Pyoderma

Piodermaids (Greek ruon-pus, derma-skin) - pustular skin diseases caused by pyogenic microorganisms, mainly staphylococci, streptococci, less often - other microorganisms.

Pyoderma - pustular skin lesions, the main causative agent of which are staphylococci, less often streptococci. Piococcal processes caused by other microorganisms are less than 1%. In addition to the virulence of streptococci and staphylococci, the different nature of their effect on the skin, which largely determines the clinical form of the disease, the general state of the organism is of great importance in the development of the process, primarily the insufficiency of humoral and cellular immunity and nonspecific protective factors, a decrease in the bactericidal function of the skin, chronic forms (furunculosis, chronic ulcerative and ulcerative vegetative pyoderma), the presence of foci of chronic infection or carriage of pathogenic Occam flora on mucous membranes, mainly nasopharynx, and also specific sensitization to piococci. It is shown that in most cases the phagotypes of pathogenic staphylococci isolated from lesions, clinically unchanged skin of patients with chronic pyoderma and from the foci of focal infection coincide. Staphylococci, sown from the nasopharynx, are the most pathogenic.

Pustular diseases of the skin and subcutaneous fat layer make up 10-15% of all diseases with temporary disability and on the frequency of treatment in dermatological institutions take first place: up to 30% in adults and up to 37% in children.

Piodermitis - diseases of the skin and subcutaneous fat layer, resulting from exogenous introduction into the skin of pyogenic cocci or pyococci (staphylococci and streptococci).

Pyoderma occurs primarily or as a complication after other diseases.

Streptococci and staphylococci are often found in the human environment (in the air, in the dust of the premises, as well as in clothing and human skin).

In case of skin lesions (abrasion, fissure, trauma), contamination of it with oily oils, dust, combustible liquids, with improper skin care, its functions, including protective ones, are violated. Development of the disease is facilitated by a decrease in the body's immune defenses, impaired sweat composition and changes in the pH of the water-lipid mantle of the skin, the composition and quantity of the sebaceous secretion, unbalanced diet, endocrine disorders (diabetes mellitus, etc.), hypovitaminosis, hypothermia, overfatigue,

On the etiologic principle distinguish staphyloderma, streptoderma and mixed - streptostafilodermii. There are the following variants of staphyloderma: superficial - osteofolliculitis, folliculitis, sycosis, etc .; deep - furuncle, carbuncle, etc.

[1], [2]

The causes and pathogenesis of pyoderma

The most common pathogens of purulent skin diseases are pyogenic microbes of staphylococcus, streptococci, less often - pneumococci, gonococci, synechymic E. Coli, etc., as well as the products of their vital activity - toxins (necrozoxime), enzymes (hyaluroidase).

In adult bowl, infection with autoflora of the skin surface, mucous membranes or from foci of chronic purulent infection (tonsillitis, otitis, sinusitis, periodontitis, etc.) occurs. Exogenous infection with pathogenic or epidemic staphylococcus strains is less common. This way of infection is noted mainly in children's groups and medical institutions.

Exogenous factors: skin contamination; violation of flow and salivation function; maceration; microtraumatism (industrial, household, skin excoriation for itching dermatoses); the action of chemicals that degrease and irritate the skin (organic solvents, lubricating oils, cooling emulsions, alkaline solutions, etc.); contaminated overalls; trophic skin disorders, as a result of disturbances in innervation and circulation.

Endogenous factors: primary and secondary insufficiency of the immunocompetent system; physical and mental overwork; malnutrition or malnutrition; neuro-endocrine disorders; use of immunosuppressive drugs; severe debilitating diseases; chronic intoxication; hypovitaminosis; diabetes; digestive diseases; dysbiosis; anemia; foci of focal infection as a source of sensitization and autoinfection.

At the first stage of infection with staphylococci, cellular micro- and macrophagal reactions prevail, as well as plasmocoagulation leading to thrombosis of lymphatic and venous small vessels confining the purulent focus.

At the second stage of infection, the fibrinolytic enzyme and hyaluronidase take effect. For staphylococcal skin lesions, the formation of deep and limited foci of suppurative or purulent-necrotic inflammation with predominant localization in the hair follicle, sebaceous or sweat glands is typical.

