Pyodermitis

Pyodermatitis (Greek pyon - pus, derma - skin) is a pustular skin disease caused by pyogenic microorganisms, mainly staphylococci, streptococci, and less commonly other microorganisms.

Pyoderma is a pustular skin lesion, the main causative agent of which is staphylococci, less often streptococci. Pyocorticoccal processes caused by other microorganisms make up less than 1%. In addition to the virulence of streptococci and staphylococci, the different nature of their impact on the skin, which largely determines the clinical form of the disease, the general condition of the body is of great importance in the development of the process, primarily the insufficiency of humoral and cellular immunity and non-specific defense factors, a decrease in the bactericidal function of the skin, especially in chronic forms (furunculosis, chronic ulcerative and ulcerative-vegetative pyoderma), the presence of foci of chronic infection or carriage of pathogenic coccal flora on the mucous membranes, mainly the nasopharynx, as well as specific sensitization to pyococci. It was shown that in most cases the phage types of pathogenic staphylococci isolated from lesions, clinically unchanged skin of patients with chronic pyoderma and from focal infection foci coincide. Staphylococci isolated from the nasopharynx have the highest pathogenicity.

Pustular diseases of the skin and subcutaneous fat layer account for 10-15% of all diseases with temporary loss of ability to work and occupy first place in terms of frequency of visits to dermatological institutions: up to 30% in adults and up to 37% in children.

Pyoderma is a disease of the skin and subcutaneous fat layer that occurs as a result of the exogenous introduction of pyogenic cocci or pyococci (staphylococci and streptococci) into the skin.

Pyoderma occurs primarily or as a complication after other diseases.

Streptococci and staphylococci are often found in the human environment (in the air, indoor dust, and on human clothing and skin).

When the skin is damaged (abrasions, cracks, injuries), contaminated with flammable oils, dust, flammable liquids, or when skin is not properly cared for, its functions, including its protective function, are disrupted. The development of the disease is facilitated by a decrease in the body's immune defense, a violation of the composition of sweat and changes in the pH of the water-lipid mantle of the skin, the composition and amount of sebum, unbalanced nutrition, endocrine disorders (diabetes mellitus, etc.), hypovitaminosis, hypothermia, overfatigue, etc.

According to the etiological principle, staphyloderma, streptoderma and mixed - streptostaphyloderma are distinguished. The following variants of staphyloderma are distinguished: superficial - osteofolliculitis, folliculitis, sycosis, etc.; deep - furuncle, carbuncle, etc.

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Causes and pathogenesis of pyoderma

Most often, the causative agents of purulent skin diseases are pyogenic microbes staphylococci, streptococci, less often pneumococci, gonococci, Pseudomonas aeruginosa, etc., as well as the products of their vital activity - toxins (necrosoxime), enzymes (hyaluronan).

In adults, infection with autoflora of the skin surface, mucous membranes or from foci of chronic purulent infection (tonsillitis, otitis, sinusitis, periodontosis, etc.) is more common. Less common is exogenous infection with pathogenic or epidemic strains of staphylococci. This route of infection is observed mainly in children's groups and medical institutions.

Exogenous factors: skin contamination; impaired sweat and sebum secretion; maceration; microtraumatism (industrial, domestic, skin excoriation in itchy dermatoses); the action of chemicals that degrease and irritate the skin (organic solvents, lubricating oils, cooling emulsions, alkaline solutions, etc.); contaminated work clothes; trophic skin disorders as a result of impaired innervation and blood circulation.

Endogenous factors: primary and secondary deficiency of the immunocompetent system; physical and mental fatigue; insufficient or inadequate nutrition; neuroendocrine disorders; use of immunosuppressive drugs; severe debilitating diseases; chronic intoxication; hypovitaminosis; diabetes; digestive diseases; dysbacteriosis; anemia; foci of focal infection as a source of sensitization and autoinfection.

At the first stage of staphylococcal infection, cellular micro- and macrophage reactions predominate, as well as plasma coagulation, leading to thrombosis of the lymphatic and venous small vessels limiting the purulent focus.

At the second stage of infection, fibrinolytic enzyme and hyaluronidase come into play. Staphylococcal skin lesions typically involve the formation of deep and limited foci of purulent or purulent-necrotic inflammation with predominant localization in the hair follicle, sebaceous or sweat glands.

