AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Background

Erysipelas is a superficial bacterial skin infection that characteristically extends into the cutaneous lymphatics. This disease has been traced back to the Middle Ages where it was referred to as "St Anthony's Fire," named after an Egyptian healer who was known for successfully treating the infection. Historically, this infection occurred on the face and was caused by Streptococcus pyogenes. However, a shift in the distribution and etiology of the disease has occurred, with most erysipelas infections now occurring on the legs and with non–group A streptococci sometimes being identified as the etiologic agents.

Pathophysiology

Bacterial inoculation into an area of skin trauma is the initial event in developing erysipelas. Thus, local factors, such as venous insufficiency, stasis ulcerations, inflammatory dermatoses, dermatophyte infections, insect bites, and surgical incisions, have been implicated as portals of entry. The source of the bacteria in facial erysipelas is often the host's nasopharynx, and a history of recent streptococcal pharyngitis has been reported in up to one third of cases. Other predisposing factors include diabetes, alcohol abuse,¹ HIV infection, nephrotic syndrome, other immunocompromising conditions, and vagrant lifestyle.

The infection rapidly invades and spreads through the lymphatic vessels. This can produce overlying skin "streaking" and regional lymph node swelling and tenderness. Immunity does not develop to the inciting organism.

Frequency

United States

Isolated cases are the rule with erysipelas, although epidemics have been reported. The incidence of erysipelas declined throughout the mid-20th century, possibly due to antibiotic development, improved sanitation, and decreased virulence. The change in distribution from the face to the lower extremities is most likely related to an aging population with risk factors such as lymphedema. Approximately 85% of cases occur on the legs rather than the face.

International

Erysipelas is somewhat more common in European countries. Isolated cases are still the rule, and distribution and etiology remain similar to that in the United States.

Mortality/Morbidity

The most common complaints during the acute infection include tenderness of the involved area, fever, chills, and swelling. Death as a direct result of erysipelas is exceedingly rare. Predisposed patients often develop local recurrence, and this can lead to disfiguring and disabling healing reactions, such as elephantiasis nostras verrucosa. This chronic warty, edematous condition is caused by lymphatic destruction from repeated infection.

Race

Erysipelas infections affect all races.

Sex

Erysipelas has been reported to be more common in females, but occurring at an earlier age in males because of their more aggressive activities. Other studies indicate that predisposing factors, rather than gender, account for any male/female differences in incidence.

Age

Cases of erysipelas have been reported in all age groups, but it does appear that infants, young children, and elderly patients are the most commonly affected groups. The peak incidence has been reported to be in patients aged 60-80 years, especially in patients who are considered high-risk and immunocompromised or those with lymphatic drainage problems (eg, after mastectomy, pelvic surgery, bypass grafting).

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

History

Patients often cannot recall an inciting event, but there may be a history of recent trauma or pharyngitis. Prodromal symptoms, such as malaise, chills, and high fever, often begin before the onset of the skin lesions and usually are present within 48 hours of cutaneous involvement. Pruritus, burning, and tenderness are typical complaints.

Physical

Erysipelas begins as a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque. The lesion classically exhibits raised sharply demarcated advancing margins. Local signs of inflammation, such as warmth, edema, and tenderness, are universal. Lymphatic involvement often is manifested by overlying skin streaking and regional lymphadenopathy. More severe infections may exhibit numerous vesicles and bullae along with petechiae and even frank necrosis. With treatment, the lesion often desquamates and can resolve with pigmentary changes that may or may not resolve over time.

Causes

Streptococci are the primary cause of erysipelas. Most facial infections are attributed to group A streptococci, with an increasing percentage of lower extremity infections being caused by non–group A streptococci. Streptococcal toxins are thought to contribute to the brisk inflammation that is pathognomonic of this infection. No clear proof has emerged that other bacteria cause typical erysipelas, although they clearly coexist with streptococci at sites of inoculation. Recently, atypical forms reportedly have been caused by Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae, Yersinia enterocolitica, and Moraxella species, and they should be considered in cases refractory to standard antibiotic therapy.

