Fact-checked by Grok 2 weeks ago

Erysipelas

Erysipelas is an acute, superficial bacterial skin infection that primarily affects the upper dermis and cutaneous lymphatics, characterized by a well-demarcated, raised, fiery red rash with edema and tenderness, often accompanied by systemic symptoms such as fever and chills.^[1]^[2] It is most commonly caused by beta-hemolytic streptococci, particularly group A Streptococcus pyogenes, which enter through breaks in the skin such as cuts, insect bites, or ulcers.^[1]^[3] The infection typically involves the face or lower extremities and has historically been known as "St. Anthony's fire" due to its intense inflammatory appearance.^[1] Clinically, erysipelas presents with rapid-onset local inflammation, including warmth, pain, and a sharply raised border that distinguishes it from deeper infections like cellulitis, though the two are often overlapping.^[3]^[2] Systemic manifestations occur in up to 40% of cases, featuring high fever, chills, malaise, and elevated white blood cell counts, with potential spread via lymphatics leading to lymphangitis.^[3] Risk factors include conditions that impair skin integrity or lymphatic drainage, such as lymphedema (with an odds ratio of 71.2), obesity, diabetes, venous insufficiency, and immunosuppression, making it more prevalent in females, the elderly, and infants.^[1]^[3] Diagnosis is primarily clinical based on the characteristic rash, with laboratory tests like blood cultures reserved for severe or complicated cases.^[1]^[2] Treatment involves prompt antibiotic therapy, with penicillin as the first-line agent for 5 to 10 days, achieving cure rates of 50–100%; intravenous administration is used for hospitalized patients with systemic involvement.^[1]^[3] Supportive measures include limb elevation, hydration, and pain management, while recurrent episodes—occurring in about 29% of cases within three years—may require prophylactic antibiotics like benzathine penicillin, reducing recurrence by up to 69%.^[1]^[3] Complications, though uncommon with early intervention, can include abscess formation, necrosis, bacteremia, or spread to deeper tissues, joints, or heart valves, underscoring the importance of prevention through skin care and management of underlying conditions.^[2]^[1] The prognosis is generally excellent with treatment, though skin healing may take weeks and leave residual peeling or pigmentation.^[2]

Clinical Features

Signs and Symptoms

Erysipelas typically presents with a sudden onset of systemic symptoms, including high fever, chills, malaise, and fatigue, which often precede the appearance of skin lesions by 48 hours.^[1] These constitutional symptoms reflect the body's inflammatory response to the infection and can be quite pronounced, leading to significant discomfort.^[4] Locally, the infection manifests as a sharply demarcated, raised erythematous plaque with a fiery red appearance, accompanied by warmth, tenderness, and edema.^[1] The affected skin feels indurated and shiny, with well-defined borders that distinguish it from surrounding healthy tissue, commonly involving the face or the lower extremities.^[4] Patients often report a burning or itching sensation in the area.^[1] The condition progresses rapidly, spreading over hours to days, and in severe cases, may develop vesicles, bullae, or petechiae on the plaque.^[1] Regional lymphadenopathy frequently accompanies the infection, with enlarged, tender lymph nodes near the affected site.^[5] These features are primarily linked to group A streptococcal invasion of the superficial skin layers.^[1]

Pathophysiology

Erysipelas is characterized by a superficial bacterial infection primarily involving the upper dermis and superficial lymphatics, initiated by beta-hemolytic streptococci that enter through breaches in the skin barrier. This leads to rapid bacterial proliferation within the lymphatic vessels, causing lymphatic obstruction and an intense local inflammatory response marked by marked edema and erythema. The infection's spread is facilitated by the bacteria's ability to invade the dermal papillae and lymphatics, resulting in well-demarcated, elevated lesions due to the accumulation of inflammatory exudate.^[1]^[6] Key to the disease's progression are bacterial virulence factors, including exotoxins and enzymes such as streptokinase and hyaluronidase, which promote tissue invasion and damage. Streptokinase activates plasminogen to plasmin, dissolving fibrin clots and enabling bacterial dissemination through the tissues, while hyaluronidase hydrolyzes hyaluronic acid in the extracellular matrix, further facilitating spread and contributing to localized edema and vasodilation. These mechanisms trigger a robust influx of neutrophils into the affected dermis, amplifying the inflammatory cascade and leading to the characteristic painful, fiery-red appearance.^[6]^[1] The inflammatory response is amplified by immune-mediated processes, particularly the release of pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), which drive systemic symptoms including fever and malaise. These cytokines, produced by activated macrophages and keratinocytes in response to bacterial antigens, promote endothelial permeability, further exacerbating edema, and stimulate acute-phase reactants in the liver, contributing to the overall host defense but also to potential tissue injury. Unlike deeper soft tissue infections such as cellulitis or necrotizing fasciitis, erysipelas remains confined to the papillary dermis and superficial lymphatics, sparing the subcutaneous fat and reticular dermis.^[7]^[1]

