristic. The edema is very dense, the fossa does not form when pressed. The color of the skin is gray, with a bluish tint. Gradually, the skin is soldered to the underlying tissues. Movement becomes difficult, then facial expressions disappear. Atrophy of the subcutaneous tissue and muscles develops. Raynaud's syndrome is often recorded. Internal organs are affected: lungs (pneumofibrosis), gastrointestinal tract (esophagus is first affected), heart, kidneys. In a laboratory study, acute phase indicators (ESR, sialic acids, CRP, fibrinogen) are increased, antinuclear factor and antinuclear antibodies are detected.

The acrosclerotic form of the disease is characterized by a chronic course. The disease usually begins with Raynaud's phenomenon, which for a long time may be its only manifestation. Later, swelling of the hands and feet appears, and then sclerodactyly. At this stage, telangiectasias may appear. Even later, the facial skin is involved in the process: the patient's face becomes amimic, the skin is stretched, gleams, the nose sharpens, the mouth opening narrows, and purse-like folds form around it. Thickening of the tongue and shortening of its frenulum are possible. A large number of telangiectasias on the face is characteristic. Of the internal organs, the esophagus is most affected early. In the early stages of its defeat, a decrease in peristalsis is detected only with fluoroscopy in the supine position or with kymography. Later, patients begin to be disturbed by the difficulty in passing the food bolus through the esophagus, associated with sclerosis of its walls. In second place in terms of frequency of lesions are the lungs. In the early stages, their defeat is detected by fluoroscopy in the form of an increase in the pulmonary pattern. Then pneumofibrosis develops with the corresponding clinical and radiological picture. Laboratory parameters at the onset of the disease in a chronic course change little, characteristic shifts are detected mainly in the later stages of the disease.

Treatment. For limited scleroderma, pathogenetic therapy is used. Typically, such patients do not need external therapy. When the disease occurs and worsens, a course of treatment with benzylpenicillin is used (500 units 000 times a day intramuscularly, 4 million units per course). Small doses of D-penicillamine are effective (28 mg per day, course duration 50-3 months).

With small-focal scleroderma, courses of unithiol are used intramuscularly. Phonophoresis of topical steroids, physiotherapy with currents are also used.

The basic tool in the treatment of acrosclerotic form of systemic scleroderma is D-penicillamine. In complex therapy, drugs that improve blood microcirculation, vitamins, and physiotherapy are used. Course treatment. All patients are subject to dispensary observation.

3. Dermatomyositis

Dermatomyositis (synonyms - Wagner's disease, Wagner-Unferricht-Hepp syndrome) is a multifactorial disease characterized by widespread, predominantly erythematous skin rashes and severe striated muscle involvement. The defeat of the internal organs in dermatomyositis is usually mild.

The disease is characterized by a chronically progressive course, leading to disability due to muscle damage. In cases of disease that occurs without a pronounced skin lesion, the term "polymyositis" is usually used. The onset of the disease is possible at any age.

Etiology and pathogenesis. Hereditary predisposition plays an important role in the development of the disease. Women get sick 3 times more often than men. Provoking factors include insolation, hypothermia, surgery, menopause, pregnancy, childbirth, trauma, and emotional stress. In the development of dermatomyositis, the increased reaction of the sensitized organism to various antigens (tumor, infectious, parasitic, chemical) is of great importance. Unlike other diffuse connective tissue diseases, autoantibodies to muscle proteins and the absence of autoantibodies to DNA are characteristic.

Clinic. Manifestations on the skin of dermatomyositis are highly diverse and have low specificity. The most common is persistent erythema (recurrent, bright red or purplish-purple). Typical localization is the face, upper chest. The development of erythroderma is possible. Subjectively, patients may note soreness of the skin in the area of ​​the rash and slight itching. Periorbital edema accompanied by erythema is typical. Of the skin manifestations, the most specific for dermatomyositis are red-violet papules on the extensor surface of the interphalangeal joints. Violet spots on the back of the hands and on the extensor surface of the elbow and knee joints are also typical. The presence of micronecrosis in the area of ​​the nail fold and the base of the nail is characteristic.

In the area of ​​the legs, there may be an accentuated venous network and a marbled skin pattern. In most cases, there is a pronounced swelling of the skin and subcutaneous fat, which often has a soft, doughy texture. The main places of localization are the face, hands, less often the feet, lower legs, torso. In addition, the skin may have urticarial elements, ecchymosis, roseola, petechiae, vesicles, and inflammatory papules. There may be scleroderma-like lesions. Simultaneously with the skin syndrome, mucous membranes are affected (conjunctivitis, rhinitis, pharyngitis).

Muscle damage usually develops gradually with the involvement of new groups. In the debut of the disease, patients are concerned about increased fatigue, muscle weakness, and myalgia. The muscles of the shoulder girdle are most often affected first: for patients, all actions associated with raising the arms are difficult. Gradually, the muscles become denser, muscle contractures develop. Usually a little later, patients notice difficulty when climbing stairs. Panmyositis gradually develops. Of great importance is the defeat of the muscles of the epiglottis, pharynx, tongue, soft palate, as this leads to dysphagia and dysphonia. Possible damage to the respiratory muscles, eye muscles.

Diagnostics. The following criteria are used to diagnose dermatomyositis:

1) weakness in the proximal muscle groups for at least 1 month;

2) myalgia for at least 1 month in the absence of sensory disturbances;

3) creatinuria more than 200 mg per day;

4) a significant increase in creatine phosphokinase and lactate dehydrogenase;

5) degenerative changes in muscle fibers;

6) characteristic skin changes.

The presence of four or more of these signs indicates a high probability of a diagnosis of dermatomyositis.

If dermatomyositis is suspected, in addition to confirming the diagnosis, it is necessary to exclude the paraneoplastic genesis of the disease.

Treatment. In the treatment of dermatomyositis, glucocorticosteroid hormone preparations are used.

LECTURE No. 7. Mycoses

Mycoses are infectious skin diseases caused by fungi. Mushrooms belong to the lower spore chlorophyll-free organisms of plant origin. Some groups of fungi are pathogenic to humans to varying degrees.

All fungi can be divided into two large groups: obligate pathogenic fungi (about 30 species) and conditionally pathogenic (mold fungi: mucor, aspergillus, penecilli). Particularly pathogenic for humans are obligate pathogenic fungi, which play an important role in the development of mycoses (22 species of trichophytons, 16 species of microsporums and 1 species of epidermophyton).

Classification. The classification of human fungal diseases is based on the depth of the lesion and the pathogen. This classification includes four groups of dermatomycosis.

1. Keratomycosis (pityriasis versicolor).

2. Dermatophytosis (microsporia, superficial trichophytosis, chronic trichophytosis, infiltrative-suppurative trichophytosis, favus, mycosis of the feet, mycosis of smooth skin, mycosis of the inguinal folds, onychomycosis).

3. Candidiasis (candidiasis of the superficial mucous membranes, skin, nail folds and nails, chronic generalized candidiasis (granulomatous), visceral candidiasis).

4. Deep mycoses (coccidiosis, histoplasmosis, blastomycosis, sporotrichosis, chromomycosis, cladosporidosis, penicillosis, aspergillosis).

1. Keratomycosis

Keratomycoses are diseases that affect the superficial sections of the stratum corneum of the epidermis, as well as hair. All keratomycosis are characterized by a chronic course and barely noticeable inflammatory phenomena. The group of keratomycosis includes pityriasis (colorful) lichen and trichosporia nodosum.

Multicolored or pityriasis versicolor is a low-contagious chronic disease of mostly young and middle-aged people, which is characterized by damage to the stratum corneum of the epidermis and a mild inflammatory reaction.

Etiology. The disease is caused by a facultatively pathogenic lipophilic yeast-like fungus. The contagiousness of this disease is very low.

Pathogenesis. The occurrence of the disease is facilitated by increased sweating, seborrhea, as well as some endocrine disorders, such as Itsenko-Cushing syndrome, diabetes mellitus, since these disorders cause changes in the physicochemical properties of the water-lipid mantle of the skin and the keratin of the stratum corneum. The disease occurs in all geographical zones, but more often in regions with hot climates and high humidity.

Clinic. The disease manifests itself as perifollicularly located round spots of different sizes, light brown in color ("café au lait") with clear boundaries. Most often, these spots are localized on the skin of the upper body (on the chest, back, scalp), less often - on the skin of the neck, abdomen and limbs. In some patients, lichen versicolor may appear as depigmented or pale brown spots.

Due to peripheral growth, the spots enlarge and merge, forming large lesions with scalloped edges. With a slight scraping, the surface of the foci begins to peel off, and small scales resemble bran. Subjective sensations are most often absent, but sometimes the patient may experience a slight itch.

The disease is characterized by a chronic course, relapses are also characteristic. In summer, under the influence of sunlight, rashes on smooth skin regress and leave behind distinct foci of depigmentation, the so-called post-parasitic leukoderma. Depigmentation of the skin that has been affected by the pathogen fungus is caused by substances that the fungus secretes, which can inhibit the formation of melanin. In people with immunosuppressive conditions of various origins, the prevalence of the process, a tendency to relapse, as well as the appearance of pityrosporum folliculitis - small follicular papules and pustules against the background of typical manifestations of the disease, are noted.

Diagnostics. The diagnosis is made based on the characteristic clinical picture and laboratory data. The main method for identifying pityriasis versicolor is the Balser test, which is considered positive when the lesions are darker in color after smearing the skin suspicious for the lesion with a 5% iodine solution. In the rays of a fluorescent lamp, the lesions glow golden yellow.

The morphology of the pathogen is very characteristic when microscopically examining scales from lesions (short, wide, curved pseudomycelium and single or clustered large spores).

Treatment and prevention. First of all, it is necessary to stop the effects of factors contributing to the disease (excessive sweating, seborrhea, endocrine disorders). Various external fungicidal preparations are recommended for therapy, sometimes in combination with keratolytic agents. Aerosol compounds (clotrimazole, ketoconazole, climbazole) are used in the form of shampoo, cream or solution. The shampoo form is most preferred. During the treatment process, it should be recommended to treat not only smooth skin with antifungal drugs, but also the scalp as the site of predominant colonization of the pityriasis versicolor pathogen.

You can also use the Demyanovich method (the skin is sequentially lubricated with a 60% solution of sodium thiosulfate and 6% hydrochloric acid), you can also rub in 2-5% sulfur-salicylic ointment, 4% boric acid solution or 10% - solution of sodium hyposulfite. When the process spreads, a tendency to relapse, resistance or intolerance to external therapy, the appearance of pityrosporum folliculitis and in people with immunosuppressive conditions, general therapy using one of the aerosol drugs is recommended: itraconazole (200 mg per day for 7 days), fluconazole (50 mg per day for 2-4 weeks) or ketoconazole (200 mg per day for 10 days).

To prevent pityriasis versicolor, in addition to eliminating the factors contributing to this disease, it is important to avoid close contact with the patient (examination of family members), as well as treating underwear and bed linen (boiling) during treatment. At the stage of convalescence, one of the modern antifungal drugs is prescribed once a month (for example, shampoos with azoles) and it is recommended to use water-alcohol shaken mixtures after washing, which contain boric acid (1-1%), resorcinol (3-1%). -nuyu), sulfur (2-5%), salicylic acid (10-1%), sodium hyposulfite (2%). Products for basic skin care for dermatological patients are also indicated, which help maintain a slightly acidic pH of the skin.

2. Dermatomycosis

Dermatomycosis is a group of fungal diseases caused by dermatophytes that parasitize humans and animals. In humans, dermatophytes affect mainly the epidermis (often the stratum corneum), as well as skin appendages - hair (microsporums and trichophytons) and nails (trichophytons and epidermophytons).

The group of dermatomycosis includes diseases such as microsporia, trichophytosis and favus.

Microsporia

It is a highly contagious disease that affects the skin and hair and is caused by various types of fungi.

The incubation period for microsporia in humans is about 2-4 days. The first sign of damage to the scalp is the appearance of foci of hair thinning. The structure of the hair in the affected areas changes: the hair becomes dull, gray, thickened and breaks off at a height of about 4-6 mm. Over time, the areas of broken hair increase peripherally, giving the hair the appearance of being trimmed.

The root part of the affected hair is surrounded by a gray coating, which consists of fungal spores. When such a hair is removed, it will look like a folded umbrella. The skin within the lesions is covered with small asbestos-like scales, which, when removed, reveal a slight erythema. Microsporia of the scalp, caused by a rusty microsporum, is characterized by a large number of foci and a tendency to merge, as well as the spread of the lesion from the scalp to the smooth skin of the face and neck.

Microsporia of smooth skin is characterized by the appearance of pink spots of round or oval shape with a diameter of about 0,5-3 cm. In the peripheral zone of the spots there are bubbles that quickly dry out to crusts. The central part of the spots is covered with scales. Due to the centrifugal growth of foci, individual elements acquire a ring-shaped shape. Along with old outbreaks, new ones arise. In rare cases, new ones appear inside old ring-shaped lesions (iris shape). Microsporia of smooth skin is clinically indistinguishable from skin lesions with superficial trichophytosis. Nail plates are very rarely affected by microsporia.

The clinical diagnosis of microsporia of the scalp is confirmed by positive results of microscopic examination of the hair, obtaining a culture of the pathogen and a distinct green glow of the affected hair during fluorescent examination. The diagnosis of smooth skin microsporia is confirmed based on the detection of mycelium and spores in skin scales from lesions and culture.

Ringworm

It is a contagious disease of humans and animals, which is caused by various types of fungi and affects the skin, hair and nails.

The causative agents of trichophytosis are divided into groups depending on the type of hair damage. There are two main groups: endotriks (fungi that affect the inner part of the hair) and ectotriks (vegetating mainly in the outer layers of the hair).

All trichophytons from the endotrix group are anthropophiles, transmitted only from person to person. They cause superficial lesions of the skin, scalp, and nails.

Ectotriks are zoophiles that parasitize mainly on animals, but can also infect humans. Compared to fungi of the endotriks group, they cause a more pronounced inflammatory reaction of the skin in humans.

According to clinical manifestations, trichophytosis can be divided into three groups: superficial, chronic and infiltrative-suppurative.

With a superficial form of trichophytosis, the lesion occurs at preschool or school age as a result of direct contact with sick children in children's institutions, as well as in a family from adults suffering from a chronic form of trichophytosis. The transmission of the disease can also be carried out indirectly - through objects and things that have been in contact with the patient. There are superficial trichophytosis of the scalp and smooth skin.

When the scalp is affected, the first noticeable sign to others is the discovery, as with microsporia, of round foci of hair thinning as a result of hair breaking off. But with trichophytosis there are more foci, and they are smaller, while one of them stands out for its size - this is the so-called maternal focus. Within the thinning area, the hair appears patchy. Changed in color, dull, gray, thickened hair with trichophytosis, unlike microsporia, breaks off at different levels and not all. Along with short broken hair (2-3 mm), seemingly unchanged, long hair is found in the lesions.

At the mouths of some hair follicles, dark gray hairs broken off low at the base are visible. More often they are localized in the temporal and occipital regions. The boundaries of the lesions are unclear. The surface of the lesion is slightly hyperemic, covered with loose pityriasis scales. When examining the scraped off scales, they reveal short thickened gray hairs, curved in the shape of commas and question marks, altered hairs that were unable to break through the scales and remained “immured” in them. Subjective sensations are usually absent, or mild itching is observed. Without treatment, the lesions gradually increase in size and can occupy large areas.

With superficial trichophytosis of smooth skin, erythematosquamous spots are found, localized mainly in open areas of the skin. In appearance, they are indistinguishable from lesions on smooth skin with microsporia. Further examination of the patient is necessary to clarify the diagnosis.

Nail plates with superficial trichophytosis are extremely rarely affected.

In some patients, untreated trichophytosis can become chronic. A disturbed autonomic nervous system and endocrinopathies play a significant role in its pathogenesis. When examining patients with chronic trichophytosis, you should pay attention to the condition of the scalp, smooth skin and nails. The most common manifestations of chronic trichophytosis of the scalp are single hair broken off at the mouths of the hair follicles at the very surface of the skin in the form of black dots, often in the occipital and temporal regions, small round atrophic scars with a diameter of 1-2 mm and slight fine-plate peeling.

On smooth skin, lesions are more often found in places most exposed to friction (on the extensor surfaces of the elbow and knee joints, on the buttocks, legs, less often on the trunk), where vaguely demarcated erythematosquamous elements of significant size with mild erythema and finely lamellar peeling of the surface are determined.

The third characteristic sign of trichophytosis is damage to the nail plates of the hands and feet (onychomycosis). Damage to the nail begins either from the free edge or from the side, less often from the base. Yellowish-white areas of various shapes appear in the nail plate, and subungual hyperkeratosis develops. The nail becomes thickened, uneven, dull, and brittle. The edge of the nail plate is jagged, the color is dirty gray, brownish, sometimes black. After the crumbly masses fall out, niches form under the nail. The nail folds are usually not changed, the eponychium is preserved.

The chronic form of trichophytosis often lasts for many years and has poor clinical manifestations. They are difficult to detect, and therefore the disease is not diagnosed for a long time.

With infiltrative-suppurative trichophytosis on the scalp, and in men also in the area of ​​\uXNUMXb\uXNUMXbgrowth of the beard and mustache, one or two sharply limited inflammatory nodes appear that protrude above the surface of the skin and are painful on palpation. At first they have a dense texture, and then soften. Their surface is covered with thick purulent-bloody crusts. The hairs that penetrate the scabs appear unchanged, but are easily pulled out when pulled. In some places, more along the periphery of the foci, follicularly located pustules are visible.

After removing the crusts along with the hair, a hemispherical inflamed surface is exposed with many enlarged mouths of hair follicles, from which a drop of pus is released when the focus is squeezed.

