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.)
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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.)
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]
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).
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.
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, if present, usually occur within 48 hours of cutaneous involvement. Pruritus, burning, tenderness, and swelling are typical complaints.
Other symptoms may include the following:
Muscle and joint pain
Nausea
Headache and other systemic manifestations of an infectious process
Associated comorbidities in erysipelas include diabetes mellitus, as well as hypertension, chronic venous insufficiency, and other cardiovascular diseases.[10]
Erysipelas involves the lower extremities in 80% of patients; the face is most often affected in the remainder of the cases.[11]
The patient may appear healthy or toxic depending on the extent of infection. Erysipelas begins as a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque, as shown in the images below.
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Well-demarcated, erythematous plaque of erysipelas. Courtesy of the US Centers for Disease Control and Prevention.
View Image
Facial erysipelas exhibiting classic fiery-red plaque with raised, well-demarcated borders.
The lesion classically exhibits a sharply raised border with abrupt demarcation from healthy skin and with advancing margins, often referred to as the step sign.[14] This is in opposition to the slightly deeper involvement seen in cellulitis, in which lesions present with limited edema and less well-defined borders. Local signs of inflammation, such as warmth, edema, and tenderness, are characteristic of this infection but may be lacking in the setting of immunosuppression. Lymphatic involvement often is manifested by overlying skin streaking and regional lymphadenopathy. Erythema is irregular, with extensions that may follow lymphatic channels (lymphangitis).
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.
In classic erysipelas, no laboratory workup is required for diagnosis or treatment. However, leukocytosis and elevations in erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are common.[1, 15] Routine blood and tissue cultures are not cost-effective, because they have an extremely low yield and the results have minimal impact on management.
Imaging studies are not usually indicated and are of low yield. Magnetic resonance imaging (MRI) and bone scintigraphy are helpful when early osteoarticular involvement is suspected. In this setting, standard radiographic findings typically are normal.
Bacterial cultures are positive in only 5% of cases, and tissue Gram stain and culture are generally not helpful. However, bacterial cultures may be useful when the diagnosis is in question or when concern for bacteremia and metastatic infection exists.
Cultures may be of benefit in patients with prosthetic heart valves, other intravascular devices, artificial joints, and in immunocompromised or toxic-appearing patients. Bacterial cultures from the portal of entry may be most helpful, especially in persons with atypical clinical presentations.[16]
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.
While most cases of erysipelas resolve without sequelae following appropriate antibiotic therapy, prompt treatment is crucial because of potentially rapid progression. Aside from administration of antibiotics, patient care includes the following:
Symptomatic treatment of aches and fever
Hydration (oral intake if possible)
Cold compresses
Elevation and rest of the affected limb: 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
Surgical care
Debridement is necessary only in severe infections with necrosis or gangrene.
Inpatient care
Hospitalization for close monitoring and intravenous antibiotics is recommended in severe cases and for infants, elderly persons, and patients who are immunocompromised. Inpatient care is also recommended for patients who are unlikely to complete the course of treatment as a result of psychosocial reasons and for those with significant comorbidities.
Streptococci cause most cases of erysipelas; thus, penicillin has remained first-line therapy.[17, 18] Penicillin administered orally or intramuscularly is sufficient for most cases of classic erysipelas and should be given for 5 days, but if the infection has not improved, treatment duration should be extended.
A first-generation cephalosporin may be used if the patient has an allergy to penicillin. Cephalosporins may cross-react with penicillin and should be used with caution in patients with a history of severe penicillin allergy, such as anaphylaxis. Clindamycin remains a therapeutic option, although clindamycin-resistant group B streptococcal isolates are well documented.[19] Erythromycin-resistant group B streptococcal isolates are common.[19]
Coverage for Staphylococcus 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.[4]
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.[20] The US Food and Drug Administration (FDA) has not approved these drugs in the United States, but they are in use in Europe.
