Erysipelas overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.
Overview
Erysipelasis is an acute inflammatory epidermal disease resulting from bacterial infection. The most common cause of erysipelas is Streptococcus pyogenes, also known as group A streptococci. Additional Streptococcus causes include Group G Streptococcus, as well as Group B and C. Rarely, erysipelas is caused by Staphylococcus aureus or Streptococcus pneumoniae. Erysipelas manifests with a characteristic rash, localized on the epidermis. Signs include erythema, edema, bullae, vesicles, and blebs. Erysipelas usually manifests on the legs, but can also be found on the face, torso, hands, feet, and toes. Patients may experience blisters, fever, chills, fatigue, headaches, vomiting, and pain, as well as redness and swelling of the affected area. Erysipelas onset begins shortly after streptococcal infection, with initial symptoms of localized lesions with erythema and edema. Advancement from the initial location is rapid, with raised and sharply demarcated boundaries from surrounding unaffected tissue. Systemic symptoms, including fever, chills, and vomiting may occur as the inflammation persists and spreads. Erysipelas must be differentiated from other inflammatory dermatological conditions that present with pain, erythema, edema, and blisters of the skin—in conjunction with other systemic conditions such as fever, chills, fatigue, headache, and vomiting. Risk factors for erysipelas are those that predispose an individual to an inflammatory reaction to Streptococcus infection, including immunocompromised status, being overweight or obese, venous insufficiency, lymphedema, having multiple deep skin lesions or ulcers, and having disruptions to the cutaneous barrier. The mainstay of therapy for erysipelas is antimicrobial therapy. Pharmacologic therapy for erysipelas includes either Penicillins, Erythromycin, or Cephalosporins. Empiric therapy for facial erysipelas includes either Vancomycin, Daptomycin, or Linezolid. Primary prevention of erysipelas involves preventing pathogenesis from streptococcal infection, as well as preventing the original streptococcal infection. The mainstay of erysipelas secondary prevention is antibiotic prophylaxis for severe cases with high frequency of recurrence. Phenoxymethylpenicillin, erythromycin, and benzathine penicillin have all demonstrated varying levels of efficacy in preventing erysipelas recurrence. More research is needed to determine standardized antibiotic selection, dosing, and interval of administration for universal application. Without treatment, the prognosis of erysipelas varies based on the presence of complications. Spread of infection below the dermis can result in hospitalization and even be life-threatening. With treatment, the prognosis of erysipelas is good; Penicillin has been shown to effectively relieve symptoms and halt progression of the disease. Complications of erysipelas occur if the infectious pathogen is not treated and it spreads below the dermis and into the bloodstream, brain, bones, kidneys, and other subcutaneous tissue.
Historical Perspective
- Erysipelas was first recognized as a disease known as "St. Anthony's Fire," named after St. Anthony in 1090 A.D.
- The cause of erysipelas, Streptococcus bacteria, was discovered by the German physician Wilhelm Busch in 1881.
- Development of erysipelas treatment began in 1882, when French microbiologist Louis Pasteur discovered rabbits' attentuating effects on Streptococcus.
Classification
There is no diagnostic classification schema for erysipelas.
Pathophysiology
Erysipelas develops from epidermal penetration of streptococcal bacteria, usually the group A streptococcus Streptococcus pyogenes. The infection occurs upon the binding of superficial ligands to the epidermal receptor cells. Dermal damages, including abrasions or lesions, allow the pathogen to adhere without being removed by natural exfoliation. A myriad of virulence factors causes bacteria to adhere to the dermis. Upon adhesion, Streptococcus pyogenes begins to invade through expression of M protein or fibronectin-binding protein. Phagocytosis is inhibited by the bacteria due to the binding of factor H and the binding of fibrinogen on the surface of the M protein. Colonization by the bacteria begins; erysipelas develops from the inflammatory response of the increased volume of leukocytes at the point of infection. The streptococcal pyrogenic exotoxins release large amounts of cytokines that result in tissue damage characteristic of erysipelas. There is evidence of genetic predisposition and susceptibility to erysipelas in an individual with a streptococcal infection. Erysipelas is associated with the following conditions associated with group A streptococcal infection, including cellulitis, necrotizing fasciitis, and toxic shock syndrome.
Causes
The most common cause of Erysipelas is Streptococcus pyogenes, also known as group A streptococci. Additional common Streptococcus causes include Group G Streptococcus, as well as Group B and C. Rarely, erysipelas is caused by Staphylococcus aureus and Streptococcus pneumoniae.
