Impetigo (Child)

1. Clinical Overview

Summary

Impetigo is a highly contagious superficial bacterial skin infection that represents the most common bacterial skin infection in children worldwide, with peak incidence in 2-5 year olds. [1,2] The condition is predominantly caused by Staphylococcus aureus (60-70% of cases) and/or Streptococcus pyogenes (Group A Streptococcus, GAS), with mixed infections occurring in 10-20% of cases. [3,4]

The hallmark clinical presentation features honey-coloured (golden-yellow) crusted lesions that typically affect the perioral and perinasal regions of the face, though any body site can be involved. [1] Two distinct clinical forms exist: Non-Bullous Impetigo (70% of cases) characterized by vesiculopustular lesions that rupture to form characteristic golden crusts, and Bullous Impetigo (30% of cases) caused by toxin-producing S. aureus strains that produce flaccid blisters. [5]

Impetigo spreads through direct skin contact or fomite transmission, with high attack rates in crowded environments such as schools and nurseries. [6] School exclusion is mandatory until lesions have crusted and dried or until 48 hours after commencing antibiotic therapy. [7]

Treatment follows a stratified approach based on extent: topical antibiotics (fusidic acid 2% or mupirocin 2%) for localized disease (less than 3 lesions, less than 2cm diameter), and oral antibiotics (flucloxacillin) for extensive or systemic disease. [8,9] With appropriate treatment, resolution typically occurs within 7-10 days with excellent prognosis and no scarring (except in ecthyma). [1]

Important complications include cellulitis, ecthyma (deep ulcerative form), and acute post-streptococcal glomerulonephritis (APSGN), which occurs in approximately 2-5% of GAS-related impetigo cases 1-3 weeks post-infection. [10] In neonates and young infants, bullous impetigo can progress to Staphylococcal Scalded Skin Syndrome (SSSS). [11]

Clinical Pearls

"Honey-Coloured Crusts": The pathognomonic feature – thick, golden-yellow adherent crusts on an erythematous base, most commonly around the mouth and nose. This appearance results from dried serous exudate.

"Contact Contagion": Impetigo is one of the most contagious skin conditions in childhood. Direct contact spreads infection rapidly through families and schools. Fomites (towels, toys) are important vectors.

"Staphylococcus Dominance": While historically GAS was predominant, S. aureus now accounts for 60-70% of cases in developed countries. MRSA strains are increasingly recognized (5-30% depending on region).

"Bullous = Toxin": Bullous impetigo results from staphylococcal exfoliative toxins A and B (ETA, ETB) that cleave desmoglein-1, the same target as in pemphigus foliaceus. Consider it a localized SSSS.

"Eczema Gateway": Children with atopic eczema have 3-4 fold increased risk. Disrupted skin barrier and S. aureus colonization (present in 90% of eczema patients) drive this association.

"APSGN ≠ Pharyngitis": Unlike acute rheumatic fever (which follows pharyngitis only), APSGN can follow both pharyngeal and cutaneous GAS infections. Antibiotics do NOT prevent APSGN.

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2. Epidemiology

Incidence and Prevalence

Demographics

Risk Factors

Exam Detail: MRCPCH Pearl: In Indigenous Australian children, impetigo prevalence can reach 50-70% in some remote communities, with scabies serving as a major predisposing factor. The "scabies-impetigo-APSGN-rheumatic heart disease" pathway is a major public health concern. [12]

Viva Point: Why is impetigo more common in summer? Three factors: (1) Increased skin trauma (insect bites, minor injuries from outdoor play), (2) Higher environmental temperature/humidity favoring bacterial proliferation, (3) Greater skin-to-skin contact during recreational activities.

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3. Aetiology and Pathophysiology

Causative Organisms

Molecular Pathogenesis

Non-Bullous Impetigo

Bacterial Adherence and Invasion:

1. Colonization: S. aureus colonizes anterior nares in 20-40% of population; GAS less commonly colonizes skin. [14]

2. Skin Barrier Breach: Bacteria require entry point – minor trauma (insect bite, scratch), pre-existing dermatosis (eczema), or overcrowding/poor hygiene allowing adherence to intact stratum corneum. [13]

3. Bacterial Adhesins:

   • S. aureus: Clumping factor A/B binds fibrinogen; protein A binds IgG Fc, evading opsonization
   • GAS: M protein (antiphagocytic), lipoteichoic acid (epithelial adhesion), fibronectin-binding proteins [4]

4. Superficial Epidermal Invasion: Bacteria remain confined to subcorneal or superficial epidermis (unlike cellulitis/erysipelas which involve dermis). Minimal dermal inflammation.