Etiology and Risk Factors

Causes

Erysipelas is predominantly caused by infection with group A beta-hemolytic Streptococcus pyogenes, a bacterium that invades the upper dermis and superficial lymphatics following disruption of the skin barrier.^[1] This organism accounts for the majority of cases, with clinical manifestations typically arising from its entry into susceptible tissues.^[8] Less commonly, other beta-hemolytic streptococci, such as groups B, C, or G, can cause erysipelas, particularly in specific populations like neonates (group B) or lower extremity infections (non-group A).^[1] In immunocompromised individuals, non-streptococcal pathogens like Staphylococcus aureus (including methicillin-resistant strains) may contribute, though evidence for their role remains limited compared to streptococci.^[4] The bacteria typically gain access through minor breaks in the skin, including abrasions, surgical wounds, ulcers, insect bites, or cracks from conditions like athlete's foot, allowing direct inoculation into the dermal layers.^[9] For facial erysipelas, entry often occurs via the nasopharynx, frequently preceded by streptococcal pharyngitis in up to one-third of cases.^[10] Historically, the incidence of facial erysipelas has declined since the mid-20th century, attributed in part to reduced transmission of streptococcal pharyngitis through improved sanitation, antibiotic use, and possible decreased bacterial virulence.^[10]

Risk Factors

Erysipelas susceptibility is heightened by various local factors that compromise skin integrity or lymphatic function. Chronic lymphedema, a major predisposing condition, impairs lymphatic drainage and creates an environment conducive to bacterial proliferation, with odds ratios as high as 71.2 in case-control studies of leg erysipelas.^[11] Venous insufficiency contributes similarly by promoting edema and stasis, increasing risk with an odds ratio of 2.9.^[11] Prior episodes of cellulitis or erysipelas further elevate recurrence risk through residual lymphatic damage.^[12] Obesity exacerbates these issues by adding mechanical pressure on tissues and worsening edema, with mean BMI significantly higher in recurrent cases (35.4 kg/m² vs. 31.2 kg/m²).^[12] Skin trauma, including wounds, ulcers, or fissured toe-web intertrigo, serves as a primary portal for bacterial entry, accounting for up to 61% of attributable risk in lower limb cases.^[11] Systemic conditions also play a critical role in host vulnerability. Diabetes mellitus, particularly insulin-dependent forms, is associated with higher recurrence rates (38.1% in recurrent vs. 20.9% in initial episodes), due to impaired immune response and neuropathy.^[13] Immunosuppression from conditions like HIV infection or treatments such as chemotherapy weakens defenses against streptococcal invasion.^[10] Nephrotic syndrome promotes generalized edema and hypoalbuminemia, further elevating risk.^[1] Demographic factors influence erysipelas incidence, with extremes of age posing particular vulnerabilities. Infants and young children are at risk due to immature immune systems, while the elderly (peaking at 60-80 years) face higher rates from age-related skin thinning and comorbidities.^[10] Recurrence is notably more common in those with underlying lymphatic damage, regardless of age.^[14] Iatrogenic risks arise from interventions disrupting lymphatic pathways. Post-surgical lymphatic obstruction, such as after mastectomy or saphenous vein excision for bypass, significantly predisposes patients.^[1] Similarly, radiotherapy, often used in breast cancer treatment, induces lymphedema that heightens recurrent erysipelas risk.^[10]

Diagnosis

Clinical Diagnosis

The clinical diagnosis of erysipelas primarily relies on a thorough history and physical examination, as the condition presents with characteristic features that allow for recognition without routine laboratory or imaging confirmation.^[1]^[4] During history taking, patients typically report an acute onset of symptoms over 24 to 48 hours, often preceded by prodromal signs such as high fever, chills, and malaise.^[1]^[4] Identifying a portal of entry is crucial, as it is frequently associated with minor skin trauma, surgical incisions, insect bites, or interdigital fissures from fungal infections, particularly in lower extremity cases.^[1]^[5] On physical examination, erysipelas is distinguished by a sharply demarcated, raised, and indurated erythematous plaque with a fiery red hue and tender, edematous margins.^[1]^[4] The lesion often exhibits a peau d'orange texture due to lymphatic obstruction and may show central clearing in some instances, though this is less common than in cellulitis.^[1]^[15] Regional lymphadenopathy and lymphangitic streaks—linear erythematous lines tracking toward lymph nodes—are frequently observed, supporting the superficial dermal involvement.^[1]^[5] Supportive laboratory tests are not essential for diagnosis but can indicate inflammation when performed. Common findings include leukocytosis, elevated C-reactive protein levels, and increased erythrocyte sedimentation rate, particularly in patients with systemic symptoms.^[1]^[15] These markers help gauge severity but do not alter the clinical diagnosis.^[4] Imaging is rarely required, as erysipelas is a superficial infection without deep extension; however, ultrasound may be used in atypical presentations to exclude abscess formation or deeper involvement.^[1]^[15] This approach ensures differentiation from conditions mimicking deeper soft tissue infections.^[5]

