Erysipelas Clinical Presentation

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

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.

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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 plaFacial erysipelas exhibiting classic fiery-red plaque with raised, well-demarcated borders.

The lesion classically exhibits raised, sharply demarcated, advancing margins. This is in opposition to the slightly deeper involvement seen in cellulitis, with which lesions present with limited edema and less well-defined borders. 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.

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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]

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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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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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