Infectious Disease · PANCE / PANRE

Erysipelas

Written & clinically reviewed by Ryan Busch, PA-C · Updated August 2026 · Report an error

Superficial cellulitis with prominent lymphatic involvement, sharply demarcated borders, and a classic 'peau d'orange' appearance — almost always streptococcal.

Also known as: erysipelas, St. Anthony's fire

Overview

Acute bacterial infection of the upper dermis and superficial lymphatics, characterized by a brilliantly erythematous, raised, sharply demarcated plaque. Caused predominantly by beta-hemolytic streptococci, especially group A (Streptococcus pyogenes); rarely groups C and G or Staphylococcus aureus.

Epidemiology

Bimodal: young children and elderly adults. More common in females. Recurrence in 10-30%, especially with persistent lymphedema.

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Question 1Infectious DiseaseMedium
A 68-year-old woman presents with one day of fever to 38.9°C (102°F), chills, and a painful, burning rash on her right cheek. She reports a recent episode of athlete's foot but no new medications, soaps, or chemical exposures. On exam, there is a brilliantly red, warm, edematous plaque over the right cheek that crosses the nasal bridge; the lesion has a sharply demarcated, raised border that can be traced with a finger, and the surface has a peau d'orange texture. Tender preauricular lymphadenopathy is present. Which of the following is the most likely diagnosis?
  • AFacial erysipelas
  • BTrigeminal zoster
  • CContact dermatitis
  • DFacial cellulitis
Reveal answer & full explanation
Correct answer: A — Facial erysipelas
  • AFacial erysipelas✓
  • BTrigeminal zoster
  • CContact dermatitis
  • DFacial cellulitis

Why Facial erysipelas is correct

  • Erysipelas is an acute beta-hemolytic streptococcal (usually group A) infection of the upper dermis and superficial lymphatics, producing a brilliantly red, raised plaque with a sharply demarcated border you can literally trace.
  • The combination of abrupt high fever and chills preceding the rash, a peau d'orange surface (edema around hair follicles), and regional lymphadenopathy is classic.
  • Facial erysipelas characteristically crosses the nasal bridge in a butterfly pattern; tinea pedis is the most common skin-barrier entry portal driving these infections.

Why the others are wrong

  • Facial cellulitis is a deeper dermal/subcutaneous infection with indistinct, poorly demarcated borders and a less intensely red, flatter appearance; the sharply raised, traceable edge here points to erysipelas instead.
  • Trigeminal zoster produces dermatomal grouped vesicles with prodromal neuropathic pain and respects the midline; an erythematous plaque that crosses the nasal bridge without vesicles argues against it.
  • Contact dermatitis is pruritus-dominant with vesicles in a geometric pattern matching an exposure and no systemic fever; this patient has high fever, pain, and no offending contactant.
Question 2Infectious DiseaseMedium
A 71-year-old woman with chronic lower-extremity lymphedema presents with one day of fever, chills, and a painful right leg. She has interdigital scaling and fissuring between her toes. On exam, temperature is 38.7°C and there is a fiery-red, warm, tender plaque on the right shin with a raised, sharply demarcated border that can be traced with a fingertip. Tender inguinal lymphadenopathy and a streak of erythema tracking up the medial thigh are noted. A clinical diagnosis of erysipelas is made. Which of the following best explains this patient's findings?
  • ABacterial proliferation within the deep dermis and subcutaneous fat
  • BStreptococcal spread through the superficial dermal lymphatics
  • CPolymicrobial invasion of the deep fascial plane with thrombosis
  • DToxin-mediated cleavage of the superficial epidermal granular layer
Reveal answer & full explanation
Correct answer: B — Streptococcal spread through the superficial dermal lymphatics
  • ABacterial proliferation within the deep dermis and subcutaneous fat
  • BStreptococcal spread through the superficial dermal lymphatics✓
  • CPolymicrobial invasion of the deep fascial plane with thrombosis
  • DToxin-mediated cleavage of the superficial epidermal granular layer

Why Streptococcal spread through the superficial dermal lymphatics is correct

  • Erysipelas is a beta-hemolytic streptococcal (usually group A, S. pyogenes) infection of the upper dermis and superficial lymphatics.
  • Organisms enter through a skin breach (here, fissured tinea pedis) and propagate within superficial dermal lymphatics; M protein, hyaluronidase, and streptolysins drive brisk inflammation.
  • This superficial lymphatic involvement produces the hallmark raised, sharply demarcated, traceable border plus lymphangitic streaking and regional lymphadenopathy that are described.

Why the others are wrong

  • Polymicrobial invasion of the deep fascial plane with thrombosis describes necrotizing fasciitis; expect pain out of proportion, rapid expansion, bullae, crepitus, and systemic toxicity rather than a sharply bordered superficial plaque.
  • Bacterial proliferation within the deep dermis and subcutaneous fat is the mechanism of cellulitis, which involves deeper tissue and characteristically has indistinct, poorly demarcated borders rather than the raised clear edge of erysipelas.
  • Toxin-mediated cleavage of the superficial epidermal granular layer describes staphylococcal scalded skin syndrome (exfoliative toxin splitting desmoglein-1), producing diffuse desquamation and a positive Nikolsky sign rather than a localized erythematous lymphangitic plaque.
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Risk factors

  • Lymphatic obstruction (post-mastectomy, filariasis, prior cellulitis)
  • Venous insufficiency, chronic leg edema
  • Skin barrier breakdown (tinea pedis is the leading entry point for lower-leg erysipelas)
  • Obesity, diabetes
  • Nephrotic syndrome (children)

Pathophysiology

Streptococci enter through minor breaks in skin and spread through the superficial dermal lymphatics, producing the characteristic raised border. Bacterial proteins (M protein, hyaluronidase, streptolysins) drive rapid lymphatic spread and brisk inflammatory response.