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

Classification and symptoms of pyoderma

There is no generally recognized classification of pyoderma. The most common and convenient in practical terms is the classification by etiological principle. According to this classification, distinguish staphylococcal, streptococcal and mixed (strepto-staphylococcal) skin lesions. In addition, each group is given surface and deep pyoderma, which can occur acutely and chronically.

To superficial pustular lesions of the skin are those nosological forms, in which the epidermis and the upper layer of the dermis are affected. With deep pyoderma, the lesion can seize not only the dermis, but also the hypodermis.

Staphylococcal pyoderma flowing sharply:

• superficial - ostiofolliculitis, superficial folliculitis, impetigo staphylococcal bullous (in children), staphylococcal pemphigoid of newborns;
• deep - deep folliculitis, boils, acute furuncle, carbuncle, hydradenitis, multiple abscesses of infants.

Staphylococcal pyoderma, which occur chronically:

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

Streptococcal pyoderma, acute:

• superficial - impetigo streptococcal, intertrigo;
• deep - ecthyma streptococcal, erysipelas.

Streptococcal pyoderma, which occur chronically:

• deep - chronic diffuse streptoderma.

Strepto-staphylococcus pyoderma flowing sharply:

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

Strepto-staphylococcal pyoderma are deep, flowing chronically (chronic atypical pyoderma):

• ulcerative chronic pyoderma and its variety - shankriform pyoderma;
• ulcerative vegetative pyoderma;
• abscessed chronic pyoderma and its variety - inverse conglobata acne.

• Staphylodermia acute, chronic.

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

Chronic staphyloderma: vulgar sycosis, chronic furunculosis.

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

Chronic diffuse streptoderma, vulgar ectima.

• Vulgar impetigo (staphyloderma and streptoderma).

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

Eruptions on the skin with pyoderma are polymorphic. The type of primary elements of the rash depends on the nature of the pathogen and the depth of the skin lesion.

[3], [4], [5], [6], [7],

Acute streptococcal skin lesions

Acute streptococcal skin lesions develop mainly in children and young women, are located more often on the face and hands, but can also be on the mucous membranes. Common diffuse forms occur. Appear in the form of small flabby bubbles (fliken) with a clear or unclear content, surrounded by a small aureole of the erythema (streptococcal impetigo). If a staphylococcal infection joins, the contents quickly become purulent (impetigo vulgaris). Streptococcus, often in association with staphylococcus, causes intertriginoznye skin lesions, as well as severe pyococcal process in children - epidemic pemphigus of newborns, manifested in the form of bullous impetigo, which can quickly occupy large areas of the skin, including creases. A clinical picture of the exotiative dermatitis of the newborn Ritter is formed. To this group of streptodermas are also post-erosive syphiloid, which is observed in children of early age, clinically characterized by erosive-papular elements that appeared on the site of the fliken, located on the genitals, buttocks and thighs, and ecthyma, which usually appears in adults, which is a pustular-ulcerative lesion skin, solitary or, less often, multiple with predominant localization on the legs.

Streptococcal skin lesions, in contrast to staphylodermia, affect the sebaceous-hair follicle and sweat glands. For them, the most typical is a superficial inflammatory lesion of smooth skin with the release of serous exudate. The main primary vysypny element with superficial streptodermia is a surface bladder. In those localizations of the skin, where the horny layer is relatively thin, the streptococcal bubble looks sluggish, flabby, it is called fliktena. In those areas of the skin where there is hyperkeratosis (the palms of the sole, okolonogtevye zones), streptococcal blisters may have a dressed appearance, sufficiently dense cover, serous or unclear content.

With deep streptococcal skin lesions, the primary voiding element can be a deep epidermodermal pustule with limited necrosis of the underlying dermis (ectema) or edematous erythema with clear, rapidly increasing areas (erysipelas).

Chronically occurring streptoderma include simple facial, zaeda, paronychia, superficial diffuse pyoderma.

Pathomorphology

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

In the bullous form of impetigo, the bubble located in the upper parts of the epidermis contains neutrophilic granulocytes and a large amount of serous exudate. Over time, the bladder may occupy almost the entire thickness of the epidermis and be covered from above with a crust. In the dermis under the bladder there is a significant infiltration of neutrophilic granulocytes with an admixture of lymphocytes.

Ecthyma is characterized by the defeat of the entire thickness of the epidermis and the underlying dermal areas with the formation of ulcers, the bottom and edges of which are densely infiltrated by lymphocytes with an admixture of a large number of neutrophilic granulocytes. The epidermis is thickened and edematous at the edges, connective tissue in the area of the ulcer can be necrotic and densely infiltrated by neutrophilic granulocytes. Capillaries of the upper part of the dermis are dilated both along the periphery and in the center of the focus, occasionally there is thrombosis.

