Epidemiology, causes and pathogenesis of erysipelas

Causes of face

Pathogen is a beta-hemolytic group A Streptococcus pyogenes. Beta-hemolytic streptococcus group A - facultative anaerobic, resistant to environmental factors, but sensitive to heating to 56 ° C for 30 minutes, to the effect of basic disinfectants and antibiotics.

Features of beta-hemolytic streptococcus strains of group A, causing an erysipelas, are not currently fully understood. The assumption that they produce toxins identical to scarlatinose was not confirmed: vaccination with erythrogenic toxin does not provide a preventive effect, and antitoxic antiscarlatinose serum does not affect the development of erysipelas.

In recent years, it has been suggested that other microorganisms participate in the development of erysipelas. For example, with bullet-hemorrhagic forms of inflammation with abundant effusion of fibrin, in addition to beta-hemolytic group A streptococcus, Staphylococcus aureus, beta-hemolytic streptococci of groups B, C, G, gram-negative bacteria (esherichia, protei) are isolated from the wound contents .

[1], [2], [3], [4]

Pathogenesis of erysipelas

The erysipelas occur against the background of a predisposition, which is probably innate and represents one of the variants of the genetically determined reaction of HRT. Frequent erysipelas are affected by people with blood group III (B). Obviously, the genetic predisposition to the erysipelas reveals itself only in the elderly (more often in women), against the background of repeated sensitization to the beta-hemolytic streptococcus of group A and its cellular and extracellular products (virulence factors) in certain pathological conditions, including those associated with involutional processes.

With the primary and repeated erysipelas, the main pathway of infection is exogenous. With a recurrent erysipelas, the pathogen spreads lymphogenically or hematogenously from the foci of streptococcal infection in the body. With frequent recurrences of erysipelas in the skin and regional lymph nodes, a chronic infection (L-form of beta-hemolytic group A streptococcus) arises. Under the influence of various provoking factors (hypothermia, overheating, trauma, emotional stress), L-forms are reversed into bacterial forms of streptococcus, which cause recurrence of the disease. With rare and late recurrences of erysipelas, reinfection and superinfection with new strains of beta-hemolytic streptococcus group A (M-types) are possible.

To provoking factors contributing to the development of the disease, include violations of the integrity of the skin (abrasions, scratches, scratches, injections, rubs, cracks, etc.), bruises, a sharp change of temperature (hypothermia, overheating), insolation, emotional stress.

Predisposing factors are:

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

Thus, the first stage of the pathological process is the introduction of beta-hemolytic group A streptococcus into the skin area when it is damaged (primary erysipelas) or infected from the focus of dormant infection (recurrent form of erysipelas) with the development of erysipelas. Endogenous infection can spread directly from the focus of an independent disease of streptococcal etiology. 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 toxinemia that causes intoxication (characterized by an acute onset of the disease with fever and chills).

In the future, the local focus of infectious-allergic skin inflammation with the participation of immune complexes (the formation of perivascularly located immune complexes containing the SZ-complement fraction), capillary lympho- and blood circulation in the skin with the formation of lymphostasis, the formation of hemorrhages and blisters with serous and hemorrhagic contents is disrupted.

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

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

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

It should be emphasized that the disease occurs only in persons who have a congenital or acquired predisposition to it. Infectious-allergic or immunocomplex mechanism of inflammation in erysipelas determines its serous or serous-hemorrhagic character. Accession of purulent inflammation indicates a complicated course of the disease.

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

When microscopic local focus of erysipelatous inflammation, serous or serous-hemorrhagic inflammation is noted (edema, small-cell infiltration of the dermis, more pronounced around the capillaries). Exudate contains a large number of streptococci, lymphocytes, monocytes and erythrocytes (with hemorrhagic forms). Morphological changes are characteristic of microcapillary arteritis, phlebitis and lymphangitis.

With erythematous-bullous and bullet-hemorrhagic forms of inflammation, an epidermal detachment occurs with the formation of blisters. When hemorrhagic forms of erysipelas in the local focus, note thrombosis of small blood vessels, diapedesis of erythrocytes in the intercellular space, abundant deposition of fibrin.

In the period of convalescence, in the uncomplicated course of erysipelas, large or small-flaked skin peeling in the region of the local inflammation focus is noted. With the recurring course of erysipelas, the connective tissue gradually grows in the dermis - as a result, the lymph drainage is broken and persistent lymphostasis develops.

Epidemiology of erysipelas

The erysipelas are a widespread sporadic disease with low contagiosity. Low contagiosity of erysipelas is associated with improved sanitary and hygienic conditions and compliance with the rules of antiseptic in medical institutions. Despite the fact that patients with erysipelas are often hospitalized in general departments (therapy, surgery), among the neighbors in the ward, in the families of patients, repeated cases of erysipelas are rarely recorded. Approximately in 10% of cases, hereditary predisposition to the disease was noted. Wound face is very rare nowadays. There is virtually no maternal newborn. For which high lethality is characteristic.

The source of the infectious agent is rarely detected, which is due to the widespread spread of streptococci in the environment. The source of the pathogen of infection in the exogenous pathway of infection may be patients with streptococcal infections and healthy bacterial carriers of streptococcus. Along with the main one. Contact mechanism for transmission of infection possible aerosol transfer mechanism (airborne droplet) with primary infection of the nasopharynx and the subsequent introduction of the causative agent on the skin by hands, as well as lymphogenous and hematogenous pathways.

With the initial face, beta-hemolytic group A streptococcus penetrates the skin or mucous membranes through cracks, intertrigo, various microtraumas (exogenous pathway). In the face face - through the cracks in the nostrils or damage to the external auditory canal, with the lower extremities face - through cracks in the interdigital spaces, on the heels or damage in the lower third of the shin. To damage include minor cracks, scratches, pinpoints and micro-traumas.

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

Currently, patients under the age of 18 register only single cases of erysipelas. From the age of 20, the incidence increases, and in the age range of 20 to 30 years, men are more likely than women, which is due to the predominance of primary erysipelas and a professional factor. The bulk of patients - people aged 50 years and older (up to 60-70% of all cases). Among the workers, manual workers predominate. The greatest morbidity is noted among locksmiths, loaders, drivers, masons, carpenters, cleaners, kitchen workers and other professionals associated with frequent microtraumatization and skin contamination, as well as abrupt temperature changes. Relatively often sick housekeepers and pensioners, who usually observe relapsing forms of the disease. The increase in morbidity is noted in the summer-autumn period.

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

Specific prevention of erysipelas is not developed. Nonspecific measures are related to the observance of rules of aseptic and antiseptic in medical institutions, with the observance of personal hygiene.

[5], [6], [7], [8]