Clinical presentation

Symptoms

  • Abrupt onset of fever, chills, malaise — often precedes rash by hours
  • Localized burning pain and tenderness
  • Bright red, hot, swollen plaque with sharply raised border

Signs / physical exam

  • Classic distribution: lower extremities (most common) or face (cheeks in 'butterfly' pattern crossing nasal bridge)
  • Sharply demarcated, raised, brilliant erythematous plaque ('peau d'orange' surface from edema around hair follicles)
  • Regional lymphadenopathy and lymphangitic streaking
  • Possible bullae in severe disease

Classic findings

A sharply demarcated, raised, fiery red facial or leg plaque with a clear edge ('the lesion you can trace') and a high fever — classic erysipelas.

Differential diagnosis

  • Cellulitis — Deeper, less sharply demarcated, often less brightly red; pathogens and treatment overlap but presentation differs
  • Contact dermatitis — Pruritus dominant, vesicles, geometric pattern matching exposure; no fever
  • Herpes zoster — Dermatomal distribution, grouped vesicles, prodromal neuropathic pain
  • Necrotizing fasciitis — Pain out of proportion, rapid expansion, bullae, crepitus, toxicity — surgical emergency
  • Erysipeloid (Erysipelothrix rhusiopathiae) — Occupational (fish, meat handlers), violaceous hand lesion without systemic toxicity; penicillin first-line
  • DRESS / fixed drug eruption — Recent drug exposure, eosinophilia, mucosal involvement

Diagnostic workup

Diagnostic criteria

Clinical: sharply demarcated, raised, brightly erythematous, warm, tender plaque with systemic symptoms.

Labs

  • Clinical diagnosis — labs not routinely required
  • CBC, CRP, ESR if hospitalized or severe
  • Blood cultures yield in ~5% — only if systemic toxicity, immunocompromise, atypical presentation
  • ASO/anti-DNase B may support recent streptococcal infection but not used acutely

Imaging

  • Not required for typical presentations
  • Ultrasound to exclude abscess if purulence suspected

Diagnostic algorithm

FeatureErysipelasCellulitis
DepthUpper dermis, lymphaticsDeeper dermis, subcutaneous fat
BorderSharply demarcated, raisedDiffuse, indistinct
ColorBrilliant red, peau d'orangePink-red, less intense
OnsetAbrupt, fever precedes rashGradual
PathogenGroup A strep (predominant)Strep or Staph (incl. MRSA)
First-line therapyPenicillin, amoxicillinCephalexin ± MRSA coverage
Clinical distinction between erysipelas and cellulitis.

Treatment

First-line

  • Penicillin remains drug of choice — narrow spectrum, predictable streptococcal coverage:
  • • Oral: penicillin VK 500 mg PO QID or amoxicillin 500 mg PO TID × 5-10 days
  • • IV: penicillin G 1-2 million units IV q6h, or ceftriaxone 1 g IV daily
  • Cephalosporins or macrolides for penicillin-allergic patients (clindamycin or azithromycin)
  • Beta-lactam for skin — cefazolin, cephalexin, dicloxacillin acceptable
  • Elevation of affected extremity speeds resolution
  • Treat underlying tinea pedis to reduce recurrence

Second-line / adjunct

  • Add MRSA coverage (vancomycin, linezolid, daptomycin) only if atypical features, purulence, or treatment failure
  • Recurrent disease (≥3 episodes/year): low-dose penicillin V 250 mg PO BID prophylaxis (PATCH trial)

Complications

  • Recurrent erysipelas with progressive lymphedema
  • Streptococcal bacteremia and sepsis
  • Post-streptococcal glomerulonephritis (rare)
  • Cavernous sinus thrombosis (facial erysipelas in the danger triangle)
  • Necrotizing fasciitis if invasive group A strep evolves

PANCE pearls

  • Facial erysipelas often crosses the nasal bridge in a butterfly pattern — distinguishes it from herpes zoster, which respects the midline.
  • Lower-leg erysipelas in an adult is overwhelmingly streptococcal; MRSA coverage usually unnecessary in non-purulent disease.
  • Treat tinea pedis (interdigital cracking) — the most common entry portal for recurrent lower-extremity erysipelas.
  • Sharply raised, well-demarcated borders distinguish erysipelas from cellulitis on physical exam.
  • Penicillin prophylaxis reduces recurrence by ~half in patients with frequent episodes (PATCH I).

References

  • IDSA 2014 — Stevens et al., Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections (Clin Infect Dis)
  • PATCH I — Thomas et al., Penicillin to prevent recurrent leg cellulitis/erysipelas (NEJM 2013)

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Commonly confused with

vs Cellulitis

Related Infectious Disease diagnoses

HIV / AIDSLyme DiseaseRocky Mountain Spotted Fever (RMSF)Infectious Mononucleosis (EBV)Cytomegalovirus (CMV)Sepsis and Septic ShockCellulitisNecrotizing FasciitisTetanusRabies Post-Exposure ProphylaxisMalariaToxoplasmosisGiardiasisCryptosporidiosis

Differentials & related conditions

Allergic and Irritant Contact DermatitisHerpes Zoster (Shingles)

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