Streptococcal skin lesions are manifested by acute serous inflammation with the formation of subcorneal vesicles or blisters - the so-called phlyctenules, prone to rapid peripheral growth and fusion.

Classification and symptoms of pyoderma

There is no generally accepted classification of pyoderma. The most common and practical classification is based on the etiological principle. According to this classification, staphylococcal, streptococcal and mixed (strepto-staphylococcal) skin lesions are distinguished. In addition, each group is divided into superficial and deep pyoderma, which can be acute or chronic.

Superficial pustular skin lesions include those nosological forms in which the epidermis and upper layer of the dermis are affected. In deep pyoderma, the lesion can affect not only the dermis, but also the hypodermis.

Staphylococcal pyoderma, acute:

• superficial - ostiofolliculitis, superficial folliculitis, staphylococcal bullous impetigo (in children), staphylococcal pemphigoid of the newborn;
• deep - deep folliculitis, furuncle, acute furunculosis, carbuncle, hidradenitis, multiple abscesses of infants.

Staphylococcal pyoderma, chronic:

• superficial - sycosis vulgaris;
• deep - chronic furunculosis (localized and general), decalving folliculitis.

Acute streptococcal pyoderma:

• superficial - streptococcal impetigo, diaper rash;
• deep - streptococcal ecthyma, erysipelas.

Streptococcal pyoderma, chronic:

• deep - chronic diffuse streptoderma.

Strepto-staphylococcal pyoderma, acute:

• superficial - impetigo vulgaris;
• deep - vulgar ecthyma.

Streptococcal-staphylococcal pyoderma, deep, chronic (chronic atypical pyoderma):

• ulcerative chronic pyoderma and its variety - chancroid pyoderma;
• ulcerative vegetative pyoderma;
• abscessing chronic pyoderma and its variety - inverse conglobate acne.

• Staphyloderma acute, chronic.

Acute staphyloderma: ostiofolliculitis, folliculitis, furuncle, acute localized furunculosis, carbuncle, hidradenitis, epidemic (staphylococcal) pemphigus of newborns, multiple abscesses in infants.

Chronic staphyloderma: vulgar sycosis, chronic furunculosis.

• Acute streptoderma: impetigo - intertriginous, annular, bullous; acute diffuse streptoderma

Chronic diffuse streptoderma, vulgar ecthyma.

• Vulgar impetigo (staphyloderma and streptoderma).

Depending on the etiology, there are streptococcal, staphylococcal and mixed, mainly staphylostreptococcal skin lesions; according to the course, they are divided into acute and (less often) chronic; according to the depth of the lesion - into superficial (mainly streptococcal) and deep, mainly staphylococcal or mixed.

Skin rashes in pyoderma are polymorphic. The appearance of the primary elements of the rash depends on the type of pathogen and the depth of the skin lesion.

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Acute streptococcal skin lesions

Acute streptococcal skin lesions develop mainly in children and young women, are most often located on the face and hands, but can also be on the mucous membranes. Common diffuse forms are encountered. They appear as small flabby bubbles (phlycten) with transparent or cloudy contents, surrounded by a small halo of erythema (streptococcal impetigo). If a staphylococcal infection joins in, the contents quickly become purulent (impetigo vulgaris). Streptococcus, often in association with staphylococcus, causes intertriginous skin lesions, as well as a severe pyogenic process in children - epidemic pemphigus of the newborn, manifested as bullous impetigo, which can quickly occupy large areas of the skin, including folds. A clinical picture of Ritter's exfoliative dermatitis of the newborn is formed. This group of streptoderma also includes syphiloid posterosive, observed in young children, clinically characterized by erosive-papular elements that have arisen at the site of phlyctena, located on the genitals, buttocks and thighs, and ecthyma, which usually occurs in adults, which is a pustular-ulcerative skin lesion, single or, less commonly, multiple, with a predominant localization on the shins.

Streptococcal skin lesions, unlike staphyloderma, affect the sebaceous hair follicle and sweat glands. They are most characterized by a predominantly superficial inflammatory lesion of smooth skin with the release of serous exudate. The main primary rash element in superficial streptoderma is a superficial blister. In those localizations of the skin where the stratum corneum is relatively thin, the streptococcal blister looks flaccid, flabby, it is called phlyctena. In those areas of the skin where there is hyperkeratosis (palms, soles, periungual areas), streptococcal blisters can have a tense appearance, a fairly dense cover, serous or cloudy contents.

