Erysipelas and cellulitis

Erysipelas and cellulitis

Introduction

Erysipelas is an acute superficial bacterial infection involving the upper dermis and superficial lymphatic vessels. It is most commonly caused by Streptococcus pyogenes (Group A Streptococcus) and other β-hemolytic streptococci without pus formation, although Gram-negative bacilli may occasionally be responsible, particularly in immunocompromised patients.

Erysipelas is considered a more superficial and sharply demarcated form of cellulitis. The infection spreads rapidly through lymphatic channels, producing characteristic raised borders.

Commonly affected sites include:

• Face (classically butterfly distribution)

• Lower limbs (most common overall)

• Upper limbs

• Umbilical stump in neonates

The disease typically presents with abrupt onset, marked systemic symptoms, and characteristic skin findings.

Etiology

Common causative organisms include:

• Streptococcus pyogenes (Group A Streptococcus)

• Group B, C, and G streptococci

• Staphylococcus aureus (secondary infection)

• Gram-negative bacilli (occasionally, especially in immunocompromised patients)

Pathophysiology

The infection develops after bacteria enter through a break in the skin, such as:

• Tinea pedis

• Skin fissures

• Ulcers

• Surgical wounds

• Insect bites

• Minor trauma

Bacteria spread through superficial lymphatics causing:

• Rapidly spreading inflammation

• Raised, sharply demarcated erythematous plaques

• Edema

• Fever and systemic toxicity

• Blistering or superficial hemorrhage in severe cases

Risk factors

Local risk factors:

• Tinea pedis

• Chronic edema or lymphedema

• Venous insufficiency

• Skin trauma

• Surgical wounds

Systemic risk factors:

• Diabetes mellitus

• Obesity

• Chronic kidney disease

• Alcoholism

• Immunosuppression

• Elderly age

• Malnutrition

Risk factors for recurrence:

• Previous erysipelas

• Chronic lymphatic damage

• Persistent fungal infection of the feet

Clinical presentation

Systemic symptoms:

• Fever

• Chills

• Malaise

• Headache

• Vomiting (especially in children)

Local findings:

• Large erythematous swelling

• Well-demarcated raised lesion

• Warm, tender, edematous skin

• Burning pain

• Regional lymphadenopathy

• Lymphangitis

• Superficial blistering secondary to edema

• Superficial hemorrhage (occasionally)

Severe disease may present with:

• High fever

• Tachycardia

• Toxic appearance

• Extensive blistering

• Rapid progression

Diagnostic criteria

Diagnosis is primarily clinical.

Major features:

• Acute onset of fever

• Raised, sharply demarcated erythematous plaque

• Tender swelling

Supportive features:

• Regional lymphadenopathy

• Superficial blistering

• Superficial hemorrhage

• Lymphangitis

Differential diagnosis

• Cellulitis

• Contact dermatitis

• Deep vein thrombosis

• Necrotizing fasciitis

• Herpes zoster

Investigations

Routine investigations are usually unnecessary in uncomplicated disease.

Consider when indicated:

• Complete blood count (CBC)

• C-reactive protein (CRP) or ESR

• Blood cultures (severe infection)

• Ultrasound (to exclude abscess)

• Doppler ultrasound (to exclude DVT)

• CT or MRI if necrotizing fasciitis is suspected

Treatment

Non-pharmacological treatment

• Bed rest

• Elevation of the affected limb

• Venous compression during the acute phase and subsequent weeks to reduce the risk of lymphedema

• Consider prophylaxis for deep venous thrombosis (DVT) depending on additional risk factors

Pharmacological treatment

Local therapy:

• Weak potassium permanganate soaks, 1:40,000 (0.025%) solution every 12 hours for 3–4 days. Each session should last 15–20 minutes.

Apply one of the following topical agents:

• Silver sulfadiazine cream once or twice daily

• Mupirocin 2% topical every 12 hours for 5–7 days

• Fusidic acid 2% topical every 12 hours for 5–7 days

Systemic antibiotics (main treatment):

• Phenoxymethylpenicillin (PO):

  • Adults: 250–500 mg every 6 hours for 5–7 days

  • Children: 25 mg/kg every 6 hours for 5–7 days

OR

• Flucloxacillin + amoxicillin (FDC) (PO):

  • Adults: 500 mg every 6 hours for 5–7 days

  • Children: 25–50 mg/kg every 6 hours for 5–7 days

Supportive treatment:

• Ibuprofen 400 mg (PO) every 6 hours for 5 days as needed for pain and inflammation.

Surgical treatment

Required only if complications develop:

• Incision and drainage of secondary abscess

• Surgical debridement for necrotic tissue

Referral

Refer urgently if there are local or systemic signs suggesting progression to necrotizing fasciitis or severe soft tissue infection, including:

• Severe pain out of proportion to examination

• Rapid progression of swelling or erythema

• Extensive blistering

• Skin necrosis

• Crepitus

• Systemic toxicity or septic shock

Complications

Local complications:

• Abscess formation

• Skin necrosis

• Ulceration

• Chronic lymphedema

• Recurrent erysipelas

Systemic complications:

• Bacteremia

• Septic arthritis

• Endocarditis

• Post-streptococcal glomerulonephritis

• Toxic shock syndrome

Prevention

• Treat tinea pedis promptly

• Maintain good skin hygiene

• Proper wound care

• Control chronic edema using compression therapy

• Moisturize dry skin to prevent fissures

• Weight reduction where appropriate

• Optimize glycemic control in patients with diabetes

• Long-term penicillin prophylaxis may be considered for recurrent erysipelas

Patient education

Advise patients to seek urgent medical attention if they develop:

• Fever above 38.5°C

• Rapid spread of redness

• Severe pain

• Blistering or black discoloration of the skin

• Confusion or generalized weakness

Advise patients to avoid:

• Massaging the affected area

• Applying irritant chemicals or traditional remedies

• Excessive walking during the acute phase

Prognosis

• Early treatment usually results in marked improvement within 48–72 hours.

• Delayed treatment increases the risk of recurrence, chronic lymphatic damage, and other complications.

• Recurrent disease may result in chronic lymphedema.