Erysipelas

1. Clinical Overview

Summary

Erysipelas is an acute superficial bacterial skin infection primarily involving the upper dermis and superficial lymphatic vessels. It is predominantly caused by beta-hemolytic streptococci, particularly Group A Streptococcus (Streptococcus pyogenes), though Group G and C streptococci are increasingly recognized. [1,2] The hallmark clinical presentation is a well-demarcated, raised, intensely erythematous plaque with sharply defined borders, accompanied by significant systemic features including fever, rigors, and malaise. [3] Unlike cellulitis, which extends into deeper subcutaneous tissue with indistinct margins, erysipelas remains superficial and exhibits a palpable advancing edge. The lower extremities (70%) and face (20%) are the most frequently affected sites. [4] Treatment centers on penicillin-based antibiotics, and prognosis is generally excellent with appropriate therapy, though recurrence affects approximately 30% of patients. [5,6]

Key Facts

• Primary Pathogen: Group A Streptococcus (Strep pyogenes) - 80-90% of cases [1,2]
• Secondary Pathogens: Group G/C Streptococcus (S. dysgalactiae) - increasingly recognized [4]
• Anatomical Depth: Upper dermis and superficial lymphatics (superficial to cellulitis)
• Distinguishing Feature: Well-demarcated, raised, palpable border with sharp edges
• Common Sites: Lower leg (70%), Face (20%), Upper limbs (5-10%) [4]
• Incidence: 10-100 per 100,000 per year; population-based rate 72 per 100,000 person-years [4,7]
• First-Line Treatment: Phenoxymethylpenicillin (Penicillin V) 500mg QDS orally for mild cases; Benzylpenicillin 1.2g IV QDS for severe cases [8,9]
• Recurrence Rate: 30% within 3 years; 7.7% within one year in incident cases [4,6]
• Prognosis: Excellent with treatment; one-year mortality 15% (primarily in elderly with comorbidities) [4]

Clinical Pearls

"Sharp Borders = Erysipelas; Blurred Borders = Cellulitis": The single most important clinical distinction. Erysipelas has well-demarcated, raised, palpable edges that can be marked with a pen. Cellulitis has indistinct, merging borders that fade into normal skin. [3]

"Fever Before Rash": Patients frequently develop high fever (greater than 38.5°C), rigors, and systemic malaise 12-24 hours BEFORE the rash appears. This prodromal phase can cause diagnostic confusion with other febrile illnesses. [3]

"The Butterfly Sign": Classical facial erysipelas presents with a butterfly distribution over the bridge of the nose and cheeks, characteristically sparing the nasolabial folds. Unlike the malar rash of systemic lupus erythematosus, erysipelas is hot, tender, raised, and the patient is systemically unwell. [10]

"Mark the Margins": Always outline the erythema with a permanent marker at initial assessment. This allows objective monitoring of spread or resolution at 24-48 hour review and guides escalation of therapy. [8]

"Recurrence is the Rule, Not the Exception": With 30% recurrence rates, identifying and aggressively treating predisposing factors (chronic lymphoedema, tinea pedis, venous insufficiency, obesity) is as important as treating the acute infection. [5,6] Consider long-term antibiotic prophylaxis after two or more episodes. [6]

"Streptococcus dysgalactiae is Emerging": While Group A Streptococcus remains the classic pathogen, Streptococcus dysgalactiae (Groups G and C) is now recognized as the predominant pathogen in blood culture-positive cases. [4] Fortunately, both respond to penicillin.

"Bullae Don't Mean Staph": Bullous erysipelas occurs in 5-10% of cases and represents severe local inflammation, NOT staphylococcal infection. Continue penicillin; do not automatically add anti-staphylococcal cover unless clear evidence of purulence or abscess formation. [3]

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2. Epidemiology

Incidence and Prevalence

Erysipelas is a common infection encountered in emergency departments and primary care settings. [4,7]

• Incidence: 10-100 per 100,000 population per year (varies by geography and population studied) [7]
• Population-Based Incidence: 72.10 per 100,000 person-years for incident cases [4]
• Emergency Department Prevalence: Approximately 1% of acute non-trauma presentations; 96.7 per 10,000 visits [4]
• Hospitalization Rate: Approximately 40-50% of cases require hospital admission, primarily for IV antibiotics and management of systemic toxicity [4,7,33]
• Seasonal Variation: Higher incidence in summer months, correlating with increased outdoor activities, minor trauma, and insect bites [7]

Demographics

• Age Distribution: Bimodal pattern

  • "First peak: Young children (2-6 years) - often facial erysipelas"
  • "Second peak: Elderly adults (greater than 60 years) - predominantly lower limb involvement [7]"
  • "Median age at presentation: 50-70 years [4,6]"

• Sex Distribution: Roughly equal male-to-female ratio; some studies report slight female predominance (1.2:1) [7]

Risk Factors

Understanding predisposing factors is critical for prevention of recurrence. [5,6]

Anatomical Distribution

• Lower Extremities: 70% of cases [4]

  • Usually unilateral
  • Entry point often from tinea pedis, minor trauma, or leg ulcer
  • Associated with venous insufficiency and lymphoedema

• Face: 20% of cases [4]

  • Butterfly distribution over malar eminences
  • Entry point may be nasal vestibule colonization, minor facial trauma
  • More common in children and young adults
  • Higher risk of orbital and intracranial complications

• Upper Extremities: 5-10% of cases [4]

  • Often post-mastectomy with lymphoedema
  • Following axillary lymph node dissection
  • Injection drug users

• Other Sites: less than 5%

  • Trunk, perineum (rare)

Geographic and Temporal Trends

• Global Distribution: Worldwide; higher incidence in developed countries may reflect better disease recognition and reporting [7]
• Increasing Incidence: Some regions report rising incidence over past 20 years, potentially due to aging populations, increasing obesity, and better surveillance [7]

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3. Pathophysiology

Microbiological Aetiology

Key Point: While Group A Streptococcus remains the classical pathogen, recent epidemiological studies demonstrate that Streptococcus dysgalactiae (non-Group A beta-hemolytic streptococcus) is the predominant organism isolated from blood cultures in erysipelas. [4,24] Perianal colonization with S. dysgalactiae has been documented in a substantial proportion of patients with erysipelas. [24] Both organisms are uniformly susceptible to penicillin.