Differential Diagnosis

Erysipelas must be differentiated from other conditions presenting with localized erythema, warmth, swelling, and pain, as these features overlap with several infectious and non-infectious entities. The primary mimic is cellulitis, which involves deeper subcutaneous tissues rather than the superficial dermis and lymphatics characteristic of erysipelas. Cellulitis typically exhibits ill-defined borders and slower progression over days, whereas erysipelas features sharply demarcated, raised, fiery red lesions that evolve rapidly within hours.^[1]^[6] Other important differentials include deep vein thrombosis (DVT), which may cause unilateral leg swelling and tenderness but lacks the intense erythema and systemic fever often seen in erysipelas; diagnosis of DVT relies on imaging such as Doppler ultrasound to confirm venous occlusion. Contact dermatitis presents with pruritic, eczematous lesions without fever or rapid spread, typically triggered by an identifiable allergen or irritant and confirmed by history or patch testing. Necrotizing fasciitis, a life-threatening emergency, is distinguished by rapid progression with skin necrosis, bullae formation, crepitus, and severe systemic toxicity, often requiring urgent surgical exploration for confirmation.^[1]^[6] Distinguishing tests include blood cultures, which yield positive results in approximately 5% of erysipelas cases, most commonly identifying β-hemolytic streptococci, and are recommended in severe or systemic presentations to detect bacteremia. Wound or lesion swabs for culture are positive in about 30% of cases, often isolating Streptococcus pyogenes, though superficial swabs may reflect colonization rather than true etiology.^[16]^[17] Erysipeloid, an occupational infection primarily affecting fish or meat handlers, must also be excluded; it is caused by Erysipelothrix rhusiopathiae and features localized, non-tender violaceous lesions on the hands without fever or lymphatic involvement, contrasting with the systemic symptoms and widespread erythema of streptococcal erysipelas. Culture from skin lesions confirms the diagnosis in erysipeloid.^[6]

Management

Treatment

The treatment of erysipelas primarily involves antibiotic therapy targeting group A beta-hemolytic Streptococcus, the most common causative pathogen. First-line treatment consists of penicillin, administered as intravenous penicillin G for severe cases or oral phenoxymethylpenicillin (penicillin V) for milder presentations, typically for a duration of 5 to 10 days.^[1]^[18]^[19] The route of administration depends on disease severity. Intravenous antibiotics are recommended for hospitalized patients, particularly those with facial involvement, significant comorbidities such as diabetes or immunosuppression, systemic toxicity, or inability to tolerate oral intake; once the patient is afebrile and clinically improving, therapy can be switched to oral antibiotics to complete the course.^[1]^[18] For patients with penicillin allergy, alternatives include clindamycin or erythromycin, selected based on local resistance patterns and patient factors, with the same general duration of 5 to 10 days.^[1]^[18]^[19] Adjunctive measures support symptom relief and recovery. Nonsteroidal anti-inflammatory drugs (NSAIDs) or acetaminophen are used to manage pain and fever, while elevation of the affected limb reduces dependent edema and promotes lymphatic drainage, particularly in lower extremity cases.^[1]^[18]^[19] Clinical response is typically expected within 48 to 72 hours of initiating antibiotics, with improvement in fever, erythema, and pain; lack of response may indicate antibiotic resistance, non-streptococcal etiology, or underlying complications such as abscess formation, necessitating further evaluation and potential adjustment of therapy.^[1]^[18]

Prevention

Preventing erysipelas involves addressing entry points for bacterial invasion and managing underlying risk factors to reduce both initial and recurrent episodes. Prompt wound care is essential, particularly for at-risk individuals such as those with skin breaks from trauma, surgery, or chronic conditions. Cleaning wounds thoroughly with soap and water, applying antiseptics, and covering them with sterile dressings can significantly lower infection risk by preventing streptococcal entry.^[20] Early identification and management of superficial skin lesions, including debridement if necessary, further supports prevention.^[20] Managing risk factors plays a central role in prophylaxis. For individuals with lymphedema or venous insufficiency, compression therapy—such as daily multilayer bandaging or stockings—has been shown to reduce recurrence rates; in a randomized trial, it lowered the hazard of cellulitis recurrence to 0.23 (95% CI 0.09-0.59) compared to education alone.^[21] In patients with diabetes, maintaining glycemic control through diet, medication, and monitoring helps mitigate impaired immune responses and skin integrity issues that predispose to infection.^[22] Similarly, weight loss in obese individuals addresses chronic edema and skin barrier compromise, forming a cornerstone of non-pharmacological prevention alongside smoking cessation.^[23] For recurrent erysipelas, typically defined as two or more episodes within three years, long-term prophylactic antibiotics are recommended. Penicillin V (250-500 mg orally twice daily) or intramuscular benzathine penicillin G (1.2-2.4 million units every 2-4 weeks) effectively reduces recurrence risk by 69% during treatment (RR 0.31, 95% CI 0.13-0.72), with a number needed to treat of 6, based on moderate-certainty evidence from multiple randomized controlled trials.^[24] This prophylaxis is often continued for 1-5 years, with alternatives like erythromycin or cephalosporins for penicillin-allergic patients.^[25] Maintaining good hygiene practices supports overall prevention efforts. Regular moisturizing to prevent dry, cracked skin, thorough handwashing, and avoiding shared personal items like towels in communal settings help minimize bacterial transmission, especially during outbreaks of streptococcal infections.^[9] No routine vaccination exists for erysipelas prevention, as group A streptococcal vaccines remain in research stages without conferring lasting immunity from prior infection. Experimental streptococcal vaccines have shown promise in reducing recurrence in small studies, but they are not currently recommended or available for clinical use.^[22]