Skin lesions caused by staphylococci, in contrast to streptococcal pyoderma have a distinct localization in the mouths of sweat glands and hair follicles.

[8], [9], [10], [11], [12], [13], [14], [15]

Acute staphylodermia

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.Other nosological forms of pustular skin lesions can manifest themselves with the same element of the rash eg follicular pustulitis ostiophalliculitis, superficial folliculitis and vulgar sycosis are manifested, and the inflammatory follicular nodule arises with folliculitis (superficial and deep) decalving Folliculitis, sometimes with a small furuncle Inflammatory node is found in the debut of a furuncle, carbuncle, multiple abscesses of infants (pseudofurunculosis) In some cases (mainly in children) at the site of penetration into the skin of staphylococcus a bubble is possible.This is due to the destruction of the bonds between the granular cells layer of epidermis with staphylococcal toxin (zaksholiatinom.) The same primary efflorescence element (bladder) is observed in superficial streptococcal pyoderma.

Acute staphyloderma can be in the form of superficial small pustular eruptions, filled with purulent contents, in the center of which is hair (ostiofolliculitis, folliculitis), or deep pustules (boils, carbuncles).

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 the sweat glands, as well as sharply delimited abscessed deep foci of lesion, located mainly on the trunk. Similar foci can be observed in adults, but in places of localization of the apocrine glands (hydradenitis). In this case, the inflammatory process is located in the deep sections of the dermis and in the subcutaneous tissue in the form of a painful tumor-like focus of infiltration, which, rapidly increasing, becomes soldered to the skin, initially unchanged, then acquiring a cyanotic red color, followed by softening and separation of purulent-bloody contents.

Staphylococcal sycosis is referred to chronic forms of staphylococcosis, characterized by the development of folliculitis on the hairy parts of the pelvis, most often in the region of the mustache and beard, sometimes accompanied by scarring (lupoid sycosis), the so-called keloid acne in the neck of Erman, localized on the posterior surface of the neck at the border with the scalp , clinically manifested by the presence of recurrent acne of similar folliculitis, located on the sclerotized thickly thickened skin; Abscessing and undermining the folliculitis of Hoffman's head, prone to abscessing, the formation of extensive lesions with fistulous movements, sclerosing and hair loss.

[16], [17]

Pyoderma vegetative

Pyoderma vegetative (this: ulcerative-inflammatory pyoderma) is characterized by the presence of septate foci, covered with sluggish granulations, vegetations located on the hands, legs and skin folds; Shankriform pyoderma usually manifests as a single ulcer of small dimensions with compaction in the base, which gives it a resemblance to syphilitic chancre, especially since its most frequent localization is the genitals and the oral cavity, and regional lymph nodes often increase.

The characteristic signs of vegetative pyoderma 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, among which are plasmocytes, lymphocytes and eosinophil granulocytes. The cells of the infiltrate penetrate the epidermis and then onto its surface, forming crusts. Some papillae of the dermis are free from infiltration, but the epidermal processes are lengthened. Differentiate the disease from vegetative pemphigus, blastomycosis, verrocus tuberculosis, bromoderm.

Histogenesis

In various forms of pyoderma, disturbances in the function of neutrophilic granulocytes, characterized by a decrease in chemotaxis, phagocytic activity, imperfect phagocytosis, the formation of polymorphous phagosomes, as well as L-transformations of pathogens, defects in the T-system of immunity with a slight increase in B-lymphocyte activity.

Weakening of immune reactivity, increase in the pathogenicity of strains of microorganisms on the skin can be facilitated by hypothermia, frequent colds, inadequate 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 effect of irrational excessive antibiotic therapy in which can change the biological properties of pyococci, including the formation of L-forms. As well as strains with increased resistance to antibiotics.

Gangrenous pyoderma

Clinically it is necrotic and gangrenous skin changes with the formation of rapidly increasing ulcerative lesions, surrounded by a cuneiform border of cyanotic color, in the zone of which pustules, palulovecicles or blisters are visible. The central focus of necrotic inflammation increases in the peripheral direction with the formation of a large ulcer.