At the height of development, mycosis is accompanied by an increase in regional subcutaneous lymph nodes and a disturbance in the general condition - malaise, increased body temperature. Sometimes there are mykids - secondary allergic nodular and spotty rashes on the trunk and limbs. After 2-3 months without treatment, the mycotic process subsides, the infiltrate resolves, scarring alopecia remains and specific immunity is formed. Similar changes develop when the beard and mustache area is affected. This disease is called parasitic sycosis.

After assessing the clinical manifestations, a standard mycological examination (microscopy and cultural diagnostics) is carried out.

General antifungal therapy for microsporia and trichophytosis is prescribed in cases where:

1) a lesion of the scalp and nail plates was revealed;

2) there are widespread foci on smooth skin (with damage to vellus hair);

3) diagnosed with infiltrative suppurative trichophytosis of the scalp;

4) external therapy turned out to be ineffective;

5) individual intolerance to externally applied fungicides was found.

General antifungal drugs for microsporia and trichophytosis include griseofulvin, terbinafine (lamizil, exifin), itraconazole (orungal), fluconazole (diflucan, mycosyst) and ketoconazole (nizoral).

Griseofulvin is recommended to take 1 tablet (0,125 g) 3-8 times a day with meals, washed down with a small amount of vegetable oil. The dosage and duration of treatment depend on the patient’s body weight and drug tolerance. The total duration of treatment for patients with microsporia is on average 6-8 weeks, and for superficial trichophytosis of the scalp 5-6 weeks.

In chronic trichophytosis, the appointment of individual pathogenetic therapy often plays a decisive role, aimed at eliminating those general disorders against which mycosis developed. In addition to long-term systemic and external therapy, vitamins (especially A, C and E), sometimes immunotherapy, are indicated.

With infiltrative-suppurative trichophytosis with allergic rashes, general antifungal and hyposensitizing therapy is prescribed.

External therapy for microsporia and trichophytosis depends on the location of the lesions (on smooth skin, scalp or nail plates), as well as the severity of the inflammatory reaction. External treatment of mycosis foci reduces the time of general treatment and reduces the possibility of infecting others.

With microsporia, superficial and chronic forms of trichophytosis of the scalp, the following groups of drugs are prescribed externally in the form of a cream, ointment, spray:

1) azoles (clotrimazole, ketoconazole, miconazole, bifonazole, econazole, isoconazole);

2) allylamines (terbinafine-lamizil, naftifine-exoderil);

3) morpholine derivatives (amorolfine (loceryl));

4) hydroxypyridone derivatives (cyclopyroxolamine-batrafen).

The hair in the affected area is shaved or cut every 10-12 days. For infiltrative-suppurative trichophytosis, after mechanical cleaning of the lesions from crusts, pus and epilation of hair on them, lotions with a 0,05% solution of chlorhexidine, a 2-3% solution of boric acid or a 0,01% solution of zinc sulfate are prescribed , 0,04% copper sulfate solution.

With the localization of lesions on smooth skin with microsporia, superficial and chronic forms of trichophytosis, the appointment of antifungal drugs in the form of a cream is indicated.

With an infiltrative-suppurative form of trichophytosis of smooth skin, staged external therapy is indicated. At the first stage, the crusts are removed and the pustules are opened. In the future, wet-drying dressings are prescribed with one of the disinfectant solutions.

As acute inflammation subsides, you can switch to gels, creams, ointments containing tar, sulfur, ichthyol, or creams and ointments with antimycotics.

In case of damage to the nail plates, adequate care is recommended, systematic filing of the affected nails. Outwardly, antifungal agents are prescribed in the form of a varnish, patch, ointment, less often - a solution, a cream. To remove nail plates, especially when prescribing general antifungal drugs with a fungistatic effect, Arabian ointment is used, which consists of potassium iodide and anhydrous lanolin, which has a selective effect on the part of the nail plate affected by the fungus and enhances peroxidation processes in the lesion.

Anti-epidemic measures for microsporia include the fight against stray cats, veterinary supervision of domestic cats and dogs, since most infections come from these animals. Given the possibility of infection of children from each other through direct contact, as well as through objects (hats, combs, towels), schoolchildren should be examined at least 2 times a year.

Preventive measures for trichophytosis include:

1) regular examinations of children in children's institutions and persons who serve these groups;

2) identification of sources of infection;

3) isolation and hospitalization of patients;

4) disinfection of things used by the patient;

5) clinical examination of patients;

6) supervision of hairdressing salons;

7) veterinary supervision of animals;

8) preventive examinations of children entering children's institutions and returning from holidays;

9) sanitary and educational work.

Favus

This is a rare chronic fungal disease of the skin and its appendages caused by an anthropophilic fungus.

In the development of the disease, chronic infections, beriberi, endocrinopathy are important. The disease begins in childhood, but since it does not tend to self-heal, it is also found in adults.

The disease is more often localized on the scalp, nails and smooth skin are less often affected.

The disease is divided into scutular (typical), pityroid and impetiginous forms.

With the scutular form, 2 weeks after infection, an itchy red spot appears around the hair, and then a shield (scutula) is formed - the main clinical sign of the favus. The scutula is a round, dry, bright yellow formation with an depression in the center, shaped like a saucer, pierced in the center with hair, consisting of elements of the fungus and cells of the desquamated stratum corneum, ranging in size from a few millimeters to 1 cm.

The lesion can involve the entire scalp, and the hair loses its shine, becomes dull, becomes twisted, becomes ashen-white, and is easily pulled out, but does not break off. Subsequently, cicatricial atrophy of the skin develops, and a border of hair 1-2 cm wide always remains along the edge of the scalp. To the listed signs should be added a specific “barn” smell coming from the patient’s head.

In the pityroid form of the favus, there are no typical scutulae or they are rudimentary. The clinical picture is dominated by abundant pityriasis peeling that occurs on slightly hyperemic skin.

The more rare impetiginous form is characterized by the presence of massive yellow “layered” crusts on the lesions, resembling impetigo crusts. In these forms, characteristic hair changes and atrophy are also observed.

There are the following clinical forms of smooth skin favus: scutular and squamous. With a rare scutular form, typical scutulae appear, which can reach considerable sizes.

The squamous form is presented in the form of limited erythematosquamous foci, resembling foci of trichophytosis. On smooth skin, favus usually does not leave atrophy.

Nail plates with favus are affected mainly in adults, more often on the hands than on the feet. Initially, a grayish-yellowish spot with a diameter of 2-3 mm appears in the thickness of the nail, which gradually increases and acquires a bright yellow color, characteristic of favous scutulae. Subungual hyperkeratosis subsequently develops, the nail plate loses its shine, becomes dull and brittle.

Untreated favus flows for many years. Damage to the internal organs is observed very rarely, mainly in malnourished and people who suffer from tuberculosis infection. Known lesions of the gastrointestinal tract, lungs, favosous lymphadenitis, favosous meningoencephalitis.

The diagnosis of favus is made on the basis of the characteristic clinical picture, the characteristic glow (dim greenish) of the affected hair when illuminated by a fluorescent lamp with a Wood's filter, as well as microscopic examination of the affected hair and obtaining a culture of the pathogen.

Mycosis stop

Mycosis of the feet is understood as a skin lesion caused by some dermatophyte and yeast fungi, which has a common localization and similar clinical manifestations. Mycosis of the feet is one of the first places among skin diseases.

Infection occurs most often in baths, showers, swimming pools, gyms with insufficient observance of sanitary and hygienic rules for their maintenance, as well as on beaches when the skin of the feet comes into contact with contaminated sand scales.

Wearing impersonal shoes without first disinfecting them and sharing towels can also lead to infection.

Pathogens are extremely stable in the environment: they can grow on wood, shoe insoles, and persist for a long time in socks, stockings, gloves, towels, and bath equipment. Mycosis of the feet usually recurs in spring and autumn and can lead to temporary disability.

Mycosis of the feet develops in the presence of predisposing exogenous and endogenous factors that favor the introduction of the fungus.

Exogenous factors include abrasions, increased sweating of the feet, which is aggravated by wearing socks made of synthetic fibers, tight, unseasonably warm shoes and leads to maceration of the stratum corneum on the feet.

Endogenous causes are associated with impaired microcirculation in the lower extremities (with atherosclerosis, obliterating endoarteritis, varicose veins of the lower extremities, autonomic imbalance, Raynaud's symptom), the state of hypovitaminosis, congenital or acquired immunosuppression (for example, with HIV infection, taking glucocorticosteroids, cytostatic, antibacterial , estrogen-progestin drugs, immunosuppressants).

Depending on the inflammatory response and localization of lesions, five clinical forms of foot mycosis are distinguished: erased, intertriginous, dyshidrotic, acute, squamous-hyperkeratotic. Often in one patient you can find a combination of them.

The erased form is usually manifested by weak peeling in the III-IV interdigital transitional folds of the feet and is accompanied by minor inflammatory phenomena. Sometimes a small superficial crack can be found in the depth of the affected interdigital fold. Slight peeling can also be expressed in the soles and lateral surfaces of the feet.

The intertriginous form resembles diaper rash. In the interdigital transitional folds of the feet, in the places of friction of the contacting surfaces of the fingers, maceration of the stratum corneum occurs, masking the hyperemia of the affected skin. There may also be blistering. This leads to detachment of the epidermis with the formation of erosion and cracks in these areas. A whitish swollen epidermis hangs over the edges of erosions in the form of a collar. The lesion is accompanied by severe itching, sometimes pain. This form of the disease can be complicated by a pyogenic infection: swelling and redness of the fingers and rear of the foot, lymphangitis, and regional adenitis appear. Sometimes this form of mycosis of the feet is complicated by erysipelas and bullous streptoderma.

The dyshidrotic form is manifested by a rash of grouped vesicles on the skin of the arches and the lateral surfaces of the feet. On the arch of the feet, they shine through a thinner stratum corneum, resembling boiled grains of rice in their appearance and size. Bubbles occur more often on unchanged or slightly reddened skin, increase in size, merge, forming larger multi-chamber cavity elements. When a secondary infection is attached, the contents of the blisters become purulent. The rash is accompanied by itching and pain. After opening the blisters, erosions are formed with fragments of epidermal covers along the edges.

The disease may be accompanied by vesicular allergic rashes, mainly on the hands, resembling eczematous manifestations. As the process subsides, the rash of fresh vesicles stops, erosions epithelialize, and slight peeling remains in the lesions.

The acute form of mycosis of the feet was identified by Ya. N. Podvysotskaya. This rare form of mycosis occurs as a result of a sharp exacerbation of dyshidrotic or intertrigenous varieties of the disease. A high degree of skin sensitization to fungal allergens occurs most often with irrational therapy of these forms of mycosis of the feet. Excessive fungicidal therapy causes a sharp increase in inflammatory and exudative changes in the foci of mycosis and beyond. The disease begins acutely, with the formation of a large number of blisters and vesicles on the skin of the feet, and then the legs, against the background of edema and diffuse hyperemia. Soon there are vesicular and bullous elements on the skin of the hands and lower third forearms. These rashes are symmetrical.

Elements of the fungus are not found in them, since they have an infectious-allergic genesis. After the opening of the cavity elements, erosions are formed, surrounded by fragments of the macerated stratum corneum. Erosions merge in places, forming extensive diffusely weeping surfaces, often with purulent discharge. The disease is accompanied by an increase in body temperature, a violation of the general condition of the patient, sharp pains in the affected feet and hands. The inguinal and femoral lymph nodes increase in size and become sharply painful.

Squamous-hyperkeratotic form of mycosis of the feet is characterized by focal or diffuse thickening of the stratum corneum of the lateral and plantar surfaces of the feet. The affected areas of the skin usually have a mild inflammatory color and are covered with small pityriasis or flour-like scales.

Peeling is usually clearly visible in the skin furrows. Some patients complain of itching in the lesions. Cracks cause pain when walking. With this form of mycosis of the feet, which is the most characteristic of the red trichophyton, there are usually no mycids.

Clinical manifestations of mycosis of the feet, caused by interdigital trichophyton, differ little from the clinic of mycosis caused by red trichophyton.

The diagnosis is established on the basis of a characteristic clinical picture and the results of a mycological study (detection of mycelium and obtaining a culture of the fungus).

As a treatment, external therapy with substances with fungicidal activity and a wide spectrum of action, such as azoles, allylamines, derivatives of ciclopirox and amorolfine, is recommended.

Pathogenetic therapy should include vasodilators and other agents that improve microcirculation, physiotherapeutic procedures aimed at improving the blood supply to the lower extremities, as well as correcting the underlying disease, against which foot mycosis developed.

Mycosis of the hands

The most common causative agent of mycosis of the feet is red trichophyton, less often - other other dermatophytes.

An important role in the occurrence of mycosis of the hands is played by injuries and impaired microcirculation in the area of ​​the distal upper extremities (with atherosclerosis, Raynaud's syndrome), as well as endocrine disorders and immunosuppressive conditions.

Clinical manifestations of lesions of the palms are similar to those of the squamous-hyperkeratotic form of mycosis of the feet. The lesion may be asymmetrical. Characterized by dryness of the skin of the palms, thickening of the stratum corneum (keratosis), floury peeling in exaggerated skin furrows, ring-shaped peeling.

Lesions can also be observed on the back of the hands in the form of areas of cyanotic erythema with scalloped or oval outlines. The edges of the foci are intermittent and consist of nodules, vesicles, and crusts. The defeat of the palms can be combined with onychomycosis of the hands.

Diagnosis, treatment and prevention are similar to those for athlete's foot.

Mycosis of smooth skin

Trichophyton red is the most common causative agent of mycosis of smooth skin.

The spread of mycosis caused by red trichophyton over smooth skin usually occurs in ascending order. Its generalization is facilitated by hormonal disorders, acquired immunodeficiency states, as well as horn formation disorders that occur with ichthyosis, keratoderma, and hypovitaminosis A.

There are three main forms of mycosis of smooth skin: erythematous-squamous, follicular-nodular and infiltrative-suppurative.

The erythematosquamous form of mycosis is characterized by the appearance of red scaly round or oval spots that tend to grow peripherally, merge and form foci of polycyclic outlines with an edematous, cherry-red color with an intermittent peripheral roller, consisting of follicular papules and pustules. The skin within the foci is poorly infiltrated, may acquire a brownish tint, covered with small scales. Against this background, grouped or single follicular papular or papulo-pustular elements of stagnant red color are located.

The follicular-nodular form of mycosis is distinguished by grouped pustular and papulo-pustular rashes that do not break off and differ little from healthy ones in appearance.

The infiltrative-suppurative form of mycosis is quite rare. According to clinical manifestations, it resembles infiltrative-suppurative trichophytosis caused by zoophilic trichophytons. At the site of the foci after their resolution, atrophy or individual scars remain.

The main means of treatment are systemic antimycotics in combination with external antifungal therapy.

Onychomycosis

This is a fungal infection of the nail plate. About half of patients with ringworm have onychomycosis.

Isolated infection of the nail plate by fungi is rare.

Usually, nail damage occurs a second time when the fungus spreads from the affected skin with mycosis of the feet, hands, chronic trichophytosis. It is also possible hematogenous drift of the fungus into the growth zone of the nail in case of injury to the nail phalanx, as well as in patients with endocrine diseases and immunodeficiency states.

In the pathogenesis of onychomycosis, circulatory disorders in the extremities play an important role. Functional and organic diseases of the nervous system, leading to disruption of tissue trophism, endocrine diseases, immunodeficiency states, some chronic skin diseases, which are characterized by horn formation disorders and nail plate degeneration, are important. Of the exogenous factors, an important role is played by mechanical and chemical injuries of the nail plates and distal extremities, as well as frostbite and chills.

Clinically, onychomycosis is manifested by a change in color, surface and shape of the nail plates. The nail fold is not affected.

In the hypertrophic form, the nail plate thickens due to subungual hyperkeratosis, acquires a yellowish color, crumbles, and its edges become jagged.

In the normotrophic variant, there are yellowish or white stripes in the thickness of the nail, while the nail plate does not change its shape, subungual hyperkeratosis is not pronounced.

The atrophic form of onychomycosis is characterized by significant thinning, detachment of the nail plate from the nail bed, the formation of voids or its partial destruction.

The diagnosis of onychomycosis is made on the basis of a characteristic clinical picture and laboratory data. The latter are obtained by microscopic examination of the affected nail scales and obtaining a culture of the fungus.

For systemic therapy of onychomycosis, one of the modern antifungal drugs is used: itraconazole (orungal), terbinafine (lamizil, exifin) and fluconazole (diflucan, mycosyst).

3. Candidiasis

Candidiasis is a disease of the skin, nails and mucous membranes, sometimes internal organs, caused by yeast-like fungi.

Infants, very old and very sick people are most susceptible to this disease. Endogenous factors predisposing to this mycosis include endocrine diseases, severe general diseases (lymphoma, leukemia, HIV infection), pathological pregnancy. Currently, the most common cause of candidiasis is the use of antibiotics with a wide spectrum of antibacterial action, glucocorticosteroids, cytostatics, hormonal contraception.

A number of exogenous factors also contribute to the development of candidiasis (high temperature, high humidity, chemicals that cause skin damage, microtrauma). Exposure to several predisposing factors at the same time significantly increases the risk of developing candidiasis.

Infection usually occurs in the birth canal, along with this, the possibility of a transplacental route of infection (congenital candidiasis) has also been proven. The occurrence of candidiasis in adults is most often associated with autogenous superinfection, but exogenous infection of the genital, perigenital areas can also occur. Dysbacteriosis and violation of the protective system of the mucous membrane and skin facilitates the attachment (adhesion) of the fungus to epitheliocytes and its penetration through the epithelial barrier.

Distinguish the following varieties of candidiasis:

1) superficial candidiasis (of the mouth, genitals, skin, nail folds and nails);

2) chronic generalized (granulomatous) candidiasis in children and adolescents;

3) chronic mucocutaneous candidiasis;

4) visceral candidiasis (damage to various internal organs and systems: candidiasis of the pharynx, esophagus and intestines, candidiasis of the bronchi and lungs).

Superficial candidiasis is a type of disease that occurs most often.