Prognosis and Complications

Prognosis

Erysipelas generally carries a favorable prognosis when treated promptly with appropriate antibiotics, with most uncomplicated cases resolving within 7 to 14 days. Symptomatic improvement, including reduced fever and pain, typically occurs within 24 to 48 hours of initiating therapy, while visible skin changes may take longer to subside, often up to 1 to 2 weeks for complete resolution.^[25] The mortality rate is low, less than 1% in treated uncomplicated cases, primarily due to the superficial nature of the infection and effective antimicrobial response.^[10] Recurrence is a notable concern, affecting up to 30% of patients within 3 years, with rates as high as 14% in the first year alone, often at the same site. The risk escalates significantly in cases involving lymphatic damage, such as preexisting lymphedema, where recurrent episodes can exceed 40% and further impair lymphatic function, creating a cycle of vulnerability.^[25]^[1] Several factors influence clinical outcomes, including the timeliness of treatment and patient characteristics. Prompt antibiotic administration reduces the need for hospitalization, which averages 5 to 7 days in moderate cases requiring inpatient care, and minimizes disease progression. Outcomes are poorer in immunocompromised individuals, who face higher risks of treatment failure, prolonged recovery, and complications necessitating intravenous therapy and extended monitoring.^[1]^[10] In the long term, even successfully treated erysipelas can lead to residual effects such as post-inflammatory hyperpigmentation, where darkened skin patches persist due to melanin deposition, or chronic edema from lymphatic disruption, particularly in recurrent or lower extremity cases. These sequelae may contribute to ongoing skin vulnerability but are generally manageable with supportive measures like compression therapy. Recurrent episodes can lead to scarring due to repeated inflammation and healing processes.^[1]^[25]

Complications

Erysipelas, if untreated or severe, can lead to various local complications at the site of infection. Abscess formation may occur, necessitating surgical drainage and debridement to prevent further tissue damage.^[1] Chronic lymphedema is another potential outcome, resulting from lymphatic obstruction and repeated episodes, which can progress to significant swelling such as elephantiasis in rare cases.^[1] Systemic complications arise when the infection spreads beyond the skin. Bacteremia can develop, particularly in immunocompromised individuals, though blood cultures often yield low positive rates and require targeted evaluation.^[1] Sepsis represents a more severe progression, demanding immediate resuscitation and comprehensive systemic management to stabilize the patient.^[1] Post-streptococcal glomerulonephritis may follow as an immune-mediated sequela, characterized by acute kidney injury, hematuria, and edema, typically resolving but potentially leading to long-term renal issues if severe.^[6] Rare but severe outcomes include progression to necrotizing fasciitis, a deep tissue infection requiring urgent surgical intervention and broad-spectrum antibiotics.^[26] Toxic shock syndrome can also emerge, driven by streptococcal toxins, presenting with multi-organ failure and necessitating intensive care.^[1] Management of these complications focuses on targeted interventions alongside continued antimicrobial therapy. For abscesses, incision and drainage are essential, often combined with debridement of necrotic tissue.^[1] Sepsis and bacteremia require supportive measures such as fluid resuscitation, vasopressors, and monitoring in an intensive care setting.^[1] In cases of post-streptococcal glomerulonephritis, supportive renal care including fluid management and monitoring for hypertension is prioritized, with most episodes self-limiting.^[6]

Epidemiology

Incidence and Demographics

Erysipelas has an estimated incidence of approximately 1 to 2 cases per 1,000 person-years in European countries, with rates varying by region and population; in European countries, it is around 200 cases per 100,000 individuals annually.^[23]^[17] As of 2025, incidence rates continue to rise in some European countries, with Denmark reporting 72.1 incident cases per 100,000 person-years.^[27] The condition is more prevalent among hospitalized patients, where bacterial skin infections like erysipelas account for a substantial proportion—up to 28% of such diagnoses in some inpatient settings.^[28] Demographically, erysipelas exhibits bimodal age distribution, with peaks among infants under 1 year and the elderly over 60 years, reflecting vulnerability at life's extremes due to immature or compromised immune responses.^[10] There is a slight female predominance overall, attributed to higher rates of leg involvement linked to conditions like venous insufficiency and lymphedema, which are more common in women.^[1]^[10] In terms of site distribution, approximately 80% of cases affect the lower limbs, while 10% to 20% involve the face, particularly in pediatric populations where facial erysipelas is more frequent.^[17]^[10]^[29] Trends indicate a decline in facial cases since the post-1950s era, coinciding with the widespread use of antibiotics and improvements in sanitation, shifting the burden toward lower extremity infections.^[1]^[10] Conversely, recurrence rates are rising in aging populations, driven by increasing prevalence of comorbidities such as obesity and chronic venous disease, with up to 46% of hospitalized patients experiencing repeats within three years.^[23]