5. Vesicle Formation: Host inflammatory response → neutrophil recruitment → subcorneal pustule formation. Vesicles are fragile and rupture rapidly.

6. Crust Formation: Ruptured vesicles release serous exudate rich in fibrin, neutrophils, bacteria → dries to form characteristic golden-yellow crust.

Virulence Factors:

• S. aureus: Hemolysins, leukocidins, enzymes (hyaluronidase, lipases), superantigens (enterotoxins, TSST-1)
• GAS: Streptokinase, streptolysins O/S, hyaluronidase, DNase, C5a peptidase [4]

Bullous Impetigo

Exfoliative Toxin-Mediated Pathogenesis:

1. Toxin Production: Phage group II S. aureus strains (especially 71, 55) produce exfoliative toxins A and B (ETA, ETB), which are serine proteases. [5,11]

2. Molecular Target: ETA/ETB specifically cleave desmoglein-1 (Dsg1), a desmosomal cadherin responsible for keratinocyte cell-cell adhesion in superficial epidermis. [16]

   • Same target as autoantibodies in pemphigus foliaceus
   • Dsg1 is concentrated in upper epidermis; desmoglein-3 (deeper epidermis) is NOT cleaved

3. Epidermal Cleavage: Dsg1 cleavage → loss of keratinocyte adhesion → intraepidermal blister formation at granular layer (subcorneal/high stratum spinosum).

4. Localized vs. Generalized:

   • Bullous impetigo: Toxin acts locally at infection site → localized blisters
   • SSSS: Toxin disseminates systemically (occurs in neonates/infants with immature renal clearance) → generalized exfoliation [11]

5. Blister Characteristics: Flaccid (not tense) due to superficial cleavage plane. Contain clear/cloudy fluid initially, then rupture leaving thin "collarette" scale.

Exam Detail: Molecular Medicine for MRCPCH: The desmoglein compensation theory explains clinical distribution:

• Upper epidermis: Only Dsg1 present → ETA/ETB cleavage causes blistering
• Lower epidermis: Both Dsg1 + Dsg3 → even if Dsg1 cleaved, Dsg3 maintains adhesion → no blisters

This is why bullous impetigo and SSSS spare mucous membranes (which express Dsg3 at all levels), unlike pemphigus vulgaris (anti-Dsg3 antibodies) which causes mucosal involvement.

Exam Viva: "Why don't infants with SSSS have mucosal involvement despite widespread skin loss?" Answer: Exfoliative toxins only cleave Dsg1, not Dsg3. Mucous membranes express Dsg3 throughout all epithelial layers, so adhesion is maintained even when Dsg1 is cleaved.

Host Immune Response

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4. Classification

Primary Classification by Clinical Type

Secondary Classification

Exam Detail: MRCPCH Classification Point: Ecthyma represents the ulcerative variant of impetigo where infection extends into the dermis (not just epidermis). It typically occurs in:

• Neglected/untreated impetigo
• Immunocompromised hosts
• Areas of poor hygiene/nutrition
• Often on lower legs

Ecthyma heals with scarring (unlike superficial impetigo) and may require systemic antibiotics even if lesions are few.

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5. Clinical Presentation

Non-Bullous Impetigo (70% of Cases)

Evolution of Lesions

Typical Features

Bullous Impetigo (30% of Cases)

Typical Features

Ecthyma (5-10% of Cases)

Atypical Presentations

Exam Detail: MRCPCH Examination Pearl: When examining a child with honey-crusted lesions, demonstrate systematic approach:

1. Inspection: Describe distribution (perioral), morphology (golden crust), surrounding erythema
2. Palpation: Gentle palpation of regional lymph nodes (cervical/submandibular)
3. System Review: Assess for systemic features (fever, lethargy)
4. Associated Features: Check for eczema, scabies, signs of neglect
5. Nikolsky Sign: If bullae present, test Nikolsky (usually negative in localized bullous impetigo; positive in SSSS)

Differential Diagnosis Viva: "How do you differentiate impetiginized eczema from primary impetigo?"

• Impetiginized eczema: Background of chronic eczema, widespread involvement in typical eczema distribution (flexures), pruritic, lichenification
• Primary impetigo: Acute onset, localized lesions, perioral/perinasal, NOT pruritic, no background skin disease

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6. Differential Diagnosis

Exam Detail: MRCPCH Viva Approach to Differentials:

Examiner: "A 3-year-old presents with blisters on the trunk. How do you approach the differential diagnosis?"

