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Lecture notes, cheat sheets
Dermatovenerology. Pustular skin diseases (most important)
Directory / Lecture notes, cheat sheets Table of contents (expand) 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. Author: Sitkalieva E.V. << Back: Viral dermatoses (Herpes viral infections. Human papillomavirus infection. Molluscum contagiosum) >> Forward: Diffuse connective tissue diseases (Lupus erythematosus. Scleroderma. Dermatomyositis)
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