Erysipelas

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

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.

• 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.
  • In 1944, scientists Fortner and Dinter published research regarding efficacy of the first erysipelas vaccine, leading to the development of additional vaccines shortly thereafter.

There is no diagnostic classification schema for erysipelas.

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.

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.

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.

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 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

There is no diagnostic screening procedure for erysipelas.

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.

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.

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 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.

There are no diagnostic electrocardiogram findings for erysipelas.

There are no x ray diagnostic findings for erysipelas.

There are no diagnostic CT findings for erysipelas.

There are no diagnostic MRI findings for erysipelas.

There are no echocardiography or ultrasound findings for erysipelas.

There are no other imaging findings associated with erysipelas.

There are no other diagnostic studies for erysipelas.

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 is not usually recommended for the 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 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 efficacy in preventing erysipelas recurrence. More research is needed to determine standardized antibiotic selection, dosing, and interval of administration for universal application.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Kalsang Dolma, M.B.B.S.[2], Luke Rusowicz-Orazem, B.S.

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. In 1944, scientists Fortner and Dinter published research regarding efficacy of the first erysipelas vaccine, leading to the development of additional vaccines shortly thereafter.

• Erysipelas was first recognized as a disease known as “St. Anthony’s Fire,” named after St. Anthony in 1090 A.D.^[1]
• The cause of erysipelas, Streptococcus bacteria, was discovered by the German physician Wilhelm Busch in 1881.^[2]

• Development of erysipelas treatment began in 1882, when French microbiologist Louis Pasteur discovered rabbits’ attentuating effects on Streptococcus.^[3]
• In 1944, scientists Fortner and Dinter published research regarding efficacy of the first erysipelas vaccine, leading to the development of additional vaccines shortly thereafter.

Many famous cases of Erysipelas have been documented throughout history, including the following:

• Father Solanus Casey, Capuchin monk and 20th Century spiritual figure, 1870-1957, USA^[4]
• Charles Lamb
• Princess Amelia, daughter of George III
• Miller Huggins, manager of the New York Yankees from 1918 until his death in 1929
• James A. Bailey
• Anne of Great Britain
• William H. Crawford, Secretary of the Treasury in the administration of President James Monroe
• John Stuart Mill, political philosopher most famous for his work On Liberty^[5]
• Judith of Swabia, daughter of the Holy Roman Emperor Henry III

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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.

There is no diagnostic classification schema for erysipelas.

There is no diagnostic classification schema for erysipelas.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

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 begin 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 of 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 individuals with streptococcal infection. Erysipelas is associated with the following conditions associated with group A streptococcal infection, including cellulitis, necrotizing fasciitis, and toxic shock syndrome.

Erysipelas develops from exotoxins released due to epidermal penetration of the pathogenic bacteria.

• Group A streptococcal infection causes erysipelas upon infiltration of the epidermis through a skin abrasion or lesion.^[1]
  • The streptococcal infection occurs upon the binding of superficial ligands to the epidermal receptor cells.
  • Epidermal damages, including abrasions or lesions, allow the pathogen to adhere without being removed by natural exfoliation.
  • Streptococcus pyogenes adheres to the dermis due to the following virulence factors:
    • Containing M protein, allowing colonization^[2]
    • Lipotechoic acid (LTA): binds with fibronectin or fibrinogen, causing adhesion of the bacteria to the dermis^[3]
    • Protein F: binds with fibronectin to mediate adhesion^[4]
    • 29-kDa fibronectin-binding protein^[5]
    • Glyceraldehyde 3-phosphate dehydrogenase^[6]
    • 70-kDa galactose-binding protein^[7]
    • Vitronectin-binding S protein^[8]
    • Collagen-binding protein^[9]
    • Serum opacity factor
    • Hyaluronate capsule^[10]
  • Upon adhesion, Streptococcus pyogenes begin 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.^[11][12]
  • Colonization of 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.^[13]