The FDA approved 3 antibiotics, oritavancin (Orbactiv), dalbavancin (Dalvance), and tedizolid (Sivextro), for the treatment of acute bacterial skin and skin structure infections. These agents are active against Staphylococcus aureus (including methicillin-susceptible and methicillin-resistant S aureus [MSSA, MRSA] isolates), Streptococcus pyogenes, Streptococcus agalactiae, and Streptococcus anginosus group (includes Streptococcus anginosus, Streptococcus intermedius, and Streptococcus constellatus), among others. For complete drug information, including dosing, see the following monographs:
Patients with acute infections involving the extremities should be encouraged to limit their activity and to keep affected limbs elevated to decrease swelling.
Most patients with erysipelas respond very well to conventional antibiotic therapy. However, in atypical infections that are unresponsive to first- and second-line agents, consultation with an infectious disease specialist is advisable. Given atypical presentations of many cutaneous diseases, dermatologist consultation should be considered in cases in which the diagnosis is in doubt.
Patients with recurrent erysipelas should be educated regarding local antisepsis and general wound care. Predisposing lower extremity skin lesions (eg, tinea pedis, toe web intertrigo, stasis ulcers, asteatotic dermatitis) 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 long-term in patients with lower extremity edema. Long-term management of lymphedema is essential.
Long-term prophylactic antibiotic therapy generally is accepted.[21, 22] Treatment regimens should be tailored to the patient. One regimen is benzathine penicillin G at 2.4 mU intramuscularly every 2-4 weeks for up to 2 years.[23] Oral penicillin or erythromycin twice daily for 4-52 weeks is an alternate regimen.[24]
The Infectious Diseases Society of America updated their guidelines for the diagnosis and management of skin and soft tissue infections in 2014. For the full guidelines, see Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America.[24]
Antibiotics should be started as soon as possible in patients with erysipelas. As previously stated, streptococci cause most cases of the disease; thus, penicillin has remained a first-line therapy.[17, 18] A first-generation cephalosporin or macrolide, such as erythromycin or azithromycin, may be used if the patient has an allergy to penicillin.
Antipyretics and analgesics may help to alleviate symptoms; these drugs ensure patient comfort and have sedating properties beneficial to patients who have sustained trauma or who experience pain.
Clinical Context:
Penicillin G procaine (Wycillin) and penicillin VK (PenVeeK) are currently recommended as first-line agents for the treatment of moderately severe infections of skin and skin structure. In adults, administer penicillin G procaine by deep intramuscular injection only into upper, outer quadrant of buttock. In infants and small children, the midlateral aspect of the thigh may be a better site for administration.
Clinical Context:
Dicloxacillin, used in the treatment of infections caused by penicillinase-producing staphylococci, is a penicillinase-resistant penicillin that will cover possible S aureus.
Clinical Context:
Nafcillin is the initial therapy for suspected penicillin G ̶ resistant streptococcal or staphylococcal infections. Use parenteral therapy initially in severe infections, and change to oral therapy as the condition warrants.
Because nafcillin may cause thrombophlebitis at the injection site, particularly in elderly patients, administer parenterally only for a short term (1-2 d); change to oral administration as clinically indicated.
Clinical Context:
Cephalexin is a first-generation cephalosporin that inhibits bacterial growth by inhibiting bacterial cell wall synthesis. This agent is bactericidal and is effective against rapidly growing organisms forming cell walls. Cephalexin is an acceptable alternative to penicillin and may be useful in patients with minor penicillin allergies.
Clinical Context:
Erythromycin is a macrolide used for penicillin-allergic individuals. It inhibits bacterial growth, possibly by blocking dissociation of peptidyl transfer ribonucleic acid (t-RNA) from ribosomes, causing RNA-dependent protein synthesis to arrest. Erythromycin is administered for the treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When twice-daily dosing is desired, half of the total daily dose may be taken every 12 hours. For more severe infections, double the dose.
Clinical Context:
Azithromycin acts by binding to the 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Nucleic acid synthesis is not affected.
Azithromycin concentrates in phagocytes and fibroblasts as demonstrated by in vitro incubation techniques. In vivo studies suggest that its concentration in phagocytes may contribute to drug distribution to inflamed tissues.
Azithromycin treats mild-to-moderate microbial infections. Plasma concentrations are very low, but tissue concentrations are much higher, giving it value in treating intracellular organisms. It has a long tissue half-life, which allows for once-daily dosing for skin and soft-tissue infections.