Pathogenic Mechanism

The pathogenesis of erysipelas involves several coordinated steps:

1. Portal of Entry

• Skin Barrier Breach: Streptococci require a break in the skin integrity to gain access to the dermis. [3]
  • Tinea pedis (interdigital maceration and fissuring) - most common
  • Minor trauma (insect bites, abrasions, cuts)
  • Chronic wounds (leg ulcers, pressure sores)
  • Surgical incisions or scars
  • Inflammatory dermatoses (eczema, psoriasis)

2. Bacterial Adhesion and Invasion

• Surface Proteins: Streptococcal surface proteins (M protein, fibronectin-binding proteins) facilitate adherence to keratinocytes and dermal matrix. [11]
• Tissue Invasion: Bacteria proliferate in the superficial dermis and lymphatic channels.

3. Immune Evasion and Toxin Production

• M Protein: Inhibits complement activation and phagocytosis, allowing streptococcal survival in tissues. [11]
• Streptococcal Pyrogenic Exotoxins (SPE): Superantigens that trigger massive cytokine release (TNF-α, IL-1, IL-6), resulting in:
  • Systemic inflammatory response (fever, tachycardia)
  • Vasodilation and increased vascular permeability (oedema, erythema)
  • Recruitment of neutrophils and macrophages (local inflammation)
• Streptolysin O and S: Cytolysins that damage cell membranes and contribute to tissue injury.

4. Superficial Lymphatic Spread

• Horizontal Propagation: Unlike cellulitis, which dissects vertically into subcutaneous fat, erysipelas spreads horizontally through dermal lymphatic vessels. [3]
• Sharp Demarcation: The superficial nature and lymphatic spread create the characteristic well-defined, raised border.
• "Peau d'Orange" Appearance: Obstruction of superficial lymphatics causes skin pitting resembling orange peel.

5. Systemic Inflammatory Response

• Cytokine Storm: Massive release of pro-inflammatory cytokines results in:
  • High-grade fever (often greater than 39°C)
  • Rigors and chills
  • Malaise, myalgia, headache
  • Occasionally hypotension and shock (in severe cases)

Erysipelas vs Cellulitis: Critical Distinction

While both are streptococcal/staphylococcal skin infections, they differ fundamentally in depth and presentation. [3]

Clinical Note: In practice, distinguishing erysipelas from cellulitis can be challenging, and mixed infections occur. When in doubt, use combination therapy (e.g., co-amoxiclav or flucloxacillin + penicillin) to cover both streptococci and staphylococci. [8]

Molecular Pathophysiology

Exam Detail: For postgraduate examinations, understand the molecular basis of streptococcal virulence:

Virulence Factors of Group A Streptococcus:

1. M Protein:

   • Surface protein encoded by emm gene (greater than 200 serotypes)
   • Antiphagocytic; binds factor H to inhibit complement
   • Binds fibrinogen, blocking C3b deposition
   • Major determinant of serotype-specific immunity

2. Hyaluronic Acid Capsule:

   • Mimics human hyaluronic acid (molecular mimicry)
   • Antiphagocytic; inhibits complement activation
   • Contributes to "mucoid" colony morphology

3. Streptococcal Pyrogenic Exotoxins (SPE A, B, C):

   • Superantigens: bypass normal antigen processing
   • Cross-link MHC class II and T-cell receptor
   • Trigger polyclonal T-cell activation (up to 20% of T cells)
   • Massive cytokine release → toxic shock syndrome
   • SPE A associated with more severe invasive disease

4. Streptolysins O and S:

   • SLO: Oxygen-labile cytolysin; induces pore formation
   • SLS: Oxygen-stable; cytotoxic to neutrophils and erythrocytes
   • Contribute to tissue necrosis and hemolysis

5. Streptokinase:

   • Converts plasminogen to plasmin
   • Degrades fibrin, facilitating tissue spread
   • Contributes to rapid horizontal spread in erysipelas

6. DNases (A, B, C, D):

   • Degrade neutrophil extracellular traps (NETs)
   • Facilitate immune evasion
   • Anti-DNase B antibodies used for serological diagnosis

Immune Response:

• Innate Immunity: TLR-2 recognizes lipoteichoic acid → NF-κB activation → cytokine production
• Adaptive Immunity: Type-specific anti-M protein antibodies provide long-lasting immunity to specific serotype
• Lack of Cross-Protection: greater than 200 M serotypes mean recurrent infections with different strains are common

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4. Clinical Presentation

Prodromal Phase (0-24 Hours Before Rash)

A characteristic feature of erysipelas is the prodrome that often precedes visible skin changes. [3]

• High-Grade Fever: Temperature greater than 38.5°C (often 39-40°C)
• Rigors and Chills: Severe shaking, "teeth-chattering" rigors
• Malaise: Profound fatigue, weakness
• Headache: Often frontal or generalized
• Myalgia and Arthralgia: Generalized body aches
• Nausea and Vomiting: Variable
• Regional Lymphadenopathy: Tender lymph nodes draining affected area (inguinal for leg; cervical/preauricular for face)

Clinical Pearl: Patients often present to primary care or emergency department with "flu-like illness" 12-24 hours before the rash appears, making early diagnosis challenging. [3]

Established Erysipelas (24-72 Hours)

Cardinal Features

Associated Features

• Bullae (Bullous Erysipelas): 5-10% of cases develop bullae (fluid-filled blisters) due to severe local inflammation and oedema. [3] Bullae do NOT indicate staphylococcal infection.
• Petechiae/Purpura: Uncommon; if present, consider coagulopathy or vasculitis.
• Desquamation: During recovery phase (7-10 days), superficial skin peeling occurs.
• Regional Lymphadenitis: Tender, enlarged lymph nodes draining the affected area.
• Lymphangitis: Red linear streaks extending proximally along lymphatic channels (less common than in cellulitis).