Gangrenous pyoderma in most patients is combined with systemic diseases: ulcerative colitis, rheumatoid arthritis, Crohn's disease, hepatitis, monoclonal gammapathy, cancer, lymphoproliferative diseases.

Pathomorphology

Histological signs are nonspecific. In the development of the morphological picture, it is possible to trace the staging corresponding to the dynamics of the clinical picture from pustules or papulesvezicula to a deep ulcer. The initial histological signs are variable. So, before the appearance of ulcers, acanthosis is detected, a dense superficial infiltration, mainly from lymphocytes, monocytes, with an admixture of neutrophilic granulocytes. Sometimes they are very many, resulting in the formation of abscesses. Subsequently, necrobiotic changes are noted in the epidermis with exocytosis, and in the dermis - sharp edema with the formation of blisters. In the vessels, in the center of focus, fibrinoid necrosis of the walls is expressed, infiltration by neutrophilic granulocytes.

In the area of ulcers - 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 from neutrophilic granulocytes. In the deeper parts of the dermis, perivascular lymphohistiocytic infiltrates with an admixture of plasma cells, less often giant cells of foreign bodies, the phenomenon of fibrinoid vascular necrosis and infiltration by neutrophilic granulocytes are observed, which some authors regard as vasculitis. When reparative changes in the area of the ulcer, vascular proliferation and the phenomenon of fibroplastic transformation are noted. Infiltrates are mainly lymphohistiocytic with an admixture of plasma cells, fibroblasts, among which there may be foreign body cells.

Differentiate gangrenous pyoderma from vegetative, for which the presence in the dermis of eosinophilic microabscesses is more characteristic.

Histogenesis

At the heart of the development of gangrenous pyoderma are immune disorders that cause immunocomplex vasculitis. This is proved by the deposition of IgM and C3 complement components in the vessels and papillary dermis layer, as well as along the dermo-epidermal zone. There are also violations of humoral and cellular immunity. When combined gangrenous pyoderma with hypergammaglobulinemia, an increase in IgA levels was noted, especially in combination with monoclonal gammapathy. Mark violation of neutrophil granulocyte function as a defect of chemotaxis or phagocytosis.

Other forms of pyoderma

Ostiophalliculitis - an acute inflammation of the hair follicle, is a pustule, centered in hair 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 shallow scar.

Decolving folliculitis is a rare form of staphylococcal injury of the hair follicle, in which chronic folliculitis without pronounced pustulization and ulceration leads to skin atrophy and persistent baldness. Etiology and pathogenesis have not been elucidated. The causative agent is Staphylococcus aureus, and additional colonization in the hair follicles of gram-negative microbial flora is also possible. This may result in a changed immunological reactivity of the organism against the background of seborrheic status, chronic focal infection, diabetes mellitus, etc. The microbial factor, apparently, is only one of the pathogenetic links in the development of this chronic process.

Furuncle - acute purulent-necrotic inflammation of the hair follicle and perifollicular connective tissue. Furuncle refers to the deep form of staphyloderma. The primary efflorescence of the furuncle is an inflammatory node that forms around the staphylococcus infected hair follicle. The onset of the disease is associated with the formation of an inflammatory purulent infiltrate around the hair follicle, which in the early stages may be small in size as folliculitis), but the process quickly captures the entire depth of the hair follicle surrounding the connective tissue and adjacent sebaceous gland and is an inflammatory congestive-hyperemic node , conically rising above the surface of the skin. Increases soreness, tearing, painful pains are possible. When localizing the boil in the face, especially on the upper lip, there is an extensive swelling around the infiltrate. On the 3rd-4th day in the center of the infiltration the fluctuation begins to be determined, a purulent fistula is formed around the hair, at the dissection of which a small amount of thick pus is secreted, a small ulcer is formed. At the bottom of this ulcer reveals a necrotic stem of a greenish color. After another 2-3 days, the necrotic stem is rejected with a small amount of blood and pus, after which soreness and inflammatory phenomena are significantly reduced. In the place of the severed necrotic stem, a deep crater ulcer forms which, after cleansing from pus and 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 located on the forearms, face, back of the neck, lower back, buttocks, hips. Usually, single furuncles are not accompanied by a violation of general health and an increase in body temperature. The exception is the furuncle of the face. Particular attention should be paid to patients with a furuncle located in the area of the lips, on the nose, in the nasolabial triangle and in the region of the external auditory canal. Mimic movements of the face, traumatization of furuncles during shaving, or attempting to squeeze them out can lead to serious complications: thrombophlebitis of facial veins. It should be noted that the anatomical features of venous outflow on the face, the presence of anastomoses with 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 formed multiple abscesses in various organs and tissues.

