Erysipelas

Etiology

• Erysipelas is a cutaneous infection classically caused by beta-hemolytic streptococcus species. It is distinct from cellulitis in that it is more superficial.
  • Up to 67% of cases are caused by Streptococcus pyogenes (Bonnetblanc, 2003).
  • Streptococcus agalactiae (Group B Streptococcus) is the most common cause in neonates.
    • Erysipelas can rarely be caused by non-Streptococcal species including Staphylococcus aureus (methicillin resistant or methicillin sensitive), Pseudomonas aeruginosa and Clostridium spp.
  • Acutely, there is significant infiltration of neutrophils into the dermis and to a lesser extent the hypodermis.
    • Infiltration of neutrophils and macrophages into the lymphatics can occur, causing lymphatic dilation.

Epidemiology

• Incidence has not been well established as cellulitis and erysipelas are not always easily differentiated. Additionally, most epidemiologic studies are done in hospitals and only include severely ill patients.
  • The combined incidence of cellulitis and erysipelas is approximately 20 per 10,000 European individuals (Bartholomeeusen, 2007).
  • The average age of onset is in the 5th decade of life.
  • There is some evidence that incidence is rising in young children and individuals over 75 years of age (Bartholomeeusen, 2007 & Stulberg, 2002)

Risk factors

• Loss of skin integrity:
  • Trauma (i.e. insect sting, abrasion)
  • Surgical wounds or prior radiation
  • Underlying dermatologic disease:
    • Dermatophytosis was found to be a significant predisposing factor for erysipelas in the primary care setting in individuals aged 45-64 (Bartholomeeusen, 2007).
    • Psoriasis
    • Eczema
  • Previous skin infection
  • Venous insufficiency with ulceration
• Lymphedema
• Nephrotic syndrome
• Pregnancy
• Nasopharyngeal infection
• Immunocompromised states:
  • Diabetes mellitus
  • Obesity
  • Alcoholism
  • Human immunodeficiency virus (HIV)
  • Transplant recipients 

History

• Individuals may experience a prodrome of fevers, chills, malaise, nausea and/or vomiting.

Clinical features

• The most common location is the leg.
  • Facial erysipelas accounts for approximately 6% of cases, making the face the second most commonly affected site (Lazzarini, 2005).
  • Facial erysipelas often appears in a malar distribution (involving the cheeks and nasal bridge)
• Erysipelas presents as the acute onset of a bright red rash with a sharply demarcated, raised border (Figure 1).
• Other features that are sometimes present include:
  • Edema, warmth, firmness and tenderness
  • Fine dimples on the affected region (similar to the skin of an orange)
  • Regional lymphadenopathy and/or lymphangitis
  • Pustules and/or bullae
  • Purpura due to bleeding into the skin

Other diagnostic studies

• The Infectious Disease Society of America does not recommend routine bacteriological skin culture as sensitivity is low (41%).
  • Blood cultures should be obtained if signs of toxicity are present or if the patient is immunosuppressed.
• Other serologic findings that support the diagnosis (but are not routinely required) include: complete blood count with differential showing leukocytosis with neutrophilia, elevated levels of procalcitonin, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR).
  • Though CRP and ESR are only elevated in approximately 50% of cases, elevated inflammatory markers are predictive of more severe disease (Lazzarini, 2005).
• A recent prospective study found that nearly 50% of patients with erysipelas were colonized with beta-hemolytic streptococcus species in the perianal area, making perianal culture a potential new diagnostic method (Trell, 2019).

• Deeper skin infections:
• Preseptal cellulitis  
• Necrotizing fasciitis
• Herpes zoster ophthalmicus
• Herpes simplex infection

• Medical therapy (Infectious Disease Society of America, 2014):
• Erysipelas is treated by empirically covering beta-hemolytic streptococcus species as they are the overwhelmingly most common inciting organism.
• Outpatient management with empiric oral penicillin V potassium for five days is used for mild disease.
• If patients have systemic symptoms, inpatient management with IV penicillin is preferred.
• Macrolides, cephalosporins, and fluoroquinolones have also shown efficacy, but are costlier.
• A systematic review including 43 studies did not find any of the above antibiotics to be more efficacious than another. This review also found a five-day course of treatment to be equally as effective as a longer course of treatment (Brindle, 2019).
• In severe cases unresponsive to initial treatment, other organisms should be suspected and antibiotics should be broadened to vancomycin plus piperacillin/tazobactam.
• Surgical therapy: surgical debridement is only required in severe, necrotizing disease.  
• Prognosis: lesions typically resolve completely over 1-2 weeks without scarring.