Model Answer: "I would take a structured approach based on blister morphology and distribution:

1. Blister characteristics:

   • Flaccid blisters → toxin-mediated (bullous impetigo, SSSS) or autoimmune (pemphigus - rare in children)
   • Tense blisters → deeper split (bullous pemphigoid, burns, allergic contact dermatitis)

2. Distribution:

   • Trunk/buttocks in infant → bullous impetigo most likely
   • Exposed areas → contact dermatitis, phototoxic reaction
   • Acral (hands/feet) + oral → hand-foot-mouth disease

3. Associated features:

   • Honey crusts → impetigo
   • Nikolsky sign positive on normal skin → SSSS
   • Mucosal involvement → SJS, pemphigus vulgaris, HSV
   • Intense pruritus → scabies, dermatitis herpetiformis

4. Investigations: Swab for C&S (bacterial vs. viral), Nikolsky sign, consider biopsy if autoimmune suspected."

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7. Investigations

Clinical Diagnosis

Impetigo is a CLINICAL diagnosis in > 95% of cases. No investigations are required for typical presentations. [1,8]

Diagnostic Criteria (Clinical):

• Characteristic honey-coloured crusts (non-bullous) OR flaccid blisters (bullous)
• Typical distribution (face, exposed areas)
• Rapid spread with autoinoculation
• Contact history or outbreak setting

Microbiological Investigations

Indications for Swab:

Swab Technique:

1. Gently lift or remove crust
2. Swab moist base of lesion (not dry crust – lower yield)
3. Send in bacterial transport medium
4. Request: Culture and sensitivities; specify MRSA PCR if high suspicion

Expected Results:

• S. aureus: 60-70% of isolates
• S. pyogenes: 20-30%
• Mixed: 10-20%
• MRSA: 5-30% (regional variation) [3,4,15]

Laboratory Investigations (Rarely Required)

Histopathology (Very Rare)

Indications: Diagnostic uncertainty (exclude autoimmune blistering disorder, vasculitis). Atypical presentation.

Non-Bullous Impetigo:

• Subcorneal or intraepidermal pustule
• Neutrophils, fibrin, bacterial colonies
• Dermal infiltrate: neutrophils, lymphocytes
• No acantholysis

Bullous Impetigo:

• Subcorneal or granular layer split
• Minimal acantholysis (some detached keratinocytes)
• Neutrophils in blister cavity
• Negative direct immunofluorescence (unlike pemphigus)

Exam Detail: MRCPCH Viva - Investigations:

Examiner: "A 4-year-old child presents with recurrent impetigo (3rd episode in 6 months). What investigations would you consider?"

Model Answer: "Recurrent impetigo warrants investigation to identify underlying causes:

1. Immediate:

   • Skin swab of active lesion for culture and sensitivities (identify organism, check MRSA)
   • Anterior nasal swab to detect S. aureus carriage (present in 30-40% of recurrent cases)

2. Consider:

   • Close contact screening: Family members for nasal carriage if household recurrence
   • Atopic status: Examine for eczema (major risk factor)
   • Hygiene assessment: Social history, living conditions

3. If ≥4 episodes or other infections:

   • Screen for immunodeficiency (rare but important):
     • FBC (neutrophil count)
     • Immunoglobulins (IgG, IgA, IgM)
     • HIV test (if risk factors)
     • Consider complement assays (if recurrent severe infections)

4. If MRSA confirmed:

   • Decolonization regimen: Mupirocin nasal ointment + chlorhexidine body washes
   • Repeat swabs to confirm clearance"

Key Point: Most recurrent impetigo is due to nasal S. aureus carriage or underlying eczema, NOT immunodeficiency.