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

Hydradenitis is a purulent inflammation of the apocrine sweat glands located in the armpits, around the nipples, behind the auricles and in the perineum. Unlike a furuncle, it does not have pustules and purulent-necrotic stem, begins with a deep infiltration in the sweat glands, capturing the subcutaneous fat layer.

Vulgar acne is a purulent inflammation of the sebaceous gland opening into the hair follicle, the primary localization is the face, chest, back.

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

Staphtococcal sycosis is a chronic skin disease, localized in the area of growth of the mustache, beard, eyelashes, eyebrows, in the nasal passages, on the pubic area. It is characterized by the recurring occurrence of folliculitis with powerful perifollicular and inflammatory filtration and hyperemia with a bluish tinge. The safety of the bands is observed, there are no scars on the skin.

Acute streptoderma is characterized by the presence of fliken, which is a flaccid bladder, surrounded by a narrow rim of hyperemia and prone to peripheral growth. In thin skin areas, the flicks are small, quickly opened with fomirovaniem merging erosion with a smooth bottom and abundant serous discharge. In open areas exudate is poured into honey-yellow crusts.

When localized on the skin with a thick horny layer (brushes, feet), flickenes reach large sizes, are filled with serous-purulent or serous-hemorrhagic contents, accompanied by a significant inflammatory reaction and edema, are often complicated by lymphangitis, lymphadenitis, increased body temperature, and changes in the hemogram. At autopsy, extensive diffuse foci of lesion with rapid peripheral growth (acute diffuse streptoderma) are given.

Chronic diffuse pyoderma has a predominant localization on the lower legs, rarely on the upper limbs and in the skin folds, characterized by a long sluggish course, clear polycyclic outlines of the foci with the cortex of the torn horny layer.

Typical diffuse infiltration is stagnant red with the presence of surface erosion, serous crusts and lamellar scales. Chronic diffuse pyoderma is often complicated by allergic rashes and eczematics of the main focus.

Vulgar ecthims are found in more weakened patients, localized mainly on the shins in the form of deep dermal pustules with insignificant peripheral infiltration, are resolved by the formation of ulcers and scars.

Impetigo streptococcal (impetigo streptogenes) is a common form of streptoderma. Primarily affects children and young women. Skin lesions usually involve open areas, the face (around the nose and mouth), the parotid zones, and limbs. The disease becomes more frequent in the warm season. In conditions of close bodily contact, streptococcal infection is easily transmitted from the patient to the healthy one. Children's groups may have epidemic outbreaks.

In the pathogenesis of streptococcal impetigo, micro- and macrotraumatism of the skin, maceration, is of great importance. Around the phlycenes and crusts there is a small corolla of hyperemia. Flickety and crusts quickly increase in size, can merge. The serous exudate of the opening flushing contaminates the surrounding skin, and the process quickly spreads. Under favorable conditions, erosion is epithelialized, the peel disappears, a small hyperaemia remains in their place, followed by light pigmentation. Strong tracks are not observed. Complications of streptococcal impetigo may be lymphangitis and regional lymphadenitis, eczematism (especially in persons prone to atopy), in children - the development of infectious-toxic glomerulonephritis.

Impetigo vulgar, or contagious (impetigo vulgaris, contagiosa), is caused by pathogenic streptococci, which determine the primary vysypnoy element - subcorneal flikenu. However, very quickly joins staphylococcal flora, leading to severe suppuration and the formation of purulent cavity elements, drying up honey-yellow or greenish crusts. Like streptococcal, vulgar impetigo is most common in children in open 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 common on the face as a result of traumatization (poor shaving), maceration (chronic rhinorrhea).

Differential diagnosis of pyoderma

Acute forms of staphylodermia (folliculitis, furuncle) should be differentiated from professional folliculitis (associated with production irritants).

Hydradenitis differs from tuberculosis scrofuloderma, which is characterized by a slight soreness subacute flow, the allocation of a small amount of pus, the predominant localization in the maxillary, supraclavicular and poluklyuchichnoy area.

Vulgar sycosis must be differentiated from parasitic sycosis, which is related to fungal diseases (pathogen-ano-anthropophilous 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 with an outcome in the scar's atrophy of the skin, persistent alopecia.

