Erysipelas A46

Frequent, acute, less frequently chronically recurrent, febrile, possibly accompanied by chills, non-pathogenic, usually asymmetric (exception facial serysipele, see Fig.), bacterial infection of the skin that can spread rapidly lymphogenically.

Beta-haemolytic streptococci of group A, as well as representatives of groups B, C and G. Recent studies indicate that staphylococci (Staphylococcus aureus) and, very rarely, pneumococci (especially in immunocompromised patients) can also play a pathogenetic role in bullous erysipelas and necrotizing forms (Bachmeyer C et al. 2012); see also MRSA.

Gram-negative pathogens (e.g. E. coli, Pseudomonas aeruginosa) can also play a pathogenetic role in rare cases, particularly in immunocompromised patients.

There are contradictory data on the incidence rates:

Incidence: 100/100,000 persons/year.

According to an American study (Ren Z et al. 2021), the incidence is:

• for adults: 2.42 to 3.55/1,000,000
• and for children: 1.14 to 2.09/1,000,000

Penetration of streptococci through skin areas with barrier disruption into the cutaneous lymph channels (often after tinea pedum or minor mechanical trauma; "erysipelas"). Persistent lymphoedema, as well as erosions due to focal dehydration of the skin, are precursors for infection (e.g. oedema after long saphenectomy during bypass operations).

Pathophysiologically, there is an open portal of entry, often lesions in areas affected by athlete's foot, rhagades, ulcers, puncture sites or erosions. Through these, the bacteria enter the superficial lymph channels and trigger an acute inflammatory skin infection with systemic involvement that often spreads extensively.

Prefers adults between the ages of 20 and 70. In larger studies, the average age is around 50 years. Children and adolescents are less frequently affected.

The possible ports of entry determine the predilection sites (especially the face and lower leg), whereby there is usually a certain distance between the erysipelas and the port of entry.

• Extremities:
  • Lower legs (about 70 % of cases)
  • Forearms (about 12 % of cases)
• Face (about 13 % of cases): especially cheek area, nasal entrance in rhinitis. (DD: dermatomyositis; systemic lupus erythematosus, rosacea)
• Trunk (about 3 % of cases)

Remark: The nasopharynx of the affected person is an important reservoir of germs (20-30 % of young adults are carriers of Streptococcus pyogenes. Nayak N et al. 2016)

Mostly asymmetrical, acute, painful, rapidly spreading, edematous dermatitis with sharply defined, extensive redness with a finger-like configuration at the edges and an intense, smooth surface. The affected area is noticeably overheated and clearly painful to the touch. If left untreated, the dermal inflammation spreads rapidly lymphogenously.

The acute infection is accompanied by chills, fever (up to 40 °C), painful lymphangitis and lymphadenitis. It is not uncommon for vesicles and hemorrhagic blisters to form as complications (erysipelas vesiculosum et bullosum).

Leukocytosis with neutrophilia, elevated ESR and CRP. ASL and anti-streptodornase B titer (ADB, anti-DNase B) increased.

Variable picture depending on the acuteity of the infection. Initial perivascular infiltrate of lymphocytes, neutrophils and scattered eosinophils. Marked edema of the upper dermis with protruding lymphatic vessels and bulging erythrocyte-filled blood vessels. The infiltrate is increasingly dominated by a neutrophil component. Erythrocyte extravasations are occasionally observed in uncomplicated infections. The hemorrhagic component may dominate in hemorrhagic erysipelas. Pathogen detection is not possible!

Clinical:

• Acute dermatitis (no fever, no lymphadenitis, itching)
• Initial zoster (important in differentiation from facial erysipelas; pain often dominant, no fever, no painful lymphadenitis, later segmental spread with vesicle or blister formation)
• Superficial thrombophlebitis (cord-like induration, fever usually absent)
• Lymphangitis acuta (characteristic linear redness along a lymphatic duct)
• Erysipelas carcinomatosum (usually board-like infiltration, lack of acuteity)
• Erysipeloid (infection is bland, localization: hands)
• Angioedema (no fever, no lymphadenitis)
• Facial erysipelas
  • Rosacea erythematosa (chronic condition, no fever, variable redness and swelling)
  • Dermatomyositis/SLE (severe chronic clinical picture with adynamia and signs of an autoimmunological disease)
  • Acute dermatitis (contact events detectable, acuteity within a few hours; vesicular dermatitis)
  • Angioedema (acute swelling, no fever, no lymphangitis, no pain)
  • Phlegmon
  • Thrombophlebitis
  • Erythema nodosum (highly painful plaques and nodules, usually no extensive redness)
  • Stasis dermatitis (in contrast to erysipelas, fever and pain are absent here)
  • Contact dermatitis (itchy erythema or plaques, in contrast to erysipelas always without fever)
  • Erysipelas-like cutaneous leishmaniasis (vacation trip; slow onset, no fever, no lymphadenitis, persistence for months, antibiotic resistance)

Histologic:

• Erysipeloid (cannot be distinguished from erysipelas; complicative components absent);
• Acute febrile neutrophilic dermatosis (diffuse, very dense, neutrophilic dermis infiltration, hemorrhages absent; clinical picture must be considered);
• Light dermatosis, polymorphic (severe dermal edema, no neutrophilia, epidermis mostly spongiotic).

