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). See the image below. (See Clinical Presentation.)[1]
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 nongroup 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.)

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 being caused by non
group A streptococci. 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.[3]
Risk factors
Predisposing factors in erysipelas include the following:

Lymphatic obstruction or edema

Saphenous vein grafting in lower extremities
Status postradical mastectomy
Immunocompromise: Including in patients who are diabetic or alcoholic[4] 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.[5, 6] 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.[7]
Erysipelas is found in lower extremities in 70-80% of patients; the face is affected in 5-20% of
patients.[10]
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.

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.
The lesion classically exhibits a sharply raised border with abrupt demarcation from healthy skin
and with advancing margins.[13] 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 universal. 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.
As previously stated, complications of erysipelas usually are not life threatening, and most cases
resolve after antibiotic therapy without sequelae. However, prompt treatment of the condition 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 patients, and patients who are immunocompromised. It is also
recommended for patients who are unlikely to complete the course of treatment as a result of
psychosocial or economic reasons or significant underlying disease.
Streptococci cause most cases of erysipelas; thus, penicillin has remained a first-line therapy.[16, 17]
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 or macrolide, such as erythromycin or azithromycin, 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.
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. [3]
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.[18] Currently, 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 recently approved 3 new 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 methicillinresistant 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:

Oritavancin

Dalbavancin
Tedizolid
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.

Acetaminophen (Tylenol, Aspirin Free Anacin, APAP 500, Acephen,

FeverAll)

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.
View full drug information

Codeine/acetaminophen (Tylenol with Codeine No. 3)

Codeine/acetaminophen is used for the treatment of mild to moderate pain.

View full drug information

Hydrocodone bitartrate and acetaminophen (Vicodin ES, Lortab, Zydone,

Norco)

This combination is used for the relief of moderate to severe pain.

Oxycodone and acetaminophen (Percocet, Endocet, Roxicet, Magnacet)

The combination of oxycodone and acetaminophen is used for the relief of moderate to
severe pain. It is the DOC for aspirin-hypersensitive patients.
View full drug information

Aspirin (Ascriptin Regular Strength, Bayer Aspirin, Aspirtab, Ecotrin)

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.
View full drug information

Ibuprofen (Addaprin, Advil, Motrin, Caldolor, Dyspel)

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.

Naproxen (Naprosyn, Aleve, Naprelan, Anaprox)

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.

Ketoprofen

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.