Erysipelas 

  • Author: Loretta Davis, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 11, 2012
 

Background

Erysipelas is a bacterial skin infection involving the upper dermis that characteristically extends into the superficial cutaneous lymphatics. Erysipelas has been traced back to the Middle Ages, where it was referred to as St. Anthony's fire, named after the Christian saint to whom those afflicted would appeal for healing. Around 1095, the Order of St. Anthony, a Roman Catholic congregation, was formed in France to care for those with the ailment. At the time, several diseases were likely grouped under this eponym, including ergotism and herpes zoster (shingles). Historically, erysipelas occurred on the face and was caused by Streptococcus pyogenes. Currently, the predominance of cases involve the legs, and although S pyogenes is still the most likely etiology, other bacteria, including non–group A Streptococcus, Staphylococcus, and even gram-negative species can be responsible.

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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.

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Epidemiology

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. 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. Death as a direct result of erysipelas is exceedingly rare.

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, likely because of their more aggressive activities and resultant skin injuries. 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).

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Contributor Information and Disclosures
Author

Loretta Davis, MD  Professor, Department of Internal Medicine, Division of Dermatology, Medical College of Georgia

Loretta Davis, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

John A Cole, MD  Resident Physician, Department of Dermatology, University of Florida College of Medicine, Gainesville, FL

John A Cole, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Keith Benbenisty, MD  Consulting Staff, Associates in Dermatology, MDs, PA

Disclosure: Nothing to disclose.

Specialty Editor Board

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Christen M Mowad, MD  Associate Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Dermatological Association, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Glen H Crawford, MD  Assistant Clinical Professor, Department of Dermatology, University of Pennsylvania School of Medicine; Chief, Division of Dermatology, The Pennsylvania Hospital

Glen H Crawford, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Phi Beta Kappa, and Society of USAF Flight Surgeons

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References
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  2. 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].

  3. 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].

  4. [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].

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  10. 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].

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  24. 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].

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Well-demarcated, erythematous plaque of erysipelas. Courtesy of the US Centers for Disease Control and Prevention.
Facial erysipelas exhibiting classic fiery-red plaque with raised, well-demarcated borders.
 
 
 
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