In deep streptococcal skin lesions, the primary rash element may be a deep epidermodermal pustule with limited necrosis of the underlying area of the dermis (ecthyma) or edematous erythema with clear, rapidly increasing boundaries (erysipelas).

Chronic streptoderma includes simple lichen of the face, angular cheilitis, paronychia, and superficial diffuse pyoderma.

Pathomorphology

In ordinary impetigo, a blister is found in the skin, located directly under the stratum corneum, containing fibrin, neutrophilic granulocytes and a small number of lymphocytes, among which there may be remnants of epidermal cells melted by proteolytic enzymes. In the late stages of the process, after the blister opens, the stratum corneum is absent, and a crust of fibrin and nuclear remnants of neutrophilic granulocytes forms in its place.

In the bullous form of impetigo, the blister, located in the upper parts of the epidermis, contains neutrophilic granulocytes and a large amount of serous exudate. Over time, the blister can occupy almost the entire thickness of the epidermis and become covered with a crust on top. In the dermis under the blister, there is significant infiltration of neutrophilic granulocytes with an admixture of lymphocytes.

Ecthyma is characterized by damage to the entire thickness of the epidermis and underlying areas of the dermis with the formation of an ulcer, the bottom and edges of which are densely infiltrated with lymphocytes with an admixture of a large number of neutrophilic granulocytes. The epidermis is thickened and edematous at the edges, the connective tissue in the ulcer area may be necrotic and densely infiltrated with neutrophilic granulocytes. The capillaries of the upper part of the dermis are dilated both at the periphery and in the center of the lesion, thrombosis is occasionally observed.

Skin lesions caused by staphylococci, unlike streptococcal pyoderma, are clearly localized in the openings of sweat glands and hair follicles.

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Acute staphyloderma

Staphylococcal skin lesions are usually associated with sebaceous hair follicles and sweat glands (apocrine and eccrine inflammatory reaction, which they cause, is purulent or purulent-necrotic. Different nosological forms of pustule skin lesions can manifest themselves in the same rash element, for example, ostiofolliculitis, superficial folliculitis and vulgar sycosis are manifested by a follicular pustule, and an inflammatory follicular nodule occurs with folliculitis (superficial and deep) decalving folliculitis, sometimes with a small furuncle. An inflammatory node is detected at the onset of a furuncle, carbuncle, multiple abscesses in infants (pseudofurunculosis). In some cases (mainly in children), a blister may form at the site of staphylococcus penetration into the skin. This is due to the destruction of the bonds between cells granular layer of the epidermis with staphylococcal toxin (zxfoliatin). The same primary rash element (blister) is observed in superficial streptococcal pyoderma.

Acute staphyloderma can be in the form of superficial small pustular rashes filled with purulent contents, in the center of which there is a hair (ostiofolliculitis, folliculitis), or deep pustules (furuncle, carbuncle).

Acute staphylococcal diseases of sweat glands are observed in children in the form of pseudofurunculosis (syn.: multiple abscesses of newborns), when pustules are formed around the excretory ducts of sweat glands, as well as sharply delimited abscessing deep lesions, located mainly on the body. Similar lesions can also be observed in adults, but in places where apocrine glands are localized (hidradenitis). In this case, the inflammatory process is located in the deep parts of the dermis and in the subcutaneous tissue in the form of a painful tumor-like infiltration focus, which, rapidly increasing, becomes fused with the skin, initially unchanged, then acquiring a bluish-red color with subsequent softening and separation of purulent-bloody contents.

Chronic forms of staphylolermia include staphylococcal sycosis, characterized by the development of folliculitis on the scalp, most often in the area of the moustache and beard, sometimes accompanied by scarring (lupoid sycosis), the so-called keloid acne of the neck of Erman, localized on the back of the neck on the border with the scalp, clinically manifested by the presence of relapsing acne-like folliculitis located on sclerotic, scallop-shaped thickened skin; abscessing and undermining folliculitis of the head of Hoffman, prone to abscessing, the formation of extensive lesions with fistulous tracts, sclerosis and hair loss.

