Erysipelas

Etiology and properties of the pathogen

The disease is caused by group A $\beta$-hemolytic streptococcus (Streptococcus pyogenes). It is a Gram-positive microbe that typically appears in chains. The bacterium is fairly stable in the external environment: it withstands drying and can persist in biological substrates for months, but is rapidly killed by boiling and contact with disinfectants.

A key feature of GAS is its ability to transform into L-forms (e.g., under the influence of certain antibiotics). This allows the microorganism to persist inside macrophages for a long time, which forms the basis for chronic, recurrent erysipelas. The main virulence factors of streptococcus:

• M-protein — inhibits phagocytosis and is the main virulence factor.
• Capsule (made of hyaluronic acid) — masks the bacterium as it resembles human tissues.
• Enzymes and toxins (streptolysins, hyaluronidase, erythrogenic toxin) — damage tissues, cause intoxication, and trigger autoimmune reactions.

Epidemiology and risk factors

Erysipelas is an anthroponotic infection with low contagiousness. The source of infection consists of patients with various streptococcal infections (tonsillitis, scarlet fever) or bacterial carriers.

Infection occurs via two main routes:

1. Exogenously (contact route) — the pathogen penetrates through microtraumas, abrasions, and cracks in the skin (typical for primary and recurrent erysipelas).
2. Endogenously (hematogenously/lymphogenously) — microbes enter the skin from existing foci of chronic infection, such as tonsillitis or dental caries (typical for recurrent erysipelas).

The development of the disease is facilitated by background conditions: chronic venous or lymphatic insufficiency, diabetes mellitus, and foot mycoses. Triggering factors ('triggers') can include hypothermia, stress, and trauma. Women and elderly individuals are more frequently affected. A summer-autumn seasonality is observed.

Mechanisms of development (Pathogenesis)

In the acute form, bacteria penetrate through damaged skin and multiply in the lymphatic capillaries of the dermis. This leads to bacteremia and the release of toxins, causing sudden fever and severe intoxication. Locally, hyperergic inflammation develops (type IV hypersensitivity), and microcirculation and lymph drainage are disrupted.

In the chronic (recurrent) form, streptococcal L-forms 'hide' in skin cells and lymph nodes. When immunity drops (stress, hypothermia), they revert back to bacterial forms. A new round of toxinemia and local inflammation occurs in the same area of the skin. Streptococcal antigens share similarities with human tissues, so the immune system begins to attack its own cells, sustaining an autoimmune inflammatory process.

Clinical presentation

The disease begins acutely, with a pronounced intoxication syndrome: chills, fever up to 39–40°C, and weakness.

A few hours (or 1–2 days) later, local symptoms appear:

• An area of bright erythema appears on the skin (most often on the lower leg or face).
• The erythema is hot to the touch, slightly raised above healthy skin, and has clear, uneven borders.
• Mild tenderness is present, more pronounced at the periphery of the lesion.
• The development of edema and enlargement of regional lymph nodes (lymphadenitis) are characteristic.

The disease can lead to serious complications: local (abscesses, phlegmon, necrosis) and systemic (sepsis, infectious-toxic shock).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Clinical classification of erysipelas forms and severity grades.
• Differential diagnosis with phlegmon, eczema, and erysipeloid.
• Principles of etiotropic antibacterial therapy.
• Pathogenetic treatment and hospitalization rules.
• Prevention of frequent disease recurrences.

Other topics in the section "Infections of the Integumentary System and Sepsis"

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