According to the localization of the lesion, they distinguish:

1) candidiasis of the mucous membranes and skin (candidiasis stomatitis, candidal glossitis, candidiasis of the corners of the mouth, candidal cheilitis, candidal vulvovaginitis, candidal balanoposthitis);

2) candidiasis of the skin and nails (candidiasis of large folds, candidal paronychia and onychia).

The most common clinical form of acute candidiasis is thrush, or pseudomembranous candidiasis. It often occurs in newborns in the first 2-3 weeks of life and in adults with the predisposing factors listed above.

Lesions are usually located on the mucous membrane of the cheeks, palate, gums. In these areas, whitish-cream crumbly plaques appear. Under them, you can find a hyperemic, less often - eroded surface. With a long-term candidal stomatitis, the plaque acquires a brown or cream color and is more firmly held on the affected mucosa.

Acute atrophic candidiasis of the oral mucosa occurs during broad-spectrum antibiotic therapy. The mucous membrane of the mouth becomes inflamed, then becomes atrophic.

These changes are accompanied by sensations of dryness of the mucosa and burning, sometimes severe pain.

Chronic hyperplastic candidiasis of the oral mucosa occurs with prolonged colonization of yeast-like fungi. On the buccal mucosa along the line of teeth closure, along the midline of the tongue and on the hard palate, rounded, thickened white plaques with an uneven, rough surface are formed, which in some places can merge.

Chronic atrophic candidiasis occurs in persons wearing a removable plastic prosthesis of the upper jaw. The mucous membrane of the prosthetic bed is hyperemic, in its central part a loose whitish-gray plaque accumulates, after the removal of which a hyperemic, sometimes eroded mucosa becomes visible.

In patients with lesions of the oral mucosa, mycosis often spreads to the corners of the mouth - candidiasis of the corners of the mouth develops. Limited erosions appear in the corners of the mouth - cracks on a slightly infiltrated base, surrounded by a fringe of slightly raised, whitened epidermis.

Candidal cheilitis is characterized by moderate swelling and cyanosis of the red border of the lips, thin grayish lamellar scales with raised edges, thinning of the skin of the lips, radial grooves, cracks.

Subjectively concerned about dryness, a slight burning sensation, sometimes pain.

Vulvovaginal candidiasis is characterized by the formation of a whitish coating on the hyperemic mucous membrane of the vulva and vagina.

A characteristic crumbly white discharge appears. Patients are disturbed by excruciating itching and burning.

Candida balanoposthitis often occurs against the background of obesity, decompensation of diabetes mellitus, in men with chronic gonorrheal and non-gonorrheal urethritis and narrow foreskin.

Numerous small pustules appear on the head and inner leaf of the foreskin against the background of hyperemia, transforming into erosions of various sizes with whitish blooms. These manifestations are accompanied by itching and burning. In the absence of adequate therapy, they can lead to inflammatory phimosis, there is a danger of joining candidal urethritis.

Candidiasis of large folds usually develops in obese people, in people with diabetes mellitus and receiving glucocorticosteroid hormones. Candidiasis of small folds, on the hands, occurs as a result of prolonged maceration.

Thin-walled, often merging pustules appear in large and small folds on hyperemic skin. In the future, erosions of a dark cherry color with a shiny surface are formed.

Candidal paronychia and onychia are the most common forms of candidiasis. With candidal onychia, there is an initial lesion of the nail fold - the occurrence of inflammatory candidal paronychia.

Subsequently, the eponychium disappears and the hyperemic nail fold hangs over the nail. When pressing on the edematous nail roller, a purulent discharge may appear from under it. Gradually, the lesion spreads to the nail plate, the change of which always begins in the proximal sections. A deformed nail with a changed color grows from under the back roller. It thickens, becomes dull, dirty-gray in color, transverse grooves appear, sometimes punctate impressions.

The presence of yeast-like fungi in patients in the lesions is determined using microscopic and cultural studies. Microscopy of native or aniline-stained preparations for candidiasis reveals a large number of budding cells, pseudomycelium or true mycelium.

To prescribe rational treatment to a patient, it is necessary to take into account the clinical form of candidiasis, its prevalence and identified predisposing factors.

In case of superficial candidiasis of the oral mucosa, genitals and perigenital area, it is necessary to find out the degree of contamination of the gastrointestinal tract with yeast. With massive colonization of the gastrointestinal tract, it is advisable to prescribe drugs to suppress their growth (natamycin, levorin, nystatin).

With local lesions of the skin and mucous membranes, they are limited to the external use of candidal preparations in rational forms. With candidal stomatitis, it is recommended to lubricate the affected mucosa with a solution of sodium tetraborate (borax) in glycerin or with a solution of an aniline dye, polyene antibiotics (nystatin) and azole derivatives in solution forms.

In acute vulvovaginitis, lotions and douching with a solution of chlorhexidine or miramistin have a quick therapeutic effect.

When skin folds are affected, external therapy is carried out depending on the severity of inflammation. First, lotions are prescribed, and then lubrication of the foci with aniline dye.

General anti-candidiasis therapy for patients with superficial candidiasis of the skin and mucous membranes is prescribed for widespread lesions of folds, smooth skin, and mucous membranes.

In case of recurrent vulvovaginal candidiasis or balanoposthitis, it is necessary to identify concomitant factors (diabetes mellitus, abnormal pregnancy), in addition, fluconazole is prescribed.

It is important to prevent candidiasis in persons with a combination of several predisposing factors: immunodeficiency, blood disease, neoplasm, etc. Great importance is attached to the treatment of intestinal dysbacteriosis, the detection and treatment of candidiasis in pregnant women, the treatment of persons with genital candidiasis and their sexual partners.

4. Deep mycoses

Fungi that cause deep mycoses belong to various generic and species groups. Many of them are dimorphic: in the external environment they exist in the form of mycelium, and in the lesions - in the parasitic (tissue) form, which differs sharply from the mycelial form in morphology. In addition to the skin, deep mycoses affect the internal organs.

The most dangerous deep mycoses include coccidioidomycosis and histoplasmosis, which cause severe lesions of the skin, mucous membranes and internal organs, often ending in the death of the patient. Other deep mycoses are caused by opportunistic fungi. The severity of their course depends on the degree of prevalence and the state of reactivity of the patient's body.

Deep mycoses are common in regions with a tropical and subtropical climate.

Deep mycoses, especially with damage to internal organs, require the appointment of a general antifungal therapy (itraconazole, fluconazole, amphotericin B).

5. Pseudomycosis

This group includes superficial (erythrasma) and deep (actinomycosis) diseases of a non-fungal nature.

erythrasma

With erythrasma, skin folds are affected. Given the significant clinical similarity and general localization, the disease must be differentiated from mycosis. Of decisive importance in the diagnosis are the examination of the foci in a lamp with a Wood filter (with a coral-red glow) and the data of microbiological studies. Treatment of erythrasma is similar to the treatment of mycosis of large folds.

Actinomycosis

The disease is caused by several types of actinomycetes. Along with the skin, internal organs can be affected. More than half of the patients have a cervicofacial form of cutaneous actinomycosis, which is manifested by gummy-nodular, tuberculous-compacted, atheromatous, abscessing and ulcerative rashes.

In treatment, high doses of penicillin and actinolysate are used for a long time.

LECTURE № 8. Psoriasis

Psoriasis, or psoriasis, is one of the most common chronic dermatoses, characterized by hyperproliferation of epidermal cells, impaired keratinization, and inflammation in the dermis.

Etiology. This is a disease of unknown etiology. One of the main hypotheses for its development is considered hereditary. It is assumed that the disease can be transmitted in an autosomal dominant manner. However, even in people with an unfavorable genotype, various provoking factors play a role in the occurrence of the disease.

1. Trauma. The occurrence of psoriatic rashes at the sites of skin injury of a physical, chemical or inflammatory nature, well known as the Koebner phenomenon.

2. Infection. The role of streptococcal and herpetic infections as the most likely variants of provoking infectious factors in psoriasis is generally recognized.

3. Endocrine factors. The peak incidence of psoriasis in puberty and menopause was noted. The development of inverse and exudative psoriasis is associated with dysfunction of the thyroid gland and adrenal cortex.

4. Insolation usually leads to clinical improvement, however, in the progressive stage of dermatosis and in patients suffering from the summer form of psoriasis, the skin process is exacerbated.

5. Medications can provoke both the onset of psoriasis and the exacerbation of the skin process.

6. Psychogenic factors can provoke both the onset of psoriasis and exacerbation of a skin or joint lesion.

7. Alcohol contributes to a more severe course of psoriasis.

8. HIV infection also causes a severe course of the disease.

Pathological signs of skin lesions in psoriasis.

1. Metabolic disorders. Violation of the content of calcium-regulating hormones predetermines the development of osteopathies and other changes characteristic of hyperparathyroidism.

Leukocyte attractants - a substance similar to leukotriene B was found in psoriatic plaques₄ and has a pronounced property to attract neutrophils.

2. Immunological mechanisms. The central pathogenetic event in psoriasis is the "mononuclear-keratinocyte" relationship, which leads to the activation of the latter with the release of inflammatory mediators and growth factor.

Pathomorphology. The changes are characterized by the following signs: infiltration of the dermis, elongation of some papillae, and the formation of glomeruli in them from full-blooded capillaries. Through diapedesis, leukocytes penetrate the epidermis and form Munro microabscesses under the stratum corneum. In the epidermis, interpapillary acanthosis, absence of the granular layer, and parakeratosis are also observed.

The peculiar morphological structure of psoriatic papules causes a triad of symptoms pathognomonic for psoriasis, which is determined by scraping the surface of the papule with a scalpel. Initially, as a result of crushing the scales, a picture is revealed that resembles that when a frozen drop of stearin is scraped off (a symptom of a stearin stain). Then, due to the absence of the granular layer, the compact lower rows of the stratum corneum peel off as a film, exposing the moist surface of the spinous layer (a symptom of the terminal film). Further scraping leads to damage to the capillaries in the elongated papillae with the appearance of droplets of blood (a symptom of blood dew).

Clinic. The primary rash in psoriasis is a flat, inflammatory epidermal-dermal papule of a round shape with clear boundaries, 1-2 mm in size, pink or deep red in color; on the lower extremities, papules often acquire a bluish tint. From the moment it appears, the surface of the papule begins to become covered with dry, loosely arranged silvery-white scales. As a result of peripheral growth, miliary papules turn into lenticular and nummular, adjacent rashes merge, forming plaques of various shapes.

In the progressive stage of psoriasis, an isomorphic irritation reaction (Kebner's symptom) is observed, which is expressed in the occurrence of psoriatic rashes at the sites of skin injury, sometimes even the most insignificant.

Over time, the formation of new papules and the peripheral growth of rashes stops, and the disease passes into the stationary stage. Evidence of growth arrest of the psoriatic element is the appearance of a pseudo-atrophic rim.

In some cases, an acute widespread rash occurs, the papules reach lenticular dimensions, and this is where the progression of the process ends (teardrop psoriasis). This course of psoriasis is usually associated with a streptococcal infection in the tonsils.

The resolution of psoriatic rashes often begins with the central part, which leads to the appearance of ring-shaped garland-shaped foci, as well as extensive foci of bizarre outlines - the stage of regression. After the rash resolves, hypopigmented spots remain in their place.

Psoriasis can affect any part of the skin, but more often it is localized on the extensor surface of the limbs, especially the elbow and knee joints, the scalp, in the sacrum. It is not uncommon for individual plaques, especially in the elbows and knees, to persist for a long time after the rest of the rash has resolved.

There are clinical varieties of ordinary psoriasis.

Seborrheic psoriasis occurs in patients with seborrhea with localization of rashes on the scalp, in the nasolabial folds, behind the auricles, in the chest area, in the skin folds. Rashes are poorly infiltrated and their boundaries are less clear than in the usual form; sebum-impregnated yellowish psoriatic scales are held on the surface, simulating a picture of seborrheic dermatitis.

Exudative psoriasis is caused by a pronounced exudative component of the inflammatory reaction, more often observed in people with increased body weight. Due to the penetration of exudate to the surface of the papules, the characteristic silvery-white appearance of the scales changes. They turn into grayish-yellowish, loose, moist cortical scales, tightly adhering to the surface of the skin.

Palmar-plantar psoriasis occurs more often in people of physical labor, which is explained by the traumatization of these areas of the skin. It may be accompanied by rashes in other areas of the skin, or it may be isolated. Clinically manifested either as ordinary psoriatic papules, or hyperkeratotic, simulating calluses. There is a continuous lesion of the skin of the palms and soles in the form of its thickening and increased keratinization.

Spotted psoriasis is characterized by mild infiltration of rashes that, after scraping off the scales, look like spots. It develops more often acutely, reminiscent of toxidermia.

Nail damage can develop in any clinical form of the disease in various ways, such as:

1) the formation of dotted depressions on the surface of the nail plates, resembling the working surface of a thimble, is due to foci of parakeratosis that form in the proximal part of the matrix;

2) changes in the type of oil stain (yellowish color of the nail bed, translucent through the nail plate) usually occurs in a progressive stage; due to histological changes in hyponychia, characteristic of psoriasis;

3) onycholysis is caused by subungual hyperkeratosis due to hyperproliferation of the epithelium of the nail bed. Clinically resembles onychomycosis;

4) leukonychia (white spots) occurs when the middle part of the matrix is ​​affected.

Psoriasis can manifest itself in severe forms.

Psoriatic erythroderma develops in patients with widespread psoriasis in a progressive stage and is a nonspecific toxic-allergic reaction, most often provoked by various irritating factors (insolation, irrational external therapy). Initially, erythema appears on areas of the skin free from psoriatic rash, then merges, occupying the entire skin. The skin is bright red, swollen, infiltrated, lichenified in places, hot to the touch, covered with large and small dry white scales. Papules and plaques become indistinguishable. The general condition of patients is sharply disturbed, the temperature rises to 38-39 ° C, thermoregulation is disrupted, water-electrolyte imbalance and hypoproteinemia develop, which can lead to heart failure.

Pustular psoriasis is characterized by the eruption of sterile pustules. The morphological basis of the disease is the accumulation of neutrophils in the epidermis (Munro microabscesses). There are two forms of pustular psoriasis: generalized (Zumbusch type) and localized (limited), palmoplantar (Barber type).

Generalized pustular psoriasis (Zumbusch type) is characterized by an acute, subacute, or sometimes chronic eruption of sterile pustules. The disease develops against the background of typical psoriatic rashes. After the resolution of the pustules, the process usually takes on its original form.

The course of the disease is severe with fever, malaise, leukocytosis, elevated ESR. Paroxysmal against the background of bright erythema, small superficial pustules appear, accompanied by burning and soreness, located both in the area of ​​​​plaques and on previously unchanged skin.

Localized pustular psoriasis (Barber type) is more common than the generalized form. One or more sharply defined plaques appear on the palms (in the thenar and hypothenar areas) and soles, within which there are numerous pustules with a diameter of 2-5 mm.

Psoriatic arthritis is one of the most severe forms of psoriasis, often leading to disability in patients. Articular involvement may develop in patients with pre-existing skin lesions simultaneously with, or precede, skin manifestations. In the future, synchronism in the development of relapses of skin lesions and arthritis may be observed.

The nature of skin rashes in psoriatic arthritis is distinguished by a number of features, in particular, a tendency to exudation, pustulization, resistance to therapy, the location of the rash in the terminal phalanges with nail damage up to onycholysis.

Treatment. Topical therapy is the use of non-irritating emollients in the form of ointment or cream after a bath or shower. Typically, emollient formulations contain low concentrations (1-2%) of salicylic acid or higher concentrations (5-6%) of lactic acid. This helps reduce peeling and restores the elasticity of the affected areas of the skin.

Topical corticosteroids have powerful anti-inflammatory, epidermostatic, anti-allergic and local anesthetic effects. They can be applied to the skin in the form of a cream (with progressive psoriasis, especially with a pronounced exudative component), ointment (with a stable lesion with severe infiltration), lotion (with localization of rashes on the scalp and face, especially with a tendency to seborrhea). If it is necessary to enhance the activity of these agents, occlusive dressings are used.

Synthetic retinoids act on the main pathogenetic links of the disease: they normalize impaired differentiation of keratinocytes, potentiate antiproliferative effects in the skin, and suppress the expression of inflammation markers.

Permissive means. Tar preparations have antimitotic, keratoplasty, anti-inflammatory, disinfectant and local irritant effects in high concentrations. Tar is used in various dosage forms (in the form of ointment, cream, lotion, paste, gel, shampoo), in various concentrations (from 1-2 to 30%, pure tar), as a single drug and in combinations with salicylic acid, dithranol and anthralin , topical corticosteroids.

Naftalan oil and its preparations, when exposed to the skin, have a softening, resolving, anti-inflammatory, disinfectant and some analgesic effect.

Hydroxianthrones. Dithranol, anthralin have a cytostatic and cytotoxic effect, which leads to a decrease in the activity of oxidative and glycolytic processes in epidermal cells, causing a decrease in the number of mitoses in the epidermis, parakeratosis and hyperkeratosis.

Systemic drug non-suppressive therapy. Hyposensitizing and detoxifying therapy. This group includes calcium preparations (citrate, gluconate, pantothenate), sodium thiosulfate, hemodez. Calcium preparations provide anti-inflammatory and hyposensitizing effects. Sodium thiosulfate has an anti-inflammatory, desensitizing effect. The drug is more active when administered intravenously. Hemodez is a water-salt solution containing low molecular weight polyvinylpyrrolidone, sodium, potassium, magnesium, chlorine ions. The mechanism of action of gemodez is due to the ability to bind toxins circulating in the blood and quickly remove them through the renal barrier.

Vitamin D3 has an active antiproliferative effect on the skin. It also normalizes the differentiation of epidermocytes, which together contributes to the resolution of psoriatic lesions.

Phototherapy. UV rays are used.

immunosuppressive therapy. Methotrexate. The action of methotrexate is based on the blockade of key steps in the biosynthesis of nucleic acids. The drug inhibits mainly DNA synthesis and cell reproduction and, to a lesser extent, RNA and protein synthesis. Used to correct excessive proliferation of epithelial cells.