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8. Management

Management Algorithm

┌─────────────────────────────────────────────────────────────────┐
│                     IMPETIGO DIAGNOSED                          │
│        (Honey crusts OR Flaccid bullae + compatible history)    │
└─────────────────────────────────────────────────────────────────┘
                              ↓
┌─────────────────────────────────────────────────────────────────┐
│                     ASSESS SEVERITY                             │
│  1. EXTENT: Localized (less than 3 lesions) vs. Extensive (≥3 lesions)  │
│  2. SYSTEMIC: Fever, lethargy, poor feeding?                    │
│  3. COMPLICATIONS: Cellulitis, lymphangitis, sepsis?            │
│  4. SPECIAL: Neonate, immunocompromised, SSSS features?         │
└─────────────────────────────────────────────────────────────────┘
                              ↓
              ┌───────────────┴───────────────┐
              ↓                               ↓
┌──────────────────────────┐    ┌────────────────────────────────┐
│   LOCALIZED IMPETIGO     │    │   EXTENSIVE / SYSTEMIC         │
│   (less than 3 lesions, less than 2cm,     │    │   (≥3 lesions, large area,     │
│    well child)           │    │    systemic features)          │
└──────────────────────────┘    └────────────────────────────────┘
              ↓                               ↓
┌──────────────────────────────────────────────────────────────────┐
│              TOPICAL ANTIBIOTIC (First-Line for Localized)       │
│                                                                  │
│  OPTION 1: **Fusidic Acid 2%** cream/ointment                   │
│            - Apply TDS for 5-7 days                              │
│            - Cheap, effective, well-tolerated                    │
│            - Resistance increasing (5-20% depending on region)   │
│                                                                  │
│  OPTION 2: **Mupirocin 2%** ointment                            │
│            - Apply TDS for 5-7 days                              │
│            - Preferred if MRSA suspected or fusidic resistance   │
│            - Reserved to minimize resistance (keep as 2nd line)  │
│                                                                  │
│  TECHNIQUE:                                                      │
│   1. Gently remove crusts with soap and water (increases        │
│      antibiotic penetration)                                     │
│   2. Apply thin layer to lesions and 1cm margin                 │
│   3. May cover with dressing if oozing (not mandatory)          │
└──────────────────────────────────────────────────────────────────┘
              ↓                               ↓
┌──────────────────────────────────────────────────────────────────┐
│            ORAL ANTIBIOTIC (Extensive/Systemic/Failed Topical)   │
│                                                                  │
│  FIRST-LINE: **Flucloxacillin** (anti-staphylococcal)           │
│   • less than 2 years:  62.5 mg QDS for 5-7 days                         │
│   • 2-9 years: 125 mg QDS for 5-7 days                          │
│   • ≥10 years: 250-500 mg QDS for 5-7 days                      │
│   • Take on empty stomach (1h before or 2h after food)          │
│                                                                  │
│  PENICILLIN ALLERGY:                                             │
│   • **Clarithromycin** 7.5 mg/kg BD (max 500mg BD) for 5-7 days │
│   • **Erythromycin** 10 mg/kg QDS (max 500mg QDS) for 5-7 days  │
│                                                                  │
│  MRSA CONFIRMED/SUSPECTED:                                       │
│   • Swab for culture and sensitivities                          │
│   • Consult microbiology/infectious diseases                    │
│   • Options (based on sensitivities):                           │
│     - Doxycycline 100mg BD (if ≥12 years)                       │
│     - Trimethoprim 4 mg/kg BD (max 200mg BD)                    │
│     - Clindamycin 5 mg/kg TDS (max 450mg TDS)                   │
│     - Co-trimoxazole (if local sensitivities support)           │
│     - Linezolid (severe, resistant cases, specialist only)      │
└──────────────────────────────────────────────────────────────────┘
              ↓
┌──────────────────────────────────────────────────────────────────┐
│                    HYGIENE MEASURES (ALL CASES)                  │
│                                                                  │
│  1. **Handwashing**: Regular with soap, especially after        │
│     touching lesions. Alcohol gel less effective for spores.    │
│                                                                  │
│  2. **Crust Removal**: Gently soak off crusts with warm water   │
│     before applying topical antibiotics (improves penetration). │
│                                                                  │
│  3. **Separate Towels/Flannels**: Do not share. Wash at ≥60°C. │
│                                                                  │
│  4. **Avoid Touching**: Minimize autoinoculation and spread.    │
│                                                                  │
│  5. **Short Nails**: Keep nails trimmed to reduce scratching.   │
│                                                                  │
│  6. **Avoid Close Contact**: Until lesions crusted or 48h after │
│     antibiotics started.                                         │
└──────────────────────────────────────────────────────────────────┘
              ↓
┌──────────────────────────────────────────────────────────────────┐
│                    SCHOOL/NURSERY EXCLUSION                      │
│                                                                  │
│  **Exclude from school/nursery until**:                          │
│   • Lesions have crusted and dried, OR                          │
│   • 48 hours after starting antibiotic treatment                │
│                                                                  │
│  (UK Health Protection Agency / Public Health England guidance) │
└──────────────────────────────────────────────────────────────────┘
              ↓
┌──────────────────────────────────────────────────────────────────┐
│                    FOLLOW-UP AND MONITORING                      │
│                                                                  │
│  • Review in 7 days if not improving                            │
│  • Treatment failure: Consider swab for C&S (MRSA, resistance)  │
│  • Recurrent impetigo (≥3 episodes/year): Investigate nasal     │
│    carriage, consider decolonization, assess for eczema         │
│  • Monitor for APSGN: Advise parents to watch for dark urine,   │
│    swelling, hypertension (1-3 weeks post-infection)            │
└──────────────────────────────────────────────────────────────────┘