Staphylococcal epidemic pemphigus of newborns should be distinguished from syphilitic pemphigus (syphilis of infancy), in which intense 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 responses.

In the differential diagnosis of streptococcal impetigo and impetigo syphilis in the secondary period, the nature of the rashes is important. With impetiginosic syphilis, there are pustular eruptions of dark red color, dense in the base, without peripheral growth, and a tendency to fuse. Eruptions are often combined with other syphilis. The diagnosis is confirmed by the detection of pale treponema and positive serological reactions.

Streptococcal impetigo (lesion of the folds) should be differentiated from candida diaper rash, which is characterized by the emergence of draining erosive surfaces of bright pink color, often covered with a whitish coating (yeast-like fungus culture). Crochets are formed as a result of the opening of the bubbles at the place of friction.

Chronic diffuse streptoderma can be transformed 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 drip-wet (micro-erosion) sites. The course is chronic, relapsing.

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

[18], [19], [20], [21], [22], [23]

Treatment of pyoderma

1. Non-drug treatment: physiotherapy, UHF, UFO.
2. Medication:
   • etiotropic (broad-spectrum antibiotics, sulfonamides, anti-staphylococcal gamma globulin);
   • pathogenetic (desensitizing and restorative means).

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

In the treatment of pyoderma, three main principles must be observed:

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

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

Indications for general antibiotic therapy

• multiple pyoderma, their rapid spread to the skin, lack of the effect of external therapy;
• the appearance of lymphangitis, enlarged and painful regional lymph nodes;
• presence of the general reaction of the body to purulent inflammation (fever, chills, malaise, weakness, etc.);
• deep uncomplicated and, especially, complicated pyoderma (threat of lympho- and hematogenous dissemination of infection, including thrombosis of venous sinuses of the brain and development of purulent meningitis);
• the relative indication (the question is solved in each case by the combination of clinical data) is the presence of mild forms of pyoderma in weakened patients on the background of immunosuppressive, radiotherapy, in HIV-infected patients, in patients with endocrine or hematological pathology. 

Systemic antibiotic therapy can be performed with drugs of a group of antibiotics or sulfonamides. The choice of these agents should preferably be carried out in accordance with the results of a microbiological study of purulent discharge from the foci of pyoderma (seeding, isolation of the pure culture of the pathogen and in vitro determination of its susceptibility to antibiotics). In the case of a technical impossibility of conducting a microbiological examination or lack of time (a sharp increase in the patient's condition and the need for urgent antimicrobial therapy), antibiotics of a wide range of action are preferred. Solving the question of the appointment of systemic antibacterial therapy, the doctor poses three main questions:

1. Which antibiotic or sulfonamide should I choose?
2. What are the side effects of the drug?
3. Is this drug shown to a particular patient (taking into account allergological anamnesis, concomitant diseases, combination with other drugs)?

The volume of external therapy of pyoderma is determined by the depth and severity of skin lesions. Thus, in acute superficial pyoderma, accompanied by the formation of surface pustules on the skin, they should be opened with subsequent immediate treatment with external antiseptics. With deep pyoderma in the infiltration stage, an authorization therapy should be prescribed, aimed at increasing the hyperemia in the focus and thereby facilitating either a quick self-infiltration or rapid abscessing. To this end, applications are applied to the developing infiltrate of ichthyol, physiotherapeutic effects - UHF, low-energy laser radiation, dry thermal procedures. It should be especially noted the undesirability of compresses, paraffin or ozocerite applications, since these procedures are accompanied by skin maceration and can cause a weighting of the purulent process. In the presence of signs of abscessing of deep pyoderma it is necessary to perform their surgical opening with subsequent drainage of the purulent cavity with the help of turunds moistened with hypertonic solution (first 1-2 days), solutions of antiseptics (furacilin, chlorhexidine, miramistin, etc.). After the appearance of active granulations, it is advisable to apply bandages with ointments containing antiseptics and biostimulants (solcoseryl, methylthiouracil, etc.).

In those cases when the pyoderma occur subacute or chronically the surface of the foci is covered with purulent crusts, they must necessarily be removed by softening with antiseptic ointment (ointment is applied to the focus for 20-30 min), followed by mechanical action with tampons moistened with 3% aqueous hydrogen peroxide solution. After removal of purulent crust, the focus is treated with an aqueous or alcoholic solution of antiseptic.