Differentiating Erysipelas overview from Other Diseases
Erysipelas must be differentiated from other inflammatory dermatological conditions that present with pain, erythema, edema, and blisters of the skin—in conjunction with other systemic conditions such as fever, chills, fatigue, headache, and vomiting.
Epidemiology and Demographics
Epidemiological and demographic information on erysipelas is not fully documented. Research in Belgium in 2004 approximated the incidence of erysipelas to be 249 per 100,000 individuals in Europe. Erysipelas primarily affects individuals older than 50 years, with median ages between 55 and 60 years old. Data are inconclusive with regard to the predominant gender among erysipelas patients; different studies have demonstrated a predominance in both males and females in different patient population samples.
Risk Factors
Risk factors for erysipelas are those that predispose an individual to an inflammatory reaction to Streptococcus infection, including:
- Immunocompromised status
- Being overweight or obese
- Venous insufficiency
- Lymphedema
- Having multiple deep skin lesions or ulcers
- Disruptions to the cutaneous barrier
Screening
There is no diagnostic screening procedure for erysipelas.
Natural History, Complications, and Prognosis
Erysipelas onset begins shortly after streptococcal infection, with initial symptoms of localized lesions with erythema and edema. Progression from the initial location is rapid, with raised and sharply demarcated boundaries from surrounding, unaffected tissue. Systemic symptoms, including fever, chills, and vomiting may occur as the inflammation persists and spreads. Complications of erysipelas occur if the infectious pathogen is not treated and it spreads below the dermis and into the bloodstream, brain, bones, kidneys, and other subcutaneous tissue. Without treatment, the prognosis of erysipelas varies based on the presence of complications. Spread of infection below the dermis can result in hospitalization and can even be life-threatening. With treatment, the prognosis of erysipelas is good; Penicillin has been shown to effectively relieve symptoms and halt progression of the disease.
Diagnosis
History and Symptoms
Erysipelas patients may experience blisters, fever, chills, fatigue, headaches, vomiting, and pain, redness and swelling of the affected area. A patient's history should be examined for obesity, venous insufficiency, lymphedema, skin ulcers and occupational/recreational exposures to skin abrasions, and breast cancer incidence, as well as mastectomy.
Physical Examination
Erysipelas manifests with a characteristic rash, localized on the epidermis. Signs include erythema, edema, bullae, vesicles, and blebs. It usually manifests on the legs, but can also be found on the face, torso, hands, feet, and toes. The patient may also be ill-appearing if systemic illness is present, such as fever, chills, or vomiting.
Laboratory Findings
Laboratory tests are not usually performed for erysipelas, as a physical examination is usually sufficient for diagnosis. However, certain laboratory tests may be performed on erysipelas patients, including those used to confirm streptococcal infection. Erysipelas patients may display markers for inflammation, such as leukocytosis.
Electrocardiogram
There are no diagnostic electrocardiogram findings for erysipelas.
X Ray
There are no x ray diagnostic findings for erysipelas.
CT
There are no diagnostic CT findings for erysipelas.
MRI
There are no diagnostic MRI findings for erysipelas.
Echocardiography or Ultrasound
There are no echocardiography or ultrasound findings for erysipelas.
Imaging Findings
There are no other imaging findings associated with erysipelas.
Other Diagnostic Studies
There are no other diagnostic studies for erysipelas.
Treatment
Medical Therapy
The mainstay of therapy for erysipelas is antimicrobial therapy. Pharmacologic therapy for erysipelas includes either Penicillins, Erythromycin, or Cephalosporins. Empiric therapy for facial erysipelas includes either Vancomycin, Daptomycin or Linezolid.
Surgery
Surgery is not usually recommended for management of Erysipelas. Surgical intervention may be indicated for management of complications related to Erysipelas, particularly those manifesting with more severe lesions that cause tissue necrosis and suppuration.
Primary Prevention
Primary prevention of Erysipelas involves preventing pathogenesis from streptococcal infection, as well as preventing the original streptococcal infection.
Secondary Prevention
The mainstay of Erysipelas secondary prevention is antibiotic prophylaxis for severe cases with high frequency of recurrence. Phenoxymethylpenicillin, erythromycin, and benzathine penicillin have all displayed varying efficacy in preventing Erysipelas recurrence. More research is needed to determine standardized antibiotic selection, dosing, and interval of administration for universal application.