Infectious Disease · PANCE / PANRE

Erysipelas

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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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

Feature	Erysipelas	Cellulitis
Depth	Upper dermis, lymphatics	Deeper dermis, subcutaneous fat
Border	Sharply demarcated, raised	Diffuse, indistinct
Color	Brilliant red, peau d'orange	Pink-red, less intense
Onset	Abrupt, fever precedes rash	Gradual
Pathogen	Group A strep (predominant)	Strep or Staph (incl. MRSA)
First-line therapy	Penicillin, amoxicillin	Cephalexin ± 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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