Methotrexate is effective only when administered orally and parenterally. It is administered orally either in one dose once a week, or this dose is divided into three doses with an interval of 12 hours. The hepatotoxic effect is pronounced in the second variant of the drug.

Cyclosporine A is a selective immunosuppressive drug. The initial dose of cyclosporine A and sandimmune-neoral should be 2,5-3 mg per 1 kg of patient body weight per day. If clinical effect and optimal effectiveness are achieved after 4-8 weeks from the start of therapy, it is recommended to continue taking the drug at the same dose.

Glucocorticosteroids. The mechanism of action of glucocorticosteroid drugs in psoriasis is their powerful anti-inflammatory effect, active immunosuppressive effect, antitoxic effect.

The dose of glucocorticoids in most cases is 40-50 mg per day in terms of prednisolone. After achieving a positive clinical effect (not necessarily complete clinical regression), the drug is gradually withdrawn. The total duration of treatment with glucocorticosteroids is short (on average no more than 2-3 weeks).

LECTURE number 9. Lichen planus

Lichen planus is a non-infectious inflammatory disease characterized by the appearance of itchy flat polygonal papules on the skin and mucous membranes. The course of the disease can be both acute and chronic.

Etiology. For this form of dermatosis, the etiology is not clear.

Pathogenesis. Currently, the pathogenesis of this dermatosis is considered as a complex participation of the following factors: infectious (viral), neuroendocrine, genetic, immune (graft-versus-host reaction), toxic-allergic (toxic effects of drugs - preparations of gold, arsenic, mercury, quinine, its derivatives , ftivazid, PAS, tetracycline), autointoxication caused by diseases of the gastrointestinal tract, diabetes mellitus, liver dysfunction, including chronic hepatitis C).

Clinic. The typical form of lichen planus is characterized by a monomorphic rash in the form of small, flat, shiny (especially in side lighting), polygonal (polygonal) papules, not prone to peripheral growth. The color of the elements is reddish-pink with a characteristic lilac or purple tint. In the center of the papules there is a small umbilical depression. On the surface of the nodules, one can find Wickham's reticulum, pathognomonic for this dermatosis, characterized by a combination of white or grayish dots and stripes. Wickham's reticulum is clearly visible under a magnifying glass after lubricating the surface of the affected area with vegetable or petroleum jelly. The formation of the mesh is explained by the uneven thickening of the granular layer. Eruptive elements can be grouped to form small plaques covered with scales, along the periphery of which new, isolated small papules appear, which is explained by the jerky nature of the appearance of rashes in this dermatosis.

Of the subjective symptoms in most patients, intense itching is noted, often general anxiety.

Typical rashes of lichen planus are usually localized on the flexor surfaces of the forearms and wrist joints, the anterior surfaces of the legs, in the sacrum, in men - on the penis.

On the red border of the lips (more often on the lower one), small, slightly flaky, purple flat plaques are formed, on the surface of which, when wetted with water or lubricated with oil, a grayish-white mesh is revealed.

The change in the nail plates with lichen planus is characterized by the formation of furrows, depressions, and areas of turbidity. Nails can become thinner and even partially or completely destroyed. The nail plates of the big toes are most often affected.

In addition to the classical form, many atypical forms of lichen planus have been described. Atypical forms of the disease include: annular, warty (verrucous), pemphigoid, atrophic, erosive-ulcerative, follicular.

The ring-shaped form of lichen planus is characterized by the presence of rashes in the form of rings. Separate papules and plaques, undergoing resolution in the center, form small rings, the central part of which may have a brown color.

The warty (verrucous) form is diagnosed with the formation (usually on the lower extremities) of purple or brownish-red plaques that rise significantly above the level of healthy skin, with an uneven surface, covered with massive horny layers. On the periphery of the plaques, individual typical papules of lichen planus can be found.

The pemphigoid (bullous) form is characterized by the appearance of blisters on papules and plaques of lichen planus, as well as on erythematous areas and unchanged skin. With this form of the disease, the general condition of the patient is often disturbed. When the rash resolves, atrophy and hyperpigmentation may remain. With the localization of elements on the scalp, the development of cicatricial alopecia is possible. Pemphigoid form of lichen planus can act as a paraneoplastic syndrome.

The atrophic form of lichen planus is diagnosed in cases where atrophy develops after resolution of primary lesions.

The erosive-ulcerative form of lichen planus is characterized by the formation of erosive-ulcerative defects on the mucous membrane of the mouth (cheeks, gums, red border of the lips) or on the skin of the legs. Erosions or small ulcers of irregular or rounded outlines with a pinkish-red surface, at the base and along their periphery, a sharply limited plaque infiltrate can persist for quite a long time.

The follicular form of lichen planus occurs in two variants: either in the form of follicular and perifollicular papules, or in the form of scarring alopecia of the scalp, as well as non-scarring alopecia of the armpits and pubis.

Lichen planus exists for a long time, many months, sometimes years. Starting acutely or subacutely, the skin lesion progresses for the first time, which is expressed in the appearance of new elements. Then comes the stationary period, usually lasting several months. Following this, the lesion begins to gradually resolve, and hyperpigmentation remains in place of papules and plaques. Acute lichen planus can regress relatively quickly, but more often becomes chronic.

Pathomorphology. In the typical form of lichen planus, hyperkeratosis, thickening of the granular layer (focal granulosis), acanthosis (elongated interpapillary processes pointed downwards - a saw-like symptom), and vacuolar degeneration of the cells of the basal layer of the epidermis are observed. The strip-like infiltrate in the upper part of the dermis is closely adjacent to the epidermis, blurring its lower border. The infiltrate contains lymphocytes and histiocytes. At the border between the epidermis and dermis, Siwatt bodies are visible - degenerated keratinocytes. Sometimes there are gap-like spaces between the epidermis and dermis.

Diagnostics. In typical cases, making a diagnosis of lichen planus is not difficult. The characteristic coloring of the elements with a lilac-pearl shade, the polygonal outlines of flat papules with an umbilical depression in the center, the presence of Wickham's mesh, the localization of lesions on the flexor surface of the forearms and often on the mucous membrane of the oral cavity and genital organs - all this almost accurately allows us to make a diagnosis of lichen planus , without even resorting to histological examination.

Treatment. Depending on the clinical form of the disease, the prevalence of the pathological process and the localization of the lesions, various treatment options for lichen planus are carried out.

1. Therapy with antimalarial drugs.

2. Therapy with aromatic retinoids (derivatives of acitretin).

3. PUVA therapy (with common forms).

4. Corticosteroid therapy (short courses in acute generalized forms).

5. Therapy with cyclosporine A (with resistance to other therapy options and generalized forms).

6. Treatment with antidepressants, tranquilizers, anxiolytics.

7. Hyposensitizing therapy with calcium preparations and antihistamines.

8. Treatment of concomitant diseases that complicate the course of dermatosis.

Outwardly, antipruritic shaken mixtures with menthol and anesthesin, corticosteroid creams and ointments are prescribed (possibly under an occlusive dressing). Large and verrucous lesions are treated with corticosteroids or cryodestruction or laser therapy is performed. In severe lesions of the oral mucosa, rinsing with a solution of cyclosporine or a corticosteroid is prescribed.

LECTURE No. 10. Syphilis

Syphilis is a chronic infectious disease that is caused by pale treponema and is characterized by a systemic lesion of the body and a staged progressive course.

1. Ways of infection

Despite successful laboratory experiments on infecting animals, under natural conditions, animals are not susceptible to syphilis. Transmission of infection in a natural way is possible only from person to person. As a source of infection, patients pose the greatest danger in the first 2 years of the disease. After 2 years of infection, the contagiousness of patients decreases, infection of contact persons occurs less frequently. A necessary condition for infection is the presence of an entrance gate - damage (microtrauma) of the stratum corneum of the epidermis or the epithelium of the mucous membrane.

There are three ways of infection transmission: contact, transfusion and transplacental. The most common infection with syphilis occurs by contact.

contact way

Infection can occur through direct (direct) contact with a sick person: sexual and non-sexual (domestic).

The most common infection occurs through direct sexual contact. The direct non-sexual route of infection is rarely realized in practice (as a result of a kiss, a bite). In domestic conditions, young children are at particular risk of infection if their parents have active forms of syphilis. Be sure to carry out preventive treatment of children who were in close contact with patients with syphilis. Cases of direct professional infection of medical workers (dentists, surgeons, obstetricians-gynecologists, pathologists) when examining patients with syphilis, performing medical procedures, contact with internal organs during operations, autopsies are rare.

Infection can occur through indirect (mediated) contact - through any objects contaminated with biological material containing pathogenic treponema. Most often, infection occurs through objects that come into contact with the oral mucosa - glasses, spoons, toothbrushes.

The risk of household infection with syphilis is real for people who are in close household contact with the patient: family members, members of closed groups. Indirect infection in medical institutions through reusable medical instruments is excluded if it is properly processed.

A patient with syphilis is contagious during all periods of the disease, starting with incubation. The greatest danger is posed by patients with primary and especially secondary syphilis, who have weeping rashes on the skin and mucous membranes - erosive or ulcerative primary syphilomas, macerated, erosive, vegetative papules, especially when located on the oral mucosa, genitals, and also in skin folds.

Dry syphilides are less contagious. Treponema is not found in the content of papulo-pustular elements. The manifestations of tertiary syphilis are practically not contagious, since they contain only single treponemas located deep in the infiltrate.

The saliva of patients with syphilis is contagious in the presence of rashes on the oral mucosa. Breast milk, semen and vaginal secretions are contagious even in the absence of rashes in the mammary glands and genitals. The secret of the sweat glands, lacrimal fluid and urine of patients do not contain treponema.

In patients with early forms of syphilis, any non-specific lesions are contagious, leading to a violation of the integrity of the skin and mucous membranes: herpetic eruptions, erosion of the cervix.

Transfusion route

Transfusion syphilis develops during the transfusion of blood taken from a donor with syphilis, and in practice it is realized extremely rarely - only in the case of direct transfusion. Drug users are at real risk of infection by sharing intravenous syringes and needles. With the transfusion route of transmission, the pathogen immediately enters the bloodstream and internal organs, so syphilis manifests on average 2,5 months after infection with immediately generalized rashes on the skin and mucous membranes. At the same time, there are no clinical manifestations of the primary period of syphilis.

Transplacental route

In a pregnant woman with syphilis, intrauterine infection of the fetus can occur with the development of congenital syphilis. In this case, treponemas penetrate the placenta immediately into the bloodstream and internal organs of the fetus. With congenital infection, the formation of a chancre and other manifestations of the primary period are not observed. Transplacental infection usually occurs no earlier than the 16th week of pregnancy, after the completion of the formation of the placenta.

2. Pathogenesis

The following variants of the course of syphilitic infection have been established: classical (staged) and asymptomatic.

Syphilis is characterized by a staged, undulating course with alternating periods of manifestation and a latent state. Another feature of the course of syphilis is progression, i.e., a gradual change in the clinical and pathomorphological picture in the direction of increasingly unfavorable manifestations.

3. Course of syphilis

Periods

During syphilis, four periods are distinguished - incubation, primary, secondary and tertiary.

The incubation period. This period begins from the moment of infection and continues until the appearance of primary syphiloma - on average 30-32 days. The incubation period may be shortened or extended compared to the stated average duration. Incubation has been described to be shortened to 9 days and extended to 6 months.

When entering the body, cells of the monocyte-macrophage system are already encountered in the area of ​​​​the entrance gate of treponema, however, the processes of recognition of a foreign agent by tissue macrophages, as well as the transmission of information by T-lymphocytes in syphilis, are impaired for several reasons: glycopeptides of the treponema cell wall are similar in structure and composition to glycopeptides human lymphocytes; treponemas secrete substances that slow down the recognition process; after introduction into the body, treponema quickly penetrate into the lymphatic capillaries, vessels and nodes, thereby avoiding the macrophage reaction; even being phagocytosed, treponema in most cases does not die, but becomes inaccessible to the body's defenses.

The early stages of syphilis are characterized by partial inhibition of cellular immunity, which contributes to the reproduction and spread of pathogens throughout the body.

Already 2-4 hours after infection, the pathogen begins to move along the lymphatic pathways and invades the lymph nodes. From the moment of infection, treponema begins to spread by hematogenous and neurogenic routes, and in the first day the infection becomes generalized. From this time on, bacteria are found in the blood, internal organs and nervous system, but in the tissues of the sick person during this period there is still no morphological response to the introduction of pathogens.

The humoral link of immunity is not able to ensure the complete destruction and elimination of pale treponema. During the entire incubation period, pathogens actively multiply in the area of ​​the entrance gate, the lymphatic system and internal organs. At the end of incubation, the number of treponemas in the body increases significantly, so patients during this period are contagious.

Primary Period. It begins with the onset of primary affect and ends with the appearance of generalized rashes on the skin and mucous membranes. The average duration of primary syphilis is 6-8 weeks, but it can be shortened to 4-5 weeks and increased to 9-12 weeks.

A few days after the onset of the primary affect, an increase and thickening of the lymph nodes closest to it is observed. Regional lymphadenitis is an almost constant symptom of primary syphilis. At the end of the primary period, approximately 7-10 days before its end, groups of lymph nodes remote from the area of ​​the entrance gate of infection increase and thicken.

During the primary period of syphilis, an intense production of antitreponemal antibodies occurs. First of all, their number in the bloodstream increases. Circulating antibodies immobilize treponemas, form membrane-attacking immune complexes, which leads to the destruction of pathogens and the release of lipopolysaccharide and protein products into the blood. Therefore, at the end of the primary - the beginning of the secondary period, some patients have a prodromal period: a complex of symptoms caused by intoxication of the body with substances released as a result of mass death of treponema in the bloodstream.

The level of antibodies in tissues gradually increases. When the amount of antibodies becomes sufficient to ensure the death of tissue treponemas, a local inflammatory reaction occurs, which is clinically manifested by widespread rashes on the skin and mucous membranes. Since that time, syphilis passes into the second stage.

Secondary period. This period begins from the moment the first generalized rash appears (on average 2,5 months after infection) and lasts in most cases for 2-4 years.

The duration of the secondary period is individual and determined by the characteristics of the patient’s immune system. Recurrences of secondary rashes can be observed 10-15 years or more after infection, while at the same time, in weakened patients, the secondary period can be shortened.

In the secondary period, the wave-like course of syphilis is most pronounced, i.e., the alternation of manifest and latent periods of the disease. During the first wave of secondary rashes, the number of treponemas in the body is the largest - they multiplied in large numbers during the incubation and primary periods of the disease.

The intensity of humoral immunity at this time is also maximum, which causes the formation of immune complexes, the development of inflammation and the massive death of tissue treponemas. The death of some pathogens under the influence of antibodies is accompanied by a gradual cure of secondary syphilides within 1,5-2 months. The disease enters a latent stage, the duration of which may vary, but on average is 2,5-3 months.

The first relapse occurs approximately 6 months after infection. The immune system again responds to the next reproduction of pathogens by increasing the synthesis of antibodies, which leads to the cure of syphilides and the transition of the disease to a latent stage. The wavelike course of syphilis is due to the peculiarities of the relationship between pale treponema and the patient's immune system.

The further course of a syphilitic infection is characterized by a continuing increase in sensitization to treponema with a steady decrease in the number of pathogens in the body.

After an average of 2-4 years from the moment of infection, the tissue response to the pathogen begins to proceed according to the Arthus phenomenon type, followed by the formation of a typical infectious granuloma - an infiltrate of lymphocytes, plasma, epithelioid and giant cells with necrosis in the center.

Tertiary period. This period develops in patients who have not received treatment at all or have not been treated sufficiently, usually 2-4 years after infection.

The balance that exists between the pathogen and the controlling immune system during the latent course of syphilis can be disturbed under the influence of adverse factors - injuries (bruises, fractures), weakening the body of the disease, intoxication. These factors contribute to the activation (reversion) of spirochetes in any part of a particular organ.

In the later stages of syphilis, the reactions of cellular immunity begin to play a leading role in the pathogenesis of the disease. These processes proceed without a sufficiently pronounced humoral background, since the intensity of the humoral response decreases as the number of treponemas in the body decreases.

Malignant course of syphilis

Severe comorbidities (such as tuberculosis, HIV infection), chronic intoxication (alcoholism, drug addiction), malnutrition, heavy physical labor and other causes that weaken the patient's body affect the severity of syphilis, contributing to its malignant course. Malignant syphilis in each period has its own characteristics.

In the primary period, ulcerative chancre is observed, prone to necrosis (gangrenization) and peripheral growth (phagedenism), there is no reaction of the lymphatic system, the entire period can be shortened to 3-4 weeks.

In the secondary period, the rash is prone to ulceration, papulo-pustular syphilides are observed. The general condition of patients is disturbed, fever, symptoms of intoxication are expressed. Often there are manifest lesions of the nervous system and internal organs. Sometimes there is a continuous recurrence, without latent periods. Treponemas in the discharge of rashes are found with difficulty.

Tertiary syphilides in malignant syphilis may appear early: one year after infection (galloping course of the disease). Serological reactions in patients with malignant syphilis are often negative, but may become positive after the start of treatment.

Re-infection with syphilis

True, or sterile, immunity does not develop with syphilis. This means that a person who has been ill can become infected again, just like a person who has never had this disease before. Re-infection with syphilis of a person who had previously been ill and completely cured is called reinfection. The latter is regarded as convincing proof of the complete curability of syphilis.

With syphilis, the so-called non-sterile, or infectious, immunity develops in the patient's body. Its essence is that a new infection is impossible while pale treponemas remain in the body.

4. Clinical manifestations

Primary Period

The following complex of clinical symptoms is characteristic of the primary period of syphilis: primary syphiloma, regional lymphadenitis, specific lymphadenitis, specific polyadenitis, prodromal phenomena.

Primary syphiloma is the first clinical manifestation of the disease that occurs at the site of the introduction of pale treponema through the skin and mucous membranes (in the region of the entrance gate).