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Pyoderma vegetans

Pyoderma vegetans (Si: ulcerative-vegetans pyoderma) is characterized by the presence of ulcerated lesions covered with flaccid granulations, vegetations, located on the hands, shins and in the area of skin folds; chancroid pyoderma usually manifests itself as a single ulcer of small size with a compaction at the base, which makes it similar to syphilitic chancre, especially since its most common localization is the genitals and oral cavity, often with an increase in regional lymph nodes.

Characteristic signs of pyoderma vegetans are pseudoepitheliomatous hyperplasia of the epidermis, as well as microabscesses in the dermis and inside the epidermis. Microabscesses contain a large number of neutrophilic granulocytes, including plasma cells, lymphocytes, and eosinophilic granulocytes. Infiltrate cells penetrate the epidermis and then onto its surface, forming crusts. Some dermal papillae are free of infiltrate, but epidermal outgrowths are elongated. The disease is differentiated from pemphigus vegetans, blastomycosis, warty tuberculosis, and bromoderma.

Histogenesis

In various forms of pyoderma, dysfunctions of neutrophilic granulocytes are revealed, characterized by a decrease in chemotaxis, phagocytic activity, imperfect phagocytosis, the formation of polymembrane phagosomes, as well as L-transformation of pathogens, defects in the T-immune system with some increase in the activity of B-lymphocytes.

Weakening of immune reactivity, increased pathogenicity of microorganism strains on the skin can be facilitated by hypothermia, frequent colds, poor nutrition with insufficient amounts of proteins, vitamins and excess carbohydrates, endogenous diseases, especially diabetes, etc. It is impossible not to take into account the adverse effects of irrational excessive antibiotic therapy, as a result of which the biological properties of pyogenic bacteria can change, including the formation of L-forms, as well as strains with increased resistance to antibiotics.

Gangrenous pyoderma

Clinically, it presents as necrotic and gangrenous changes in the skin with the formation of rapidly enlarging ulcerative lesions surrounded by a ridge-shaped bluish border in which pustules, palulovesicles or blisters are visible. The central focus of necrotic inflammation increases in the peripheral direction with the formation of a large ulcer.

In most patients, gangrenous pyoderma is combined with systemic diseases: ulcerative colitis, rheumatoid arthritis, Crohn's disease, hepatitis, monoclonal gammopathy, cancer, lymphoproliferative diseases.

Pathomorphology

Histological signs are non-specific. In the development of the morphological picture, one can trace the stages corresponding to the dynamics of the clinical picture from a pustule or papulovesicle to a deep ulcer. The initial histological signs are variable. Thus, before the ulcer appears, acanthosis, a dense superficial infiltrate, mainly of lymphocytes, monocytes, with an admixture of neutrophilic granulocytes are detected. Sometimes there are very many of them, resulting in the formation of abscesses. Later, necrobiotic changes with increased exocytosis are noted in the epidermis, and a sharp edema with the formation of blisters is observed in the dermis. In the vessels, in the center of focus, fibrinoid necrosis of the walls, their infiltration with neutrophilic granulocytes are expressed.

In the ulcer area there is necrosis of its edges with hyperplasia of the epidermis, the bottom is covered with necrotic masses and inflammatory elements, mainly neutrophilic granulocytes. In the dermis, in addition to perivascular lymphocytic infiltrates, there are abscesses of neutrophilic granulocytes. In the deeper parts of the dermis there are perivascular lymphohistiocytic infiltrates with an admixture of plasma cells, less often giant cells of foreign bodies, phenomena of fibrinoid necrosis of vessels and their infiltration with neutrophilic granulocytes, which is assessed by some authors as vasculitis. With reparative changes in the ulcer area there is proliferation of vessels and phenomena of fibroplastic transformation. Infiltrates are mainly lymphohistiocytic with an admixture of plasma cells, fibroblasts, among which there may be cells of foreign bodies.

Gangrenous pyoderma is differentiated from vegetative pyoderma, which is more characterized by the presence of eosinophilic microabscesses in the dermis.