• Ocular complications (rare):
• Endogenous endophthalmitis due to hematogenous spread of Streptococcus pyogenes infection has been reported in the literature (Costa, 2015).
• Chronic periocular lymphedema.
  • This mostly occurs with recurrent disease as lymphatic drainage becomes permanently impaired.
  • Although this is a rare complication, a case report demonstrated improvement of periocular lymphedema, without intervention, over several months (Buckland, 2006).
• Other complications
• Abscess formation
• Focal necrosis
• Bacteremia
  • Blood cultures return positive in less than 5% of cases (Bonnetblanc, 2003).
• Infections at distant sites (i.e. infective endocarditis)
• Post-streptococcal glomerulonephritis
• Cavernous sinus thrombosis
• Streptococcal toxic shock syndrome
• Deep vein thrombophlebitits
  • Occurs in less than 5% of cases (Bonnetblanc, 2003).
• Compartment syndrome
  • Usually related to infection with Clostridium spp.
  • Can compromise the airway and circulation if the large vessels of the neck are involved.
• 3-year recurrence rates are up to 30% in patients hospitalized for severe disease and approximately 16% in the those who receive outpatient treatment for mild to moderate disease (Bartholomeeusen, 2007).
  • High recurrence rates may be caused by the persistence of toxins in lymphatic channels due to impaired lymphatic drainage.  
  • Long term penicillin prophylaxis can be considered in these cases.  

Photograph courtesy of D@nderm Atlas of Clinical Dermatology.

Figure 1. Erysipelas presenting as an intensely erythematous, demarcated rash involving the periocular region.

• Bonnetblanc J & Bedane C. Erysipelas recognition and management. Am J of Clin Dermatology. 2003; 4(3): 157-163.
• Bartholomeeusen S, Vandenbroucke J, Truyers C, Buntinx F. Epidemiology and comorbidity of erysipelas in primary care. Dermatology. 2007;215:118–122.
• Stulberg D, Penrod, M, Blanty, RA. Common bacterial skin infections. Am Fam Physician. 2002 Jul 1;66(1):119-125.
• Morris AD. Cellulitis and erysipelas. BMJ Clin Evid. 2008;1708.
• Batista M & Goncalo M. The rash that presents as a red swollen face. Clinics in Dermatology. 2020; 38(1): 63-78.
• Bishara J, Golan-Cohen A, Robenshtok E, et al. Antibiotic use in patients with erysipelas: a retrospective study. Isr Med Assoc J 2001; 3: 722-4.
• Brindle R, Williams MO, Barton E. Assessment of Antibiotic Treatment of Cellulitis and Erysipelas: A Systematic Review and Meta-analysis. JAMADermatol. 2019;155(9):1033-1040.
• Karakonstantis S. Is coverage of S. aureus necessary in cellulitis/erysipelas? A literature review. Infection. 2020;48:183–191.
• Stevens D, Bisno A, Chambers H. Executive Summary: Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America. Clinical Infectious Diseases. 2014; 59(2): 147-159.
• Lazzarini L, Conti E, Tositti G & de Lalla F. Erysipelas and cellulitis: clinical and microbiological spectrum in an Italian tertiary care hospital. J Infect. 2005;51(5):383-9.
• Trell K, Rignér S, Wierzbicka M, et al. Colonization of β-hemolytic streptococci in patients with erysipelas-a prospective study. Eur J Clin Microbiol Infect Dis. 2019;38(10):1901‐1906.
• Costa JF, Marques JP, Marques M, Quadrado MJ. Endogenous endophthalmitis secondary to erysipelas. BMJ Case Reports. 2015: bcr2014209252.
• Buckland G, Carlson J, Meyer D. Persistent Periorbital and Facial Lymphedema Associated With Group A [beta]-Hemolytic Streptococcal Infection (Erysipelas). Ophthal Plast Reconstr Surg. 2007;23(2):161-163.