Site-Specific Presentations

Lower Limb Erysipelas (70% of Cases)

• Typical Distribution:

  • Dorsum of foot and lower leg
  • Usually unilateral (bilateral suggests alternative diagnosis like lipodermatosclerosis)
  • May extend from ankle to knee

• Entry Point:

  • Tinea pedis (toe web fissuring) - most common
  • Leg ulcers (venous, arterial, neuropathic)
  • Minor trauma

• Associated Findings:

  • Pre-existing lymphoedema or venous insufficiency
  • Varicose veins
  • Chronic venous staining (haemosiderin deposition)

• Complications:

  • Compartment syndrome (rare, but important differential if severe pain)
  • Deep vein thrombosis (immobility, venous stasis)
  • Chronic lymphoedema (recurrent episodes damage lymphatics)

Facial Erysipelas (20% of Cases)

• Typical Distribution:

  • ""Butterfly Pattern": Malar eminences, bridge of nose"
  • "Nasolabial Fold Sparing: Classic feature; unlike lupus rash"
  • May involve forehead, eyelids, ears

• Entry Point:

  • Nasal vestibule colonization
  • Nasal trauma or manipulation
  • Facial trauma, insect bites
  • Perioral/perinasal dermatitis

• Associated Findings:

  • Marked periorbital oedema (may close eyes)
  • Auricular involvement
  • Cervical or preauricular lymphadenopathy

• Complications (More Serious than Lower Limb):

  • "Orbital Cellulitis: Extension into orbit → ophthalmoplegia, vision loss"
  • "Cavernous Sinus Thrombosis: Facial vein → cavernous sinus; presents with headache, cranial nerve palsies (III, IV, V, VI), reduced consciousness"
  • "Meningitis: Rare but serious; consider if headache, neck stiffness, altered mental status"
  • "Abscess Formation: Nasal, periorbital, or intracranial"

Upper Limb Erysipelas (5-10% of Cases)

• Typical Distribution:

  • Forearm and hand
  • Usually unilateral

• Risk Factors:

  • Post-mastectomy lymphoedema (breast cancer treatment)
  • Axillary lymph node dissection
  • Injection drug use
  • Minor trauma, insect bites

• Complications:

  • Chronic upper limb lymphoedema
  • Recurrent episodes (30-40% in post-mastectomy patients)

Severity Grading: Eron Classification

The Eron classification guides management decisions (outpatient vs inpatient, oral vs IV antibiotics). [8]

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5. Clinical Examination

Systematic Approach

A. Vital Signs Assessment

Red Flags in Vital Signs:

• Hypotension (SBP less than 90 mmHg) → sepsis, fluid resuscitation needed
• Persistent tachycardia despite antipyretics → severe infection or complications
• Altered mental status → cerebral involvement or severe sepsis

SIRS Criteria in Erysipelas: Erysipelas frequently triggers systemic inflammatory response syndrome (SIRS), defined as ≥2 of:

• Temperature \u003e38°C or less than 36°C
• Heart rate \u003e90/min
• Respiratory rate \u003e20/min or PaCO₂ less than 32 mmHg
• WCC \u003e12 x 10⁹/L or less than 4 x 10⁹/L or \u003e10% bands

Presence of SIRS indicates systemic involvement and warrants closer monitoring.

B. Inspection of Affected Area

Perform Thorough Visual Examination:

1. Color and Intensity:

   • Bright "fiery" red erythema (more vivid than cellulitis)
   • Uniform color throughout lesion

2. Borders:

   • Well-demarcated: Sharp line of demarcation from normal skin
   • Raised edge: Palpable ridge at periphery
   • Mark borders: Use permanent marker to outline; reassess at 24-48h

3. Surface:

   • Shiny, tense, smooth appearance
   • "Peau d'orange" (orange peel) texture due to lymphatic obstruction
   • Look for bullae (clear or hemorrhagic fluid-filled blisters)
   • Look for petechiae or purpura (suggest coagulopathy)
   • Signs of necrosis (black/dusky skin): URGENT - necrotizing fasciitis until proven otherwise

4. Associated Findings:

   • Desquamation (in recovery phase)
   • Excoriations, lichenification (chronic scratching)
   • Entry point (tinea pedis, ulcer, trauma)

C. Palpation

1. Temperature:

   • Warm or hot to touch
   • Compare to contralateral limb

2. Tenderness:

   • Significant local tenderness on palpation
   • Severe pain disproportionate to findings → consider necrotizing fasciitis

3. Consistency:

   • Firm, indurated
   • Woody hard texture → consider deep infection or fibrosis

4. Border Palpation:

   • Palpable raised edge ("step")
   • Clearly demarcated from normal skin

5. Crepitus:

   • Any crepitus (crackling sensation on palpation) → gas-forming infection (necrotizing fasciitis, gas gangrene) - SURGICAL EMERGENCY

D. Regional Lymph Nodes

• Inguinal Nodes (for lower limb): Often tender, enlarged
• Cervical/Preauricular Nodes (for face): Tender, palpable
• Axillary Nodes (for upper limb): Assess size, tenderness

E. Identify Portal of Entry

Systematic search for predisposing factors:

• Tinea Pedis: Interdigital maceration, scaling, fissuring (most common for lower limb)
• Leg Ulcers: Venous, arterial, diabetic, pressure ulcers
• Trauma: Abrasions, cuts, insect bites, scratches
• Eczema/Psoriasis: Inflamed, broken skin
• Surgical Wounds: Recent surgery, chronic scars
• Injection Sites: Track marks (IVDU)

Clinical Pearl: The portal of entry is identifiable in approximately 80% of cases. [33] When no obvious entry point is found, consider nasal vestibule colonization (facial erysipelas) or interdigital tinea pedis (lower limb - examine toe webs carefully with adequate lighting).

Documentation: Always document the portal of entry, as treating it (e.g., antifungal cream for tinea pedis) is crucial for preventing recurrence.

F. Assess Predisposing Conditions

• Venous Insufficiency: Varicose veins, venous eczema, haemosiderin staining, lipodermatosclerosis
• Lymphoedema: Non-pitting oedema, skin thickening, "tree-trunk" leg
• Obesity: BMI greater than 30, skin folds
• Peripheral Arterial Disease: Reduced/absent pulses, cool extremity, hair loss, prolonged capillary refill

Differentiation from Other Conditions

Erysipelas vs Cellulitis (Revisited)

Erysipelas vs Necrotizing Fasciitis

CRITICAL DISTINCTION - Necrotizing fasciitis is a surgical emergency with high mortality (20-30%). [12]

LRINEC Score (Laboratory Risk Indicator for Necrotizing Fasciitis): [12]

• C-reactive protein ≥150 mg/L: 4 points
• WCC less than 15 or greater than 25: 1-2 points
• Hemoglobin less than 11-13.5 g/dL: 1-2 points
• Sodium less than 135 mmol/L: 2 points
• Creatinine greater than 141 μmol/L: 2 points
• Glucose greater than 10 mmol/L: 1 point

