Impetigo
Superficial bacterial skin infection (S. aureus or S. pyogenes) producing honey-colored crusted erosions; highly contagious in children.
Also known as: impetigo, non-bullous impetigo, bullous impetigo, ecthyma
Overview
Highly contagious superficial bacterial skin infection caused predominantly by Staphylococcus aureus and Streptococcus pyogenes. Classified as non-bullous (most common), bullous, or ecthyma (ulcerative deeper variant).
Epidemiology
Most common bacterial skin infection in children ages 2-5; peak incidence in summer/fall. Affects ~140 million people globally. Bullous impetigo predominantly in neonates and young children. Higher rates in crowded conditions, hot/humid climates, and individuals with atopic dermatitis.
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Risk factors
- Disrupted skin barrier — atopic dermatitis, scabies, insect bites, abrasions, varicella
- Crowded living, daycare, sports involving skin contact (wrestling, football)
- Hot humid climates, poor hygiene
- Diabetes, immunosuppression
- Nasal carriage of S. aureus (especially MRSA)
Pathophysiology
Non-bullous impetigo: bacteria invade skin through breaks in barrier, producing intraepidermal pustules that rupture and crust. Bullous impetigo: S. aureus phage group II produces exfoliative toxin (ET-A) that cleaves desmoglein-1 in the granular layer → flaccid bullae. Ecthyma: deeper dermal invasion → ulcerative crusted lesion that heals with scar.
Clinical presentation
Symptoms
- Minimal systemic symptoms; rarely fever (unless extensive)
- Local pruritus, mild discomfort
- Lesions noticed by parents or coaches
Signs / physical exam
- Non-bullous: thin-walled vesicle/pustule on erythematous base → rapidly ruptures → erosion with honey-colored (yellow-brown) crust; face (perioral, perinasal), extremities; well-demarcated; minimal surrounding inflammation
- Bullous: flaccid clear/cloudy bullae 1-5 cm on intact skin (no erythematous base required) that rupture leaving collarette of scale and varnish-like brown crust; trunk, extremities, intertriginous areas; neonates and young children
- Ecthyma: punched-out ulcer with adherent yellow-gray crust and surrounding violaceous halo; lower extremities; heals with scarring
- Regional lymphadenopathy in 90% of non-bullous cases
Classic findings
Honey-colored crust on superficial erosions in a child; flaccid bullae with brown varnish-like crusts (bullous form).
Differential diagnosis
- Herpes simplex (HSV) — Grouped vesicles on erythematous base, prodromal tingling, recurrent in same site; Tzanck/PCR positive
- Varicella — Generalized eruption in different stages, fever, vesicles on erythematous base ('dew drop on rose petal')
- Contact dermatitis with secondary infection — Pattern matches exposure; pruritus predominant before crusting
- Tinea corporis with secondary infection — Annular plaque with peripheral scale; KOH positive
- Pemphigus / pemphigoid (bullous DDx) — Older adult, widespread bullae, painful mucosae (pemphigus); DIF positive
- Stevens-Johnson syndrome (bullous DDx) — Mucosal involvement, drug exposure, systemic symptoms
- Staphylococcal scalded skin syndrome (SSSS) — Diffuse erythema and superficial desquamation; positive Nikolsky; fever; young child
- Ecthyma gangrenosum (vs ecthyma) — Necrotic ulcer with black eschar in neutropenic patient; Pseudomonas bacteremia
Diagnostic workup
Diagnostic criteria
Clinical: characteristic honey-colored crusted lesions or flaccid bullae in a typical patient; culture confirms organism and susceptibility.