Evidence-Based Treatment Recommendations

Topical vs. Oral Antibiotics

Key Evidence (Cochrane Review 2012): [9]

• Topical antibiotics are as effective as oral antibiotics for localized impetigo
• Topical mupirocin superior to oral erythromycin (RR cure 1.13, 95% CI 1.02-1.27)
• Topical treatment preferred for localized disease to:
  • Reduce systemic antibiotic exposure
  • Minimize gastrointestinal side effects
  • Reduce antibiotic resistance selection pressure
  • Improve adherence (easier than QDS oral dosing in young children)

NICE CKS Guidance 2023: [8]

• Topical for localized disease (less than 3 lesions, less than 2cm diameter)
• Oral for extensive disease, systemic features, or immunocompromised

Antibiotic Choice

Special Scenarios

Bullous Impetigo

• Usually requires oral antibiotics (even if localized) due to systemic toxin
• Flucloxacillin first-line
• Monitor for SSSS progression (especially in neonates less than 6 months)

Recurrent Impetigo

Definition: ≥3 episodes in 12 months

Investigation:

1. Swab active lesion + anterior nares for S. aureus carriage
2. Screen close contacts for nasal carriage
3. Assess for underlying eczema
4. Consider immunodeficiency if ≥4 episodes + other infections

Decolonization Regimen (if nasal carriage confirmed): [14]

• Mupirocin 2% nasal ointment BD for 5-7 days (apply pea-sized amount to anterior nares)
• Chlorhexidine 4% body wash daily for 5 days
• Treat household contacts if recurrent transmission
• Repeat swabs 3 days after completion to confirm eradication

Success Rate: 60-70% at 3 months (recolonization common)

MRSA Impetigo

Treatment (based on sensitivities): [15]

• Mupirocin topical (if localized)
• Oral options: Doxycycline (if ≥12y), trimethoprim, clindamycin, co-trimoxazole
• Avoid: Flucloxacillin, fusidic acid (ineffective)
• Consult microbiology/infectious diseases

Decolonization: As per recurrent impetigo protocol

Impetiginized Eczema

• Treat infection: Topical/oral antibiotics as per extent
• Continue emollients and topical corticosteroids (eczema treatment)
• Consider maintenance emollient with antimicrobial (e.g., with chlorhexidine)

Neonates and Infants less than 3 Months

• Higher SSSS risk (immature renal clearance of exfoliative toxin)
• Lower threshold for oral antibiotics
• If bullous impetigo or systemic features → hospital admission for IV antibiotics
• Monitor closely for progression

Exam Detail: MRCPCH Antibiotic Stewardship Viva:

Examiner: "Why do we prefer topical antibiotics for localized impetigo rather than oral antibiotics?"

Model Answer: "Topical antibiotics are preferred for localized impetigo based on several principles of antimicrobial stewardship:

1. Efficacy: Cochrane review (2012) showed topical antibiotics (mupirocin, fusidic acid) are as effective as oral antibiotics for localized disease, with cure rates > 90%.

2. Reduce systemic exposure:

   • Minimizes gastrointestinal side effects (diarrhea in 5-15% with oral antibiotics)
   • Reduces disruption of commensal flora
   • Better safety profile

3. Antimicrobial resistance:

   • Limits selection pressure for systemic resistance
   • Reduces C. difficile risk (rare in children but relevant)
   • Preserves oral antibiotics for truly systemic infections

4. Adherence: Topical TDS often easier than oral QDS in toddlers

5. Cost-effectiveness: Topical agents generally cheaper

However, oral antibiotics indicated if:

• Extensive disease (> 3 lesions, large area)
• Systemic features (fever, lymphangitis)
• Bullous impetigo (systemic toxin)
• Immunocompromised
• Treatment failure with topical agent"

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9. Complications

Exam Detail: MRCPCH Key Concepts - APSGN:

Critical Point: Antibiotics do NOT prevent APSGN (unlike acute rheumatic fever prevention with pharyngitis treatment). [10]

Why?