Geographic Distribution

Erysipelas exhibits a higher incidence in temperate climates and developed countries, where aging populations contribute significantly to prevalence rates. In Europe, for instance, the age-standardized incidence has risen notably, from 71.5 per 100,000 in 2000 to 111.3 per 100,000 in 2016, primarily driven by increases among individuals aged 75 and older. This pattern aligns with demographic shifts in regions like the United States and Europe, where improved sanitation has reduced overall rates but not offset the impact of longevity and comorbidities.^[10]^[30]^[31] In some tropical settings, such as case reports from Burkina Faso, erysipelas presents as facial dermohypodermitis associated with insect bites or poor hygiene that facilitate bacterial entry through minor skin disruptions, where limited access to prompt care can exacerbate progression to necrotizing forms. These presentations contrast with the predominantly lower limb involvement seen elsewhere, underscoring environmental influences like vector exposure in resource-constrained settings.^[32] Outbreaks of erysipelas occur in institutional settings, particularly nursing homes housing vulnerable elderly residents and post-operative wards where surgical sites serve as entry points. In long-term care facilities, acute bacterial skin infections like erysipelas are prevalent due to factors such as immobility and shared environments, contributing to cluster transmissions. Similarly, post-surgical erysipelas has been documented at high rates following procedures like vulvar carcinoma treatment, with incidence up to three times higher in affected cohorts.^[33]^[34] Socioeconomic factors elevate erysipelas risk in low-income areas, where limited access to wound care and hygiene resources hinders prevention of skin barrier breaches. In African contexts, neglected wounds and intertrigo from poor sanitation are key local risk factors for lower limb cellulitis and erysipelas, amplifying incidence in underserved communities. Global patterns reflect how economic disparities perpetuate higher burdens in these settings, independent of climatic variations.^[35]^[6]

History

Historical Overview

The term erysipelas originates from the ancient Greek words erysibē (ἐρυσίβη), meaning "red," and pelas (πέλας), meaning "skin," literally translating to "red skin," a description reflecting the condition's characteristic fiery erythema.^[36] This nomenclature first appeared in medical literature around the 5th century BCE, when Hippocrates described erysipelas as an acute skin inflammation, often linked to wounds and termed "traumatic erysipelas," distinguishing it from other non-wound-related cutaneous lesions.^[37] In his Epidemics (Book III), Hippocrates provided the earliest recorded account of an erysipelas epidemic, noting its rapid spread and association with fever and local tenderness.^[38] Roman physician Galen, in the 2nd century CE, further refined these descriptions by differentiating erysipelas from phlegmonous (suppurative or gangrenous) inflammations, classifying both under broader inflammatory categories while emphasizing non-necrotic cellulitis as the core presentation.^[37] During the medieval period, erysipelas became colloquially known as "St. Anthony's fire" due to its burning pain and visible red inflammation, a term also applied to ergotism—a toxic condition from Claviceps purpurea-infected rye causing gangrenous symptoms—and occasionally herpes zoster, leading to diagnostic confusion among these "fiery" afflictions.^[39] The Knights Hospitaller of St. Anthony specialized in treating such conditions using remedies like pork fat applications, amid widespread epidemics in Europe where poor hygiene exacerbated surgical site infections and postpartum cases.^[39] By the 19th century, erysipelas was recognized as a significant postoperative risk and linked to puerperal fever; Ignaz Semmelweis, in the 1840s, observed that decaying matter from erysipelas cases transmitted via unwashed hands caused puerperal sepsis in maternity wards, dramatically reducing mortality through chlorine hand disinfection after connecting the diseases' shared etiology.^[40] In the late 19th century, microbiological advances clarified erysipelas as a bacterial infection; in 1884, Friedrich Julius Rosenbach isolated chain-forming cocci from erysipelas lesions and named the pathogen Streptococcus pyogenes, establishing its role in suppurative skin diseases.^[41] The 20th century brought transformative treatments: sulfonamides in the 1930s lowered mortality from approximately 10-15%, but penicillin's introduction in the 1940s proved even more effective against S. pyogenes, boosting cure rates to over 95% and reducing overall mortality to less than 1% in treated cases, shifting erysipelas from a potentially fatal scourge to a manageable condition.^[42]^[43]^[44] This evolution marked the transition from symptomatic management and contagion control to targeted antimicrobial therapy, fundamentally altering the disease's prognosis.