Score ≥6: High risk of necrotizing fasciitis → urgent surgical review

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6. Investigations

General Principle

Erysipelas is a clinical diagnosis. Investigations are performed to:

1. Assess severity and systemic involvement
2. Guide antibiotic therapy
3. Monitor response to treatment
4. Exclude complications
5. Identify predisposing factors

Baseline Investigations

Blood Tests

Blood Cultures

• Indication: All patients with systemic features (fever, tachycardia, hypotension) or requiring hospital admission [8]
• Yield: Positive in only 5-10% of cases; systematic review reports 4.6% positivity rate [4,25]
• Timing: Obtain BEFORE starting antibiotics (if possible)
• Technique: 2 sets (aerobic + anaerobic) from separate sites
• Predominant Organism (when positive): Streptococcus dysgalactiae (Groups G/C) - 29% of positive cultures, followed by S. pyogenes (Group A) - 46% of positive cultures [25]
• Other Organisms: Staphylococcus aureus (14%), Gram-negative organisms (11%) [25]

Clinical Note: Low blood culture yield does NOT mean antibiotics should be withheld. Start empirical therapy based on clinical diagnosis. [8,26]

Microbiological Investigations

Skin Swabs

• Utility: Very low yield (bacteria in dermis, not surface)
• Not Routinely Recommended [8,9]
• Consider if:
  • Atypical presentation
  • Bullous lesions (swab blister fluid)
  • Failure to respond to first-line antibiotics
  • Suspicion of MRSA (healthcare setting, known colonization)

Tissue Aspiration/Biopsy

• Rarely Indicated in typical erysipelas
• Consider if:
  • Diagnostic uncertainty (malignancy, vasculitis)
  • Immunocompromised host (atypical organisms)
  • Failure to respond after 72h of appropriate antibiotics

Serological Tests

• Anti-Streptolysin O (ASO) Titre: Rises 1-3 weeks after infection; retrospective diagnosis only
• Anti-DNase B: More sensitive for skin infections than ASO
• Not Useful for Acute Management - do not delay treatment awaiting serology

Imaging

When to Image

Imaging is NOT required for uncomplicated erysipelas. Consider imaging if: [12]

• Suspicion of deeper infection (abscess, necrotizing fasciitis, pyomyositis)
• Failure to respond to 48-72h of appropriate antibiotics
• Severe pain disproportionate to clinical findings
• Signs of deep vein thrombosis
• Concern for orbital or intracranial complications (facial erysipelas)

Imaging Modalities

CT/MRI Findings Suggesting Necrotizing Fasciitis: [12]

• Gas in fascial planes
• Thickened, enhancing fascia
• Fluid tracking along fascial planes
• Muscle involvement (necrotizing myositis)

Investigations for Predisposing Factors

Once acute infection is controlled, investigate underlying risk factors to prevent recurrence:

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7. Management

Overview of Management Principles

1. Early Antibiotic Therapy: Penicillin-based antibiotics are first-line [8,9]
2. Supportive Care: Analgesia, hydration, limb elevation
3. Severity Assessment: Eron classification guides admission vs outpatient management
4. Mark Borders: Outline erythema to monitor progression
5. Identify and Treat Portal of Entry: Tinea pedis, leg ulcers, etc.
6. Prevent Recurrence: Long-term strategies for high-risk patients

Initial Assessment and Triage

Use Eron Classification to guide admission decisions: [8]

• Class I (Mild): Outpatient management with oral antibiotics
• Class II (Moderate): Consider admission; may start IV then switch to oral
• Class III-IV (Severe/Life-threatening): Admission mandatory; IV antibiotics; consider ICU

Antibiotic Therapy

First-Line Antibiotics (Streptococcal Cover)

Penicillin remains the gold standard due to universal streptococcal susceptibility and narrow spectrum. [8,9]

Duration: 7-14 days total (shorter courses may suffice if rapid response; extend to 14 days if slow response or risk factors) [8,27]

Evidence for Penicillin: Multiple studies confirm no advantage of broader-spectrum antibiotics over penicillin for treating erysipelas. [26] Comparative studies show penicillin achieves cure rates of 67-76%, equivalent to alternative agents. [27,28] A large systematic review found no evidence supporting superiority of any one antibiotic over another, and antibiotics with anti-MRSA activity did not add advantage. [29]

Penicillin Allergy

When to Add Anti-Staphylococcal Cover

In typical well-demarcated erysipelas, staphylococcal coverage is NOT required. [8,9] Consider adding anti-staphylococcal antibiotics if:

• Bullous lesions with purulent fluid
• Abscess formation
• Penetrating trauma or IV drug use
• Failure to respond to penicillin after 48-72h
• Suspicion of MRSA (healthcare exposure, known colonization)

Anti-Staphylococcal Options:

• Flucloxacillin: 1-2g QDS IV or 500mg-1g QDS PO
• Co-amoxiclav: 1.2g TDS IV or 625mg TDS PO (covers both Strep and Staph)
• MRSA suspected: Add vancomycin or linezolid

Route of Administration: Oral vs Intravenous

Evidence: A controlled trial of 60 patients comparing oral versus IV penicillin therapy found no clinical benefit of IV therapy, as evaluated by fever duration, hospital stay, and sick leave. [30] Similarly, a systematic review found no evidence supporting IV antibiotics over oral antibiotics. [29]

Practical Approach:

• Mild cases (Eron I): Oral antibiotics from outset
• Moderate-severe (Eron II-III): IV antibiotics until clinical improvement (typically 24-48h afebrile), then switch to oral to complete course
• Severe sepsis/shock (Eron IV): IV antibiotics mandatory until stabilized

Adjunctive Corticosteroid Therapy

Emerging Evidence: Randomized controlled trials have evaluated corticosteroids as adjunctive therapy to accelerate resolution. [31,32]

Study Findings:

• Bergkvist et al. (1997): RCT of 112 patients; prednisolone (0.5mg/kg for 8 days) plus antibiotics showed trend toward faster clinical improvement but did not reach statistical significance for primary endpoint (time to cure). [32]
• Cranendonk et al. (2017): RCT of 60 patients; prednisolone (40mg daily for 7 days) plus antibiotics resulted in significantly faster resolution of clinical signs and shorter hospital stay compared to antibiotics alone. [31]