Histogenesis

The development of gangrenous pyoderma is based on immune disorders causing immune complex vasculitis. This is proven by the deposition of IgM and C3 complement component in the vessels and papillary layer of the dermis, as well as along the dermo-epidermal zone. Humoral and cellular immunity disorders have also been detected. When gangrenous pyoderma is combined with hypergammaglobulinemia, an increase in the IgA level is noted, especially in combination with monoclonal gammopathy. A disorder of the function of neutrophilic granulocytes is noted in the form of a defect in chemotaxis or phagocytosis.

Other forms of pyoderma

Ostiofolliculitis is an acute inflammation of the hair follicle, which is a pustule, pierced by a hair in the center and surrounded by a narrow border of erythema.

Folliculitis is a purulent inflammation of the hair follicle, characterized by the presence of a painful inflammatory infiltrate at the base of the pustule. Deep folliculitis can leave a small scar.

Folliculitis decalvans is a rare form of staphylococcal lesion 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 fully understood. Staphylococcus aureus is considered to be the causative agent; 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, diabetes mellitus, etc. The microbial factor is apparently only one of the pathogenetic links in the development of this chronic process.

Furuncle is an acute purulent-necrotic inflammation of the hair follicle and perifollicular connective tissue. Furuncle is a deep form of staphyloderma. The primary rash element of a furuncle is an inflammatory node that forms around a 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), but the process quickly captures the entire depth of the hair follicle, the surrounding connective tissue and the adjacent sebaceous gland and is an inflammatory congestive-hyperemic node, cone-shaped, rising above the surface of the skin. Pain increases, twitching, pulsating pains are possible. When the furuncle is localized in the face area, especially on the upper lip, extensive edema is noted around the infiltrate. On the 3rd-4th day, a fluctuation begins to be determined in the center of the infiltrate, a purulent fistula is formed around the hair, when opened, a small amount of thick pus is released, a small ulcer is formed. At the bottom of this ulcer, a greenish necrotic core is revealed. After another 2-3 days, the necrotic core is rejected with a small amount of blood and pus, after which the pain and inflammation are significantly reduced. At the site of the rejected necrotic core, a deep crater-shaped ulcer is formed, which, after cleansing from pus and remnants of necrotic masses, is performed by granulation, a retracted scar is gradually formed, the size and depth of which depends on the size of the necrosis in the center of the furuncle. A furuncle can occur in any area of the skin where there are hair follicles. Single furuncles are usually localized on the forearms, face, back of the neck, lower back, buttocks, thighs. Usually, single furuncles are not accompanied by a deterioration in general health and an increase in body temperature. An exception is a furuncle of the face. Particular attention should be paid to patients who have a furuncle in the lip area, on the nose, in the nasolabial triangle and in the area of the external auditory canal. Facial movements, trauma to furuncles during shaving or an attempt to squeeze them out can lead to serious complications: thrombophlebitis of the veins of the face. It should be noted that the anatomical features of venous outflow on the face, the presence of anastomoses with the cavernous sinus of the brain, can lead to even 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.

Carbuncle is a purulent-necrotic inflammation of several hair follicles and surrounding tissue, accompanied by general intoxication and ending in scarring after 2-3 weeks.

Hidradenitis is a purulent inflammation of the apocrine sweat glands located in the armpits, around the nipples, behind the ears and in the perineum. Unlike a furuncle, it does not have a pustule or purulent-necrotic core, and begins with a deep infiltrate in the sweat glands, capturing the subcutaneous fat layer.

Acne vulgaris is a purulent inflammation of the sebaceous glands that opens into the hair follicle, predominantly localized on the face, chest, and back.

Staphylococcal pemphigus of newborns manifests itself on the 3rd-7th day after birth in the form of blisters with their subsequent opening and the formation of extensive erosions on the body, skin folds. The disease is accompanied by general intoxication and can lead to septic complications.

Staphtococcosis is a chronic skin disease, localized in the area of growth of the moustache, beard, eyelashes, eyebrows, in the nasal passages, on the pubis. Characterized by recurrent occurrence of folliculitis with powerful perifollicular and inflammatory infiltration and hyperemia with a bluish tint. Preservation of stripes is observed, there are no scars on the skin.

Acute streptoderma is characterized by the presence of phlyctenas, which are flaccid bubbles surrounded by a narrow rim of hyperemia and prone to peripheral growth. In areas of thin skin, the phlyctenas are small, quickly open up with the formation of merging erosions with a smooth bottom and abundant serous discharge. In open areas, the exudate dries into honey-yellow crusts.

