Clinical Overview

Impetigo is the most common bacterial skin infection in children, highly contagious and characterized by rapid onset non-inflammatory vesicopustular lesions that rupture into golden-yellow or honey-colored crusts. Two morphologic variants: nonbullous (70% of cases, nonexudative) and bullous (30% of cases, exudative with flaccid bullae containing seropurulent fluid). Both result from Group A Streptococcus (GAS) or Staphylococcus aureus colonization through minor skin barrier disruption.

Epidemiology

Impetigo affects 111 million children annually worldwide, peak incidence 2-6 years. Males and females equally affected. Higher prevalence in tropical/subtropical climates (warm, humid environments) and resource-limited settings (2-10% prevalence in children vs. <1% in developed nations). Predisposing factors: poor hygiene, malnutrition, overcrowding, pre-existing skin disease (eczema, scabies, insect bites), immunosuppression. GAS predominant (60%), followed by S. aureus (25%), and both organisms (15%). MRSA increasingly common (5-10% in some regions). Contagious period: until 48 hours after effective antibiotic initiation or while open lesions present. Attack rate household contacts 40-70%. Complications: acute post-streptococcal glomerulonephritis (APSGN) develops in 1-5% (particularly non-M-protein-producing GAS strains), acute rheumatic fever (ARF) rare (<1%). Post-streptococcal sequelae more common with impetigo than pharyngitis.

Pathophysiology

Impetigo results from colonization of skin by GAS/STSA through minor barrier disruption (insect bite, abrasion, eczema, scabies). GAS produces pyogenic exotoxins (SPE-A, SPE-C) driving superantigen-mediated immune response with massive IL-1, TNF-alpha, and IL-6 release. Streptokinase (fibrinolytic enzyme) and hyaluronic acid capsule enhance tissue invasion. S. aureus produces alpha-toxins (cell membrane lysis), PVL (leukocyte apoptosis), and enterotoxins. Both organisms induce rapid neutrophilic recruitment creating purulent exudate. Bullous impetigo (exfoliative toxin-producing strains) characterized by exfoliative toxins A/B (ETXN-A, ETXN-B) causing intraepidermal acantholysis creating flaccid bullae. Rheumatogenic GAS M-types (particularly M49, M60, M61) associated with APSGN susceptibility; however, impetigo-derived strains vary geographically in nephritogenic potential.

Clinical Presentation

Nonbullous impetigo (70%): begins as erythematous macule or papule progressing to vesicopustule within 24-48 hours. Rapid rupture (lesion lifespan hours to days) leaves characteristic golden or honey-colored crust on erythematous base (pathognomonic finding). Satellite lesions develop through autoinoculation. Regional lymphadenopathy in 80% (non-suppurative). Distribution: exposed areas (face, extremities, shins), particularly around nose and mouth. Minimal systemic toxicity; afebrile in 90%.

Bullous impetigo (30%): begins as vesicle or small flaccid bullae. Bullae contain clear yellow serous fluid initially, becoming turbid/seropurulent. Rupture creates erosion or shallow ulcer without adherent crust (distinguishes from nonbullous). Flaccid bullae rupture easily, larger area of denudation. Systemic toxicity more common (fever in 20-30%). Perirectal involvement in 20%, potentially causing anal itching/bleeding.

Diagnosis

Diagnosis primarily clinical based on characteristic golden crusting (nonbullous) or flaccid bullae (bullous). Bacterial culture: swab underlying erythematous base beneath crust for nonbullous; fluid from intact bulla for bullous impetigo. Sensitivity 80-95% if properly obtained. Identify organism and assess antibiotic susceptibility, particularly MRSA detection. Rapid strep antigen/PCR increasingly used; nucleic acid amplification superior sensitivity (95%) to culture in some studies. Serology: anti-streptococcal antibodies (elevated ASO titers, anti-hyaluronidase, anti-streptokinase) support GAS diagnosis; however, not required clinically. Consider baseline serum creatinine and urinalysis (hematuria/proteinuria) to screen for APSGN given complication risk.