There is evidence of increased susceptibility to erysipelas in individuals with streptococcal infection, due to the following genetic factors:^[14]

• Human leukocyte antigen (HLA) Class II and T-cell receptor Vβ variation can cause differing susceptibility due to their influence on Super antigen production, contributing the to severity of cytokine release from inflammation.^[13]
• The region Angiotensin II receptory type 1 (AGRT1) on the chromosome 3q22 has been shown to reveal susceptibility to developing erysipelas by determining an individual’s cytokine response to Streptococcus pyogenes infection.^[14]

Erysipelas is associated with the following streptococcal conditions:^[15]

• Cellulitis
• Necrotizing fasciitis
• Toxic shock syndrome

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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.

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 and Streptococcus pneumoniae.

Erysipelas is usually caused by by β-hemolytic Streptococcus infection—particularly Streptococcus pyogenes, also known as group A streptococci.^[1][2]

Additional Streptococcus causes include the following:

• Group G Streptococcus^[3]
• Group B Streptococcus infection^[4]
• Group C Streptococcus infection^[5]

Rarely, erysipelas is caused by the following:

• Staphylococcus aureus^[6]
• Streptococcus pneumoniae^[7]

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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.

Erysipelas must be differentiated from other inflammatory dermatological conditions that present with pain, erythema, edema, and blisters of the skin, as well as other systemic conditions such as fever, chills, fatigue, headache, and vomiting.

• Erysipelas must be differentiated from other causes of lower limb edema like chronic venous insufficiency, acute deep venous thrombosis, lipedema, myxedema, lymphatic filariasis and causes of generalized edema.

Diseases	Symptoms							Signs	Gold standard Investigation to diagnose
	History	Onset	Pain	Fever	Laterality	Scrotal swelling	Symptoms of primary disease
(Cellulitis-erysipelas-skin abscess)	Acute painful swelling Fever	Acute	+	+	Unilateral	–	–	Tenderness, hotness, and may be fluctuation if abscess formed. Lymphangitis in nearby lymph nodes. Toxemia and fever in severe cases. Cellulitis involves the deeper dermis and erysipelas involves the upper dermis.[1]	Usually it doesn’t need any laboratory tests to diagnose.[2] Blood cultures are warranted for patients in the following circumstances:[3] Systemic toxicity Extensive skin or soft tissue involvement Underlying comorbidities persistent cellulitis In patients with recurrent cellulitis, serologic testing for beta-hemolytic streptococci is a good diagnostic tool.[4]
Lymphatic filariasis	History of living in endemic area or travelling to it	Chronic	+	+	Bilateral	+	–	Hepatomegaly Lymphedema Elephantiasis Lymphangitis Hydrocele Scrotal elephantiasis Lymphadenopathies Rhonchi may be present in patients with Pulmonary tropical eosinophilia syndrome.	Preparing blood smears Thick smears Thick smears consist of a thick layer of dehemoglobinized (lysed) red blood cells (RBCs). Thick smears allow a more efficient detection of parasites (increased sensitivity). Thin smears consist of blood spread in a layer such that the thickness decrease. By the ultrasound, the following findings can be observed: Dilated lymphatic channels Living worms tend to be in motion which called “filarial dance” sign.
Chronic venous insufficiency	History of untreated varicose veins Painful bilateral lower limb swelling that increases with standing and decreases by rest and leg elevation.	Chronic	+	–	Bilateral	+ (If congenial)	–	Typical varicose veins Skin change distribution correlate with varicose veins sites in the medial side of ankle and leg Reduction of swelling with limb elevation.	Duplex ultrasound will demonstrate typical findings of venous valvular insufficiency
Acute deep venous thrombosis	History of prolonged recumbency Classic symptoms of DVT include acute unilateral swelling, pain, and erythema	Acute	+	–	Unilateral	–	May be associated with primary disease mandates recumbency for long duration	Dilated superficial veins Difference in calf diameter is twice as likely to have DVT(most impotant sign )[5] Calf pain on passive dorsiflexion of the foot (Homan’s sign) isn’t realiable sign.	Compression ultrasonography (CUS) with doppler is the diagnostic test of choice D-dimer level is used for unprobable cases
Lipedema	Family history especially in women; X-linked dominant or autosomal dominant condition.[6] Abnormal deposition of fat and edema and easy bruising.	Chronic	+	–	Bilateral	–	–	Tender with palpation Negative Semmer sign to differentiate from lymphedema.[7] Pinching the skin on the upper surface of the toes. If it is possible to grasp a thin fold of tissue then it is negative result. In a positive result, it is only possible to grasp a lump of tissue.	MRI offers strong qualitative and quantitative parameters in the diagnosis of lipedema [8]
Myxedema	History of untreated hypothyroidism. Infiltration of the skin with glycosaminoglycans with associated water retention.	Chronic	+	–	Bilateral	–	+ (hypothyroidism )	Pretibial myxedema	Thyroid function tests.
Other causes of generalized edema	History of chronic general condition (cardiac-liver-renal)	Chronic	–	–	Bilateral	–	+		According to the primary cause ( Echo- LFTs– RFT)

