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Erysipelas

  • Author: Loretta Davis, MD; Chief Editor: William D James, MD  more...
 
Updated: Jun 29, 2016
 

Background

Erysipelas is a bacterial skin infection involving the upper dermis that characteristically extends into the superficial cutaneous lymphatics. It is a tender, intensely erythematous, indurated plaque with a sharply demarcated border. Its well-defined margin can help differentiate it from other skin infections (eg, cellulitis).[1] See the image below. (See Clinical Presentation.)

Well-demarcated, erythematous plaque of erysipelas Well-demarcated, erythematous plaque of erysipelas. Courtesy of the US Centers for Disease Control and Prevention.

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, but cases today most often involve the legs. The group A streptococcal bacterium Streptococcus pyogenes causes most of the facial infections; although it can also cause erysipelas on the legs, an increasing percentage of lower extremity infections are now being caused by non–group A streptococci. (See Pathophysiology and Etiology.)

Patient education

Instruct patients to rest, elevate the affected area, and use cold compresses 4 times daily for 48 hours. Patients should return or see a primary care physician if they are experiencing an increase in pain, fever and chills, redness, or other new symptoms. (See Treatment and Medication.)

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Pathophysiology and Etiology

Pathophysiology

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.

Etiology

Streptococci are the primary cause of erysipelas.[2] Most facial infections are attributed to group A streptococci, while an increasing percentage of lower extremity infections are caused by non–group A streptococci. Erysipelas in newborns is often caused by group B streptococci, which may also be responsible for perineal and lower-trunk erysipelas occurring in postpartum women.[3] Streptococcal toxins are thought to contribute to the brisk inflammation that is typical of this infection. No clear proof has emerged that other bacteria cause erysipelas, although they coexist with streptococci at sites of inoculation.

The role of Staphylococcus aureus, and specifically methicillin-resistant S aureus (MRSA), 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.[4]

Risk factors

Predisposing factors in erysipelas include the following:

  • Lymphatic obstruction or edema
  • Saphenous vein grafting in lower extremities
  • Status postradical mastectomy
  • Immunocompromise: Including patients who are diabetic or alcoholic [5] or who have human immunodeficiency virus (HIV)
  • Arteriovenous insufficiency
  • Paretic limbs
  • Nephrotic syndrome
  • Vagrant lifestyle

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.

Preexisting lymphedema is a clear-cut risk factor for erysipelas. Recurrent erysipelas complicating the lymphedema from breast cancer treatment is well documented.[6, 7] Lymphoscintigraphy in patients with a first-time episode of lower extremity erysipelas has documented lymphatic impairment in affected and nonaffected legs. Thus, subclinical lymphatic dysfunction is also a risk factor for erysipelas.[8]

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Epidemiology

Occurrence in the 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.[9] However, an increasing incidence of the condition has been noted since the late 1980s.

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 80% of cases of erysipelas occur on the legs rather than the face.

International occurrence

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

Race-, sex-, and age-related demographics

Erysipelas infections affect persons of all races. The condition has been reported to be more common in females but to occur at an earlier age in males (likely because of a greater incidence of skin injuries in younger males).[10] Other studies indicate that predisposing factors, rather than gender, account for any male/female differences in incidence.

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

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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. (The disease may also resolve spontaneously, without treatment.)

Complications of erysipelas may include the following:

  • Gangrene/amputation
  • Chronic edema
  • Scarring
  • Bacteremia sepsis
  • Scarlet fever
  • Pneumonia
  • Abscess [1, 11]
  • Embolism
  • Meningitis
  • Death

The most common complications of erysipelas include abscess, gangrene, and thrombophlebitis.[12] 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.[13]

Local recurrence has been reported in up to 20% of patients with predisposing conditions, and this can lead to disfiguring and disabling sequelae, such as elephantiasis nostras verrucosa. This chronic warty, edematous condition is caused by lymphatic destruction from repeated infection.

Although generally easily and successfully treated with oral antibiotics, with a mortality rate of less than 1% in treated cases, erysipelas can be fatal when associated with bacteremia in very young, elderly, or immunocompromised patients.

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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 Dermatologist, Private Practice, Valdosta, GA

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

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Acknowledgements

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

Disclosure: Nothing to disclose.

Francis Counselman, MD Program Director, Chair, Professor, Department of Emergency Medicine, Eastern Virginia Medical School

Francis Counselman, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Association of Academic Chairs of Emergency Medicine (AACEM), Norfolk Academy of Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary; Assistant Professor, Department of Family Medicine, McGill University

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Canadian Association of Emergency Physicians, and Society for Academic Emergency Medicine

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.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers 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, New York Academy of Medicine, and Sigma Xi

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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.

References
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  2. Bernard P. Management of common bacterial infections of the skin. Curr Opin Infect Dis. 2008 Apr. 21(2):122-8. [Medline].

  3. Matz H, Orion E, Wolf R. Bacterial infections: uncommon presentations. Clin Dermatol. 2005 Sep-Oct. 23 (5):503-8. [Medline].

  4. 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].

  5. Jorup-Ronstrom C. Epidemiological, bacteriological and complicating features of erysipelas. Scand J Infect Dis. 1986. 18(6):519-24. [Medline].

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  7. 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. 2009 Jun. 18(2):63-5. [Medline].

  8. 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. 2008 Jun. 158(6):1210-5. [Medline].

  9. Ellis H. The last year before the dawn of antibiotics. Br J Hosp Med (Lond). 2009 Aug. 70(8):475. [Medline].

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  13. Coste N, Perceau G, Leone J, et al. Osteoarticular complications of erysipelas. J Am Acad Dermatol. 2004 Feb. 50(2):203-9. [Medline].

  14. Bien P, De Anda C, Prokocimer P. Comparison of Digital Planimetry and Ruler Technique To Measure ABSSSI Lesion Sizes in the ESTABLISH-1 Study. Surg Infect (Larchmt). 2014 Apr. 15(2):105-10. [Medline].

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  16. Leppard BJ, Seal DV, Colman G, Hallas G. The value of bacteriology and serology in the diagnosis of cellulitis and erysipelas. Br J Dermatol. 1985 May. 112(5):559-67. [Medline].

  17. Bishara J, Golan-Cohen A, Robenshtok E, Leibovici L, Pitlik S. Antibiotic use in patients with erysipelas: a retrospective study. Isr Med Assoc J. 2001 Oct. 3(10):722-4. [Medline].

  18. Vos MD, Bos RR, Vissink A. [A sudden redness and swelling of the face]. Ned Tijdschr Tandheelkd. 2009 Jul. 116(7):383-6. [Medline].

  19. Phares CR, Lynfield R, Farley MM, Mohle-Boetani J, Harrison LH, Petit S, et al. Epidemiology of invasive group B streptococcal disease in the United States, 1999-2005. JAMA. 2008 May 7. 299 (17):2056-65. [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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