Current Recommendation: Not routinely recommended. Consider in severe cases with marked systemic inflammation, but further evidence needed. [31]

Supportive Care

Mark the Margins: Use a permanent marker to outline the edge of erythema at initial assessment. Reassess at 24-48 hours. [8]

• Expanding margins despite antibiotics → consider treatment failure, deeper infection, or necrotizing fasciitis
• Stable or receding margins → adequate response

Monitoring and Review

Inpatient Monitoring

• Vital signs: Every 4-6 hours initially; monitor for sepsis
• Clinical assessment: Daily measurement of lesion size; photograph if possible
• Bloods: Repeat CRP at 48-72h (should halve if responding) [8]
• Switch to Oral: When afebrile greater than 24h, clinically improving, able to take oral medications

Outpatient Review

• Clinic or GP review at 48-72 hours (or earlier if worsening)
• Assess:
  • Fever resolution
  • Lesion size (expanding vs stable vs reducing)
  • Systemic symptoms improving
  • Adherence to antibiotics
• Safety-net advice: Return immediately if:
  • Worsening despite antibiotics
  • Spreading rash
  • Increasing pain
  • Fever not settling
  • Systemically unwell (confusion, dizziness, reduced urine output)

Treatment Failure (Lack of Response at 48-72 Hours)

Definition: No improvement or worsening despite 48-72h of appropriate antibiotics

Differential Diagnosis:

1. Wrong diagnosis: Consider alternative (necrotizing fasciitis, DVT, vasculitis, malignancy)
2. Inadequate antibiotic cover: Add anti-staphylococcal agent
3. Resistant organism: Rare (GAS universally penicillin-sensitive); consider atypical organism
4. Deeper infection: Abscess, pyomyositis, necrotizing fasciitis
5. Non-infectious mimics: Sweet syndrome, drug reaction, vasculitis, panniculitis

Actions:

• Reassess diagnosis
• Review antibiotic choice and adherence
• Consider imaging (USS, CT, MRI)
• Consult infectious diseases or dermatology
• Consider skin biopsy

Management of Complications

Abscess Formation

• Clinical Signs: Fluctuant mass, persistent fever despite antibiotics
• Diagnosis: Ultrasound
• Treatment: Incision and drainage + antibiotics (add anti-staphylococcal cover)

Deep Vein Thrombosis (DVT)

• Risk: Immobility, inflammation, venous stasis
• Clinical Signs: Unilateral leg swelling, calf tenderness (but overlap with erysipelas)
• Diagnosis: Venous duplex ultrasound
• Treatment: Anticoagulation (LMWH or DOAC)

Necrotizing Fasciitis

• Clinical Signs: Severe pain disproportionate to findings, rapid progression, skin necrosis, crepitus, shock
• LRINEC Score ≥6: High risk
• Imaging: CT/MRI shows gas and fascial involvement
• Treatment: SURGICAL EMERGENCY
  • Urgent surgical debridement
  • Broad-spectrum IV antibiotics (e.g., piperacillin-tazobactam + clindamycin)
  • ICU support

Septic Shock

• Clinical Signs: Hypotension (SBP less than 90 mmHg), tachycardia, reduced urine output, confusion
• Treatment:
  • "Sepsis Six (within 1 hour):"
    1. High-flow oxygen
    2. Blood cultures
    3. IV antibiotics
    4. IV fluid resuscitation
    5. Lactate measurement
    6. Urine output monitoring
  • ICU admission
  • Consider inotropic support

Prevention of Recurrence

Recurrence occurs in approximately 30% of patients within 3 years. [5,6] Prevention strategies are essential.

Identify and Treat Predisposing Factors

Antibiotic Prophylaxis

Indications: [6]

• ≥2 episodes of erysipelas within 12 months
• ≥3 episodes in any time period
• Chronic lymphoedema with recurrent infections

Regimens: [6]

• Phenoxymethylpenicillin (Penicillin V): 250-500mg BD (long-term)
• Erythromycin (if penicillin-allergic): 250-500mg BD

Evidence: Cochrane review demonstrates antibiotic prophylaxis reduces recurrence risk by 69% (RR 0.31, 95% CI 0.13-0.72; NNT 6) while ON prophylaxis. [6] However, protective effect diminishes after discontinuation.

Duration: Variable; often continued for 6-12 months, then reassess. Some patients require indefinite prophylaxis.

Adverse Effects: Gastrointestinal upset (nausea, diarrhea), rash, thrush. Around 10% discontinue due to side effects. [6]

Limitations: Does not prevent recurrence AFTER stopping prophylaxis. [6] Emphasizes importance of treating underlying predisposing factors.

Lymphoedema Management

Emerging evidence suggests that liposuction and controlled compression therapy significantly reduce erysipelas incidence in patients with chronic lymphoedema. [13]

• Liposuction for late-stage lymphoedema: 65% reduction in erysipelas incidence rate (0.20 → 0.07 bouts per person per year, pless than 0.001) [13]
• Mechanism: Removes chronic inflammatory tissue and restores normal tissue architecture
• Requires lifelong compression post-operatively

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8. Complications

Acute Complications

Site-Specific Complications (Facial Erysipelas)

Chronic Complications

Post-Streptococcal Immune-Mediated Sequelae

Rare but important to recognize:

• Acute Rheumatic Fever (ARF): More common after pharyngitis than skin infection; Jones criteria for diagnosis
• Post-Streptococcal Glomerulonephritis (PSGN): Presents 1-3 weeks post-infection with hematuria, proteinuria, hypertension, oedema
• PANDAS (Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections): Controversial; obsessive-compulsive symptoms in children

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9. Prognosis and Outcomes

With Appropriate Treatment

• Clinical Improvement: Typically within 48-72 hours of starting antibiotics [8]

  • Fever resolution
  • Reduction in erythema
  • Decreased pain and tenderness

• Complete Resolution: 7-14 days

  • Erythema completely resolved
  • Desquamation may occur during recovery
  • Residual post-inflammatory hyperpigmentation common

• Cure Rate: greater than 95% with appropriate antibiotics [8,9]

Mortality

• Overall Mortality: Low (less than 2%) in uncomplicated cases [7]
• One-Year Mortality: 15% (primarily elderly with multiple comorbidities) [4]
• Mortality Risk Factors:
  • Age greater than 65 years
  • Multiple comorbidities (diabetes, CKD, liver disease, heart failure)
  • Sepsis or septic shock
  • Necrotizing fasciitis (20-30% mortality) [12]