Clinical Context:
Clindamycin is a lincosamide for the treatment of serious skin and soft-tissue staphylococcal infections. It is also effective against aerobic and anaerobic streptococci (except enterococci). Clindamycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. Clostridium difficile-associated diarrhea is a potential adverse effect.
Penicillin is the standard therapy for typical erysipelas, although coverage for Staphylococcus aureus should be considered in the appropriate setting.
Clinical Context:
This is the drug of choice (DOC) for treating pain in patients with documented hypersensitivity to aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs), who are diagnosed with upper gastrointestinal disease, or who take oral anticoagulants.
Clinical Context:
The combination of oxycodone and acetaminophen is used for the relief of moderate to severe pain. It is the DOC for aspirin-hypersensitive patients.
Clinical Context:
Aspirin blocks prostaglandin synthetase action, which in turn inhibits prostaglandin synthesis and prevents the formation of platelet-aggregating thromboxane A2; it acts on the hypothalamic heat-regulating center to reduce fever.
Clinical Context:
Ibuprofen is usually the DOC for treating mild to moderate pain, if no contraindications exist. It is one of the few NSAIDs indicated for fever reduction.
Clinical Context:
Naproxen is used for the relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing COX activity, which results in decreased prostaglandin synthesis.
Clinical Context:
Ketoprofen is used for relief of mild to moderate pain and inflammation. Small dosages are indicated initially in small patients, elderly patients, and patients with renal or liver disease. Doses higher than 75 mg do not increase the therapeutic effects. Administer high doses with caution, and closely observe the patient's response.
Pain control is essential to quality patient care. Analgesics and antipyretics ensure patient comfort, promote pulmonary toilet, and have sedating properties beneficial to patients who have sustained trauma or who experience pain.
What is erysipelas?Why is erysipelas called St. Anthony’s fire?Where on the body does erysipelas occur?What instructions should be given to patients during initial treatment of erysipelas?What is the pathophysiology of erysipelas?What is the role of streptococcal infection in the pathogenesis of erysipelas?What are the risk factors for erysipelas?What is the initial molecular event in the pathogenesis of erysipelas?What is the role of lymphedema in the etiology of erysipelas?What is the incidence of erysipelas in the US?What is the global incidence of erysipelas?How does the incidence of erysipelas vary among demographic groups?What is the prognosis of erysipelas?What are the complications of erysipelas?What is the prevalence local recurrences of erysipelas and how does the disease progress?Which factors increase the risk of mortality from erysipelas?What are the signs and symptoms of erysipelas?What are the comorbidities of erysipelas?Which physical findings suggest erysipelas?How is erysipelas differentiated from cellulitis?What are the differential diagnoses for Erysipelas?How is erysipelas diagnosed?What is the indication for bacterial cultures in the workup of erysipelas?Which histologic findings are characteristic of erysipelas?How is erysipelas treated?When is debridement indicated in the treatment of erysipelas?When is inpatient care indicated in the treatment of erysipelas?What is the first-line therapy for erysipelas?When is a first-generation cephalosporin indicated in the treatment of erysipelas?When should a Staphylococcus aureus etiology be considered during the treatment of erysipelas?Which medications are used in Europe to treat erysipelas?Which antibiotics have FDA approval for the treatment of erysipelas?What activity modifications are needed during treatment of erysipelas?Which specialists should be consulted regarding the treatment of erysipelas?How is recurrent erysipelas managed?What guidelines are available for the diagnosis and management of erysipelas?When should antibiotic therapy be initiated for erysipelas?When are antipyretics and analgesics indicated in the treatment of erysipelas?Which medications in the drug class Analgesics-Antipyretics are used in the treatment of Erysipelas?Which medications in the drug class Antibiotics are used in the treatment of Erysipelas?
Loretta S Davis, MD, Professor and Chair, Department of Dermatology, Medical College of Georgia, Augusta University
Disclosure: Nothing to disclose.
Coauthor(s)
John A Cole, MD, Dermatologist, Private Practice, Valdosta, GA
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
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
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
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