The appearance of an erosive or ulcerative defect is preceded by the appearance of a small hyperemic inflammatory spot, which after 2-3 days turns into a papule. These changes are asymptomatic and are not noticed by either the patient or the doctor. Soon after the appearance of the papule, the epidermis (epithelium) covering it undergoes disintegration, and an erosion or ulcer is formed - the primary syphiloma itself. The depth of the defect depends on the severity and nature of the tissue reaction to the introduction of the pathogen.

Clinical features of a typical primary syphiloma.

1. Primary syphiloma is an erosion or superficial ulcer.

2. Primary syphilomas are single or single (2-3 elements).

3. Primary syphiloma has round or oval outlines.

4. Primary syphiloma usually measures 5-15 mm in size. There are also dwarf primary affects with a diameter of 1-3 mm. Giant chancre with a diameter of up to 4-5 cm or more are ulcerative, covered with serous-hemorrhagic or purulent-hemorrhagic crusts and have extragenital or perigenital localization.

5. Having reached a certain size, primary syphiloma does not tend to grow peripherally.

6. The boundaries of primary syphiloma are even, clear.

7. The surface of the primary syphiloma has a bright red color (the color of fresh meat), sometimes covered with a dense coating of grayish-yellow color (the color of spoiled fat).

8. The edges and bottom of erosive syphiloma lie on the same level. The edges and bottom of the ulcerative chancre are separated from each other by the depth of the defect.

9. The bottom of the primary syphiloma is smooth, covered with scanty transparent or opalescent discharge, giving it a kind of mirror or lacquer sheen.

10. At the base of primary syphiloma there is a dense elastic infiltrate, clearly demarcated from the surrounding tissues and extending 2-3 mm beyond the syphiloma.

11. Primary syphiloma is not accompanied by subjective sensations. Soreness in the area of ​​primary affect appears when a secondary infection is attached.

12. There are no acute inflammatory skin changes around the primary syphiloma.

Localization of primary syphilomas: primary syphilomas can be located on any part of the skin and mucous membranes where the conditions for the introduction of treponemas have developed, i.e., in the area of ​​​​the entrance gate of infection. By localization, primary syphilomas are divided into genital, perigenital, extragenital and bipolar.

Atypical primary syphilomas. In addition to primary affects with a typical clinical picture and its many varieties, atypical chancres can be observed that do not have the characteristic signs inherent in typical syphilomas. These include indurative edema, chancre-felon, chancre-amygdalite. Atypical forms of syphilomas are rare, have a long course and often cause diagnostic errors.

Indurative edema is a persistent specific lymphangitis of small lymphatic vessels of the skin, accompanied by symptoms of lymphostasis.

It occurs in the genital area with a richly developed lymphatic network: in men, the foreskin and scrotum are affected, in women, the labia majora, and very rarely, the small lips, clitoris, and lips of the pharynx of the cervix.

Chancre panaritium is localized on the distal phalanx of the finger and has a great resemblance to the banal panaritium. It is characterized by the formation of an ulcer on the dorsum of the terminal phalanx of the finger. Deep - down to the bone - an ulcer with uneven, tortuous and undermined edges, lunate or horseshoe-shaped. The bottom of the ulcer is pitted, covered with purulent-necrotic masses, crusts, there is abundant purulent or purulent-hemorrhagic discharge with an unpleasant odor.

Chancre-amygdalite is a specific unilateral enlargement and significant thickening of the tonsil without a defect on its surface. The tonsil has a stagnant red color, but is not accompanied by diffuse hyperemia.

There are the following complications of primary syphiloma:

1) impetiginization. A hyperemic corolla appears along the periphery of the syphiloma, the tissues acquire pronounced puffiness, the brightness of the element increases, the discharge becomes abundant, serous-purulent or purulent, there is a burning sensation, soreness in the area of ​​syphiloma and regional lymph nodes;

2) balanitis and balanoposthitis - in men, vulvitis and vulvovaginitis - in women. High humidity, constant temperature, the presence of a nutrient medium in the form of smegma in the preputial sac contribute to the reproduction of microorganisms and the development of clinical manifestations of balanitis - inflammation of the skin of the glans penis. In women, secondary infection contributes to vulvovaginitis;

3) phimosis. In men who have not undergone circumcision, the inflammatory process of the skin of the preputial sac due to the developed lymphatic network often leads to phimosis - narrowing of the foreskin ring. Inflammatory phimosis is characterized by a bright diffuse hyperemia, mild swelling and an increase in the volume of the foreskin, as a result of which the penis acquires a cone-shaped shape, becomes painful;

4) paraphimosis, which is an infringement of the glans penis by a narrowed ring of the foreskin, drawn to the coronal sulcus. Occurs as a result of forced exposure of the head during phimosis. This leads to a violation of the blood and lymph flow, aggravation of the edema of the preputial ring and severe pain in the penis;

5) gangrenization. Syphiloma undergoes necrotic decay, which is clinically expressed by the formation of a scab of a dirty gray, brown or black color, tightly soldered to the underlying tissues and painless;

6) phagedenism, which begins with the appearance of a larger or smaller area of ​​necrosis against the background of an ulcer. But the necrotic process is not limited to the chancre and extends not only in depth, but also beyond the syphiloma.

Regional lymphadenitis. It is an enlargement of the lymph nodes that drain the site of primary syphiloma. This is the second clinical manifestation of primary syphilis.

specific lymphangitis. It is an inflammation of the lymphatic vessel from a hard chancre to regional lymph nodes. This is the third component of the clinical picture of primary syphilis.

Specific polyadenitis. At the end of the primary period of syphilis, patients develop a specific polyadenitis - an increase in several groups of subcutaneous lymph nodes remote from the area of ​​​​the entrance gate of infection.

Prodromal syndrome. Approximately 7-10 days before the end of the primary period and during the first 5-7 days of the secondary period, general symptoms are observed due to intoxication as a result of the massive presence of treponemes in the bloodstream. It includes fatigue, weakness, insomnia, decreased appetite and performance, headache, dizziness, irregular fever, myalgia, leukocytosis and anemia.

Secondary period

The secondary period of syphilis is characterized by a complex of such clinical manifestations as spotted syphilis (syphilitic roseola), papular syphilis, papulo-pustular syphilis, syphilitic alopecia (baldness), syphilitic leucoderma (pigmented syphilis).

Spotted syphilide, or syphilitic roseola. This is the most common and earliest manifestation of the secondary period of the disease. The roseate rash appears gradually, in spurts, 10-12 elements per day. The rash reaches full development in 8-10 days, lasts on average 3-4 weeks without treatment, sometimes less or more (up to 1,5-2 months). The roseate rash resolves without leaving a trace.

Syphilitic roseola is a hyperemic inflammatory spot. The color of roseola varies from pale pink to deep pink, sometimes with a bluish tint. Most often it has a pale pink, faded color. Long-existing roseola acquires a yellowish-brown tint. The size of the spots ranges from 2 to 25 mm, with an average of 5-10 mm. The outlines of roseola are round or oval, the boundaries are unclear. The spots do not grow peripherally, do not merge, and are not accompanied by subjective sensations. There is no peeling.

Roseolous rash is localized mainly on the lateral surfaces of the trunk, chest, in the upper abdomen. Rashes can also be observed on the skin of the upper thighs and flexor surface of the forearms, rarely on the face.

In addition to the typical roseolous syphilis, its atypical varieties are distinguished: elevating, confluent, follicular and scaly roseola.

Elevating (towering) roseola, urticarial roseola, exudative roseola. In this form, the spots appear to rise slightly above the level of the skin and become similar to an urticarial rash with urticaria.

Drain roseola. It occurs with a very abundant rash of spots, which, due to the abundance, merge with each other and form continuous erythematous areas.

Follicular roseola. This variety is a transitional element between roseola and papule. Against the background of a pink spot, there are small follicular nodules in the form of dotted granularity of copper-red color.

Flaky roseola. This atypical variety is characterized by the appearance of lamellar scales on the surface of the spotty elements, resembling crumpled tissue paper. The center of the element appears somewhat sunken.

Papular syphilide. Occurs in patients with secondary recurrent syphilis. Papular syphilide also occurs with secondary fresh syphilis; in this case, papules usually appear 1-2 weeks after the onset of roseola rash and are combined with it (maculopapular syphilide). Papular syphilides appear on the skin in spurts, reaching full development in 10-14 days, after which they exist for 4-8 weeks.

The primary morphological element of papular syphilis is a dermal papule, sharply delimited from the surrounding skin, regularly rounded or oval in shape. In shape, it can be hemispherical with a truncated top or pointed. The color of the element is initially pink-red, later becoming yellowish-red or bluish-red. The consistency of the papules is densely elastic. Elements are located in isolation, only when localized in folds and irritation, there is a tendency for their peripheral growth and merging.

There are no subjective sensations, but when pressing on the center of a newly appeared papule with a blunt probe, pain is noted.

Depending on the size of the papules, four types of papular syphilis are distinguished.

Lenticular papular syphilide. This is the most common variety, which is characterized by a rash of papules with a diameter of 3-5 mm, observed in both secondary fresh and recurrent syphilis.

Miliary papular syphilis. This variety is extremely rare, its appearance is considered evidence of a severe course of the disease.

The morphological element is a cone-shaped papule of dense consistency with a diameter of 1-2 mm, located around the mouth of the hair follicle. The color of the elements is pale pink, as a result of which they stand out slightly against the surrounding background.

Nummular papular syphilide. This manifestation of the disease occurs mainly in patients with secondary recurrent syphilis. The rashes appear in small numbers and are usually grouped. The morphological element is a hemispherical papule with a flattened apex with a diameter of 2-2,5 cm. The color of the elements is brownish or bluish-red, rounded in outline. When nummular papules resolve, pronounced skin pigmentation remains for a long time.

Plaque papular syphilis. It occurs very rarely in patients with secondary recurrent syphilis. It is formed as a result of peripheral growth and fusion of nummular and lenticular papules that are exposed to external irritation. Most often, plaque-like syphilis is formed in the area of ​​​​large folds - on the genitals, around the anus, in the inguinal-femoral fold, under the mammary glands, in the armpits.

Papulo-pustular syphilis. It is observed in debilitated patients suffering from alcoholism, drug addiction, severe concomitant diseases, and indicates a severe, malignant course of syphilis.

The following clinical varieties of papulopustular syphilis are distinguished: acneiform (or acneiform), smallpox (or varioliform), impetigo-like, syphilitic ecthyma, syphilitic rupee. Superficial forms of papulo-pustular syphilis - acne-like, pox-like and impetigo-like - are most often observed in patients with secondary fresh syphilis, and deep forms - syphilitic ecthyma and rupee - are observed mainly in secondary recurrent syphilis and serve as a sign of a malignant course of the disease. All varieties of pustular syphilides have an important feature: they have a specific infiltrate at their base. Pustular syphilides arise as a result of the collapse of papular infiltrates, so it is more correct to call them papulo-pustular.

Syphilitic alopecia. There are three clinical varieties of alopecia: diffuse, small-focal and mixed, which is a combination of small-focal and diffuse varieties of alopecia.

Diffuse syphilitic alopecia is characterized by an acute general thinning of the hair in the absence of any skin changes. Hair loss usually starts at the temples and spreads to the entire scalp. In some cases, other areas of the hairline are also subject to baldness - the areas of the beard and mustache, eyebrows, eyelashes. The hair itself also changes: it becomes thin, dry, dull. The severity of diffuse alopecia varies from barely noticeable hair loss, slightly exceeding the size of the physiological change, to complete loss of all hair, including vellus.

Small focal syphilitic alopecia is characterized by the sudden, rapidly progressive appearance on the scalp, especially in the area of ​​the temples and the back of the head, of many randomly scattered small foci of hair thinning with a diameter of 0,5-1 cm. Bald spots have irregularly rounded outlines, do not grow along the periphery and do not merge with each other. The hair in the affected areas does not fall out completely, only a sharp thinning occurs.

Syphilitic leukoderma, or pigment syphilide. This is a kind of skin dyschromia of unknown origin that occurs in patients with secondary, mainly recurrent, syphilis. A typical localization of leukoderma is the skin of the back and sides of the neck, less often - the anterior wall of the armpits, the area of ​​the shoulder joints, the upper chest, and back. Diffuse yellowish-brown hyperpigmentation of the skin first appears on the affected areas. After 2-3 weeks, whitish hypopigmented spots with a diameter of 0,5 to 2 cm of round or oval shape appear on the hyperpigmented background. All spots are approximately the same size, located in isolation, and are not prone to peripheral growth and fusion.

There are three clinical varieties of pigmented syphilis: spotted, mesh (lace) and marbled. In spotted leukoderma, hypopigmented patches are separated from each other by wide layers of hyperpigmented skin, and there is a pronounced difference in color between hyper- and hypopigmented areas. With a mesh form, hypopigmented spots are in close contact with each other, but do not merge, remaining separated by thin layers of hyperpigmented skin. At the same time, narrow areas of hyperpigmentation form a grid.

In leukoderma marble, the contrast between hyper- and hypopigmented areas is negligible, the boundaries between the white patches are indistinct, and the overall impression is of dirty skin.

Damage to the nervous system. Neurosyphilis is usually divided into early and late forms, depending on the nature of the pathomorphological changes observed in the nervous tissue. Early neurosyphilis is a predominantly mesenchymal process affecting the meninges and vessels of the brain and spinal cord.

It usually develops in the first 5 years after infection. Early neurosyphilis is characterized by the predominance of exudative-inflammatory and proliferative processes.

Damage to internal organs. Syphilitic lesions of internal organs in early syphilis are inflammatory in nature and are similar in morphological pattern to changes occurring in the skin.

Damage to the musculoskeletal system. Lesions of the skeletal system, mainly in the form of ossalgia, less often - periostitis and osteoperiostitis, are localized mainly in the long tubular bones of the lower extremities, less often - in the bones of the skull and chest.

Tertiary period

Damage to the skin and mucous membranes in tertiary active syphilis is manifested by tuberculous and gummy rashes.

Tubercular syphilide. It can be located on any part of the skin and mucous membranes, but the typical places of its localization are the extensor surface of the upper limbs, torso, face. The lesion occupies a small area of ​​the skin, is located asymmetrically.

The main morphological element of tubercular syphilis is a tubercle (a dense, hemispherical, cavityless formation of a rounded shape, densely elastic consistency). The tubercle is formed in the thickness of the dermis, sharply demarcated from apparently healthy skin, has a size of 1 mm to 1,5 cm. The color of the tubercles is first dark red or yellowish-red, then becomes bluish-red or brownish. The surface of the elements is at first smooth, shiny, later on it appears small-lamellar peeling, and in case of ulceration - crusts. There are no subjective sensations. Fresh elements appear along the periphery of the focus.

The following clinical varieties of tubercular syphilis are distinguished: grouped, serping (creeping), tubercular syphilis with a platform, dwarf.

Grouped tubercular syphilide is the most common type. The number of tubercles usually does not exceed 30-40. The tubercles are at different stages of evolution, some of them have just appeared, others have ulcerated and become crusty, and others have already healed, leaving scars or cicatricial atrophy.

Due to the unequal growth of the tubercles and the different depths of their occurrence in the dermis, individual small scars differ in color and relief.

Serping tubercular syphilis. The lesion spreads over the surface of the skin either eccentrically or in one direction, when fresh bumps appear at one pole of the lesion.

In this case, the individual elements merge with each other into a dark red horseshoe-shaped roller raised above the level of the surrounding skin with a width of 2 mm to 1 cm, along the edge of which fresh tubercles appear.

Tuberous syphilide platform. Individual tubercles are not visible; they merge into plaques 5-10 cm in size, of bizarre shape, sharply demarcated from the unaffected skin and rising above it.

The plaque has a dense texture, brownish or dark purple color. The regression of the tubercular syphilis with a platform occurs either dry, with the subsequent formation of cicatricial atrophy, or through ulceration with the formation of characteristic scars.

Dwarf tubercular syphilide. Rarely observed. It has a small size of 1-2 mm. The tubercles are located on the skin in separate groups and resemble lenticular papules.

Gummous syphilide, or subcutaneous gumma. This is a node that develops in the hypodermis. The characteristic places of localization of gums are the shins, head, forearms, sternum. There are the following clinical varieties of gummy syphilis: isolated gums, diffuse gummous infiltrations, fibrous gums.

Isolated gumma. Appears in the form of a painless node measuring 5-10 mm, spherical in shape, densely elastic consistency, not fused to the skin. Gradually increasing, the subcutaneous gum adheres to the surrounding tissue and skin and protrudes above it in the form of a hemisphere.

The skin over the gumma first becomes pale pink, then brownish-red, purple. Then a fluctuation appears in the center of the gumma, and the gumma opens. When opened, 1-2 drops of sticky, yellow liquid with crumbly inclusions are released from the gummosa node.

Hummous infiltrations. They arise independently or as a result of the merger of several gums. Hummous infiltrate disintegrates, ulcerations merge, forming an extensive ulcerative surface with irregular, large-scalloped outlines, healing with a scar.

Fibrous gums, or periarticular nodules, are formed as a result of fibrous degeneration of syphilitic gums. Fibrous gummas are localized mainly in the area of ​​the extensor surface of large joints in the form of formations of a spherical shape, very dense consistency, ranging in size from 1 to 8 cm. They are painless, mobile, the skin above them is not changed or slightly pinkish.

Late neurosyphilis. It is a predominantly ectodermal process affecting the nervous parenchyma of the brain and spinal cord. It usually develops after 5 years or more from the moment of infection. In late forms of neurosyphilis, degenerative-dystrophic processes predominate. The actual late forms of neurosyphilis include: dorsal tabes - the process of destruction of the nervous tissue and its replacement with connective tissue, localized in the posterior roots, posterior columns and membranes of the spinal cord; progressive paralysis - degenerative-dystrophic changes in the cerebral cortex in the frontal lobes; taboparalysis - a combination of symptoms of dorsal tabes and progressive paralysis. In the tertiary period, lesions of the meninges and blood vessels can still be observed.