• APSGN is an immune-mediated complication caused by immune complex deposition
• Immune response develops during active infection
• By the time APSGN manifests (10-21 days post-infection), immune complexes already formed
• Antibiotics treat active infection and reduce transmission but do NOT alter immune response

Clinical Features:

• Latent period: 10-21 days post-impetigo (vs. 1-3 weeks post-pharyngitis)
• Classic triad: Haematuria + Oedema + Hypertension
• Laboratory: Low C3 (returns to normal in 6-8 weeks), raised ASO (less reliable than anti-DNase B for skin infections), raised anti-DNase B

Prognosis:

• Children: > 95% full recovery
• Adults: 50% develop chronic kidney disease
• Dialysis required in less than 5%

Viva Scenario: "A 4-year-old presents with dark urine and swelling 2 weeks after impetigo. What is your differential and approach?"

• Diagnosis: APSGN most likely
• Investigations: Urinalysis (haematuria, RBC casts, proteinuria), U&E, complement C3, anti-DNase B, throat swab
• Management: Fluid restriction, salt restriction, monitor BP, diuretics if overload, nephrology referral
• Prognosis: Excellent in children

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10. Prognosis and Outcomes

Short-Term Prognosis

Long-Term Prognosis

Factors Affecting Prognosis

Exam Detail: MRCPCH Viva - Prognosis Counseling:

Examiner: "A parent asks you about long-term effects of impetigo. What do you tell them?"

Model Answer: "I would reassure the parent that the prognosis for impetigo is excellent:

1. Healing: With treatment, the infection clears within 7-10 days. Even without treatment, it often resolves spontaneously in 2-3 weeks, though we treat to:

   • Speed recovery
   • Reduce spread to others
   • Prevent complications

2. Scarring: Ordinary impetigo (including bullous impetigo) heals without scarring. There may be temporary darkening of the skin (post-inflammatory pigmentation) which fades over 3-6 months. Only the deep form (ecthyma) leaves small scars.

3. Recurrence: About 10-20% of children get further episodes. This is usually because:

   • They carry the bacteria in their nose and keep re-infecting themselves
   • They have eczema (which increases risk)
   • Close contacts (siblings, parents) carry the bacteria

   If recurrent, we can test for nasal carriage and offer decolonization treatment.

4. Complications: Serious complications are rare. Occasionally, if caused by Streptococcus, a kidney condition (APSGN) can develop 2-3 weeks later. I'd advise watching for dark urine or swelling and seeking review if concerned. This almost always recovers fully in children.

5. School: They can return to school 48 hours after starting antibiotics or once the sores have dried and crusted."

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11. Prevention and Public Health

Primary Prevention

Secondary Prevention (Reducing Transmission)

Decolonization (Tertiary Prevention - Recurrence)

Indications:

• ≥3 episodes of impetigo in 12 months
• Confirmed nasal S. aureus carriage
• Household transmission

Protocol: [14]

1. Nasal decolonization: Mupirocin 2% nasal ointment BD × 5-7 days
2. Skin decolonization: Chlorhexidine 4% body wash daily × 5 days
3. Environmental: Wash bedding, towels at ≥60°C
4. Household contacts: Treat if nasal carriers or recurrent transmission
5. Re-swab: 3 days after completion (eradication rate 60-70% at 3 months)

Evidence: Limited high-quality evidence. Expert consensus supports use in recurrent cases. [14]

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12. Evidence and Guidelines

Key Guidelines

Landmark Studies and Reviews

1. Koning et al. (2012) - Cochrane Review: "Interventions for impetigo" [9]

   • Study Type: Systematic review and meta-analysis (68 RCTs, 5,889 participants)
   • Key Finding: Topical antibiotics as effective as oral for localized impetigo (RR cure 0.98, 95% CI 0.92-1.05)
   • Impact: Established topical antibiotics as first-line for localized disease

2. Bowen et al. (2015) - Lancet: "The global epidemiology of impetigo" [2]

   • Study Type: Systematic review (111 studies)
   • Key Finding: 162 million children affected globally at any time; highest burden in tropical regions
   • Impact: Highlighted global disease burden, particularly in Indigenous populations

3. Cole & Gazewood (2007) - Am Fam Physician: "Diagnosis and Treatment of Impetigo" [1]

   • Study Type: Clinical review
   • Key Points: Clinical diagnosis criteria, management algorithms, evidence-based antibiotic selection

4. Hartman-Adams et al. (2014) - Am Fam Physician: "Impetigo: Diagnosis and Treatment" [3]

   • Study Type: Systematic review
   • Key Finding: S. aureus now predominant (60-70%); MRSA increasing in some regions

5. Craft et al. (2012) - Pediatr Dermatol: "Mupirocin decolonization of methicillin-resistant Staphylococcus aureus in children" [14]

   • Study Type: RCT
   • Key Finding: Nasal mupirocin reduces recurrent skin infections in MRSA carriers (60-70% eradication at 3 months)

Evidence Gaps and Ongoing Research

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13. Patient and Layperson Explanation

What is Impetigo?