Labs
- Clinical diagnosis usually sufficient
- Gram stain and culture of exudate (especially in suspected MRSA, treatment failure, severe disease, outbreaks)
- Anti-DNase B and anti-streptolysin O titers (rising in post-streptococcal glomerulonephritis surveillance — not routine)
- Urinalysis 1-3 weeks after streptococcal impetigo if PSGN suspected (hematuria, edema, HTN)
Imaging
- Not indicated
Diagnostic algorithm
| Variant | Hallmark | Therapy |
|---|---|---|
| Non-bullous | Honey-colored crusts on face/extremities | Topical mupirocin × 5 d (limited); oral cephalexin/dicloxacillin × 7 d (extensive) |
| Bullous | Flaccid bullae → varnish-like brown crust (toxin-mediated) | Oral cephalexin/dicloxacillin; admit neonates |
| Ecthyma | Punched-out ulcer with adherent crust, scars on healing | Oral antibiotics × 7-10 d; local wound care |
| MRSA-suspected | Treatment failure, purulent, abscess | Clindamycin, TMP-SMX, or doxycycline based on susceptibilities |
Treatment
First-line
- Limited (≤5 lesions, small body area, non-bullous): topical mupirocin 2% ointment TID × 5 days OR topical retapamulin 1% ointment BID × 5 days OR topical ozenoxacin 1% cream BID × 5 days
- Extensive, bullous, ecthyma, or treatment failure (systemic antibiotics × 7 days): cephalexin 25-50 mg/kg/day divided QID (pediatric) or 250-500 mg QID (adult); dicloxacillin 12.5 mg/kg/day pediatric or 250-500 mg QID adult — covers MSSA and S. pyogenes
- Penicillin-allergic (non-anaphylactic): cephalexin acceptable; (anaphylactic): clindamycin 10-30 mg/kg/day pediatric or 300-450 mg QID adult, or doxycycline (≥8 years)
- MRSA suspected: clindamycin (check D-test for inducible resistance), trimethoprim-sulfamethoxazole, doxycycline, linezolid; mupirocin remains effective for many MRSA strains
- Hygiene: hand washing, nail trimming, separate towels and bedding, cover lesions; school exclusion until 24 hours of antibiotics or lesions crusted over
- Decolonization for recurrent: intranasal mupirocin BID × 5 days + chlorhexidine washes + household decontamination
Bullous impetigo (neonates)
- Low threshold for hospital admission, IV antibiotics (nafcillin, oxacillin, vancomycin if MRSA risk)
- Differentiate from staphylococcal scalded skin syndrome which requires broader management
Ecthyma
- Systemic antibiotics (as above) × 7-10 days
- Local wound care with gentle debridement
- Counsel: heals with scarring (unlike standard impetigo)
Second-line / adjunct
- Mupirocin resistance documented in some regions — fusidic acid or retapamulin are alternatives
- Bleach baths for recurrent disease in atopic dermatitis patients
- Treat underlying skin disease (scabies, eczema)
Complications
- Cellulitis, lymphangitis, bacteremia
- Post-streptococcal glomerulonephritis (PSGN) — 1-5% incidence after streptococcal skin infection, 1-3 weeks post-infection; antibiotic treatment does NOT prevent PSGN once infection established
- Acute rheumatic fever is NOT a complication of streptococcal impetigo (unlike pharyngitis)
- Staphylococcal scalded skin syndrome (SSSS) from toxin spread
- Scarlet fever
- Permanent scarring from ecthyma
- Recurrence with persistent nasal/skin S. aureus colonization
PANCE pearls
- Honey-colored crust on a child's face = impetigo. Topical mupirocin × 5 days is sufficient for limited disease.
- Bullous impetigo is caused by S. aureus exfoliative toxin (same family that produces SSSS); the bullae are typically on intact-appearing skin without erythematous halo.
- Antibiotic treatment of streptococcal impetigo does NOT prevent post-streptococcal glomerulonephritis once infection is established — but does prevent transmission and other complications.
- Recurrent impetigo warrants S. aureus decolonization (intranasal mupirocin + chlorhexidine).
- Ecthyma heals with scarring; standard impetigo does not.
References
- IDSA 2014 — Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America (Stevens et al., Clin Infect Dis 2014)
- AAP Red Book 2024 — American Academy of Pediatrics Red Book — Staphylococcal and Streptococcal Skin Infections (2024 update)
- AAFP 2014 — Impetigo: Diagnosis and Treatment (Hartman-Adams, Banvard, Juckett, Am Fam Physician 2014)
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