Erisipelas

01Pathophysiology

Erysipelas is a bacterial infection of the upper dermis and superficial lymphatic vessels, almost exclusively caused by Group A Streptococcus (GAS). The organism gains entry through a breach in the skin barrier, which can be as subtle as tinea pedis between the toes, a small scratch, or a chronic venous stasis ulcer. This is why vignettes often mention a seemingly minor wound or fungal infection of the feet before the dramatic skin findings appear.

Once GAS penetrates the epidermis, it produces a set of virulence factors that promote rapid horizontal spread through the superficial tissue planes. Streptokinase dissolves fibrin clots that would otherwise wall off the infection. Hyaluronidase breaks down hyaluronic acid in the connective tissue ground substance, opening pathways for bacterial dissemination. Streptolysins O and S damage host cell membranes and impair the local immune response.

The reason the borders of erysipelas are sharply demarcated and raised is directly tied to its anatomical plane of infection. Because the bacteria spread laterally through the superficial lymphatics and upper dermis, the advancing edge of infection creates a distinct step-off between inflamed and uninflamed tissue. This is the single most important physical finding that separates erysipelas from deeper soft tissue infections.

The "peau d'orange" (orange peel) texture develops because edema accumulates in the dermis, but the skin is tethered at hair follicle insertion points. The surrounding swollen tissue bulges outward while the tethered points remain depressed, creating the characteristic dimpled surface. This same mechanism explains peau d'orange in inflammatory breast cancer, and examiners appreciate when students understand the shared pathologic basis.

Lymphatic involvement also explains why patients with pre-existing lymphatic compromise (post-mastectomy lymphedema, chronic venous insufficiency, prior episodes of erysipelas that damaged the lymphatics) are at high risk of recurrence. Each episode of erysipelas further damages the lymphatic drainage, creating a vicious cycle of impaired clearance, stasis, and reinfection.

Systemically, GAS releases pyrogenic exotoxins that stimulate a robust cytokine response, which is why patients often present with high fever, rigors, and leukocytosis even when the skin lesion is still relatively small. This mismatch between the degree of systemic illness and the apparent size of the lesion is a common exam clue.

02Classification and Clinical Manifestation

Clinical presentation by severity:

03Diagnostic Workup

Erysipelas is fundamentally a clinical diagnosis. The combination of an acutely tender, bright red plaque with well-demarcated, raised borders in a febrile patient is considered diagnostic. In exam vignettes, you will rarely be asked to order advanced testing. Instead, the question tests whether you can recognize the clinical picture and initiate treatment without delay.

That said, you should order a CBC and CRP as baseline supportive labs. CRP is particularly valuable because it correlates with disease severity and serves as a marker of treatment response. If the CRP fails to decline after 48 to 72 hours of appropriate antibiotics, you should suspect a complication such as abscess formation or an incorrect diagnosis.

Blood cultures are obtained in moderate-to-severe presentations, especially if the patient has sepsis features or is immunocompromised. The yield is low (around 5%), but a positive culture changes the picture because it confirms bacteremia and may prompt longer courses of IV therapy.

The most accurate test is a punch biopsy with tissue culture, but this is almost never performed in clinical practice or tested as a "next step" on exams. It is reserved for cases that fail standard therapy or have an atypical appearance that raises concern for alternative diagnoses such as cutaneous lymphoma or deep fungal infection.

One important workup consideration: always inspect the interdigital web spaces for tinea pedis. Identifying and treating the portal of entry is essential to preventing recurrence. Examiners frequently include this detail in the vignette as a clue or test whether you address the underlying predisposing factor.

04Management and Treatment

Acute stabilization begins with determining whether the patient can be managed as an outpatient or requires hospitalization. Patients with high fevers, hemodynamic instability, inability to tolerate oral medications, or significant comorbidities should be admitted for IV penicillin G. The classic exam scenario presents a relatively well-appearing patient with uncomplicated erysipelas, and the answer is oral penicillin V or amoxicillin as an outpatient.

Penicillin remains the drug of choice because GAS has not developed clinically meaningful penicillin resistance. This is a frequently tested concept. Even though broader-spectrum antibiotics exist, penicillin is the correct answer for uncomplicated streptococcal erysipelas. Choosing a fluoroquinolone or vancomycin when penicillin is an option is a classic wrong answer on exams.

For patients with a true penicillin allergy (anaphylaxis, angioedema), the alternatives are clindamycin or a macrolide. Clindamycin is generally preferred given the increasing prevalence of macrolide-resistant GAS strains. First-generation cephalosporins (cephalexin 500 mg PO every 6 hours) can be used if the penicillin allergy is non-anaphylactic (e.g., rash only), because the cross-reactivity rate between penicillins and first-generation cephalosporins is very low.

Long-term management focuses on two goals: treating modifiable risk factors and preventing recurrence. For the exam, the high-yield points are:

1. Treat tinea pedis aggressively with topical antifungals to eliminate the portal of entry.

2. Manage chronic edema with compression stockings, leg elevation, and treatment of underlying venous insufficiency.

3. Initiate prophylactic antibiotics in patients with two or more episodes of erysipelas. The standard regimen is low-dose penicillin V twice daily. Intramuscular benzathine penicillin every 3 to 4 weeks is an alternative for patients with adherence concerns.

The "next best step" logic that examiners commonly test: if a patient on appropriate antibiotics shows no improvement after 48 to 72 hours, consider imaging (ultrasound or CT) to evaluate for a deeper abscess that requires drainage, or reconsider the diagnosis entirely.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common way students lose points on erysipelas questions is by confusing it with cellulitis. Both are bacterial skin infections, both involve erythema and fever, and both affect the lower extremities. The examiners know this is confusing, and the entire question is built around whether you can identify the border characteristics. If the vignette describes "sharply demarcated," "well-defined," or "raised borders," the answer is erysipelas. If the borders are "indistinct," "spreading," or "diffuse," the answer is cellulitis. Train yourself to look for this phrase immediately.

A second trap involves the facial butterfly distribution. When a vignette describes bilateral cheek and nasal bridge erythema, many students reflexively select lupus. The discriminator is the clinical context: erysipelas presents acutely with fever and a toxic appearance, and the borders are raised and palpable. Lupus malar rash spares the nasolabial folds, is not associated with acute febrile illness, and lacks the raised, indurated edge.

A third testing angle is the management question where students over-treat. Because erysipelas is caused by GAS (which remains penicillin-sensitive), the correct answer is simple penicillin, not a broad-spectrum antibiotic. Selecting vancomycin, piperacillin-tazobactam, or a fluoroquinolone for uncomplicated erysipelas is the wrong answer. The exception is if the vignette suggests MRSA involvement (purulent drainage, abscess, history of MRSA colonization), which would shift the diagnosis away from classic erysipelas toward a staphylococcal process.

Finally, watch for the recurrence prevention question. A patient with their third episode of lower extremity erysipelas and known lymphedema who asks "how do we stop this from happening again" is being tested on prophylactic penicillin and treatment of predisposing conditions (tinea pedis, compression therapy for edema). The core competency here is recognizing that erysipelas damages lymphatics with each episode, creating a self-perpetuating cycle, and that breaking this cycle requires both antimicrobial prophylaxis and addressing the underlying lymphatic or venous compromise.