• Erysipelas must be differentiated from other inflammatory dermatological conditions that present with pain, erythema, edema, and blisters of the skin, as well as other systemic conditions such as fever, chills, fatigue, headache, and vomiting.^[9]

Disease	Findings
Cellulitis	Presents with nearly identical symptoms to erysipelas, and is also usually caused by Streptococcus or Staphylococcus bacteria.[10] Differentiated from erysipelas by its manifestation beneath the epidermis in the dermal layer of the skin; infection can spread to the subcutaneous fat, bones, joints, and muscles of the affected area. The area of inflammation is not as sharply visibly demarcated as those characteristic of erysipelas, due to the deeper manifestation in the skin. Can lead to complications with poor prognosis including osteomyelitis, lymphangitis, endocarditis, and meningitis.
Necrotizing fasciitis	Presents with more severe epidermal signs and symptoms than erysipelas. Necrotizing fasciitis patients usually present with erythema, edema, blisters, pain, suppuration, and clear signs of tissue necrosis (dark violet/blue to black in appearance).[11] Left untreated, necrotizing fasciitis usually leads to subcutaneous nerve destruction; a patient communicating more pain than is visibly apparent or manifested on the epidermis is indicative of nerve damage preceding or disproportionate to visible evidence.[12] In addition to antibiotics, immediate therapeutic surgery is required to prevent morbidity from necrotizing fasciitis.
Shingles	Presents with itching, pain, and tingling on a single side of the body or face, which will develop into a rash with blisters. It can also present with fever, chills, headache, and nausea.[13]. Differentiated from erysipelas by its cause (Varicella zoster virus infection) and is usually self-limited; antiviral therapy and analgesics are indicated to shorten the duration and severity of symptoms, which will usually self-resolve within 7-10 days. Recognition and diagnosis of shingles is important to prevent complications, including postherpetic neuralgia.[14]
Angioedema	An edematous condition that involves swelling occurring below the epidermis, including the dermis and mucous membranes.[15] Angioedema usually presents with edema near the eyes and lips, as well as the hands, feet, and throat.[16] Can present similarly to erysipelas if epidermal welts and blisters form in the regions of edema, as well as cause abdominal pain.[17] Differentiated from erysipelas in that the cause is primarily an allergic reaction to a variety of possible allergens, including pollen, food, or medication. While angioedema is usually self-limited and will resolve itself upon the cessation of exposure to the allergen, treatment with antihistamines, epinephrine, or corticosteroids must be administered to prevent life-threatening complications, including asphyxiation if the edema occurs in the throat.[17]
Contact dermatitis	An inflammatory condition of the epidermis resulting from direct contact with an allergen or irritant. Contact dermatitis is similar to erysipelas due to the usual presentation of erythema, blisters, itching, pain, and discharge. Differentiated from erysipelas by its cause: an allergic response by contact to a specific surface or entity. There is no indication of bacterial infection. Common causes include chemicals from cosmetic and hygienic products, fabrics, metals, and animal hair or skin. Therapy involves avoiding the original cause and application of topical or oral corticosteroids and analgesics.[18]
Inflammatory breast cancer	Presents with edema and erythema of the breast, as well as itching, pain, and tenderness from the inflammation.[19] Differentiated from erysipelas by the fact that inflammation is usually limited to the breast. Additional differential criteria include development of “ridges” on the breast, giving the appearance of an orange peel. It is urgent to differentiate and diagnose inflammatory breast cancer to begin immediate chemotherapy, radiation therapy, and/or surgery when indicated.