Late visceral syphilis. In the tertiary period of syphilis, limited gummas or diffuse gummous infiltrations can occur in any internal organ, and various dystrophic processes can also be observed. The morphological basis of lesions in late visceral syphilis is an infectious granuloma.

Damage to the musculoskeletal system. In the tertiary period, the musculoskeletal system may be involved in the process.

The main forms of bone damage in syphilis.

1. Hummous osteoperiostitis (lesion of spongy bone):

1) limited;

2) diffuse.

2. Hummous osteomyelitis (damage to spongy bone and bone marrow):

1) limited;

2) diffuse.

3. Non-gummous osteoperiostitis.

Most often, the tibia is affected, less often the bones of the forearm, collarbone, sternum, skull bones, and vertebrae. Damage to muscles in the form of gummous myositis and joints in the form of acute or chronic synovitis or osteoarthritis in the tertiary period are rare.

5. Latent syphilis

Latent syphilis is diagnosed on the basis of positive results of serological reactions in the absence of active manifestations of the disease on the skin and mucous membranes, signs of a specific lesion of the nervous system, internal organs, and the musculoskeletal system.

Latent syphilis is divided into early (with a disease duration of up to 1 year), late (more than 1 year) and unspecified, or unknown (it is not possible to determine the timing of infection). This time division is due to the degree of epidemiological danger of patients.

6. Congenital syphilis

Congenital syphilis occurs as a result of infection of the fetus during pregnancy through the transplacental route from a mother with syphilis. A pregnant woman with syphilis can transmit Treponema pallidum through the placenta, starting from the 10th week of pregnancy, but usually intrauterine infection of the fetus occurs in the 4-5th month of pregnancy.

Congenital syphilis is most often observed in children born to sick women who have not been treated or received inadequate treatment. The likelihood of congenital syphilis depends on the duration of the infection in a pregnant woman: the fresher and more active the syphilis in the mother, the more likely the unfavorable ending of pregnancy for the unborn child. The fate of a fetus infected with syphilis may be different. Pregnancy may end in stillbirth or live birth with disease manifestations occurring immediately after delivery or somewhat later. It is possible to give birth to children without clinical symptoms, but with positive serological reactions, who subsequently develop late manifestations of congenital syphilis. Mothers who have had syphilis for more than 2 years can give birth to a healthy baby.

Syphilis of the placenta

With syphilis, the placenta is hypertrophied, the ratio of its mass to the mass of the fetus is 1:4-1:3 (normally 1:6-1:5), the consistency is dense, the surface is lumpy, the tissue is fragile, flabby, easily torn, the color is motley. It is difficult to find treponema in placental tissue, so to detect the pathogen, material is taken from the umbilical cord, where treponema is always found in large quantities.

Fetal syphilis

The changes that have occurred in the placenta make it functionally defective, unable to ensure normal growth, nutrition and metabolism of the fetus, resulting in its intrauterine death in the 6-7th month of pregnancy. The dead fruit is expelled on the 3rd or 4th day, usually in a macerated state. A macerated fetus, compared to a normally developing fetus of the same age, is significantly smaller in size and weight. The skin of stillborns is bright red, folded, the epidermis is loosened and easily slides off in large layers.

Due to the massive penetration of pale treponema, all internal organs and the skeletal system of the fetus are affected. A huge number of treponema found in the liver, spleen, pancreas, adrenal glands.

Early congenital syphilis

If a fetus affected by a syphilitic infection does not die in utero, then the newborn may develop the next stage of congenital syphilis - early congenital syphilis. Its manifestations are detected either immediately after birth or during the first 3-4 months of life. In most cases, newborns with severe manifestations of early congenital syphilis are not viable and die in the first hours or days after birth due to functional inferiority of internal organs and general exhaustion.

Clinical signs of early congenital syphilis are detected on the part of the skin, mucous membranes, internal organs, musculoskeletal system, nervous system, and generally correspond to the period of acquired syphilis.

The appearance of a newborn with early congenital syphilis is almost pathognomonic. The child is poorly developed, has a small body weight, the skin due to the lack of subcutaneous tissue is flabby, folded. The face of the infant is wrinkled (senile), the skin is pale earthy or yellowish, especially on the cheeks. Due to hydrocephalus and due to premature ossification of the skull bones, the size of the head is sharply increased, the fontanel is tense, and the skin veins of the head are dilated. The child's behavior is restless, he often screams, develops poorly.

Lesions of the skin and mucous membranes can be represented by all varieties of secondary syphilides and special symptoms characteristic only of early congenital syphilis: syphilitic pemphigoid, diffuse skin infiltrations, syphilitic rhinitis.

Massive bone stratification on the anterior surface of the tibia as a result of repeatedly recurring osteoperiostitis ending in ossification leads to the formation of a falciform protrusion and the formation of false saber tibiae. Periostitis and osteoperiostitis of the skull bones can lead to various changes in its shape. The most typical are the buttock-shaped skull and the Olympian forehead.

In patients with early congenital syphilis, various forms of damage to the nervous system can be observed: hydrocephalus, specific meningitis, specific meningoencephalitis, cerebral meningovascular syphilis.

The most typical form of damage to the organ of vision is damage to the retina and choroid - specific chorioretinitis. With ophthalmoscopy, mainly along the periphery of the fundus, small light or yellowish spots are found, alternating with dotted pigment inclusions. The visual acuity of the child does not suffer.

Late congenital syphilis

This form occurs in patients who previously had signs of early congenital syphilis, or in children with a long asymptomatic course of congenital syphilis. Late congenital syphilis refers to symptoms that appear 2 years or more after birth. Most often they develop between 7 and 14 years, after 30 years they rarely occur.

The clinical picture of active late congenital syphilis is generally similar to acquired tertiary syphilis: tuberculous and gummous syphilis, lesions of the nervous system, internal organs, and the musculoskeletal system, as in tertiary syphilis, can be observed. But along with this, with late congenital syphilis, there are special clinical signs that are divided into reliable, probable and dystrophies.

Reliable signs of late congenital syphilis, resulting from the direct impact of treponema on the child's organs and tissues, include parenchymal keratitis, specific labyrinthitis, and Hutchinson's teeth.

Probable signs of late congenital syphilis include Robinson-Fournier radial perioral striae, true saber tibia, saddle nose, buttock-shaped skull, syphilitic gonitis. Probable signs are taken into account in combination with reliable or in combination with data from a serological examination, anamnesis.

Dystrophies (stigmas) arise as a result of the indirect effect of the infection on the organs and tissues of the child and are manifested by their abnormal development. They acquire diagnostic value only when the patient simultaneously reveals reliable signs of late congenital syphilis, positive serological reactions. The most characteristic dystrophies are the following: a sign of Avsitidia - a thickening of the thoracic end of the clavicle, more often the right one; axifoidia (Keira's symptom) - the absence of the xiphoid process of the sternum; Olympic forehead with very convex frontal tubercles; high (Gothic) hard palate; symptom of Dubois - Gissar, or infantile little finger, - shortening and curvature of the little finger inward due to hypoplasia of the fifth metacarpal bone; hypertrichosis of the forehead and temples.

7. Diagnosis of syphilis

The main diagnostic criteria:

1) clinical examination of the patient;

2) detection of pale treponema in the serous discharge of weeping syphilides of the skin and mucous membranes by examining the native drug crushed drop by dark-field microscopy;

3) results of serological reactions;

4) confrontation data (survey of sexual partners);

5) results of trial treatment. This diagnostic method is rarely used, only in late forms of syphilis, when other methods of confirming the diagnosis are not possible. With early forms of syphilis, trial treatment is unacceptable.

8. Principles of syphilis therapy

Early forms of syphilis are completely curable if the patient is given therapy that is adequate to the stage and clinical form of the disease. In the treatment of late forms of the disease, in most cases, clinical recovery or stabilization of the process is observed.

A specific treatment can only be given to a patient if the diagnosis of syphilis is clinically justified and confirmed in accordance with the criteria listed above. There are the following exceptions to this general rule:

1) preventive treatment, which is carried out in order to prevent the development of the disease to persons who have had sexual or close household contact with patients with early forms of syphilis, if no more than 2 months have passed since the contact;

2) prophylactic treatment prescribed for pregnant women who are ill or have had syphilis, but not taken off the register, in order to prevent congenital syphilis in a child, as well as children born to mothers who did not receive prophylactic treatment during pregnancy;

3) trial treatment. It can be prescribed for the purpose of additional diagnostics in case of suspected late specific damage to the internal organs, nervous system, sensory organs, musculoskeletal system in cases where it is not possible to confirm the diagnosis with laboratory tests, and the clinical picture does not allow to exclude the possibility of a syphilitic infection.

The drugs of choice for the treatment of syphilis are currently antibiotics of the penicillin group:

1) durant (extended) penicillin preparations - the group name of benzathine benzylpenicillin (retarpen, extensillin, bicillin-1), ensuring that the antibiotic stays in the body for up to 18-23 days;

2) drugs of medium duration (procaine-benzylpenicillin, novocaine salt of benzylpenicillin), which ensure the stay of the antibiotic in the body for up to 2 days;

3) preparations of water-soluble penicillin (benzylpenicillin sodium salt), ensuring that the antibiotic remains in the body for 3-6 hours;

4) combination preparations of penicillin (bicillin-3, bicillin-5), ensuring that the antibiotic remains in the body for 3-6 days.

The most effective preparations are water-soluble penicillin, the treatment of which is carried out in a hospital in the form of round-the-clock intramuscular injections or intravenous drip. The volume and duration of therapy depend on the duration of the syphilitic infection. Therapeutic concentration of penicillin in the blood is 0,03 IU / ml and above.

In case of intolerance to drugs of the penicillin group, treatment of patients with syphilis is carried out with reserve antibiotics that have a wide spectrum of action - semi-synthetic penicillins (ampicillin, oxacillin), doxycycline, tetracycline, ceftriaxone (rocephin), erythromycin.

Specific treatment for syphilis should be complete and vigorous. Medicines should be prescribed in strict accordance with the approved instructions for the treatment and prevention of syphilis - in sufficient single and course doses, observing the frequency of administration and the duration of the course.

At the end of treatment, all patients are subject to clinical and serological monitoring. During observation, patients undergo a thorough clinical examination and serological examination every 3-6 months.

LECTURE No. 11. Tuberculosis of the skin

Tuberculosis of the skin is a group of diseases that differ in clinical and morphological manifestations and outcome, caused by mycobacteria of human tuberculosis, less often of bovine type.

Etiology. Mycobacterium tuberculosis is a short, straight or slightly curved, acid-fast bacilli about 2,5 microns in length. Mycobacteria are characterized by polymorphism, do not form spores, and their virulence varies significantly.

Etiology and pathogenesis. Infection most often occurs aerogenously, but it is also possible through the gastrointestinal tract. It is extremely rare that Mycobacterium tuberculosis initially enters directly into the skin. At the site of introduction of mycobacteria, a primary affect is formed, then the lymph nodes are affected, and a primary tuberculosis complex is formed. In the future, dissemination of mycobacteria or, with a favorable outcome, local spread with subsequent encapsulation and petrification, leading to persistent healing, is possible.

Mycobacterium tuberculosis enters the skin more often secondarily (endogenously), rarely - primarily (exogenously).

Most forms of skin tuberculosis are the result of hematogenous spread (in pulmonary or extrapulmonary tuberculosis) from primary or secondary foci. Both dissemination of Mycobacterium tuberculosis throughout the body (including from skin to skin) and metastatic spread are possible.

The result of the dissemination of the pathogenic beginning is the so-called tuberculides (in which the intensity of immunity is very high and mycobacteria quickly die, having time to cause a reaction).

It is practically impossible to detect the causative agent of tuberculosis in the skin in such cases. Tuberculin tests are sharply positive. Lesions do not tend to grow peripherally and are relatively easy to treat.

With a metastatic entry of the pathogen into a specific area of ​​\uXNUMXb\uXNUMXbthe skin (tuberculous lupus, some cases of scrofuloderma), single lesions develop (focal, localized forms). An important feature of these variants of tuberculous skin lesions is the tendency to peripheral growth.

With exogenous contact of the pathogen with the skin, the following forms of skin tuberculosis may develop:

1) tuberculous chancre (primary tuberculosis of the skin). Currently almost never found. Observed in newborns who were not infected (i.e., immunity and infectious allergies were absent) and became infected during ritual circumcision or piercing of the earlobes;

2) verrucous (warty) tuberculosis. It develops as a result of the introduction of mycobacteria into the damaged skin of pathologists or butchers in the presence of formed infectious immunity and allergies (the primary focus is called the "tubercle of pathologists" or "cadaveric tubercle").

In patients with bacillary tuberculosis of various internal organs (lungs, kidneys, gastrointestinal tract), mycobacteria can get on the skin. In such cases, the following forms may develop:

1) verrucous (warty) tuberculosis. The most common cause of skin lesions is sputum on the back of the hands. Occurs in immunocompromised patients;

2) ulcerative tuberculosis (tuberculosis of the skin and mucous membranes). With cavernous tuberculosis or a primary focus in the lungs, mycobacteria with sputum enter the oral mucosa. In people with tuberculosis of the genitourinary organs, mycobacteria get on the genitals, and in patients with the gastrointestinal tract - on the skin of the perianal region. In these cases, the pathogen is easily detected on the surface of the ulcers (in smears and cultures).

Clinic. The following forms of skin tuberculosis are distinguished: tuberculous lupus, colliquative tuberculosis of the skin, warty tuberculosis of the skin, ulcerative tuberculosis of the skin and mucous membranes, papulo-necrotic tuberculosis, indurative tuberculosis, lichenoid tuberculosis. The first four diseases are focal (localized) forms, and the remaining three are disseminated.

Tuberculous lupus (lupus vulgaris, lupus tuberculosis of the skin). The most common form of localized skin tuberculosis.

The most commonly affected skin is the face, especially the wings and tip of the nose, cheeks, upper lip, auricles and neck. The skin of the extremities and trunk is affected much less frequently. Foci are single or few. The primary element is a tubercle (lupoma) of a brownish-yellow color. Similar lupomas are quickly formed around, located very close. After a few weeks or months, a plaque of various sizes with scalloped edges forms. A smooth white superficial scar gradually forms in the center, resembling crumpled tissue paper.

Tuberculous lupus is characterized by a symptom of the probe: when pressed with a blunt probe on the affected surface, a persistent retraction is formed.

Collicative tuberculosis, scrofuloderma - the result of hematogenous or lymphogenous spread. Allocate secondary and primary scrofuloderma. Secondary is the result of Mycobacterium tuberculosis entering the subcutaneous lymph nodes, and only then into the skin. The most common localization is in the region of the collarbones, sternum, and neck. Primary scrofuloderma occurs as a result of metastatic hematogenous entry of Mycobacterium tuberculosis directly into the subcutaneous tissue.

The primary element is a node in the subcutaneous tissue, the skin over which is not changed at first, and then acquires a red-yellow translucent color. Caseous necrosis is formed in the center. The knot softens and opens. Discharge is copious, crumbly-purulent. The resulting ulcer has soft undermined edges and is covered with yellowish-white caseous masses that adhere very tightly. Along the periphery, similar rashes appear, ulcers merge. The process ends with a characteristic scarring: bridge-like scars are formed.

Warty tuberculosis. May be the result of autoinoculation. The lesions are exclusively on the back of the hands. The primary element is the papule. Lesions of various sizes, with a clear boundary. Three zones are distinguished: in the central part there are warty growths up to 0,5-1 cm high, cracks, crusts, possible scarring, along the periphery there is a swollen purple shiny zone in the form of a border.

Ulcerative tuberculosis of the skin and mucous membranes. Manifestations are localized on the oral mucosa, genital organs, in the perianal region. Painful ulcers are formed with scalloped outlines, undermined edges and a bottom dotted with yellowish nodules. Ulcers are painful when eating, defecation, urination. Mycobacterium tuberculosis is easily detected in the discharge of ulcers.

Papulo-necrotic tuberculosis. Clinically very close to papulo-necrotic vasculitis, but flows for years. Exacerbates in cold weather. Papules the size of lentils are covered with crusts that fall off. Exodus - stamped scars. Typical localization - extensor surfaces of the limbs, buttocks, face.

Indurative tuberculosis, indurative erythema of Bazin. Vasculitis of deep vessels of tuberculous etiology. Usually happens in women. Nodules are formed with the capture of subcutaneous tissue and dermis. The skin above them is not changed at first, then it becomes reddish-bluish. Knots are dense, painless. Between them, you can feel the strands (endo- and periphlebitis). The most common localization is the lower third of the posterior surface of the legs. The nodes sometimes ulcerate, leaving a smooth retracted scar after resolution.

Lichenoid tuberculosis, lichen scrofula. It develops in children and adolescents with active tuberculosis of the internal organs. Small, often grouped, sometimes merging nodules are formed. Localization - chest, back.

Diagnostics. In addition to clinical manifestations and medical history, a histological examination of the affected skin, a bacterioscopic method, detection of foci of tuberculosis in internal organs, and serological tests (tuberculin tests) help establish a final diagnosis.

In some cases, it is possible to obtain a culture of the pathogen and positive results of infection of guinea pigs, which is an absolute confirmation of the diagnosis.

Treatment. Treatment of patients with skin tuberculosis begins in a specialized hospital after a thorough examination. After the diagnosis is established, combination treatment with anti-tuberculosis drugs (isoniazid with rifampicin, ftivazide with rifampicin) is prescribed. Duration of treatment is 9-12 months. Subsequently, two two-month courses of therapy are carried out annually for 5 years. An important component of complex therapy is nutritional therapy. Additionally, vitamins, iron supplements, hepato- and angioprotectors, and drugs that improve blood microcirculation are prescribed.

In senile patients with a variety of comorbidities, poor tolerance to anti-tuberculosis drugs, a good result can be achieved with long-term monotherapy with one of the derivatives of GINK - (for example, ftivazid) in medium doses. With a formed cosmetic defect, a corrective operation is indicated.