Treatment Algorithm

Localized Nonbullous Impetigo (<10 lesions, <100cm² total area): Topical antibiotic monotherapy adequate for uncomplicated cases. Mupirocin 2% ointment applied 3 times daily x 7 days: 95% efficacy in comparative trials, superior or equivalent to oral antibiotics. Requires good compliance; patient/parent education essential. Alternative: bacitracin ointment, though less effective than mupirocin. Cover lesions with bandage to prevent autoinoculation. Monitor for systemic signs; switch to systemic therapy if spreading rapidly or systemic symptoms develop.

Nonlocalized or Bullous Impetigo: Systemic antibiotics first-line. Nonbullous: amoxicillin 500mg (or 25mg/kg pediatric) 2-3 times daily OR cephalexin 500mg (25mg/kg pediatric) 4 times daily x 7-10 days. Both effective GAS/MSSA coverage. Bullous impetigo often STSA-derived (exfoliative toxin-producing): same empiric therapy covers MSSA; however, if MRSA suspected (prior antibiotics, healthcare exposure): add TMP-SMX 1-2 DS tablets (pediatric: TMP 4-6mg/kg) twice daily x 7-10 days. Amoxicillin-clavulanate 875-125mg twice daily alternative providing MSSA coverage; less first-line given broader spectrum and cost.

MRSA-Positive Impetigo: TMP-SMX (first-line), clindamycin 300-450mg 3 times daily (25mg/kg pediatric), or if beta-lactam allergy: cephalexin still covers MSSA but not MRSA. For documented MRSA: change to TMP-SMX or clindamycin. Fluoroquinolones (levofloxacin) avoid in children due to tendinopathy risk; reserve for adults with allergy/intolerance. Duration: 7-10 days typically sufficient.

Systemic Toxicity/Complications: Fever, rapid spreading, or signs of sepsis warrant empiric broad-spectrum therapy: cefazolin 1-2g IV q6-8h (or pediatric 25mg/kg) PLUS vancomycin if MRSA risk. Blood cultures indicated. Hospitalization for IV antibiotics if concerned for invasive disease/sepsis.

Prognosis

Impetigo: excellent prognosis with appropriate topical/systemic antibiotics. 90-95% clinical cure by day 7-10. Scarring rare in nonbullous; minimal scarring in bullous (resolves within weeks). APSGN develops 1-5% with peak incidence 3-4 weeks post-infection (hematuria, proteinuria may persist months but renal function typically normalizes). ARF rare (<1%) with impetigo-derived GAS. Recurrence 10-15% if predisposing factors (eczema, poor hygiene) persist or autoinoculation continues.

When to See a Dermatologist

Dermatologists recognize impetigo clinically and initiate therapy. Refer for: diagnostic uncertainty, treatment failure, complicated cases with systemic manifestations, or recurrent impetigo requiring investigation of predisposing factors.

Frequently Asked Questions

Q: Is impetigo contagious?
A: Highly contagious. Spread through direct contact with open lesions or drainage. Keep infected child home until 48 hours after antibiotics started. Prevent autoinoculation by keeping lesions covered and fingernails trimmed.

Q: Can impetigo cause serious complications?
A: Rarely. APSGN (glomerulonephritis) develops 1-5% with impetigo—higher than pharyngitis. Scarring minimal. Invasive infection/sepsis very rare with prompt treatment. Monitor for hematuria/proteinuria as APSGN marker.

Q: Should I use topical or systemic antibiotics?
A: Localized nonbullous (few lesions): mupirocin ointment adequate. Bullous, widespread, or systemic symptoms: systemic antibiotics (amoxicillin, cephalexin) required. Discuss with provider to determine appropriate approach.

Q: How long until it's not contagious?
A: With antibiotics: child non-contagious after 48 hours of effective therapy and may return to school/daycare. Without treatment: remains contagious while lesions present (weeks), so prompt diagnosis/treatment critical.

References

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