Erysipelas A46

Author: Prof. Dr. med. Peter Altmeyer

Co-Autors: Dr. med. Jeton Luzha, Hadrian Tran

All authors of this article

Last updated on: 25.09.2022

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Synonym(s)

Cellulite; erysipelas; Erysipelas; Erysipelas gangrenous; Erysipelas phlegmonous; Facial Rose; Mucosal erysipelas; Rose; Rotlauf; Streptodermia cutanea lymphatica

Definition
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Frequent, acute, less frequently chronic recurrent, febrile, possibly accompanied by chills, non-pathogenic, usually asymmetric, bacterial local infection of the skin that may spread rapidly lymphogenically.

Pathogen
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Beta-hemolytic streptococci of group A, as well as representatives of groups B, C, and G. Recent studies indicate that in bullous erysipelas and in necrotizing forms, staphylococci (Staphylococcus aureus) and, very rarely, pneumococci (especially in immunocompromised patients) may also play a pathogenetic role (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, especially in immunosuppressed patients.

Occurrence/Epidemiology
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There are contradictory data on the incidences:

Incidence: 100/100,000 persons/year.

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

  • for adults: 2.42 to 3.55/1,000,000
  • and for children: 1.14 to 2.09/1.000.000

Etiopathogenesis
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Penetration of streptococci through barrier-disrupted skin into cutaneous lymphatic ducts (often after tinea pedum or minor mechanical trauma; "erysipelas"). Persistent lymphedema, including erosions due to focal desiccation of the skin, are pathogens for infection (e.g., edema after long saphenectomy for bypass surgery).

Pathophysiology
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Pathophysiologically, there is an open port of entry. Common ports of entry are athlete's foot, rhagades, ulcers, puncture sites or erosions. Entry through the portal allows the bacteria to enter the lymphatic vessels, and from here the bacteria can spread and cause inflammation of the skin.

Manifestation
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Preferably adults between the ages of 20 and 70 . Lj. In larger studies the average age is about 50 years. Children and adolescents are less frequently affected.

Localization
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The possible entry sites determine the predilection sites (mainly face and lower leg), whereby there is usually a certain distance between erysipelas and the entry site.

Note: a major source as a reservoir of germs is the nasopharynx of the affected persons themselves (germ carriers of Str. pyogenes are 20-30% of young eadults - Nayak N et al. 2016).

Clinical features
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Usually asymmetric, acute painful, rapidly spreading, edematous dermatitis with sharply demarcated, areal, marginally also finger-shaped configured, intense, surface-smooth redness. The affected area is markedly hyperthermic and hypersensitive to palpation. If left untreated, there is rapid spread of dermal inflammation. The acute infection is accompanied by chills, fever (up to 40 °C) and painful lymphangitis and lymphadenitis. Not infrequently, complicating vesicles and hemorrhagic blistering may occur (erysipelas vesiculosum et bullosum).

Laboratory
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Leukocytosis with neutrophilia, BSG and CRP elevation. ASL and anti-streptodornase B(ABD) titers elevated.

Histology
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Variable picture depending on the acuteity of the infection. Initial perivascular infiltrate from lymphocytes, neutrophils and isolated eosinophils. Prominent edema of the upper dermis with dilated lymphatic vessels and bulging erythrocyte-filled blood vessels. Increasingly the infiltrate is dominated by a neutrophil component. Occasionally erythrocyte extravasations are observed in uncomplicated infections. The hemorrhagic component may dominate in hemorrhagic erysipelas. Pathogen detection is not successful!

Diagnosis
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Clinical picture with the typical triad (E = erythema; F = fever; L = lymphadenitis)

Differential diagnosis
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Clinical:

  • acute dermatitis (no fever, no lymphadenitis, itching)
  • initial zoster (important in differentiation from facial serysipelas; pain often predominant, no fever, no painful lymphadenitis, later pathological segmental spread with vesicle or blister formation)
  • superficial thrombophlebitis (cord-like induration, fever usually absent)
  • lymphangitis acuta (characteristic linear redness along a lymphatic pathway)
  • Erysipelas carcinomatosum (usually board-like infiltration, acuity absent)
  • Erysipeloid (infection proceeds blandly, localization - hands)
  • Angioedema (no fever, no lymphadenitis)
  • Facial erysipelas
    • Rosacea erythematosa (chronic condition, no fever, alternating redness and swelling)
    • Dermatomyositis/SLE(severe chronic condition with adynamia and signs of autoimmunologic disease)
    • Acute dermatitis (contact history detectable, acute 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).