The role of Staphylococcus aureus, and specifically methicillin-resistant S aureus, remains controversial. No conclusive evidence demonstrates a pathogenic role for staphylococci in typical erysipelas. The infection's predictable response to penicillin, even when S aureus is present, argues against S aureus as an etiologic agent. However, analogous to what occurs in bullous impetigo or staphylococcal scalded skin syndrome, exotoxins from coexisting S aureus may account for the clinical presentation of bullous erysipelas.²

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Other Problems to be Considered

Erysipelas can be differentiated from cellulitis by its characteristically raised advancing edges and sharply demarcated borders, reflecting its more superficial nature. Cellulitis has no lymphatic component and exhibits indiscreet margins.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab Studies

• In classic erysipelas, no laboratory workup is required for diagnosis or treatment.
• Routine blood and tissue cultures are not cost-effective because they have an extremely low yield and results have a minimal impact on management. Cultures are perhaps best reserved for very immunosuppressed hosts in whom an atypical etiologic agent might be more likely.³
• Bacterial cultures from the portal of entry may be most helpful in persons with atypical clinical presentations.

Imaging Studies

• Imaging studies are not usually indicated and are of low yield. MRI and bone scintigraphy are helpful when early osteoarticular involvement is suspected. In this setting, standard radiographs are typically normal.

Histologic Findings

The histologic hallmarks of erysipelas are marked dermal edema, vascular dilatation, and streptococcal invasion of lymphatics and tissues. This bacterial invasion results in a dermal inflammatory infiltrate consisting of neutrophils and mononuclear cells. The epidermis is often secondarily involved. Rarely, bacterial invasion of local blood vessels may be seen.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Medical Care

• Elevation and rest of the affected limb are recommended to reduce local swelling, inflammation, and pain.
• Saline wet dressings should be applied to ulcerated and necrotic lesions and changed every 2-12 hours, depending on the severity of the infection.
• Streptococci cause most cases of erysipelas; thus, penicillin has remained first-line therapy.⁴ Penicillin administered orally or intramuscularly is sufficient for most cases of classic erysipelas and should be given for 10-20 days.
• A cephalosporin or macrolide, such as erythromycin or azithromycin, may be used if the patient has an allergy to penicillin. Cephalosporins may cross-react with penicillin first-generation cephalosporins and should not be used in patients with a history of severe penicillin allergy, urticarial reactions, or anaphylaxis.
• Hospitalization for close monitoring and intravenous antibiotics is recommended in severe cases and in infants, elderly patients, and patients who are immunocompromised.
• Coverage for S aureus is not usually necessary for typical infections, but it should be considered in patients who do not improve with penicillin or who present with atypical forms of erysipelas, including bullous erysipelas. Some authors believe that facial erysipelas should be treated empirically with a penicillinase-resistant antibiotic, such as dicloxacillin or nafcillin, to cover possible S aureus infection, but supporting evidence for this recommendation is lacking.²
• Two drugs, roxithromycin and pristinamycin, have been reported to be extremely effective in the treatment of erysipelas. Several studies have demonstrated greater efficacy and fewer adverse effects with these drugs compared with penicillin.⁵ Currently, the Food and Drug Administration has not approved these drugs in the United States, but they are in use in Europe.
• Patients with recurrent erysipelas should be educated regarding local antisepsis and general wound care. Predisposing lower extremity skin lesions (eg, tinea pedis, stasis ulcers) should be treated aggressively to prevent superinfection. Use of compression stockings should be encouraged for as long as 1 month in previously healthy patients and for the long-term in patients with preexisting lower extremity edema. Long-term prophylactic antibiotic therapy generally is accepted, but no true guidelines are available. Treatment regimens should be tailored to the patient. One reported regimen is benzathine penicillin at 2.4 MU intramuscularly every 3 weeks for up to 2 years.⁶

Surgical Care

Debridement is necessary only in severe infections with necrosis or gangrene.

Consultations

Most patients with erysipelas respond very well to conventional antibiotic therapy. However, in atypical infections that are unresponsive to first- and second-line agents, an infectious disease consult may be useful.

Activity

Patients with acute infections involving the extremities should be encouraged to limit their activity and keep the limb elevated to decrease swelling.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

The objective of pharmacotherapy is to reduce morbidity and to prevent complications.

