Erysipelas

Synonym: St Anthony's Fire.

It is caused by a beta-haemolytic streptococcal infection of skin and underlying lymphatics but it is not always a Lancefield group A infection. The name St Anthony's fire comes from the Egyptian healer of the Middle Ages who could cure it. Traditionally the infection has tended to affect the face but more recently about 85% are seen on the legs.¹

It is presumably inoculated into the skin. Predisposing factors include venous insufficiency especially with leg ulcers, inflammatory dermatoses, dermatophyte infections and insect bites. On the face the source of the bacteria is often the nasopharynx. Other predisposing factors include diabetes, alcohol abuse, immune compromise including chemotherapy and steroids, nephrotic syndrome, and an unhygienic, especially a vagrant lifestyle.

It tends to occur in sporadic cases rather than outbreaks. The incidence declined during the 20th century, probably due to antibiotics, a less virulent streptococcus and more hygienic life styles. It tends to affect women more than men but men tend to be affected at an earlier age. This seems to be related to risk factors rather than an inherent gender difference in susceptibility. It is more common among the young and the elderly with a peak incidence between 60 and 80 years.

• There may have been a recent nasopharyngeal infection or trauma to the leg but often no precipitating cause is noted. Athlete's foot may well be the portal of entry.²
• Malaise, chills, and high fever often precede any skin lesion.
• Within 48 hours there is a sudden and rapid onset with pruritis, burning, and tenderness.
• The lesions start as a small erythematous patch that progresses to a fiery-red, indurated, tense, and shiny plaque. There are raised, sharply demarcated advancing margins and they rapidly enlarge over 3 to 6 days. There is rubor, calor and dolor with local oedema. The overlying skin shows streaking and there is regional lymphadenopathy as the lymphatics are involved.
• It may become deeper red with a bruise-like appearance and bright red leading edge.
• There are also fever, chills, joint pain, tiredness and loss of appetite.
• Severe infections may produce numerous vesicles and bullae along with petechiae and even frank necrosis.
• With treatment, the lesion often shows desquamation and there may be pigmentary changes that do not always resolve with time.

• Erysipelas can be differentiated from cellulitis by its characteristically raised advancing edges and sharply demarcated borders, reflecting its more superficial nature. Cellulitis has no lymphatic component and exhibits indiscreet margins.
• It is important to differentiate it from necrotising fasciitis that is a much more serious condition that can be associated³ with much tissue necrosis and disseminated intravascular coagulation.
• Contact dermatitis
• Angioedema has no fever or tenderness.
• Herpes zoster has classical lesions and a dermatome distribution.
• H. influenzae cellulitis usually affects areas around mouth and eyes and in children less than 2 years of age. Bacteraemia is common so patients appear toxic.
• Erysipeloid (infection by Erysipelothrix rhusiopathiae from dead animals) has a slow onset, limited spread, no systemic symptoms or history of exposure.

Usually the diagnosis is purely clinical and no investigations are required.⁴ If there is an atypical presentation or failure to respond to treatment then cultures from possible portals of entry may be valuable. Most infections are streptococcal and respond to standard therapy but Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae, Yersinia enterocolitica, and Moraxella species are occasionally found.

• Oral penicillin is the drug of choice with erythromycin if allergic. Give for 10 to 14 days or until the rash is completely resolved and asymptomatic.
• Elevation and rest of the affected limb are recommended to reduce local swelling, inflammation, and pain.
• Saline wet dressings should be applied to ulcerated and necrotic lesions and changed every 2 to 12 hours, depending on the severity of the infection.
• Hospital admission for close monitoring and intravenous antibiotics is recommended in severe cases and in infants, elderly patients, and patients who are immunocompromised.
• Antibiotics to cover Staphylococcus aureus are not usually necessary for infections off the face, but should be considered in patients who do not improve with penicillin. Some authors believe that facial erysipelas should be treated empirically with a penicillinase-resistant antibiotic to cover for possible S. aureus infection.

The most common complications of erysipelas include abscess, gangrene, and thrombophlebitis. Less common complications at less than 1%, include acute glomerulonephritis, endocarditis, septicaemia, and streptococcal toxic shock syndrome.

The centre of the erythema starts to clear within 7 to 10 days and returns to normal. Skin may exfoliate with possible impetiginous lesions or hyperpigmentation that may be permanent.

Local recurrence has been reported in up to 20% of patients with predisposing conditions.

Recurrence is relatively common in immunocompromised patients and may justify prophylactic therapy if frequent or severe.