Introduction
Background
Erysipelas is a superficial bacterial skin infection that characteristically extends into the cutaneous lymphatics. Erysipelas 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, erysipelas occurred on the face and was caused by Streptococcus pyogenes. However, a shift in the distribution and etiology of erysipelas 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.
Preexisting lymphedema is a clear-cut risk factor for erysipelas. Recurrent erysipelas complicating the lymphedema from breast cancer treatment is well documented.2,3 Lymphoscintigraphy in patients with a first-time episode of lower extremity erysipelas has documented lymphatic impairment in both affected and nonaffected legs. Thus, subclinical lymphatic dysfunction is a risk factor for erysipelas.4
In erysipelas, 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.5 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 of erysipelas 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 persons of 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
History
Patients often cannot recall an inciting event, but a history of recent trauma or pharyngitis may be elicited. 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, as shown in the image below.
Facial erysipelas exhibiting classic fiery-red plaque with raised, well-demarcated borders.
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.6
More on Erysipelas |
 Overview: Erysipelas |
| Differential Diagnoses & Workup: Erysipelas |
| Treatment & Medication: Erysipelas |
| Follow-up: Erysipelas |
| Multimedia: Erysipelas |
| References |
| Next Page » |
References
Jorup-Ronstrom C. Epidemiological, bacteriological and complicating features of erysipelas. Scand J Infect Dis. 1986;18(6):519-24. [Medline].
Vignes S, Dupuy A. Recurrence of lymphoedema-associated cellulitis (erysipelas) under prophylactic antibiotherapy: a retrospective cohort study. J Eur Acad Dermatol Venereol. Aug 2006;20(7):818-22. [Medline].
Pereira de Godoy JM, Azoubel LM, Guerreiro Godoy Mde F. Erysipelas and lymphangitis in patients undergoing lymphedema treatment after breast-cancer therapy. Acta Dermatovenerol Alp Panonica Adriat. Jun 2009;18(2):63-5. [Medline].
[Best Evidence] Damstra RJ, van Steensel MA, Boomsma JH, Nelemans P, Veraart JC. Erysipelas as a sign of subclinical primary lymphoedema: a prospective quantitative scintigraphic study of 40 patients with unilateral erysipelas of the leg. Br J Dermatol. Jun 2008;158(6):1210-5. [Medline].
Ellis H. The last year before the dawn of antibiotics. Br J Hosp Med (Lond). Aug 2009;70(8):475. [Medline].
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].
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].
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].
Vos MD, Bos RR, Vissink A. [A sudden redness and swelling of the face]. Ned Tijdschr Tandheelkd. Jul 2009;116(7):383-6. [Medline].
Bernard P, Plantin P, Roger H, 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].
Sjoblom AC, Eriksson B, Jorup-Ronstrom C, Karkkonen K, Lindqvist M. Antibiotic prophylaxis in recurrent erysipelas. Infection. Nov-Dec 1993;21(6):390-3. [Medline].
Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. Nov 15 2005;41(10):1373-406. [Medline].
Coste N, Perceau G, Leone J, et al. Osteoarticular complications of erysipelas. J Am Acad Dermatol. Feb 2004;50(2):203-9. [Medline].
Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med. Jan 25 1996;334(4):240-5. [Medline].
Bonnetblanc JM, Bedane C. Erysipelas: recognition and management. Am J Clin Dermatol. 2003;4(3):157-63. [Medline].
Bratton RL, Nesse RE. St. Anthony's Fire: diagnosis and management of erysipelas. Am Fam Physician. Feb 1 1995;51(2):401-4. [Medline].
Chartier C, Grosshans E. Erysipelas. Int J Dermatol. Sep 1990;29(7):459-67. [Medline].
Chartier C, Grosshans E. Erysipelas: an update. Int J Dermatol. Nov 1996;35(11):779-81. [Medline].
Elston DM. Epidemiology and prevention of skin and soft tissue infections. Cutis. May 2004;73(5 Suppl):3-7. [Medline].
Grosshans EM. The red face: erysipelas. Clin Dermatol. Apr-Jun 1993;11(2):307-13. [Medline].
Hammar H, Wanger L. Erysipelas and necrotizing fasciitis. Br J Dermatol. Apr 1977;96(4):409-19. [Medline].
Ronnen M, Suster S, Schewach-Millet M, Modan M. Erysipelas. Changing faces. Int J Dermatol. Apr 1985;24(3):169-72. [Medline].
Torok L. Uncommon manifestations of erysipelas. Clin Dermatol. Sep-Oct 2005;23(5):515-8. [Medline].
Zeglaoui F, Dziri C, Mokhtar I, 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].
Further Reading
Keywords
erysipelas, nonnecrotizing dermohypodermitis, non-necrotizing dermohypodermitis, acute bacterial dermohypodermitis