Notable Cases

One notable historical case of erysipelas involved Queen Anne of Great Britain, who died in 1714 from complications including suppressed gout leading to erysipelas, an abscess, and fever.^[39] Similarly, Pope Gregory XVI succumbed to facial erysipelas in 1846 after an initial mild attack rapidly worsened, highlighting the disease's potential lethality before modern antibiotics.^[39] Another prominent victim was Princess Amelia, the youngest daughter of King George III, who contracted severe erysipelas in 1810 amid underlying tuberculosis, resulting in widespread rash and her death at age 27.^[45] In 19th-century obstetrics, puerperal erysipelas emerged as a devastating form of the disease, often linked to streptococcal infections transmitted during childbirth and contributing to high maternal mortality rates in hospitals.^[46] Hungarian physician Ignaz Semmelweis observed that handwashing with chlorinated lime solutions dramatically reduced puerperal fever cases, including erysipelas outbreaks, at Vienna General Hospital's maternity ward, dropping mortality from 18% to under 2% by interrupting cadaveric particle transmission from autopsies.^[46] This intervention marked a pivotal milestone in infection control, though Semmelweis faced resistance until Louis Pasteur later confirmed the streptococcal etiology shared with erysipelas.^[47] In the late 20th century, erysipelas outbreaks were documented among post-mastectomy breast cancer patients, underscoring the heightened risk due to lymphedema from axillary lymph node dissection, which impairs lymphatic drainage and facilitates bacterial entry.^[48] A retrospective study of 26 cases reported recurrent episodes in nearly one-third of patients, with initial symptoms of fever and inflammatory erythema appearing an average of five years post-treatment, often requiring prolonged antibiotic therapy and compression to manage lymphedema exacerbation.^[48] These instances emphasized the need for vigilant skin care and prophylactic measures in lymphedema-prone individuals to prevent recurrent cellulitis-like presentations of erysipelas.^[49] Culturally, erysipelas has been depicted in art as "St. Anthony's fire" owing to its intense burning pain and fiery red rash, evoking the saint's temptations by flames in medieval iconography.^[50] Religious artworks, such as Michelangelo's The Torment of Saint Anthony, portray the condition through inflamed skin and demonic fire motifs, symbolizing affliction cured by the saint's intercession, while pigs in these scenes allude to folk remedies using their fat for erysipelas treatment.^[51] This nomenclature and visual tradition persisted into the Renaissance, reflecting erysipelas's historical terror as a divine or demonic scourge before its bacterial cause was understood.^[52]

