Epidemiology, causes and pathogenesis of rye

Causes of erysipelas

The causative agent of erysipelas is beta-hemolytic streptococcus group A (Streptococcus pyogenes). Beta-hemolytic streptococcus group A is a facultative anaerobe, resistant to environmental factors, but sensitive to heating to 56 °C for 30 minutes, to the effects of basic disinfectants and antibiotics.

The characteristics of the strains of beta-hemolytic streptococcus group A that cause erysipelas have not been fully studied at present. The assumption that they produce toxins identical to scarlet fever toxins has not been confirmed: vaccination with erythrogenic toxin does not provide a prophylactic effect, and antitoxic scarlet fever serum does not affect the development of erysipelas.

In recent years, it has been suggested that other microorganisms are involved in the development of erysipelas. For example, in bullous-hemorrhagic forms of inflammation with abundant fibrin exudate, along with beta-hemolytic streptococcus group A, Staphylococcus aureus, beta-hemolytic streptococci of groups B, C, G, gram-negative bacteria (Escherichia, Proteus) are isolated from the wound contents.

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Pathogenesis of erysipelas

Erysipelas occurs against the background of a predisposition, which is probably congenital and represents one of the variants of a genetically determined reaction to DTH. People with blood group III (B) suffer from erysipelas more often. Apparently, a genetic predisposition to erysipelas reveals itself only in old age (more often in women), against the background of repeated sensitization to beta-hemolytic streptococcus group A and its cellular and extracellular products (virulence factors) in certain pathological conditions, including those associated with involutional processes.

In primary and recurrent erysipelas, the main route of infection is exogenous. In recurrent erysipelas, the pathogen spreads lymphogenously or hematogenously from foci of streptococcal infection in the body. With frequent relapses of erysipelas, a focus of chronic infection (L-forms of beta-hemolytic streptococcus group A) occurs in the skin and regional lymph nodes. Under the influence of various provoking factors (hypothermia, overheating, trauma, emotional stress), L-forms revert to bacterial forms of streptococcus, which cause relapses of the disease. In rare and late relapses of erysipelas, reinfection and superinfection with new strains of beta-hemolytic streptococcus group A (M-types) are possible.

Provoking factors that contribute to the development of the disease include damage to the integrity of the skin (abrasions, scratches, combs, pricks, abrasions, cracks, etc.), bruises, sudden changes in temperature (hypothermia, overheating), insolation, emotional stress.

Predisposing factors include:

• background (concomitant) diseases: mycosis of the feet, diabetes mellitus, obesity, chronic venous insufficiency (varicose veins), chronic (acquired or congenital) insufficiency of the lymphatic vessels (lymphostasis), eczema, etc.;
• the presence of foci of chronic streptococcal infection: tonsillitis, otitis, sinusitis, caries, periodontal disease, osteomyelitis, thrombophlebitis, trophic ulcers (more often with erysipelas of the lower extremities);
• occupational hazards associated with increased trauma, contamination of the skin, wearing rubber shoes, etc.;
• chronic somatic diseases, as a result of which anti-infective immunity decreases (more often in old age).

Thus, the first stage of the pathological process is the introduction of beta-hemolytic streptococcus group A into a skin area when it is damaged (primary erysipelas) or infected from a dormant infection site (recurrent form of erysipelas) with the development of erysipelas. Endogenously, the infection can spread directly from the site of an independent disease of streptococcal etiology. The reproduction and accumulation of the pathogen in the lymphatic capillaries of the dermis corresponds to the incubation period of the disease.

The next stage is the development of toxemia, which causes intoxication (characterized by an acute onset of the disease with an increase in temperature and chills).

Subsequently, a local focus of infectious-allergic inflammation of the skin is formed with the participation of immune complexes (the formation of perivascularly located immune complexes containing the complement fraction C3), capillary lymph and blood circulation in the skin is disrupted with the formation of lymphostasis, the formation of hemorrhage and blisters with serous and hemorrhagic contents.

In the final stage of the process, the bacterial forms of beta-hemolytic streptococcus are eliminated by phagocytosis, immune complexes are formed, and the patient recovers.

In addition, it is possible that foci of chronic streptococcal infection may form in the skin and regional lymph nodes with the presence of bacterial and L-forms of streptococcus, which causes chronic erysipelas in some patients.