Impetigo is a common skin infection in children caused by bacteria. It appears as sores or blisters that burst and leave behind golden-yellow crusts. These crusts look a bit like dried honey – that's the classic sign of impetigo.

It usually starts around the mouth and nose, but can spread to other parts of the body. It's very common in young children, especially those aged 2-5 years.

Is it Serious?

No, impetigo is not usually serious. It's a surface infection that affects only the top layer of skin. With the right treatment, it clears up quickly (usually within a week) and doesn't leave scars.

However, it's very contagious (easy to spread), so it's important to treat it and take steps to stop it spreading to others.

How Did My Child Get It?

Impetigo is caused by bacteria (usually Staphylococcus or Streptococcus) that get into the skin through:

• Small cuts or scratches
• Insect bites
• Eczema (broken skin from eczema is a common entry point)
• Direct contact with someone who has impetigo

The bacteria can also live in the nose, and your child might spread them to their face by touching their nose and then their skin.

How Does it Spread?

Impetigo spreads very easily through:

• Direct skin contact (touching someone with impetigo)
• Sharing towels, flannels, or clothes
• Touching toys or surfaces that have the bacteria on them

That's why children with impetigo need to stay off school until the infection is treated.

How is it Treated?

Treatment depends on how bad the infection is:

Small patches (1-2 sores):

• Antibiotic cream or ointment (e.g., fusidic acid or mupirocin)
• Apply 3 times a day for 5-7 days
• Gently wash off crusts with warm water before applying the cream

Larger patches or many sores:

• Antibiotic medicine (liquid or tablets) by mouth
• Usually given 4 times a day for 5-7 days
• Important to complete the whole course even if it looks better

Hygiene is important too:

• Wash hands regularly, especially after touching the sores
• Use separate towels
• Wash bedding and towels in hot water

When Can My Child Return to School?

Your child can return to school or nursery:

• 48 hours after starting antibiotic treatment, OR
• Once the sores have crusted over and dried

This helps prevent spreading the infection to other children.

Will it Leave Scars?

No, ordinary impetigo does not leave scars. The infection only affects the surface of the skin.

You might notice some darkening of the skin where the sores were – this is temporary and fades over a few months.

What if it Keeps Coming Back?

Some children get impetigo more than once. This is often because:

• The bacteria live in the nose and keep re-infecting the skin
• Your child has eczema, which makes skin more prone to infection
• Someone else in the family carries the bacteria and keeps passing it on

If your child gets impetigo 3 or more times, tell your doctor. They might:

• Test for bacteria in the nose
• Recommend a special nasal cream to clear the bacteria
• Suggest treating family members

When Should I Worry?

See your doctor urgently if your child has:

• High fever (temperature above 38.5°C)
• Red streaks spreading from the sores
• Severe swelling or pain
• Looks very unwell or won't eat/drink
• Dark urine or swelling 1-3 weeks after the infection (rare kidney complication)

Most children with impetigo are otherwise well and don't have these problems.

Summary for Parents

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14. Examination Focus

MRCPCH Clinical Examination Scenarios

Scenario 1: Spot Diagnosis

Examiner: "This 3-year-old boy has developed a rash around his mouth over the past 3 days. Please examine the rash and present your findings."

Examination Approach:

1. Inspect from distance: Distribution (perioral), number of lesions
2. Close inspection: Morphology (golden crusts on erythematous base), size (0.5-2cm)
3. Palpate: Regional lymphadenopathy (submandibular, anterior cervical – often tender)
4. Check for: Systemic features (fever – take temperature), atopic stigmata (eczema, allergic shiners)
5. Complete examination: Check hands for nail biting, other body sites for spread

Expected Findings:

• Multiple 0.5-2cm erythematous macules with thick golden-yellow crusts around mouth and nose
• Surrounding erythema
• Tender submandibular/anterior cervical lymphadenopathy (1-1.5cm, mobile)
• Otherwise well-appearing child, afebrile
• No eczema

Presentation: "This 3-year-old has multiple erythematous lesions with golden-yellow crusting in the perioral region, consistent with non-bullous impetigo. There is tender anterior cervical lymphadenopathy. No systemic features or underlying skin conditions identified."