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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.

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 regards to the predominant gender in erysipelas patients; studies have shown both a predominance in males and females in different patient population samples.

Research in Belgium in 2004 approximated the incidence of erysipelas to be 249 per 100,000 individuals in Europe.^[1]

Erysipelas primarily affects individuals older than 50 years of age.

• Research from November 1988 – October 1990 in Sweden indicated a median age of 61 years old for erysipelas patients.^[2]
• Research in Greece from 1999-2002 indicated a median age of 54.5 years old for erysipelas patients.^[3]
• Research in Hungary from 2001-2002 indicated a median age of 59 years old for erysipelas patients.^[4]

Data are inconclusive with regards to the predominant gender in erysipelas patients.

• Studies have shown both a predominance in males and females in different patient population samples.^[4][3][2]

There is no racial predilection to erysipelas.

There is no geographic predilection to erysipelas.

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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.

Risk factors for erysipelas are those that predispose one 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 disruptions to the cutaneous barrier.

The following risk factors contribute to an individual’s predisposition to erysipelas:^[1][1]

• Immunocompromised status
• Being overweight or obese^[1]
• Experiencing a disruption of the cutaneous barrier
• Venous insufficiency
• Lymphedema^[2]
• History of mastectomy^[3]
• Having multiple deep skin lesions or ulcers, particularly in the leg^[2]

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

There is no diagnostic screening procedure for erysipelas.

There is no diagnostic screening procedure for erysipelas.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Luke Rusowicz-Orazem, B.S.

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.

Erysipelas onset begins shortly after streptococcal infection.^[1]

• An initial lesion forms with localized erythema and edema
• Progression from the initial location is rapid, with raised and sharply demarcated boundaries from surrounding unaffected tissue
• Untreated, the lesions will spread, while the initial manifestation resolves
• Systemic symptoms, including fever, chills, and vomiting may occur as inflammation persists and spreads

If left untreated, erysipelas will not usually be self-resolved and can lead to life-threatening complications.^[2]

Complications of erysipelas occur if the infectious pathogen is not treated, including the following:

• Increased severity of lesions, including haemorrhagic, bullous, abscessing, and necrotic (necrotizing fasciitis)^[3][4]
• Osteoarticular complications, including bursitis, osteitis, tendinitis, and arthritis^[5]
• Bacteremia, resulting from spread of infection from the epidermis to the bloodstream^[6]
• Septic shock^[7]
• Chronic, recurrent erysipelas due to increased susceptibility from damaged cutaneous lymph vessels^[8]
• Meningitis (if the infection is localized in the face and spreads below the dermis and into the brain and spinal cord)
• Gangrene
• Acute glomerulonephritis^[9]
• Thrombophlebitis^[10]
• Lymphatic damage and lymphedema^[2]
• Streptococcal toxic shock syndrome^[1]
• Myocarditis^[11]

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.^[12]

With treatment, the prognosis of erysipelas is good.

• Penicillin has been shown to effectively relieve symptoms and halt the progression of the disease.^[13]

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