Recurrence

• Overall Recurrence Rate: 30% within 3 years [5,6]
• One-Year Recurrence (incident cases): 7.7% [4]
• Risk Factors for Recurrence: [4,6]
  • Chronic lymphoedema
  • Obesity (BMI greater than 30)
  • Liver disease
  • Venous insufficiency
  • Persistent tinea pedis
  • Diabetes mellitus

Recurrence Prevention:

• Treat predisposing factors aggressively
• Antibiotic prophylaxis (reduces recurrence by 69% while on treatment) [6]
• Compression therapy for lymphoedema
• Emollients and skin care
• Weight loss in obese patients

Long-Term Outcomes

• Chronic Lymphoedema: Develops in 10-20% of patients with recurrent lower limb erysipelas [13]
• Quality of Life: Impaired in patients with recurrent episodes due to pain, immobility, time off work, psychological impact
• Economic Burden: Recurrent hospitalizations, prolonged antibiotic courses, lost productivity

Adherence to Guidelines Improves Outcomes

A large prospective study demonstrated that adherence to antibiotic guidelines (penicillin-based therapy) was associated with:

• Reduced poor outcomes: 6.3% vs 12.7% (p=0.007)
• Protective effect in logistic regression: OR 0.48 (95% CI 0.26-0.89) [1]

Risk factors for poor outcome: [1]

• Peripheral arterial disease: OR 4.80
• Bacteremia: OR 5.21

Clinical Implication: Penicillin remains first-line therapy with excellent outcomes when used appropriately. [1,26,29]

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10. Differential Diagnosis

When evaluating suspected erysipelas, consider the following differentials:

Infectious Mimics

Non-Infectious Inflammatory Conditions

Malignancy

Drug Reactions

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11. Special Populations

Immunocompromised Patients

Patients with HIV/AIDS, chemotherapy, organ transplant, or on immunosuppressive medications (corticosteroids, biologics) have:

• Higher risk of severe, atypical, or disseminated infection
• Broader organism spectrum (consider Gram-negatives, fungi)
• Higher risk of treatment failure and complications
• Management: Lower threshold for admission, IV antibiotics, broader empirical cover, infectious diseases consultation

Diabetics

• Higher risk of erysipelas (2-3x)
• More likely to have polymicrobial infection (add anti-staphylococcal cover)
• Risk of diabetic foot complications
• Management: Optimize glycemic control, assess for neuropathy and vascular disease, podiatry input

Pregnancy

• Group B Streptococcus may be causative (postpartum)
• Safe antibiotics: Penicillin, cephalosporins
• Avoid: Quinolones, tetracyclines
• Management: Low threshold for admission; involve obstetrics

Elderly

• Higher risk of severe disease and complications
• More likely to have comorbidities (heart failure, CKD)
• Higher one-year mortality (15%) [4]
• Management: Lower threshold for admission, careful fluid balance, monitor renal function

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12. Patient Education and Layperson Explanation

What is Erysipelas?

Erysipelas is a bacterial skin infection that affects the surface layers of the skin. It is caused by bacteria called streptococcus (the same bacteria that cause strep throat). The infection causes a bright red, hot, swollen area of skin with a clearly defined edge.

What Causes It?

The bacteria enter the skin through a small break, such as:

• Athlete's foot (cracked skin between the toes) - the most common entry point
• Cuts, grazes, or insect bites
• Leg ulcers or sores
• Dry, cracked skin from eczema

What Are the Symptoms?

• Sudden high fever (often before the rash appears), chills, and feeling very unwell
• A bright red, hot, painful, swollen area of skin
• The edge of the redness is sharply defined (you can trace it with your finger)
• Most commonly affects the face or lower leg

How is it Different from Cellulitis?

Erysipelas is very similar to cellulitis, but:

• Erysipelas affects the surface layers of skin and has a clear, sharp edge
• Cellulitis affects deeper layers and has a blurred, fading edge

Both are treated with antibiotics, so your doctor may use the terms interchangeably.

How is it Treated?

Antibiotics are very effective - usually penicillin tablets taken 4 times daily for 7-14 days. [8]

If you are very unwell, you may need:

• Hospital admission
• Antibiotics through a drip (IV)
• Fluids and pain relief

Self-Care at Home:

• Rest with the affected limb raised (if it's your leg, lie down with your leg on pillows above your heart)
• Take paracetamol for pain and fever
• Drink plenty of fluids
• Continue antibiotics for the full course, even when you feel better

How Long Does it Take to Get Better?

You should start to feel better within 2-3 days of starting antibiotics. The redness will gradually fade over 1-2 weeks. If you're not improving after 48 hours, contact your doctor.

Can it Come Back?

Yes - about 1 in 3 people get erysipelas again, especially if there's an underlying problem like:

• Chronic leg swelling (lymphoedema)
• Athlete's foot
• Varicose veins
• Obesity

Preventing Recurrence:

• Treat athlete's foot with antifungal cream
• Use moisturiser daily to prevent dry, cracked skin
• Keep skin clean and dry
• Compression stockings if you have leg swelling (start after infection clears)
• Weight loss if overweight
• Long-term antibiotics (preventive dose) if you've had 2 or more episodes

When Should I Seek Urgent Medical Attention?

Contact your doctor or go to A&E immediately if:

• The rash is spreading rapidly despite antibiotics
• You develop severe pain
• You feel confused, dizzy, or very unwell
• You have difficulty breathing
• You develop black or dark purple areas on the skin

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13. Evidence and Guidelines

Key Guidelines

1. NICE Clinical Knowledge Summaries: Cellulitis and Erysipelas [8]

   • Outlines diagnostic criteria, antibiotic choices, and admission criteria
   • Recommends penicillin as first-line therapy
   • Advises oral therapy for mild cases, IV for severe

2. British Association of Dermatologists Guidelines [9]

   • Comprehensive guideline on erysipelas and cellulitis management
   • Evidence-based antibiotic recommendations
   • Emphasis on predisposing factor management

3. Infectious Diseases Society of America (IDSA) Guidelines on Skin and Soft Tissue Infections [14]

   • Differentiates purulent vs non-purulent infections
   • Empirical antibiotic recommendations based on organism

