Impetigo Diagnosis and Treatment

Clinical Manifestations

Nonbullous impetigo is caused by Staphylococcus aureus or Streptococcus pyogenes, or both in combination, and begins as erythematous papules that rapidly evolve into vesicles and pustules 1
Bullous impetigo is caused exclusively by toxin-producing strains of S. aureus and is characterized by fragile, thin-roofed vesicopustules that form when toxins cleave the dermal-epidermal junction 1
Ecthyma is a deeper infection than impetigo, caused by S. aureus and/or streptococci, and begins as vesicles that rupture, resulting in circular, erythematous ulcers with adherent crusts 1

Cultures of vesicle fluid, pus, erosions, or ulcers may be obtained to establish the cause, especially in cases of treatment failure, suspected MRSA, or recurrent infections 1, 2
Topical mupirocin 2% ointment applied three times daily for 5-7 days is the first-line treatment for localized impetigo 2, 3
Oral antibiotics should be used when impetigo is extensive, involves multiple sites, topical therapy is impractical, treatment with topical antibiotics has failed, or systemic symptoms are present 2, 3
For methicillin-susceptible S. aureus (MSSA), dicloxacillin or cephalexin may be used 2, 3, 4
For methicillin-resistant S. aureus (MRSA), clindamycin, trimethoprim-sulfamethoxazole (TMP-SMX), or doxycycline may be used 4, 2, 3
When streptococci alone are the cause, penicillin is the drug of choice, and for penicillin-allergic patients, a macrolide or clindamycin is recommended 1

Systemic antimicrobials should be used during outbreaks of poststreptococcal glomerulonephritis to help eliminate nephritogenic strains of Streptococcus pyogenes 4
Oral antibiotic dosing should be adjusted by weight for children 2
Tetracyclines (doxycycline, minocycline) should not be used in children under 8 years of age 2

Topical treatment should be used for 5-7 days 2, 3
Oral antibiotics should be administered for 5-10 days 3
Re-evaluate if no improvement after 48-72 hours of therapy 2, 3
Lesions should be kept covered with clean, dry bandages and good personal hygiene maintained to prevent spread 2, 3

Folliculitis differs from impetigo by being more superficial, with inflammation and pus confined to the epidermis rather than extending through the dermis, according to the Infectious Diseases Society of America 5
Furuncles (boils) are deeper infections of hair follicles with suppuration extending into subcutaneous tissue, presenting as inflammatory nodules rather than superficial crusted lesions, as noted by the Infectious Diseases Society of America 5
Ecthyma represents a deeper variant of impetigo itself, caused by S. aureus and/or streptococci, characterized by circular erythematous ulcers with adherent crusts rather than superficial vesicles, as described by the Infectious Diseases Society of America 5
Atopic dermatitis with secondary bacterial infection (impetiginized eczema) represents secondary impetigo superimposed on underlying eczematous lesions, according to the Infectious Diseases Society of America 5

Nonbullous impetigo is caused by Staphylococcus aureus, Streptococcus pyogenes, or both, presenting as erythematous papules that rapidly evolve into vesicles, then pustules, and finally characteristic thick honey-colored crusts, as noted by the Infectious Diseases Society of America 5
Lesions typically occur on exposed areas, most frequently the face and extremities, according to the Infectious Diseases Society of America 5
Pustules gradually enlarge and break down over 4-6 days before forming crusts, as described by the Infectious Diseases Society of America 5
Regional lymphadenitis may occur, but systemic symptoms are usually absent, as noted by the Infectious Diseases Society of America 5

Topical antibiotics are superior to placebo and equal or superior to oral antibiotics for localized disease, with a relative risk of 2.24 (95% CI 1.61-3.13), as reported by the Infectious Diseases Society of America 5

A thorough history of chemical exposure (occupational, cleaning products, industrial chemicals, accidental contact) is the most reliable way to differentiate a chemical burn from primary impetigo. [Clinical Infectious Diseases] 6
Chemical burns initially present with tissue necrosis, eschar formation, or ulceration that have well‑demarcated borders and appear before any signs of infection. [Clinical Infectious Diseases] 7
The typical progression of a chemically‑induced burn is: first, tissue injury; then, after several days, purulent drainage or impetiginous changes develop as a secondary infection. [Clinical Infectious Diseases] 8 9
Pain is prominent from the onset in chemical burns because of direct tissue injury, whereas uncomplicated impetigo is usually painless unless the lesion overlies a joint. [Clinical Infectious Diseases] 8

When the clinical picture is atypical, early biopsy or aspiration of the lesion for histologic and microbiologic analysis should be performed to confirm the diagnosis. [Clinical Infectious Diseases] 6
Prior to diagnostic sampling or treatment, debridement of any overlying eschar down to a clean ulcer base is recommended, because thick crusts can mask underlying pathology. [Clinical Infectious Diseases] 9
Clinicians should avoid assuming that purulent drainage automatically indicates primary impetigo; purulence more often reflects secondary infection of a pre‑existing burn. [Clinical Infectious Diseases] 8

Immediate copious irrigation and decontamination of any residual chemical agent is essential at presentation. [Clinical Infectious Diseases] 7
Surgical debridement of necrotic tissue is indicated when local infection cannot be controlled by conservative measures. [Clinical Infectious Diseases] 7
Systemic antibiotic therapy is required for burns that have become secondarily infected; topical agents alone are insufficient. [Clinical Infectious Diseases] 7