Important features of the pathogenesis of frequently recurring erysipelas are considered to be the formation of a persistent focus of streptococcal infection in the patient's body (L-form); changes in cellular and humoral immunity; a high level of allergization (hypersensitivity type IV) to beta-hemolytic streptococcus group A and its cellular and extracellular products.

It should be emphasized that the disease occurs only in individuals with a congenital or acquired predisposition to it. The infectious-allergic or immune complex mechanism of inflammation during erysipelas determines its serous or serous-hemorrhagic nature. The addition of purulent inflammation indicates a complicated course of the disease.

In erysipelas (especially in hemorrhagic forms), the activation of various links of hemostasis (vascular-platelet, procoagulant, fibrinolysis) and the kallikrein-kinin system acquires important pathogenetic significance. The development of intravascular blood coagulation, along with the damaging effect, has an important protective value: the inflammation focus is delimited by a fibrin barrier, preventing further spread of infection.

Microscopy of a local erysipelas focus reveals serous or serous-hemorrhagic inflammation (edema; small-cell infiltration of the dermis, more pronounced around the capillaries). The exudate contains a large number of streptococci, lymphocytes, monocytes and erythrocytes (in hemorrhagic forms). Morphological changes are characterized by a picture of microcapillary arteritis, phlebitis and lymphangitis.

In erythematous-bullous and bullous-hemorrhagic forms of inflammation, the epidermis peels off with the formation of blisters. In hemorrhagic forms of erysipelas, thrombosis of small blood vessels, diapedesis of erythrocytes into the intercellular space, and abundant fibrin deposition are observed in the local lesion.

During the convalescence period with uncomplicated erysipelas, large or small plate-like peeling of the skin is observed in the area of the local inflammation. With recurrent erysipelas, connective tissue gradually grows in the dermis - as a result, lymph flow is disrupted and persistent lymphostasis develops.

Epidemiology of erysipelas

Erysipelas is a widespread sporadic disease with low contagiousness. Low contagiousness of erysipelas is associated with the improvement of sanitary and hygienic conditions and compliance with antiseptic rules in medical institutions. Despite the fact that patients with erysipelas are often hospitalized in general departments (therapy, surgery), among neighbors in the ward, in the families of patients, repeated cases of erysipelas are rarely registered. In about 10% of cases, hereditary predisposition to the disease is noted. Wound erysipelas is currently extremely rare. Erysipelas of newborns, which is characterized by high mortality, is practically absent.

The source of the infectious agent is rarely detected, which is associated with the widespread distribution of streptococci in the environment. The source of the infectious agent in the exogenous route of infection can be patients with streptococcal infections and healthy carriers of streptococcus bacteria. Along with the main contact mechanism of infection transmission, an aerosol mechanism of transmission (airborne route) is possible with primary infection of the nasopharynx and subsequent transfer of the pathogen to the skin by hands, as well as by the lymphogenous and hematogenous route.

In primary erysipelas, beta-hemolytic streptococcus group A penetrates the skin or mucous membranes through cracks, diaper rash, various microtraumas (exogenous route). In facial erysipelas - through cracks in the nostrils or damage to the external auditory canal, in lower extremity erysipelas - through cracks in the interdigital spaces, on the heels or damage to the lower third of the shin. Damage includes minor cracks, scratches, pinpoint pricks and microtraumas.

In recent years, there has been an increase in the incidence of erysipelas in the United States and a number of European countries.

Currently, only isolated cases of erysipelas are registered in patients under 18 years of age. From the age of 20, the incidence increases, and in the age range from 20 to 30 years, men get sick more often than women, which is associated with the prevalence of primary erysipelas and professional factors. The majority of patients are people aged 50 and older (up to 60-70% of all cases). Among workers, manual workers predominate. The highest incidence is noted among mechanics, loaders, drivers, bricklayers, carpenters, cleaners, kitchen workers and people of other professions associated with frequent microtraumatization and contamination of the skin, as well as sudden changes in temperature. Housewives and pensioners get sick relatively often, who usually have recurrent forms of the disease. An increase in morbidity is noted in the summer-autumn period.

Post-infection immunity is fragile. Almost a third of patients experience recurrent disease or relapse of the disease due to autoinfection, reinfection, or superinfection with strains of group A β-hemolytic streptococcus that contain other variants of the M protein.

There is no specific prevention of erysipelas. Non-specific measures are related to compliance with the rules of asepsis and antisepsis in medical institutions, and personal hygiene.

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