A hemorrhagic component can be seen as a worsening of the infection.

Blistering with very exudative inflammatory reaction: see below Erysipelas bullous

Phlegmon: see below Erysipelas phlegmonous (blurred accumulations of pus along the anatomical lines)

Gangrenous erysipelas (erysipelas gangraenosum): dreaded necrotizing form of the disease

Necrotizing fasciitis: as a severe, rapidly progressing, life-threatening soft tissue infection

Septic erysipelas: sepsis with endocarditis and possibly glomerulonephritis (<5%) originating from the erysipelas of the skin.

Facial erysipelas: particularly feared variant of erysipelas, especially if the erysipelas begins over the nasal saddle. Possible spread to the orbit.

Erysipelas recurrence (see below erysipelas, recurrent): Recurrences are observed in 10 % of cases within 6 months (30 % within 3 years).

Chronic recurrent erysipelas: Recurrent erysipelas is preferentially observed in patients with comorbidities, including hypertension, obesity, CVI and diabetes (Li A et al. 2021). With recurrent erysipelas, there is a risk of secondary lymphoedema with all the resulting possible secondary conditions(papillomatosis cutis lymphostatica, macrocheilia).

Streptococcal allergic, systemic sequelae: acute streptococcal glomerulonephritis

Systemic antibiotics see Table 1.

Heparinization during bed rest. Antipyretic and, if necessary, analgesic measures with paracetamol (e.g. Ben-u-ron Tbl.) 3 times/day 500-1000 mg p.o.

If swelling persists from the 3rd-5th day after antibiotic treatment, manual and, if necessary, additional intermittent lymphatic drainage.

Remember! No lymph drainage in an acute inflammatory state! Spread of germs!

In the case of recurrent erysipelas: treatment of the acute symptoms, followed by regular penicillin cycles and lymphoedema treatment for 1 year.

see below Erysipelas, recurrent

Bed rest, cooling and elevation of the affected body part. Once the acute inflammation has subsided, supportive lymph drainage may be indicated. In the case of facial erysipelas, speech is prohibited and a passaged diet is indicated.

Moist compresses with antiseptic additives such as polihexanide (Serasept, Prontoderm), quinolinol solution(e.g. Chinosol 1:1000), R042 or potassium permanganate solution(light pink). Renew every 2 hours! Permanent and consistent treatment of the entry point (e.g. tinea pedis).

Favorable with sufficient antibiotic therapy. If there is a predisposition (untreated tinea, lymphoedema, chronic venous insufficiency), there is a risk of recurrence, usually in the same location. Any underlying disease must be treated accordingly.

Another possible cause of recurrence is intracellular uptake and persistence of streptococci. As β-lactam antibiotics only achieve bactericidal concentrations in the extracellular space, it may be necessary to additionally use intracellularly active antibiotics such as clindamycin, macrolides and rifampicin. The combination of clindamycin or rifampicin together with penicillin is currently proving to be the most effective combination for the treatment of group A streptococcal infections (see also erysipelas, recurrent).

System therapy in erysipelas

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2. Brennecke S, Hartmann M, Schofer H, Rasokat H, Tschachler E, Brockmeyer NH (2005) Treatment of erysipelas in Germany and Austria--results of a survey in German and Austrian dermatological clinics. J Dtsch Dermatol Ges 3: 263-270
3. Hadzovic-Cengic M et al.(2012) Cellulitis--epidemiological and clinical characteristics. Med Arch 66(3 Suppl 1):51-53
4. Krasagakis K et al. (2006) Bullous erysipelas: clinical presentation, staphylococcal involvement and methicillin resistance. Dermatology 212: 31-35
5. Li A et al (2021) Risk factors of recurrent erysipelas in adult Chinese patients: a prospective cohort study. BMC Infect Dis 21:26.
6. Nayak N et al (2016) Clinical implications of microbial biofilms in chronic rhinosinusitis and orbital cellulitis.BMC Ophthalmol 16:165.

7. Parajuli N et al (2020) Case Report: Erysipeloid Cutaneous Leishmaniasis Treated with Oral Miltefosine. Am J Trop Med Hyg 104:643-645.

8. Ren Z et al (2021) Burden, risk factors, and infectious complications of cellulitis and erysipelas in US adults and children in the emergency department setting. J Am Acad Dermatol 84:1496-1503.
9. Schwartz MN (2004) Cellulitis. N Eng J Med 350: 904-912.
10. Segnitz A et al (2010) Afebrile erysipelas under etanercept. Akt Dermatol 35: 444-446
11. Sunderkotter C, Herrmann M, Jappe U (2006) Antimicrobial therapy in dermatology. J Dtsch Dermatol Ges 4: 10-27.