When localized on skin with a thick horny layer (hands, feet), phlyctenae reach large sizes, are filled with serous-purulent or serous-hemorrhagic contents, are accompanied by a significant inflammatory reaction and edema, and are often complicated by lymphangitis, lymphadenitis, increased body temperature, and changes in the hemogram. When opened, they give extensive diffuse lesions with rapid peripheral growth (acute diffuse streptoderma).

Chronic diffuse pyoderma is predominantly localized on the shins, less often on the upper limbs and in skin folds, and is characterized by a long, sluggish course, clear polycyclic outlines of lesions with a border of exfoliating stratum corneum.

Typical diffuse infiltration of a stagnant red color with the presence of superficial erosions, serous crusts and lamellar scales. Chronic diffuse pyoderma is often complicated by allergic rashes and eczematization of the main lesion.

Vulgar ecthyma occurs in weaker patients, is localized mainly on the shins in the form of deep dermal pustules with slight infiltration along the periphery, and resolves with the formation of ulcers and scars.

Impetigo streptogenes is a common and superficial form of streptoderma. It mainly affects children and young women. Skin lesions usually affect exposed areas, the face (around the nose and mouth), parotid areas, and limbs. The disease becomes more frequent in the warm season. In conditions of close physical contact, streptococcal infection is easily transmitted from a sick person to a healthy person. Epidemic outbreaks are possible in children's groups.

In the pathogenesis of streptococcal impetigo, micro- and macrotraumatism of the skin and maceration are of great importance. A small halo of hyperemia is noticeable around the phlyctena and crusts. Phlyctena and crusts quickly increase in size and can merge. Serous exudate of opening phlyctena infects the surrounding skin, and the process quickly spreads. Under favorable conditions, erosions epithelialize, crusts fall off, and a small hyperemia remains in their place, then light pigmentation. No persistent traces are observed. 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.

Impetigo vulgaris, or contagiosa, is caused by pathogenic streptococci, which cause the primary rash element - subcorneal phlyctena. However, staphylococcal flora joins very quickly, leading to pronounced suppuration and the formation of purulent cystic elements that dry up into honey-yellow or greenish crusts. Like streptococcal impetigo, vulgar impetigo is most often found in children on exposed areas of the body. With close physical contact, especially in children's groups, mass outbreaks of vulgar impetigo are possible. In adults, this process is more often found on the face as a result of trauma (poor shaving), maceration (chronic rhinitis with rhinorrhea).

Differential diagnostics of pyoderma

Acute forms of staphyloderma (folliculitis, furuncle) should be differentiated from occupational folliculitis (associated with industrial irritants).

Hidradenitis differs from tuberculous scrofuloderma, which is characterized by minor pain, subacute course, release of a small amount of pus, predominant localization in the submandibular, supraclavicular and subclavian region.

Vulgar sycosis must be differentiated from parasitic sycosis, which is a fungal disease (causative agent - zooanthropophilic fungus of the genus Ecthothrix). It is characterized by a violent inflammatory reaction in the lesion with the formation of an infiltrate, purulent melting of the hair follicle resulting in cicatricial atrophy of the skin, persistent baldness.

Staphylococcal epidemic pemphigus of newborns should be distinguished from syphilitic pemphigus (syphilis of infancy), in which tense blisters filled with serous-hemorrhagic contents have a dense infiltrated base and are located mainly on the palms and soles. In addition, syphilitic manifestations are confirmed by the detection of the pathogen and positive serological reactions.

In the differential diagnosis of streptococcal impetigo and impetiginous syphilis in the secondary period, the nature of the rash is of great importance. In impetiginous syphilis, pustular rashes of a dark red color, dense at the base, without peripheral growth, and a tendency to merge are observed. The rashes are often combined with other syphilides. The diagnosis is confirmed by the detection of pale treponema and positive serological reactions.

Streptococcal impetigo (damage to the folds) should be differentiated from candidal diaper rash, which is characterized by the appearance of confluent erosive surfaces of a bright pink color, often covered with a whitish coating (culture of yeast-like fungi). Crusts are formed as a result of the opening of blisters at the site of friction.