Drug Category: Antibiotics

Penicillin is the standard therapy for typical erysipelas, although coverage for S aureus should be considered in the appropriate setting.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Complications

The most common complications of erysipelas include abscess, gangrene, and thrombophlebitis. Less common complications (<1%) are acute glomerulonephritis, endocarditis, septicemia, and streptococcal toxic shock syndrome. Rare osteoarticular complications involve joints contiguous with the erysipelas plaques and include bursitis, osteitis, arthritis, and tendinitis.⁷

Prognosis

The prognosis for patients with erysipelas is excellent. Complications of the infection usually are not life threatening, and most cases resolve after antibiotic therapy without sequelae. However, local recurrence has been reported in up to 20% of patients with predisposing conditions.

MULTIMEDIA

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Media file 1:  Facial erysipelas exhibiting classic fiery-red plaque with raised, well-demarcated borders.
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Media type:  Photo

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

1. Jorup-Rönström C. Epidemiological, bacteriological and complicating features of erysipelas. Scand J Infect Dis. 1986;18(6):519-24. [Medline].
2. Krasagakis K, Samonis G, Maniatakis P, Georgala S, Tosca A. Bullous erysipelas: clinical presentation, staphylococcal involvement and methicillin resistance. Dermatology. 2006;212(1):31-5. [Medline].
3. Leppard BJ, Seal DV, Colman G, Hallas G. The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas. Br J Dermatol. May 1985;112(5):559-67. [Medline].
4. Bishara J, Golan-Cohen A, Robenshtok E, Leibovici L, Pitlik S. Antibiotic use in patients with erysipelas: a retrospective study. Isr Med Assoc J. Oct 2001;3(10):722-4. [Medline].
5. Bernard P, Plantin P, Roger H, Sassolas B, Villaret E, Legrain V, et al. Roxithromycin versus penicillin in the treatment of erysipelas in adults: a comparative study. Br J Dermatol. Aug 1992;127(2):155-9. [Medline].
6. Sjöblom AC, Eriksson B, Jorup-Rönström C, Karkkonen K, Lindqvist M. Antibiotic prophylaxis in recurrent erysipelas. Infection. Nov-Dec 1993;21(6):390-3. [Medline].
7. Coste N, Perceau G, Léone J, Young P, Carsuzaa F, Bernardeau K, et al. Osteoarticular complications of erysipelas. J Am Acad Dermatol. Feb 2004;50(2):203-9. [Medline].
8. Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med. Jan 25 1996;334(4):240-5. [Medline].
9. Bonnetblanc JM, Bédane C. Erysipelas: recognition and management. Am J Clin Dermatol. 2003;4(3):157-63. [Medline].
10. Bratton RL, Nesse RE. St. Anthony's Fire: diagnosis and management of erysipelas. Am Fam Physician. Feb 1 1995;51(2):401-4. [Medline].
11. Chartier C, Grosshans E. Erysipelas. Int J Dermatol. Sep 1990;29(7):459-67. [Medline].
12. Chartier C, Grosshans E. Erysipelas: an update. Int J Dermatol. Nov 1996;35(11):779-81. [Medline].
13. Elston DM. Epidemiology and prevention of skin and soft tissue infections. Cutis. May 2004;73(5 Suppl):3-7. [Medline].
14. Grosshans EM. The red face: erysipelas. Clin Dermatol. Apr-Jun 1993;11(2):307-13. [Medline].
15. Hammar H, Wanger L. Erysipelas and necrotizing fasciitis. Br J Dermatol. Apr 1977;96(4):409-19. [Medline].
16. Ronnen M, Suster S, Schewach-Millet M, Modan M. Erysipelas. Changing faces. Int J Dermatol. Apr 1985;24(3):169-72. [Medline].
17. Török L. Uncommon manifestations of erysipelas. Clin Dermatol. Sep-Oct 2005;23(5):515-8. [Medline].
18. Zeglaoui F, Dziri C, Mokhtar I, Ezzine N, Kharfi M, Zghal M, et al. Intramuscular bipenicillin vs. intravenous penicillin in the treatment of erysipelas in adults: randomized controlled study. J Eur Acad Dermatol Venereol. Jul 2004;18(4):426-8. [Medline].

Article Last Updated: Feb 11, 2008