References

[1]
Erysipelas - StatPearls - NCBI Bookshelf
Erysipelas is a skin infection involving the dermis layer of the skin, but it may also extend to the superficial cutaneous lymphatics.Introduction · History and Physical · Evaluation · Treatment / Management
[2]
Erysipelas: MedlinePlus Medical Encyclopedia
### Erysipelas Summary
[3]
Cellulitis and erysipelas - PMC - PubMed Central - NIH
It causes local signs of inflammation, such as warmth, erythema, pain, lymphangitis, and frequently systemic upset with fever and raised white blood cell count.
[4]
Erysipelas - Dermatologic Disorders - Merck Manuals
Erysipelas is characterized clinically by shiny, raised, indurated, and tender plaques with distinct margins. · There is also a bullous form of erysipelas.
[5]
Cellulitis and erysipelas - Symptoms, diagnosis and treatment
Jun 10, 2025 · Key diagnostic factors · skin discomfort · macular erythema · disruption of cutaneous barrier · raised bright-red erythema with clearly demarcated ...
[6]
Impetigo, Erysipelas and Cellulitis - Streptococcus pyogenes - NCBI
Feb 10, 2016 · Cellulitis and erysipelas can be mild or moderately severe, while necrotizing fasciitis, myonecrosis and StrepTSS are life-threatening. This ...
[7]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5420430/
[8]
Streptococcus pyogenes Impetigo, Erysipelas, and Cellulitis - NCBI
Sep 7, 2022 · In most cases, the infecting agent is S. pyogenes, but similar lesions can be caused by groups C or G streptococci. Rarely, group B ...Abstract · Anatomical Relationship of... · Streptococcal Virulence...
[9]
Overview: Erysipelas and cellulitis - InformedHealth.org - NCBI - NIH
Jul 8, 2025 · Erysipelas and cellulitis are skin infections that can develop if bacteria enter through a break in the skin. Both infections make your skin swell, become red ...Introduction · Symptoms · Causes and risk factors · Effects
[10]
Erysipelas: Background, Pathophysiology and Etiology, Epidemiology
Jun 19, 2020 · Erysipelas is a bacterial skin infection involving the upper dermis that characteristically extends into the superficial cutaneous lymphatics.Background · Pathophysiology and Etiology · Epidemiology
[11]
Risk factors for erysipelas of the leg (cellulitis): case-control study
This first case-control study highlights the major role of local risk factors (mainly lymphoedema and site of entry) in erysipelas of the leg.
[12]
In Search of Risk Factors for Recurrent Erysipelas and Cellulitis of ...
The most common complication of erysipelas is recurrence of the infection. The recurrence occurs in up to 41% of patients in 5 years [8]. A number of ...
[13]
Comorbidities as Risk Factors for Acute and Recurrent Erysipelas
Mar 15, 2019 · The most significant risk factors are local-Chronic oedema/lymphedema, history of ulcer, coexisting ipsilateral dermatitis, PAOD, chronic ulcer, fungal ...
[14]
Erysipelas: A common potentially dangerous infection - ResearchGate
Aug 9, 2025 · Erysipelas, a beta-hemolytic streptococcal infection of the skin and subcutaneous tissue, was once a common disease but nearly disappeared ...
[15]
Recurrent erysipelas: risk factors - PubMed
Results: The recurrent cases occurred mainly in the lower limb with several risk factors that were statistically more common than in the single episode group ...
[16]
Erysipelas Workup: Approach Considerations, Bacterial Cultures ...
Jun 19, 2020 · In classic erysipelas, no laboratory workup is required for diagnosis or treatment. However, leukocytosis and elevations in erythrocyte sedimentation rate (ESR ...
[17]
A systematic review of bacteremias in cellulitis and erysipelas
Results: For erysipelas, 4.6% of 607 patients had positive blood cultures, of which 46% were Streptococcus pyogenes, 29% were other β-hemolytic streptococci ...
[18]
Recurrent erysipelas - risk factors and clinical presentation - PMC
May 18, 2014 · The most prominent risk factor for recurrence was lymphedema and other conditions causing a chronic impairment of the defence against microbes.
[19]
Erysipelas Treatment & Management - Medscape Reference
Penicillin administered orally (PO) or intramuscularly (IM) is sufficient for most cases of classic erysipelas. The drug is usually given for 5 days, but if the ...
[20]
Erysipelas - Dermatologic Disorders - MSD Manuals
Erysipelas is characterized clinically by shiny, raised, indurated, and tender plaques with distinct margins. · There is also a bullous form of erysipelas.
[21]
Clinical Guidance for Group A Streptococcal Cellulitis - CDC
Aug 5, 2025 · Chickenpox and shingles; Chronic skin conditions (e.g., eczema); Fungal skin infections (e.g., athlete's foot); Injection drug use; Injuries and ...
[22]
Compression Therapy to Prevent Recurrent Cellulitis of the Leg
Aug 12, 2020 · This small, single-center, unblinded trial showed that compression therapy prevented the recurrence of cellulitis in patients with chronic edema ...
[23]
Recurrent Erysipelas: Clinical Challenges and Strategies for ... - MDPI
If first-line prophylaxis fails, some guidelines suggest clindamycin 150 mg once daily, cephalexin 125 mg once daily, doxycycline 50 mg once daily, or ...
[24]
Recurrent Erysipelas: Clinical Challenges and Strategies for ...
Oct 8, 2025 · Erysipelas can result in a range of local complications, including recurrent infections, abscesses, cellulitis, skin necrosis, superficial ...
[25]
Interventions for the prevention of recurrent erysipelas and cellulitis
Blood cultures are even less productive, with only 2% to 4% of cultures showing positive bacterial growth. Furthermore, blood culture ... exp Erysipelas/ or ...
[26]
Acute cellulitis and erysipelas in adults: Treatment - UpToDate
Jun 13, 2025 · Beta-hemolytic streptococci cause most cases of cellulitis and erysipelas, but cellulitis is sometimes caused by Staphylococcus aureus and ...Contributors · Print · 23 · 45,46
[27]
Erysipelas: a common potentially dangerous infection - PubMed
