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 1DermatologyMedium
A 65-year-old male presents with sudden onset of a sharply demarcated, painful, raised, erythematous lesion on his face. He has fever and leukocytosis. Which of the following is the most likely diagnosis?
AErysipelas
BContact dermatitis
CNecrotizing fasciitis
DCellulitis
EHerpes zoster
Reveal answer & full explanation
Correct answer: A — Erysipelas
AErysipelas✓
BContact dermatitis
CNecrotizing fasciitis
DCellulitis
EHerpes zoster
Why Erysipelas is correct
Superficial dermal cellulitis with prominent lymphatic involvement, caused almost exclusively by group A Streptococcus.
Hallmark is a sharply demarcated, raised, brightly erythematous border, classically on the face or lower extremity.
Systemic signs such as fever and leukocytosis are typical and often precede the skin findings.
Responds to penicillin, amoxicillin, or a first-generation cephalosporin for streptococcal coverage.
Why the others are wrong
Cellulitis — confused-with erysipelas; deeper infection with ill-defined, non-raised borders and more often staphylococcal, so it lacks the sharp demarcation described.
Necrotizing fasciitis — right-concept-wrong-severity; features pain out of proportion, crepitus, and rapid systemic toxicity requiring emergent surgical debridement.
Contact dermatitis — anchoring on erythema; a non-infectious eruption without fever or leukocytosis that follows the pattern of allergen or irritant exposure.
Herpes zoster — anchoring on age and a painful facial eruption; zoster produces grouped vesicles on an erythematous base in a unilateral dermatomal band, often after prodromal burning pain, rather than a raised, sharply demarcated plaque, and prominent fever with leukocytosis favors a bacterial infection.
Additional high-yield points
Erysipelas vs cellulitis: erysipelas is more superficial with a raised, sharply bordered plaque; cellulitis is deeper with indistinct margins.
Cellulitis more often requires anti-staphylococcal coverage in addition to strep coverage.
Facial erysipelas warrants close monitoring given proximity to the orbit and cavernous sinus.
Question 2Infectious 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?
ALupus malar rash
BFacial erysipelas
CFacial cellulitis
DTinea faciei
ETrigeminal zoster
Reveal answer & full explanation
Correct answer: B — Facial erysipelas
ALupus malar rash
BFacial erysipelas✓
CFacial cellulitis
DTinea faciei
ETrigeminal zoster
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 classic entry portal for lower-extremity erysipelas, whereas facial erysipelas more often follows streptococcal nasopharyngeal infection or a minor break in the facial skin.
Why the others are wrong
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.
Tinea faciei can spread from tinea pedis by autoinoculation, which makes her athlete's foot tempting, but it is an afebrile, usually pruritic, slowly enlarging annular plaque with scale and central clearing that is KOH-positive for hyphae; it does not cause abrupt high fever and chills, a warm peau d'orange surface, or tender regional lymphadenopathy.
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.
Lupus malar rash — the erythema crossing the nasal bridge mimics the butterfly rash of acute cutaneous lupus, but a malar rash is typically bilateral and photo-distributed and spares the nasolabial folds; abrupt high fever and chills with a hot, painful, peau d'orange plaque, a sharply raised border, and tender preauricular nodes point to streptococcal infection instead.
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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
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 2-4 million units IV q4-6h, or ceftriaxone 1 g IV daily
Penicillin allergy: cephalexin or cefazolin if the prior reaction was not immediate-type or severe; clindamycin if it was. Macrolides (azithromycin) are unreliable because group A strep resistance is common
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 (N Engl J Med 2013;368:1695-1703)
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