LECTURE No. 12. Leprosy

Leprosy (synonyms: leprosy, Hansen's disease) is a chronic disease that usually affects the skin, mucous membranes of the upper respiratory tract and the peripheral nervous system. Currently, leprosy is most common in Africa, Asia and South America. In Russia, there are sporadic cases of the disease.

Etiology. The causative agent is an acid-fast, rod-shaped bacterium belonging to the Mycobacterium family. The microorganism is stable in the external environment. It is still not possible to cultivate the pathogen in an artificial medium. Mycobacterium leprosy multiplies intensively only during laboratory infection in the tissues of an armadillo. The causative agent of leprosy is intracellular parasites of macrophages. A long incubation period is associated with a low growth rate of microorganisms.

Pathogenesis. Leprosy is a mildly contagious, low-pathogenic disease. Subclinical infection is common. No more than a third of people are susceptible to leprosy. Relatives of patients become ill more often, which confirms a genetic predisposition to the disease.

The main route of transmission is considered to be airborne. The entrance gate is the mucous membrane of the upper respiratory tract. Transepithelial penetration of pathogens is also possible. Accidental infection can occur through a tattoo, smallpox vaccination, or surgery. Men get sick 2-3 times more often than women.

The resistance of the infected organism and the virulence of the pathogen determine the form of the disease. The hormonal background matters: the first manifestation may be shortly after puberty, during pregnancy or after childbirth. During these periods, new lesions may appear and old lesions become more active.

Immunity in leprosy is cellular in nature, it is minimal in lepromatous and dimorphic leprosy and maximal in patients with tuberculoid leprosy.

In cases where the shortest "slow incubation period" between inoculation and the appearance of an open lesion can be established, it is 2-3 years. It is assumed that minor infection stimulates cellular immunity, resulting in the development of the tuberculoid variant of the disease. Massive invasion puts pressure on the immune potential, resulting in the development of the lepromatous type.

Clinic. There are several clinical forms of the disease. These are lepromatous leprosy, tuberculoid leprosy, borderline or dimorphic leprosy and undifferentiated leprosy.

Lepromatous type. The most severe form. It is characterized by polymorphism of clinical manifestations, especially in the skin. In addition to the skin, the nasal mucosa, oral cavity, nasopharynx, larynx, sometimes trachea, lymph nodes, peripheral nerve trunks, organs of vision, hearing, urogenital, and sometimes internal organs are affected.

The first manifestations of the disease are usually rounded or irregularly shaped erythematous spots with a shiny surface, which may be rusty in color. The most characteristic localization is the face, extensor surfaces of the hands, forearms, and legs.

Symmetry of rashes is characteristic. In the future, infiltration appears, plaques with normal sensitivity or hyperesthesia are formed. Due to the increased function of the sebaceous glands, the surface of the plaques is oily and shiny. Sweating is reduced (later it disappears completely).

After 3-5 years, eyebrows and vellus hair on the plaques fall out. Possible loss of mustache and beard. With diffuse infiltration of the facial skin, natural wrinkles and folds deepen, the brow ridges protrude sharply, the nose is thickened, the cheeks and lips have a lobed appearance. Usually the scalp, elbow and popliteal fossae, and armpits are not affected.

In the area of ​​infiltrates, single or multiple tubercles and nodes (lepromas) are formed, sharply demarcated, painless. They can be dermal and hypodermal (at first they are detected only on palpation), their consistency is densely elastic. In the future, nodes and tubercles sluggishly, without pronounced inflammatory phenomena, ulcerate. Similar rashes can appear on intact skin.

On the mucous membranes, as well as on the skin, the process can begin with the development of individual lepromas or diffuse lepromatous infiltration. All this leads to the formation of scars and deformities.

Often the spleen is enlarged, there may be damage to the liver, kidneys, lungs, orchiepididymitis often manifests in men, damage to the prostate gland, spermatic cords is possible. Characterized by lymphadenitis, periostitis (especially of the tibia, ulna, ribs), leading to fractures, fractures, deformities of the joints, shortening and deformation of the phalanges.

The course of the disease is chronic, with exacerbations that are provoked by hormonal changes, surgical interventions, errors in therapy. During exacerbations, there is a rise in body temperature, an increase and soreness of the lymph nodes, brightness, disintegration of infiltrates, new rashes.

The nervous system is affected relatively late - in the form of symmetrical polyneuritis. Gradually, infiltration of the entire nerve trunk occurs, as it develops, sensitivity is lost until complete anesthesia. In the later stages, there may be trophic and motor disorders.

Tuberculoid form. The skin, peripheral nervous system, and rarely the internal organs are affected. The causative agent is detected by histological examination of organs, in skin scrapings. The causative agent is absent in the nasal mucosa.

This form is characterized by a rash of small reddish-cyanotic flat polygonal papules. Often, merging, they form figures (discs, rings, half rings). A peripheral ridge is characteristic (the outer edge is, as it were, raised, clearly defined, more saturated in color, and the inner edge is "blurred", indistinctly passes into the central pale part of the lesion). There may be plaques, tubercles resembling a lupoma. Peeling, erythematous and depigmented rashes are possible. Reduced sensitivity in the elements of the rash and often around them. At first, mild hyperesthesia develops, then thermal, pain and tactile sensitivity sequentially disappear. Sweating decreases, then stops. Hair becomes dull and may fall out. Localization is asymmetric, in any area.

Border leprosy. Immune reactivity in this form of the disease varies widely and changes under the influence of stress, infections, exhaustion. All this is reflected in the clinical manifestations of target tissues.

Undifferentiated leprosy is an unstable clinical form in which the skin is affected, the spots (hypo- and hyperpigmented) are not sensitive to pain and temperature. The main feature is multiple nerve lesions. After a few years, this form becomes either tuberculoid or lepromatous.

Diagnostics. The main signs are clinical changes in the skin. Caution should also be with a decrease and disappearance of sensitivity in certain areas of the skin, parasthesias, mild contractures of the 5th, 4th and 3rd fingers, beginning muscle atrophy, pasty hands and feet, persistent lesions of the nasal mucosa.

Confirmatory methods are bacterioscopic and histological. For bacterioscopic examination in the lepromatous type, scrapings are taken from the nasal mucosa. Additionally, functional tests are carried out with histamine for sweating (weakly expressed), nicotinic acid (inflammation), mustard plaster (no reaction) and detection of sensitivity dissociation in the lesion.

The lepromine test (intradermal injection of a suspension of leprosy mycobacteria obtained by homogenizing leprosy) is not diagnostic. It is carried out to assess the immune response and differential diagnosis of various types of leprosy: the test is positive in the tuberculoid variant and negative in the lepromatous variant (with dimorphic leprosy, both positive and negative results are possible).

Treatment. Depending on the type of disease, treatment is carried out in a leper colony or at the place of residence (for minor skin manifestations of abacillary leprosy). Combination treatment, a course with the use of anti-leprosy drugs (diaphenylsulfone, solusulfone, diucifone and other sulfone derivatives): courses of 6 months with breaks of 1 month.

For multibacterial leprosy, start with rifampicin or clofazimine and then move on to sulfones. In addition, solusulfone, benemycin, ethionamide, lampren can be used.

The effectiveness of treatment is assessed based on the results of bacterioscopic control and histological examination. The average duration of therapy is 3-3,5 years.

Prevention. General prevention consists of improving the standard of living of the population, early detection, isolation and treatment of patients. Contact persons are examined and observed for at least 7 years. Preventive chemotherapy with sulfones is carried out. Men who have been in contact with leprosy patients are not subject to conscription into the army.

LECTURE No. 13. Eczema

Eczema is understood as a chronic persistently relapsing skin disease, manifested by a characteristic eczematous inflammatory reaction of the skin (in the form of grouped small vesicles) caused by various exogenous and endogenous factors that lead to the development of polyvalent skin sensitivity in patients.

In true eczema, skin allergy tests fail to identify the specific allergen that directly caused the inflammatory response. Eczematous lesions appear at the sites of application of several standard allergens.

Etiology and pathogenesis. Eczema is a disease of the whole body with characteristic manifestations on the skin. The same clinical forms of eczema (nummular, dyshidrotic eczema, eczematide) may have different etiologies and pathogenesis, on the basis of which the classification of eczema has been developed.

1. Predominantly exogenous eczema:

1) eczema of the hands and feet;

2) dyshidrotic;

3) professional.

2. Predominantly endogenous eczema:

1) eczema of the hands and feet;

2) dyshidrotic;

3) nummular (plaque);

4) eczematid (abortive plaque).

3. Microbial eczema:

1) nummular (plaque);

2) eczematid (abortive plaque);

3) paratraumatic;

4) varicose;

5) mycotic;

6) intertriginous.

Predominantly exogenous eczema can be of allergic and non-allergic origin. In allergic genesis, an allergic reaction is a manifestation of delayed-type hypersensitivity in response to repeated exposure to allergens with suppression of cellular and humoral immunity. Often, exogenous eczema develops as a result of allergic contact dermatitis with its frequent relapses and the formation of polyvalent sensitization and autosensitization in the patient. With reduced skin tolerance to irritants, a non-allergic inflammatory eczematous reaction occurs in places of constantly repeated exposure to subtoxic agents (alkalis, detergents, organic solvents, some mineral oils, as well as water, humid and cold air, mechanical irritation).

In endogenous (atopic) eczema, constitutional (endogenous) influences prevail, which are genetically predetermined and regulate the functions of the immune, hormonal, neurovegetative systems, as well as the structural and functional properties of the skin. There are violations of cellular and humoral immunity.

In an extensive third group - microbial eczema - its various clinical forms are combined. In this group, the occurrence of an eczematous reaction is equally influenced by both an exogenous factor (microbial flora) and an endogenous factor - an acquired temporary local disorder in the regulation of skin functions. Long-acting chronic dystrophic disorders in the skin or subtoxic effects as a result of cumulation lead to local disturbances in its function and structure.

Clinic. Eczema can begin acutely or chronically and then usually lasts a long time with a tendency to relapse. Any area of ​​the skin can be affected, but more often eczema occurs in open areas accessible to various environmental influences (on the hands, face, feet, legs). Regardless of the location, the morphological manifestations of the disease remain the same. The only exception is eczema of the palms and soles, where due to the thickness of the stratum corneum of the epidermis, eczema manifests itself not as microvesicles, but as large multi-chamber blisters.

In the acute phase, eczema is manifested by a rash on hyperemic and slightly swollen skin of small, closely grouped papules that quickly transform into tiny vesicles (the so-called microvesicles), which are located in groups and do not merge with each other. Quickly opening, the bubbles form small point erosions that separate the serous exudate. As the process subsides, small-drop wetting decreases, some of the vesicles, without opening, dry up with the formation of serous crusts, a small, bran-like peeling appears (subacute phase).

Since eczema develops in jerks, all of the listed primary elements of the rash (erythema, ephemeral micropapules, microvesicles) and secondary ones (erosion with small droplets of weeping, serous crusts, pityriasis scales) are usually present in the lesion at the same time. All this determines the polymorphism of rashes characteristic of eczema: true and false (evolutionary).

As the process progresses, the lesions, which have different sizes and usually blurred outlines, increase due to peripheral growth. Rashes appear in symmetrical areas and in the distance. Morphologically, secondary rashes are most often represented by erythematosquamous or papulovesicular elements, although macular, small-papular and bullous rashes are also possible. These rashes usually regress without a trace 2-3 weeks after the acute manifestations in the main focus have subsided. In some cases, eczema can reach significant spread. Subjectively, patients in the acute stage of eczema are bothered by a burning sensation and itching of the skin, and when acute inflammatory phenomena subside, they are bothered by painful itching.

The predominance of small yellowish crusts and bran-like scales in clinical manifestations characterizes the regression of the disease. In the future, complete resolution of rashes or transition to the chronic stage of the disease is possible. In this case, infiltration, peeling and thickening of the affected area of ​​the skin increase, the skin pattern (lichenification) intensifies. The color of the skin takes on a stagnant color with a brownish tinge. With an exacerbation in the focus, small vesicles, punctate erosions and crusts appear again against the background of active hyperemia.

The course of eczema is characterized by duration, a tendency to chronicity and frequent relapses. Exacerbation can not always be associated with the irritating effect of contact allergens. The influence of neuroreflex, immune and endocrine disorders is more clearly revealed. The course of eczema is influenced by psycho-emotional overload, immune and endocrine dysfunctions, foci of chronic infection and some other concomitant diseases. The emerging state of increased skin sensitivity to exogenous stimuli, manifested by polyvalent sensitization, does not remain constant all the time. It gradually changes depending on the severity of compensatory and adaptive mechanisms. This leads to the undulating course of the disease characteristic of eczema.

Hand eczema occurs in patients with a history of atopic dermatitis.

The dyshidrotic form of eczema is formed on the palms and soles more often in individuals with a pronounced imbalance of the autonomic nervous system (with increased sweating, persistent red dermographism, vascular lability) and with atopy. Exacerbations are more often observed in the winter season, although some relapses occur in hot weather.

Dyshidrotic eczema may occur initially, but patients often have a history of allergic dermatitis. The skin of the palms and soles is affected, however, in some cases, a gradual transition of rashes to the lateral surfaces of the fingers and the back surface of the hands and feet is possible. The clinical feature of this form of eczema is large, pea-sized, dense multi-chamber blisters, which is due to the thick stratum corneum. Therefore, there is no hyperemia and swelling. Bubbles persist for a long time without opening. The lesion gradually spreads to the interdigital spaces and the rear of the hands and feet. In this localization hyperemia and puffiness are already expressed, there are small superficial rapidly opening vesicles and erosions with a characteristic small droplet weeping.

If a pyogenic infection joins, the contents of the cavity elements become purulent, regional lymphangitis and lymphadenitis occur, body temperature rises, and the general condition of the patient worsens. After epithelialization of erosions on the palms and soles, relapses of dyshidrotic eczema are manifested by the formation of already small bubbles under a thin stratum corneum.

Occupational eczema results from skin contact with chemicals in a work environment. It usually develops after relapses of occupational allergic dermatitis, clinically no different from eczema of another origin.

Nummular, or plaque, eczema occurs on the skin of the extremities, less often the trunk, where round, sharply limited from the surrounding skin, slightly raised erythematous plaques with a diameter of 1,5-3 cm or more are formed, consisting of closely grouped small papules, microvesicles and small erosions located on hyperemic skin. The edges of the plaques are finely scalloped with a narrow whitish border of the exfoliated stratum corneum (the result of the evolution of small bubbles formed along the edge). Within the plaques there is abundant fine-droplet weeping. As the severity of inflammation decreases, the exudate dries out to form serous crusts. The prevalence of rashes varies; a long, chronically relapsing course is typical.

Eczematid is an abortive form of plaque eczema, it is characterized by the formation of round, oval and irregularly shaped pink spots of various sizes on the skin. Their surface is completely covered with bran-like and small-lamellar scales. Separate dotted serous crusts are found among the scales. When scraping the surface of the focus, small erosions are revealed, indicating hidden microvesiculation. The rash is usually accompanied by itching. The course is long. In unfavorable cases, the transformation of eczematid foci into typical nummular eczema is possible.

In some cases, microbial eczema develops as a result of eczematization of chronic microbial or fungal skin lesions: streptococcal diaper rash, chronic diffuse streptoderma, infected wounds, fistulas, dyshidrotic form of mycosis of the feet, superficial candidiasis of the folds. At the same time, in the area of ​​\uXNUMXb\uXNUMXbthe infectious lesion of the skin, rashes characteristic of eczema with small droplets of persistent weeping are formed. At the beginning, characteristic manifestations of a microbial (fungal) disease and eczema are simultaneously present in the lesion. In the future, eczematous phenomena increase, spread, while the symptoms of the initial bacterial (fungal) skin lesions gradually disappear.

Paratraumatic eczema develops around wounds, trophic ulcers, fistulas.

Varicose (or hypostatic) eczema develops on the shins in persons with varicose symptom complex. Dystrophically changed skin over varicose veins is more often affected.

Mycotic eczema usually develops against the background of long-term mycosis of the feet (dyshidrotic and intertriginous forms). In its development, the combined effect of several exogenous (sensitization by metabolic products of fungi and pyococci, local antifungal drugs) and endocrine factors (atopy, vascular and endocrine disorders) is essential. Eczematous rashes first appear in the areas of localization of mycosis, and then gradually spread.

Intertriginous eczema is eczema that occurs in large folds, perigenital and perianal areas. It develops as a result of eczematization of an intertriginous lesion due to the association of microbial and fungal microflora within the same focus.

Treatment. In each specific case, it is necessary to establish which exogenous and endogenous factors have a significant impact on the reactivity of the skin, on the compensatory and adaptive mechanisms of the body. In cases where predominantly exogenous factors dominate, it is important to eliminate as much as possible exposure to the skin of various contact allergens, as well as simple irritants (irritants).

If a patient has one of the forms of eczema, which is part of the group of a predominantly endogenous variant of the disease, in addition to the maximum protection of the skin from allergens and irritants, it is important to prescribe a treatment that is used for exacerbations of atopic dermatitis (antihistamines, sedatives, hypnotics, desensitizing agents). With microbial eczema, it is important to rationally influence the initial microbial (fungal) lesion, identify and normalize local disorders (microcirculatory, neurotrophic)

in the regulation of the protective function of the skin. With widespread persistent eczema, short-term administration of small doses of a glucocorticosteroid drug is possible. When localizing foci on the limbs, reflex physiotherapeutic procedures are prescribed for the corresponding paravertebral nodes.

External treatment is carried out taking into account the stage of eczema in the same way as patients with allergic dermatitis. The choice of forms and means of external therapy depends on the severity and characteristics of the inflammatory reaction of the skin. It should be borne in mind that with eczema, intolerance to both conventional pharmacological agents (including topical steroids) and indifferent medicinal bases often develops. In case of secondary infection and microbial eczema, the development of which was preceded by a pyococcal (mycotic) process in the skin, antimicrobial (antimycotic) agents should be used. In uncomplicated cases of eczema, short-term use of modern corticosteroid drugs with the highest safety index is justified. In some cases, combined preparations containing a topical corticosteroid and an antibiotic or antiseptic may be used.