Erysipelas is an acute superficial cutaneous cellulitis that commonly occurs not only in elderly and immunocompromised persons, but also in neonates and small ...
[28]
Common Bacterial Skin Infections - AAFP
Jul 1, 2002 · Bacterial skin infections are the 28th most common diagnosis in hospitalized patients. ... The incidence of erysipelas is rising ...
[29]
Erysipelas - an overview | ScienceDirect Topics
Bacteria may gain access to the epidermis through cracks in the skin, abrasions, cuts, burns, insect bites, surgical incisions, and intravenous catheters. The ...
[30]
[PDF] Trends in the epidemiology of erysipelas in Slovenia
Erysipelas is a relatively common infection of the upper dermis and superficial lymphatics. The affected area is tender and in-.
[31]
Primary and Recurrent Erysipelas—Epidemiological Patterns in a ...
Jul 27, 2025 · Results: The majority of erysipelas cases (85.4%) involved the lower limbs, with a higher prevalence in men. Upper extremities were mostly ...
[32]
A series of four cases and a review of the literature - ResearchGate
Management of necrotizing and non-necrotic bacterial erysipelas of the face in tropical areas: A series of four cases and a review of the literature. August ...
[33]
Common infections in nursing homes: a review of current issues and ...
Acute bacterial infections in NHs include cellulitis, erysipelas and necrotizing fasciitis. Chronic wound infections, which are more common, include infected ...
[34]
High Incidence of Erysipelas After Surgical Treatment for Vulvar ...
Erysipelas occurs frequently in patients who undergo surgical treatment for vulvar carcinoma. The risk of erysipelas is 3 times higher in patients who undergo ...
[35]
Risk factors and complications of lower limb cellulitis in Africa
Local risk factors of cellulitis reported were: disruption of the skin barrier, neglected wounds, toe-web intertrigo, leg ulcers, use of depigmentation drugs ...<|control11|><|separator|>
[36]
Etymologia: Streptococcus - Volume 22, Number 11—November 2016
Nov 11, 2016 · ... erysipelas (Greek for “red skin”). The genus Streptococcus (Figure) was named by Austrian surgeon Theodor Billroth, who in 1874 described ...
[37]
Erysipelas (VIII.50) - The Cambridge World History of Human Disease
For the past century or so, however, erysipelas has commonly referred to infection of the derma with a streptococcal organism, usually Streptococcus pyogenes.Missing: decline pharyngitis
[38]
The Etiology of Erysipelas | Annals of Internal Medicine - ACP Journals
In his "Epidemion" Book III, Hippocrates made the first written record of an epidemic of erysipelas, in... Formats available. You can view the full content in ...Missing: ancient | Show results with:ancient
[39]
One holy man, one eponym, three distinct diseases. St. Anthony's ...
The original writings of Hippocrates, from the 4th century BC, describe the disease erysipelas (ἐρυσίπελας, i.e., red skin) (26) and, in fact, streptococcal ...Ergotism · Erysipelas · Discussion
[40]
Puerperal Fever | Death in Childbirth - Oxford Academic
It was first discovered by Ignaz Semmelweis, who also showed its contagiousness and who discovered an antisepsis against it. Puerperal fever may be considered ...
[41]
History of Streptococcal Research - Streptococcus pyogenes - NCBI
Feb 10, 2016 · Streptococcal diseases have been known for centuries, although their delineation into separate disease entities did not begin to occur until the 16 th century ...Missing: facial | Show results with:facial
[42]
Skin and Soft Tissue Infections: Modern Evolution of an Ancient ...
However, analysis of historical data has demonstrated that the mortality rate of cellulitis (or “erysipelas” as it was called prior to the 1950s) was ~11% in ...
[43]
Mortality from Erysipelas Before and After the Introduction of...
... In the pre-antibiotic era, bacteremia was common, with mortality as high as 15%. The introduction of sulfona-mides into clinical use in the 1930s changed the ...
[44]
Antimicrobial Agents for Complicated Skin and Skin-Structure ... - NIH
For cellulitis/erysipelas, cure rates were 66% (95% CI, 64%–68%) without antibiotics and 98% (95% CI, 96%–99%) for penicillin-treated patients, and penicillin ...
[45]
Princess Amelia (1783-1810) - Blog | Regency History
May 29, 2012 · By eighteen, she was also suffering from erysipelas, a painful bacterial skin infection also known as St Anthony's fire. All kinds of ...
[46]
“No Good Deed Goes Unpunished”: Ignaz Semmelweis and the ...
May 16, 2016 · The connection between the nature of puerperal fever and erysipelas was first suggested, to the best of our knowledge, by the French surgeon ...
[47]
The Most Unspeakable Terror - Dartmouth Medicine Magazine
That was left to Semmelweis and ultimately to Pasteur, who in 1879 isolated and characterized streptococcus as the cause of puerperal fever and erysipelas. The ...
[48]
Erysipelas after breast cancer treatment (26 cases) - PubMed
Dec 1, 2005 · Lymphedema occurred in eighteen patients. The first signs were fever and shivering in 25 patients. The clinical aspect was an inflammatory ...
[49]
Cellulitis after axillary lymph node dissection for carcinoma of the ...
We present a series of patients who developed cellulitis following axillary lymph node dissection for carcinoma of the breast.<|separator|>
[50]
Anthony Abbot (Anthony of Egypt) in Art - Christian Iconography
Jun 13, 2022 · 5 Butler and Duchet-Suchaux explain the flame as related to "St. Anthony's Fire," the disease erysipelas, outbreaks of which were said to be ...Missing: depictions | Show results with:depictions
[51]
Integrating the Integumentary System with the Arts: A Review of ...
Apart from syphilis, another infectious disease represented in paintings is erysipelas, or “St. Anthony's fire,” depicted in the Torment of St. Anthony ...
[52]
This pig is on fire: A late medieval pig in Leiden's Pieterskerk
Nov 2, 2018 · ... erysipelas, both of which became known as "St Anthony's fire". As a result, Anthony is often depicted among flames: Saint Anthony surrounded ...