Histological:

Complication(s)
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  • A hemorrhagic component may be considered an exacerbation of the infection.
  • Blistering with very exudative inflammatory reaction: see below Erysipelas bullous.
  • Phlegmonous: see below. Erysipelas phlegmonous (fuzzy collections of pus along the anatomical guide rails).
  • Gangrenous erysipelas (Erysipelas gangraenosum): dreaded necrotizing course.
  • Necrotizing fasciitis as a severe, rapidly progressive, life-threatening soft tissue infection.
  • Septic erysipelas: sepsis with endocarditis and possibly glomerulonephritis (<5%) originating from the erysipelas of the skin.
  • Facial erysipelas: a particularly dreaded variant of erysipelas, especially when the erysipelas begins above the nasal saddle. In this case, spread to the orbita is possible.
  • Erysipelas recurrence (see below Erysipelas, recurrent): Recurrences are observed within 6 months in 10% of cases (30% within 3 years).
  • Chronic recurrent erysipelas: Recurrent erysipelas is preferentially observed in patients with co-morbidities including hypertension, obesity, CVI, and diabetes (Li A et al 2021). Recurrent erysipelas carries the risk of secondary lymphedema with all the possible sequelae that may result(papillomatosis cutis lymphostatica, macrocheilia).
  • Streptococcal allergic systemic sequelae: acute streptococcal glomerulonephritis .

Therapy
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Systemic antibiosis 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.

In case of persistent swelling, manual and, if necessary, additional intermittent lymphatic drainage with apparatus from the 3rd-5th day after antibiosis.

Notice! No lymphatic drainage in acute inflammation! Germs are spread!

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

S.u. Erysipelas, recurrent.

General therapy
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Bed rest, cooling and elevation of the affected body part. After the acute inflammatory reaction has subsided, lymph drainage can be supportive. In the case of facial erysipelas, speaking is forbidden and the indication for passed fare exists.

External therapy
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Moist envelopes 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 rehabilitation of the entry portal (e.g. Tinea pedis).

Progression/forecast
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Under sufficient antibiotic therapy favorable. In case of predisposition (untreated tinea, lymphedema, chronic venous insufficiency) danger of recurrence. An existing underlying disease must be treated accordingly.

Tables
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System therapy for erysipelas

Pharmaceutical substance and sample preparation

Dose

Therapy duration

Uncomplicated course

Penicillin V (e.g. Megacillin)

1.5-3 million IU/day p.o. in 3-4 ED

10 days

Complicated course or chronic recurrence

Penicillin G (e.g. Penicillin Grünenthal)

15-30 million IU/day in 3-4 ED (max. 30 mega/day)

until healed

Complicated course/penicillin allergy

Vancomycin

40-60 mg/kg/day in 2-3 ED

until healed

Mixed infections

Oxacillin (e.g. Infectostaph)

4 times/day 1 g (max. 8 g) i.v. or i.m.

10 days

cephalosporins such as cefotaxime (e.g. claforan)

2-3 times/day 2 g i.v.

Until healing

Combination of cefuroxime (e.g. cefuroxime hexal) + gentamicin (e.g. refobacin)

2 times/day 1.5 g i.v. + 240 mg/day i.v.

Until healing

Penicillin allergy

Erythromycin (e.g. erythrocin)

4 times/day 0,5-1 g p.o.

10 days

Clarithromycin (e.g. Klacid)

2 times/day 250-500 mg p.o.

Literature
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  1. Bachmeyer C et al. (2012) Érysipèle à Streptococcus pneumoniae révélateur d'une infection par le virus de l'immunodéficience humaine. Press Med 41:883-884.
  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. 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.
  8. Schwartz MN (2004) Cellulitis. N Eng J Med 350: 904-912.
  9. Segnitz A et al (2010) Afebrile erysipelas under etanercept. Akt Dermatol 35: 444-446
  10. Sunderkotter C, Herrmann M, Jappe U (2006) Antimicrobial therapy in dermatology. J Dtsch Dermatol Ges 4: 10-27.

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

Authors

Last updated on: 25.09.2022