Chronic diffuse streptoderma can transform into microbial eczema. The latter is characterized by the appearance of microvesicles against the background of hyperemia and edema, their subsequent opening and the formation of areas of droplet weeping (microerosion). The course is chronic, recurrent.

Vulgar ecthyma must be differentiated from syphilitic. The latter is characterized by the absence of pain, dark red color, infiltrated base, as well as detection of the syphilis pathogen in the ulcer and positive serological reactions.

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Treatment of pyoderma

1. Non-drug treatment: physiotherapy, UHF, UV radiation.
2. Drug treatment:
   • etiotropic (broad-spectrum antibiotics, sulfonamides, antistaphylococcal gamma globulin);
   • pathogenetic (desensitizing and tonic agents).

Externally: solutions of aniline dyes, pure ichthyol, ointments containing antimicrobial agents.

In the treatment of pyoderma, it is necessary to follow 3 main principles:

1. Address the cause of pyoderma, i.e. carry out etiotropic (antimicrobial) treatment.
2. Eliminate predisposing factors (pathogenetic therapy) - correction of carbohydrate metabolism, elimination of vitamin deficiency, treatment of foci of chronic infection, immunostimulating therapy, etc.
3. Prevent the spread of infection to unaffected areas of the skin (temporarily prohibit washing and visiting swimming pools; prohibit compresses, massage and any cosmetic procedures in the area of pyoderma; treat unaffected skin around the pyoderma lesions with antiseptics).

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

Indications for general antibacterial therapy

• multiple pyoderma, their rapid spread across the skin, lack of effect of external therapy;
• the appearance of lymphangitis, enlarged and painful regional lymph nodes;
• the presence of a general reaction of the body to purulent inflammation (increased body temperature, chills, malaise, weakness, etc.);
• deep uncomplicated and, especially, complicated pyoderma (threat of lympho- 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 specific case based on the totality of clinical data) is the presence of mild forms of pyoderma in weakened patients against the background of immunosuppressive, radiation therapy, in HIV-infected patients, in patients with endocrine or hematological pathology.

Systemic antibacterial therapy can be carried out with antibiotics or sulfonamides. It is advisable to select these agents in accordance with the results of a microbiological study of purulent discharge from pyoderma foci (sowing, isolation of a pure culture of the pathogen and determination of its sensitivity to antibiotics in vitro). In case of technical impossibility of conducting a microbiological study or lack of time (sharp deterioration of the patient's condition and the need for urgent antimicrobial therapy), preference is given to broad-spectrum antibiotics. When deciding on the appointment of systemic antibacterial therapy, the doctor asks himself three main questions:

1. Which antibiotic or sulfanilamide should I choose?
2. What are the side effects of the drug?
3. Is this drug indicated for a specific patient (taking into account the allergy history, concomitant diseases, combination with other drugs)?

The volume of external therapy for pyoderma is determined by the depth and severity of the skin lesion. Thus, in acute superficial pyoderma, accompanied by the formation of superficial pustules on the skin, they should be opened with subsequent immediate treatment with external antiseptics. In deep pyoderma at the infiltration stage, resolving therapy should be prescribed, aimed at increasing hyperemia in the lesion and thereby promoting either rapid self-resolution of the infiltrate or rapid abscess formation. For this purpose, applications of ichthyol to the forming infiltrate, physiotherapeutic effects - UHF, low-energy laser radiation, dry thermal procedures are used. It should be especially noted that compresses, paraffin or ozokerite applications are undesirable, since these procedures are accompanied by maceration of the skin and can cause aggravation of the purulent process. If there are signs of abscess formation in deep pyoderma, they should be surgically opened with subsequent drainage of the purulent cavity using turundas soaked in a hypertonic solution (the first 1-2 days), antiseptic solutions (furacilin, chlorhexidine, miramistin, etc.). After the appearance of active granulation, it is advisable to apply dressings with ointments containing antiseptics and biostimulants (solcoseryl, methylthiouracil, etc.).

In cases where pyoderma occurs subacutely or chronically, the surface of the lesions is covered with purulent crusts, they must be removed by softening with an antiseptic ointment (the ointment is applied to the lesion for 20-30 minutes) followed by mechanical action with tampons soaked in a 3% aqueous solution of hydrogen peroxide. After removing the purulent crusts, the lesion is treated with an aqueous or alcoholic solution of antiseptic.