Impetigo

A common, highly contagious superficial bacterial skin infection predominantly caused by Staphylococcus aureus and less commonly Streptococcus pyogenes. Presents with golden-crusted lesions (non-bullous) or flaccid blisters (bullous). Most common in children aged 2–6 years. Treated with topical fusidic acid or hydrogen peroxide cream; oral flucloxacillin for extensive disease.

Key Facts

Most common bacterial skin infection in children: peak age 2–6 years S. aureus: predominant cause (~80%); S. pyogenes also implicated Non-bullous impetigo (~70%): golden/honey-coloured crusts, often perioral/perinasal Bullous impetigo (~30%): flaccid blisters caused by S. aureus exfoliative toxins — neonates/infants Topical hydrogen peroxide 1% cream: first-line for localised, non-bullous impetigo (NICE CKS 2020) Topical fusidic acid 2%: second-line topical — TDS for 5 days; resistance increasing Oral flucloxacillin 500 mg QDS for 5–7 days: for extensive or systemic impetigo Highly contagious: exclude from school/nursery until lesions crusted over or 48 hours after starting antibiotics

Overview

Key Facts

Impetigo is a superficial skin infection that is extremely common in childhood. It is highly contagious and can spread rapidly in schools and nurseries. It is important to distinguish from more serious skin infections and to be aware of rare post-streptococcal complications.

Epidemiology

  • Most common bacterial skin infection in children
  • Peak age: 2–6 years
  • More common in summer/autumn (warm, humid conditions)
  • Affects ~2–3% of children annually in UK
  • Can occur at any age; common secondary infection of eczema ('eczema herpeticum' is different — HSV)

Aetiology

  • S. aureus: ~80% of cases; sole pathogen in bullous impetigo
  • S. pyogenes (Group A Streptococcus): ~10–20%; may cause post-streptococcal glomerulonephritis (NOT rheumatic fever)
  • MRSA: increasingly recognised cause in community-acquired impetigo
  • Risk factors: pre-existing skin condition (eczema, scabies), minor trauma, warm/humid environment, crowding

Pathophysiology

  • Bacteria colonise damaged skin (abrasion, insect bite, eczema) → superficial infection of epidermis
  • Non-bullous: mixed S. aureus/S. pyogenes → inflammatory response → serous exudate → characteristic golden crust
  • Bullous: S. aureus exfoliative toxins (ETA/ETB) → cleavage within epidermis (desmoglein 1 cleavage) → flaccid blisters (same mechanism as SSSS but localised)

Clinical Presentation

Non-Bullous Impetigo (70%)

  • Begins as erythematous macules → vesicles/pustules → rupture → characteristic golden/honey-coloured crusts
  • Usually perioral, perinasal, or on exposed skin
  • Regional lymphadenopathy may be present
  • May spread by autoinoculation (finger-to-face)

Bullous Impetigo (30%)

  • Flaccid, clear or cloudy fluid-filled blisters 1–3 cm
  • Rupture easily → leave thin, lacquer-like crust with erythematous base
  • More common in neonates and infants
  • Usually on trunk, axillae, flexures

Secondary Impetiginisation

  • Bacterial superinfection of pre-existing skin condition (eczema, scabies, herpes, chickenpox)
  • Golden crusting developing on top of chronic skin disease

Red Flags

  • Systemic symptoms (fever, malaise) — consider cellulitis, abscess, or bacteraemia
  • Widespread bullous impetigo in neonate — exclude staphylococcal scalded skin syndrome (SSSS)
  • Post-streptococcal glomerulonephritis: haematuria, oedema, hypertension 1–3 weeks after streptococcal impetigo
  • Treatment failure — consider MRSA

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Eczema (infected)Chronic history, flexural, with secondary crustingClinical
Herpes simplexGrouped vesicles on erythematous base, painfulViral swab PCR
Bullous pemphigoid (in adults)Tense blisters, elderly, Nikolsky −veBiopsy, DIF
SSSS (in neonates)Widespread erythema, Nikolsky +ve, sheet-like desquamationClinical, biopsy
Contact dermatitisDistribution matches allergen; vesicles, no golden crustPatch testing
Tinea corporisAnnular, advancing scaly edge, central clearingKOH microscopy

Diagnosis / Investigation

Bedside

  • Clinical diagnosis: usually straightforward from characteristic appearance
  • Swab for MC&S: if treatment failure, recurrent episodes, or suspected MRSA; take swab from beneath crust

Bloods

  • Not routinely required for uncomplicated impetigo
  • ASOT/anti-DNase B: if post-streptococcal glomerulonephritis suspected
  • U&Es, urinalysis: if PSGN suspected (haematuria, proteinuria, renal impairment)

Biopsy

  • Not required — clinical diagnosis

Special Tests

  • Nasal swab: for S. aureus carriage if recurrent impetigo — treat with mupirocin nasal ointment TDS for 5 days

Management

Non-Pharmacological

  • Hygiene measures: regular handwashing, avoid sharing towels/flannels
  • Wound care: gently remove crusts with warm water and clean cloth
  • School exclusion: until lesions crusted over, or 48 hours after starting antibiotics
  • Avoid touching/scratching lesions — prevents autoinoculation and spread

Pharmacological

Localised, non-bullous impetigo:

  • Topical hydrogen peroxide 1% cream (Crystacide): first-line (NICE CKS) — apply BD-TDS for 5 days; effective, no resistance concerns
  • Topical fusidic acid 2% cream/ointment: second-line — TDS for 5 days; increasing S. aureus resistance (~20%)
  • Topical mupirocin 2%: alternative, especially if MRSA suspected

Extensive, bullous, or systemically unwell:

  • Flucloxacillin 500 mg QDS (adult) or 12.5–25 mg/kg QDS (child) for 5–7 days: first-line oral
  • Clarithromycin 250–500 mg BD for 5 days: if penicillin-allergic
  • Co-amoxiclav: if mixed streptococcal/staphylococcal suspected

Recurrent impetigo:

  • Mupirocin 2% nasal ointment TDS for 5 days + chlorhexidine body wash for 5 days — S. aureus decolonisation
  • Treat whole household if recurrent

Referral Criteria

  • Rarely needed — manage in primary care
  • Dermatology: if diagnostic uncertainty or treatment-resistant
  • Paediatrics: neonatal impetigo, suspected SSSS, systemically unwell child

Prognosis

  • Excellent: self-limiting even without treatment in many cases; resolves faster with antibiotics
  • Heals without scarring
  • Post-streptococcal glomerulonephritis: rare (~1–5% after streptococcal impetigo); usually self-limiting
  • Rheumatic fever does NOT follow skin streptococcal infections (only throat)
  • Recurrence: common; consider nasal S. aureus decolonisation
  • SSSS (in neonates): potentially life-threatening if not recognised

Other Relevant Information

Impetigo Treatment Ladder

SeverityFirst-LineAlternative
Localised non-bullousHydrogen peroxide 1% creamFusidic acid 2%
Extensive non-bullousOral flucloxacillinOral clarithromycin
BullousOral flucloxacillinOral clarithromycin
RecurrentDecolonisation (mupirocin nasal + chlorhexidine)
MRSA suspectedTopical mupirocin + oral doxycycline/co-trimoxazole

Complications of Impetigo

ComplicationFrequencyFeatures
CellulitisUncommonSpreading erythema, systemic upset
PSGNRareHaematuria, oedema, HTN 1–3 weeks later
SSSS (neonates)RareWidespread erythema, desquamation
AbscessUncommonFluctuant, tender collection