4. European Dermatology Forum Guidelines [15]

   • Evidence-based diagnostic and treatment algorithms
   • Prophylaxis recommendations for recurrent erysipelas

Landmark Studies and Systematic Reviews

Antibiotic Efficacy

Klotz et al. (2019): Prospective cohort of 630 cases of erysipelas/cellulitis demonstrated that adherence to antibiotic guidelines (penicillin-based) was associated with favorable outcomes (OR 0.48, 95% CI 0.26-0.89, p=0.007). [1]

Morris AD (2008): BMJ Clinical Evidence review confirms penicillin as first-line therapy for streptococcal erysipelas. [3]

Prophylaxis for Recurrent Erysipelas

Dalal et al. (2017) - Cochrane Review: Systematic review of 6 RCTs (573 participants) assessing antibiotic prophylaxis for recurrent cellulitis/erysipelas. [6]

Key Findings:

• Antibiotic prophylaxis reduces recurrence risk by 69% while on treatment (RR 0.31, 95% CI 0.13-0.72; NNT 6)
• Reduced incidence rate by 56% (RR 0.44, 95% CI 0.22-0.89)
• Increased time to next episode (HR 0.51, 95% CI 0.34-0.78)
• Protective effects diminish after discontinuation (RR 0.88 post-prophylaxis)
• Common adverse effects: GI upset, rash, thrush (~10% discontinuation rate)
• Evidence Quality: Moderate certainty

Clinical Implication: Prophylaxis is effective while being taken, but does not provide lasting protection after cessation. Treating underlying predisposing factors is critical.

Sjöblom et al. (1993): Early RCT demonstrating that antibiotic prophylaxis reduces recurrence by approximately 50%. [5]

Epidemiology

Tang et al. (2025): Population-based cohort study from Denmark (223,618 acute visits) reporting erysipelas incidence of 72.10 per 100,000 person-years and one-year mortality of 15%. [4]

Key Findings:

• Erysipelas prevalence: 1% of ED visits
• Predominant organism in blood cultures: Streptococcus dysgalactiae
• One-third had prior hospitalization for erysipelas
• 7.7% recurrence within one year
• Obesity and liver disease are risk factors for recurrence

Lymphoedema and Erysipelas

Karlsson et al. (2022): Prospective study of 124 patients with lower extremity lymphoedema undergoing liposuction and controlled compression therapy. [13]

Key Findings:

• 65% reduction in erysipelas incidence rate (0.20 → 0.07 bouts per person per year, pless than 0.001)
• Period prevalence dropped from 52% to 23%
• Complete reduction of excess limb volume
• Similar findings in upper limb lymphoedema

Clinical Implication: Surgical management of chronic lymphoedema significantly reduces erysipelas risk.

Necrotizing Fasciitis

Wong et al. (2004): Developed the LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score, validated for distinguishing necrotizing fasciitis from severe cellulitis/erysipelas. [12]

Key Findings:

• LRINEC score ≥6: High risk of necrotizing fasciitis (PPV 92%, NPV 96%)
• Components: CRP, WCC, Hb, Na, Cr, Glucose

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14. Viva and Exam Preparation

Exam Detail: ### High-Yield Exam Topics

MRCP / FRACP / Emergency Medicine

1. Differentiate Erysipelas from Cellulitis:

   • Answer: Erysipelas is superficial (upper dermis + lymphatics) with well-demarcated, raised borders; cellulitis is deeper (subcutaneous) with indistinct borders. Erysipelas is predominantly streptococcal; cellulitis is mixed Staph/Strep. [3]

2. First-Line Antibiotic for Erysipelas:

   • Answer: Phenoxymethylpenicillin (Penicillin V) 500mg QDS orally for mild cases; Benzylpenicillin 1.2g QDS IV for severe cases. [8,9]

3. Why Penicillin for Erysipelas, but Flucloxacillin for Cellulitis?:

   • Answer: Erysipelas is almost exclusively streptococcal (penicillin-sensitive); cellulitis has significant Staph aureus component (requiring anti-staphylococcal cover). [1,3]

4. Evidence for Prophylactic Antibiotics in Recurrent Erysipelas:

   • Answer: Cochrane review (Dalal 2017) shows prophylactic penicillin reduces recurrence by 69% while on treatment (NNT 6), but effect diminishes after stopping. [6]

5. LRINEC Score and When to Use It:

   • Answer: Laboratory Risk Indicator for Necrotizing Fasciitis; score ≥6 suggests necrotizing fasciitis. Components: CRP ≥150, WCC less than 15 or greater than 25, Hb less than 11-13.5, Na less than 135, Cr greater than 141, Glucose greater than 10. Used when necrotizing fasciitis is in the differential. [12]

6. Most Common Pathogen in Blood Culture-Positive Erysipelas:

   • Answer: Streptococcus dysgalactiae (Group G/C Streptococcus), followed by S. pyogenes (Group A). [4]

7. Red Flags in Erysipelas Requiring Urgent Intervention:

   • Answer: Severe pain disproportionate to findings (necrotizing fasciitis), crepitus, skin necrosis, septic shock, facial involvement with orbital signs (cavernous sinus thrombosis risk). [12]

8. Management of Erysipelas in Penicillin-Allergic Patient:

   • Answer:
     • Non-anaphylactic allergy: Clarithromycin 500mg BD or erythromycin 500mg QDS
     • Anaphylactic allergy: Clindamycin 300-450mg QDS PO or 600mg TDS IV [8]

MRCS / FRCS / Surgical Exams

1. When Does Erysipelas Require Surgical Intervention?:

   • Answer: Rarely. Indications: Abscess formation (I&D), necrotizing fasciitis (urgent debridement), compartment syndrome (fasciotomy). [12]

2. Necrotizing Fasciitis: Diagnosis and Management:

   • Answer: Clinical: severe pain, rapid progression, systemic toxicity. LRINEC ≥6. Imaging: CT/MRI (gas in fascia). Management: Urgent surgical debridement + broad-spectrum IV antibiotics (pip-tazo + clindamycin) + ICU support. [12]

3. Difference Between Necrotizing Fasciitis Type I and Type II:

   • Answer:
     • Type I: Polymicrobial (anaerobes + Gram-negatives); often post-surgical or in diabetics
     • Type II: Monomicrobial Group A Streptococcus; younger, previously healthy; "flesh-eating bacteria" [12]

MRCGP / Primary Care

1. Eron Classification and Admission Criteria:

   • Answer:
     • Class I: Outpatient oral antibiotics
     • Class II: Consider admission or IV antibiotics
     • Class III-IV: Admission mandatory, IV antibiotics [8]

2. Red Flags for Immediate Hospital Referral:

   • Answer: Sepsis (hypotension, confusion, oliguria), rapid spread despite antibiotics, severe pain, crepitus, skin necrosis, immunocompromised, facial involvement with orbital signs. [8]

3. Preventing Recurrent Erysipelas in Primary Care:

   • Answer: Treat tinea pedis, manage lymphoedema (compression), weight loss, emollients, treat venous insufficiency. Prophylactic penicillin V 250-500mg BD if ≥2 episodes. [6,8]

Model Viva Answers

Examiner: "You see a 65-year-old woman in the emergency department with a 24-hour history of fever, rigors, and a painful red swollen left lower leg. How do you approach this case?"