LECTURE No. 14. Tumors of the skin

Skin tumors are non-inflammatory neoplasms that consist of structural elements of the skin that do not tend to regress. All tumors are divided into epithelial, neuroectodermal and mesenchymal. Distinguish tumors benign, malignant and intermediate forms - potentially malignant (precancrosis of the skin). In the group of precancroses, obligate (pigmented xeroderma and Dubrey's melanosis) and facultative (chronic dermatitis caused by the action of carcinogens, radiation skin lesions, senile keratoma, skin horn, keratoacanthoma, leukoplakia, kraurosis, chronic cheilitis, pigmented nevi) are distinguished.

1. Epithelial tumors

Nevus warty

Limited lesions with a brownish-brown verrucous surface. May be multiple, there is no favorite localization; sometimes arranged linearly.

Keratosis seborrheic

Appears at the age of 30-40 years. Brownish-brown or almost black formations with a papillomatous surface, sharply limited, covered with fatty scales. Rise above the level of healthy skin.

Localization: closed areas of the skin, less often - the face, scalp.

Keratoma senile

Facultative precancrosis that occurs in the elderly and old people.

Dense dry nodules of brownish or gray color, covered with scales, when removed, a warty surface is exposed. Prone to peripheral growth with the formation of large plaques.

Localization: open areas of the skin (face, back surface of the hands).

Cutaneous horn

Precancrosis. In elderly people, in open areas (lips, nose, cheeks, auricles), horny brownish cones are localized on a wide base. The appearance of a peripheral inflammatory zone is one of the signs of malignancy.

Keratoacanthoma (sebaceous mollusk)

It is more common in people over 40 years of age. There is a connection with insolation. Solitary hemispherical nodules or nodules of pinkish color of unchanged skin, in the center of which there is a depression filled with horny masses.

Localization: exposed areas of the skin (face, hands). Spontaneous regression is possible.

Leukoplakia

Precancrosis of the mucous membranes of the oral cavity, less often - of the genitourinary organs. Development is promoted by traumatization (dentures, smoking, insolation). There are the following forms: leukoplakia of smokers (nicotinic stomatitis), flat, warty and erosive-ulcerative.

The onset is preceded by a limited inflammatory response. In the future, the focus becomes dense, elevated, acquires a whitish color. The smooth surface gradually becomes verrucous with cracks and erosions.

Epithelioma calcific Malherba

A benign tumor that develops in the epidermal cyst as a result of an embryonic anomaly in the development of the epidermis. Deep single nodule of unaltered skin color, slowly growing. As a result of the deposition of calcium salts, it acquires a dense texture and can turn into a skin osteoma.

Predominant localization: head, limbs.

Basalioma

Nevoid formation with local destructive changes in the skin, prone to relapses. Solitary, rarely multiple tumor, clinically occurring in several variants.

Nodular ulcer - the most common. Nodules with a waxy tint and telangiectasia grow slowly. Gradually, the center ulcerates and becomes covered with a dense crust, which, when removed, causes bleeding. On the periphery there is an elevated roller, consisting of nodules ("pearls").

Pigmentary - characterized by a dark brown color of the focus.

Sclerosing - a raised, dense, scleroderma-like plaque that may ulcerate over time.

Superficial - multiple foci, superficial, eczema-like.

Localization: face, neck, less often - other areas. Mucous membranes are not affected.

Bowen's disease (Bowen's cancer)

Isolated single sharply limited reddish-brown plaque, raised above the skin surface. Covered with a crust, under which a granular (velvety) surface is found. Often the plaque has a warty or eczema-like character. Develops slowly, turns into spinocellular carcinoma.

Localization: torso, eyelids, genitals.

Keyr's disease (Erythroplasia of Keyr)

Intraepidermal spinocellular carcinoma. The focus is bright red with sharp borders and a granular surface. Develops slowly; metastases to the lymph nodes.

Localization: glans penis, preputial sac, vulva, oral mucosa.

Paget's cancer

An erythematous eroded lesion with sharp borders, a weeping surface, scales and crusts, resembling microbial eczema. Dense nodes are palpated in the underlying tissue; regional (axillary) lymph nodes are enlarged. The breast nipple is retracted. Mostly women are ill.

Localization: nipple area and surrounding skin.

Spinalioma (spinocellular cancer)

Development is often preceded by chronic cheilitis, leukoplakia (precancrosis). Men are predominantly ill. There are 2 clinical forms.

1. Tumor form - dense (cartilaginous consistency), rapidly growing nodes with a papillomatous surface and ridge-like edges.

2. Ulcerative form - rapid decay leads to the formation of superficial or deep ulcers with clear edges, a bumpy bottom, growing along the periphery. Metastasizes lymphogenously.

Localization: open areas of the skin (back of the nose, lips, eyelids, auricles, back of the hands).

Pseudocarcinomatous hyperplasia

Benign proliferation of the epithelium in chronic dermatoses of various etiologies. Clinically resembles spinalioma.

2. Tumors of the glands of the skin and hair follicle

Sweat gland tumors

Tumors emanating from eccrine (eccrine poroma, eccrine spiradenoma, syringoepithelioma) and apocrine glands (syringoma, syringoadenoma, papillary hydroadenoma, syringocystadenoma). They develop from the excretory ducts of the sweat glands. Most of them are single hemispherical formations of the color of unchanged skin or slightly erythematous, not prone to ulceration (except for syringoadenoma) and relapses after removal. The diagnosis is established on the basis of histological examination.

Syringoma is characterized by a multiplicity of small nodules up to millet grain size, which are cysts of the excretory ducts. Light translucent rashes are located on the face, chest, abdomen, thighs. Occurs in women during puberty.

Tumors of the sebaceous glands

Fordyce disease. On the red border and mucous membrane of the lips and oral cavity there are small yellowish hemispherical nodules.

Nodular hyperplasia of the sebaceous glands. Small yellowish nodules on the face (usually on the chin) that occur in older people.

Sebaceous gland adenoma. A solitary tumor the size of a hazelnut, hemispherical in shape, the color of unchanged skin. Most often located on the face.

Atheroma. Retention cyst of the sebaceous glands. Tumor-like formation prone to infection.

Hair follicle tumors

Hair nevus. It occurs predominantly on the face in the form of a small pigmented nodule with a large amount of hair.

Trichoepithelioma. During puberty, single or multiple yellowish papules appear on the face (less often the limbs). May be combined with nevus pilaris.

Cylinder. Multiple, less often solitary tumors the size of a pigeon egg, dense consistency with a smooth surface. Grouping, the nodes form conglomerates that cover the head in the form of a tuberous cap (“turban tumors”). Localization: scalp, less often - face.

3. Neuroectodermal tumors

Pigmented nevi

Skin changes of a patchy or papular nature, due to the accumulation of nevus or pigment cells in the epidermis and dermis. The clinical picture is varied. The following varieties are distinguished: borderline nevus (localized mainly on the palms, soles and in the ano-genital region); intraepidermal (the most frequent and varied clinical picture with a smooth or papillomatous surface); mixed.

Nevus blue

Nodules of a bluish-gray color with sharp borders, located more often on the face, limbs. Their surface is smooth and rounded.

The Mongolian spot is one of the varieties of the blue nevus. Bluish-brown spots without a clear outline, determined at birth and disappearing with age.

juvenile melanoma

A single limited nodule of a hemispherical or flat shape of pinkish-red or yellowish-brown color of various shades. On the periphery - erythematous corolla with telangiectasias. Hair growth is absent. It occurs more often in children. The flow is benign.

Localized on any part of the skin.

Melanosis precancerous Dubrey

Limited brown or black pigment spot with irregular outlines without compaction. Grows slowly. It is an obligate precancrosis of melanoblastoma. Occurs in older people.

Localization: face, chest, less often - other areas.

Melanoma (melanoblastoma)

The most malignant tumor that metastasizes by lympho- or hematogenous route. It develops most often on the basis of pigmented nevi after their traumatization or intense insolation. Signs of malignancy: accelerated growth of the pigment spot, discoloration (darkening or decrease in pigmentation), the phenomenon of reactive inflammation (erythema corolla), the appearance of child nodules, increased vulnerability and bleeding, itching. Formed melanoma can be superficial or nodular - a dark brown or black formation that rises above the skin with a mirror or rough surface. However, there are poorly pigmented melanomas. It grows rapidly and ulcerates early.

4. Tumors of mesenchymal tissue

Tumors of adipose tissue

Lipoma. Benign tumor. The node is the color of unchanged skin or a yellowish tint, soft, often lobular, painless. Often there are multiple tumors.

Fibrolipoma. Fibrous tissue develops, and therefore the tumor has a dense consistency.

Liposarcoma. Multiple nodes or diffuse infiltration in the subcutaneous tissue without clear outlines. The course is malignant. Metastases to visceral organs.

Dermatofibroma. Slightly raised dense nodules of brown color, dense consistency.

Fibroma. Nodes the color of unaltered skin. A hard fibroma is isolated - dense whitish nodules; soft - papillomatous soft formations on a thin stalk with a wrinkled surface.

Keloid. A benign neoplasm of connective tissue - fibroma. It develops as an independent process (primary keloid), as well as after thermal burns, wounds, operations and during the resolution of certain skin diseases (boils, acne). A dense, limited formation with a smooth surface, sometimes with bizarre outlines. The color is purplish-red, later whitish. Itching occurs in the initial phases.

Fibrosarcoma. The course is malignant. Metastasizes to lymph nodes and visceral organs. Dense yellowish-brown nodules with a smooth surface, located isolated or in groups.

Tumors of muscle tissue

Leiomyomas. Tumors arising from smooth muscle fibers. There are multiple leiomyomas of smooth muscles of the skin, solitary leiomyomas of the genitals and breast nipples, and solitary vascular ones. Dense nodes, painful on palpation, capable of contracting when irritated. The course is benign.

Leiomyosarcoma. Painless single large node with unclear contours. The course is malignant.

5. Tumors of the blood and lymph vessels

Skin angioma

Benign vascular formation of nevoid origin. There are such clinical forms as: flat angioma (vascular spots with telangiectasias); cavernous (a soft towering tumor of a purple-red color - a "blood sponge", is easily injured); stellate (reminiscent of the outlines of a spider); ruby dots (dark red small dotted nodules on the trunk, less often on the face); tuberous (purple-red tumor-like nodules on the face); verrucous (has hyperkeratotic growths on the surface).

Osler's disease

A congenital disease that is manifested by multiple telangiectasias of the skin, mucous membranes and internal organs, a tendency to bleeding.

Hemangioma pyogenic

Considered as one of the atypical forms of pyoderma. It is a capillary hemangioma. A rounded, hazelnut-sized formation of soft or dense consistency, whitish-gray or purple-red, sometimes has a stalk. Easily ulcerated and bleeds, covered with a dark brown crust. Localization: fingers, back surface of the hands, red border of the lips.

Glomus angioma of Bare - Masson

A benign tumor, located almost always on the tips of the fingers in the area of ​​​​the nail bed. It is characterized by sharp paroxysmal pain.

Mibelli's angiokeratoma

Multiple dark red vascular nodules up to a pea size with a warty surface and horny scales, when removed, bleeding occurs. More often young women are ill. Localization: the back surface of the hands and fingers, auricles. Fabry trunk angiokeratoma is a rare variant of angiokeratoma. Rashes are disseminated in the form of small horny nodules of dark red color, resembling beads. When injured, they bleed. Combined with hypertension, kidney and heart damage.

Lymphangioma

Tumor-like soft nodule or nodule with a smooth or bumpy surface of the color of unchanged skin, if damaged, a clear liquid is released.

Kaposi's angioreticulosis

Bluish-red spots that resemble nevoid formations transform into nodes and plaques ranging in size from a pea to a plum, rising above the level of healthy skin. Gradually they acquire a brownish-red hue. As a result of the merger, large foci are formed.

The surface of the lesions may be smooth or warty, covered with scales. Characterized by the presence of telangiectasias and hemorrhages. Ulcers that do not heal for a long time may form. Elephantiasis often develops. Multiple nodes are located symmetrically, mainly on the feet and legs, less often on the upper limbs and mucous membranes. Men are ill mainly at advanced age. The course is chronic progressive with involvement of visceral organs in the process.

Histopathology. In the dermis, the blood vessels are dilated and there are many new growths. Perivascular infiltration by lymphoid and plasma cells; hemosiderin deposition. Differentiate with fungal mycosis and lymphoreticular skin diseases.

Treatment. Penicillin injections of 20-30 million units per course, radiotherapy (up to 2000 rads per course), prospidin 75-100 mg per day (up to 2000-3000 mg per course); preparations of resokhin (delagil, chloroquine, hingamine), arsenic, vitamins B1 and D. It is also advisable to include corticosteroids in complex treatment. Surgical removal of nodes.

Nevi are not subject to treatment. In some cases, removal is performed for cosmetic reasons, with trauma and a tendency to rebirth. Benign tumors can be removed surgically, electrocoagulation or cryodestruction.

Treatment of keloids: chipping the focus with lidase, a suspension of hydrocortisone and other steroids; excision followed by radiation therapy; electrophoresis of potassium iodide, phonophoresis of collagenase or hydrocortisone; cryotherapy.

Treatment of basaliomas should be differentiated. In superficial forms, ointments with cytostatics are widely used (0,5% colhamic or methotrexate, 5% fluorouracil or fluorofur). Nodular-ulcerative variants undergo cryosurgical treatment; in some cases, radiation therapy and surgical removal are used.

Malignant neoplasms of the skin are subject to treatment in a specialized oncological institution.

The therapy is based on the principle of complexity (surgical removal, radiation therapy, polychemotherapy, general strengthening treatment).

LECTURE No. 15. Principles of external therapy

1. External therapy

External therapy is a very important (sometimes the only or main), but most often auxiliary method of treating dermatological diseases.

1. The doctor's knowledge of pathomorphological changes in skin lesions allows you to choose etiotropic or pathogenetically substantiated treatment.

2. A clear understanding of the pharmacological properties of the active substance and the basis of its action is a prerequisite for successful treatment.

3. The choice of dosage forms and drugs depends on the phase of the pathological process (acute or chronic stages, the stage of progression, stabilization or regression), the existing primary and secondary elements of skin lesions (spots, papules, tubercles, nodes, blisters, pustules, vesicles, erosions, ulcers or scars), i.e. from the clinical picture of the lesion.

4. The prescription of drugs should be dynamic (careful monitoring of the patient is necessary).

5. When prescribing, individual intolerance must be taken into account. Starting treatment, you should use lower concentrations of drugs, gradually increasing them.

6. A new drug and the same drug, but in a new form, should be applied only after the removal of the previous one.

7. External treatment should be carried out until complete clinical recovery.

8. When prescribing external agents simultaneously with general therapy, it is necessary to take into account the possibility of synergism or antagonism of their effects.

9. When starting external treatment, it is necessary to first clean the affected skin and remove secondary layers: scales, crusts, fragments of blisters. It is necessary to clean the skin carefully, using a staged, rather than forcible removal of scales, crusts, necrotic masses.

10. A doctor who does not specifically deal with dermatological problems should not dilute or mix forms in order to avoid obtaining a form with incompatible components.

2. Forms of external medicines

1. Solutions (lotions). The main component of this dosage form is water. Any soluble medicinal substances of various mechanisms of action are added depending on the purpose of therapy. Solutions can be alcoholic (with the addition of alcohol) or soapy (shampoo). Used as lotions, compresses, washes, cauterizations.

2. Chatterboxes - shaken solutions. The main component is water, but insoluble, powdery substances (talc, zinc oxide, starch) are also added. They dry out the skin very much, so oils (glycerin, vaseline or olive oil) are often added to them.

3. Powders - fine powders (talc, zinc starch, dermatol, xeroform).

4. Pastes - the composition includes solid nutrients in powder form in an amount of at least 50%, which are evenly mixed with the ointment base (in an amount of 10-50%). Pastes may contain one or more medicinal substances. Ointment base - petroleum jelly, anhydrous lanolin, naphthalan, spermaceti, lard, cocoa butter, vaseline, sunflower, peach, olive, apricot, castor oil, fish oil.

5. Ointment - they differ from pastes in having a lower solids content (from 1% to 40%) and a higher content of bases (80-90%).

6. Crema - emulsions, which consist of a solution of oil in water or water in oil. You can enter any medicinal substances into them, as well as fragrances (cosmetic creams). There are creams in which medicinal substances are introduced in the form of liposomes. Liposomes are microcapsules with bilayer lipid membrane walls. They are made from plant seeds (sunflower), from lecithin, egg white, filled with biologically active substances, vitamins and moisture. They penetrate well into the skin, even into the deep layers, are well absorbed, reacting with the components of membranes and cells.

7. Gels (jelly) - semi-solid colloidal solutions or suspensions.

8. Bandages - the basis includes (except for fat) wax or rosin, often resins, rubber. The consistency of the patch is very thick and sticky. Before use, the patch is heated. Attaches tightly to the skin and holds firmly.

9. Laki Liquids that dry quickly on the surface of the skin to form a thin film. They are used for deep and limited effects on tissues (nails, calluses, warts). They contain various medicinal substances.

10. Aerosols - dispersed systems with a gaseous medium (freon, mixture of gases, nitrogen). Depending on the particle size of the dispersed phase, aerosols are divided into highly dispersed (0,5-5 microns), medium dispersed (5-20 microns) and low dispersed (20-100 microns). They allow for even distribution of medicinal substances, prevent their crystallization and are more stable than other forms. They are less adsorbed and have the greatest surface effect.

11. Drug carriers through the skin - dimexide, collagenase, hyaluronidase. They are used with an integral stratum corneum of the epidermis along with other drugs for the purpose of their deep penetration.

Author: Sitkalieva E.V.

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