Candidate: "This presentation is highly suggestive of erysipelas or cellulitis - acute bacterial skin infections. I would take a focused history and examination to confirm the diagnosis, assess severity, and identify predisposing factors.

In the history, I'd ask about:

• Onset and progression of symptoms (rapid onset with systemic symptoms suggests erysipelas)
• Fever, rigors, malaise
• Predisposing factors: previous episodes, lymphoedema, venous insufficiency, tinea pedis, leg ulcers, diabetes, immunosuppression
• Recent trauma or insect bites

On examination, I'd assess:

• Vital signs: fever, tachycardia, hypotension (sepsis?)
• Inspect the leg: well-demarcated raised border with bright red erythema suggests erysipelas; indistinct borders suggest cellulitis. I'd mark the borders with a pen.
• Palpate: warm, tender, palpable raised edge. Check for crepitus (necrotizing fasciitis)
• Look for entry point: tinea pedis, ulcers, trauma
• Regional lymph nodes: inguinal adenopathy

Investigations:

• FBC, CRP, U&E, glucose, blood cultures (if systemically unwell)
• Imaging is not routinely needed unless concern for deeper infection

Management depends on severity (Eron classification):

• If mild (Class I): oral penicillin V 500mg QDS for 7-14 days, outpatient with 48-hour review
• If moderate-severe (Class II-III): admission, IV benzylpenicillin 1.2g QDS, supportive care (fluids, analgesia, limb elevation)
• Mark the margins and reassess at 24-48 hours

Address predisposing factors: treat tinea pedis, manage lymphoedema, optimize diabetes control

Safety-net: advise to return if worsening, spreading, or not improving by 48 hours."

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Examiner: "Why do we use penicillin for erysipelas but flucloxacillin for cellulitis?"

Candidate: "This reflects the different microbiological aetiology of the two conditions.

Erysipelas is almost exclusively caused by beta-hemolytic streptococci - primarily Group A Streptococcus pyogenes, and increasingly Group G and C Streptococcus dysgalactiae. These organisms are uniformly susceptible to penicillin, making it the ideal first-line agent due to its narrow spectrum and lack of resistance.

Cellulitis, in contrast, involves deeper tissues and has a mixed aetiology. Staphylococcus aureus accounts for 40-50% of cases, while streptococci account for 30-40%. Since S. aureus produces beta-lactamases, flucloxacillin (a beta-lactamase-resistant penicillin) is required for anti-staphylococcal cover.

In practice, the distinction can be challenging, and there's overlap. If there's diagnostic uncertainty, co-amoxiclav provides cover for both organisms."

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Examiner: "What is the evidence for prophylactic antibiotics in recurrent erysipelas?"

Candidate: "The key evidence comes from the 2017 Cochrane systematic review by Dalal and colleagues, which analyzed six randomized controlled trials involving 573 participants with recurrent erysipelas or cellulitis.

Key findings:

• Antibiotic prophylaxis (primarily penicillin) reduced the risk of recurrence by 69% while patients were on treatment (RR 0.31, NNT 6)
• It reduced the incidence rate by 56% and significantly increased time to next episode
• The quality of evidence was rated as moderate

However, a critical limitation is that the protective effect diminished after prophylaxis was stopped. Post-prophylaxis, there was no significant difference in recurrence rates.

Clinical implications:

• Prophylaxis is indicated for patients with ≥2 episodes within 12 months
• Typical regimen: penicillin V 250-500mg twice daily for 6-12 months
• Equally important is addressing underlying predisposing factors - treating tinea pedis, managing lymphoedema with compression, weight loss, and skin care - as these provide more sustainable protection."

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15. References

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2. Newberger R, Hollingshead CM. Group A Streptococcal Infections. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2025. PMID: 32644666

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4. Tang AHR, Lassen AT, Skjot-Arkil H, et al. Epidemiology of erysipelas and necrotising soft tissue infections. Dan Med J. 2025;72(9):A02250077. doi:10.61409/A02250077

5. Sjöblom AC, Eriksson B, Jorup-Rönström C, Karkkonen K, Lindqvist M. Antibiotic prophylaxis in recurrent erysipelas. Infection. 1993;21(6):390-393. doi:10.1007/BF01728930 PMID: 8132368

6. Dalal A, Eskin-Schwartz M, Mimouni D, et al. Interventions for the prevention of recurrent erysipelas and cellulitis. Cochrane Database Syst Rev. 2017;6(6):CD009758. doi:10.1002/14651858.CD009758.pub2 PMID: 28631307

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8. National Institute for Health and Care Excellence. Cellulitis - acute. NICE Clinical Knowledge Summaries. 2024. Available at: https://cks.nice.org.uk/topics/cellulitis-acute/

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29. Jenkins TC, Sabel AL, Sarcone EE, Price CS, Mehler PS, Burman WJ. Assessment of Antibiotic Treatment of Cellulitis and Erysipelas: A Systematic Review and Meta-analysis. JAMA Dermatol. 2019;155(9):1033-1040. doi:10.1001/jamadermatol.2019.1884 PMID: 31188407

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31. Cranendonk DR, Lavrijsen APM, Prins JM, Wiersinga WJ. Corticosteroid Therapy in Combination with Antibiotics for Erysipelas: A Double-Blind, Placebo-Controlled Randomized Clinical Trial. J Infect Dis. 2019;219(8):1256-1264. doi:10.1093/infdis/jiy643 PMID: 29527848

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Topic: Erysipelas
Lines: 1,397
Citations: 33