Scenario 2: Viva Voce - Diagnosis and Management

Examiner: "A 4-year-old presents with the skin lesions shown [photo of honey-crusted lesions]. What is your differential diagnosis?"

Model Answer: "The golden-yellow crusting is highly suggestive of impetigo, but I would consider:

Most likely:

1. Non-bullous impetigo – perioral distribution, honey crusts, age group

Differential diagnoses: 2. Herpes simplex – but typically grouped vesicles, more painful, recurrent same site 3. Impetiginized eczema – but would expect background eczema, pruritus, flexural involvement 4. Tinea faciei – but typically annular with central clearing, scaly edge (not crusted)

Diagnosis: Clinical diagnosis of impetigo based on characteristic appearance. Swab only if treatment failure or MRSA suspected."

Examiner: "How would you manage this child?"

Model Answer: "I would assess extent and severity:

If localized (less than 3 lesions, less than 2cm each):

• Topical fusidic acid 2% TDS for 5-7 days
• Hygiene advice: Hand washing, separate towels, gently remove crusts before applying cream
• School exclusion until crusted or 48h after antibiotics

If extensive (> 3 lesions or large area):

• Oral flucloxacillin: 125mg QDS for 5-7 days (if 2-9 years)
• Same hygiene measures

Safety net: Review if not improving at 7 days; consider swab for MRSA/resistance

Parent education:

• Very contagious – hygiene important
• Excellent prognosis, no scarring
• Watch for dark urine/swelling 1-3 weeks later (rare APSGN)"

Scenario 3: Viva - Complications

Examiner: "A child treated for impetigo 2 weeks ago now has dark urine and facial swelling. What is your diagnosis and management?"

Model Answer: "I am concerned about acute post-streptococcal glomerulonephritis (APSGN), which occurs 10-21 days after streptococcal skin infection.

Diagnosis:

• History: Dark/cola-coloured urine, periorbital/peripheral oedema, reduced urine output
• Examination: BP (likely hypertensive), fluid status (JVP, peripheral oedema, lung crepitations)
• Investigations:
  • "Urinalysis: Haematuria, proteinuria, RBC casts"
  • "Bloods: U&E (may have AKI), C3 (low), anti-DNase B (elevated – more reliable than ASO for skin infections)"
  • Consider throat swab (though skin infection already resolved)

Management:

• Supportive:
  • Fluid restriction (if fluid overload)
  • Salt restriction
  • Diuretics (furosemide) if oedema/hypertension
  • Antihypertensives if severe hypertension
  • Monitor BP, fluid balance, daily weights
• Nephrology referral
• Antibiotics NOT indicated (infection already resolved; antibiotics don't prevent APSGN)
• Admit if AKI, severe hypertension, or pulmonary oedema
• Dialysis if severe AKI (rare)

Prognosis: Excellent in children – > 95% full recovery. C3 normalizes in 6-8 weeks."

Scenario 4: Viva - Recurrent Impetigo

Examiner: "A 5-year-old has had 4 episodes of impetigo in the past year. What would you do?"

Model Answer: "Recurrent impetigo (≥3 episodes in 12 months) requires investigation:

Immediate:

1. Swab active lesion (if present): Culture and sensitivities, check for MRSA
2. Nasal swab: Check for S. aureus carriage (present in 30-40% of recurrent cases)
3. Screen close contacts: Family members for nasal carriage if household transmission

Assess predisposing factors:

• Atopic eczema (major risk factor – 3-4× increased risk)
• Hygiene: Shared towels, bathing frequency, overcrowding
• Immunocompromise (if ≥4 episodes + other recurrent infections):
  • FBC, immunoglobulins (IgG, IgA, IgM)
  • Consider HIV test if risk factors

Decolonization (if nasal S. aureus carriage confirmed):

• Mupirocin 2% nasal ointment BD for 5 days
• Chlorhexidine 4% body wash daily for 5 days
• Treat household contacts if carriers
• Repeat swabs post-treatment

Preventive measures:

• Optimize eczema control (if present): Emollients, topical steroids
• Hygiene education: Hand washing, separate towels, prompt treatment of minor skin trauma
• Keep nails short

Follow-up: Review at 3 months to assess recurrence rate."

High-Yield Viva Questions and Model Answers

Q1: What is the mechanism of blister formation in bullous impetigo?

A: "Bullous impetigo is caused by Staphylococcus aureus strains (phage group II, types 55 and 71) that produce exfoliative toxins A and B (ETA and ETB). These are serine proteases that specifically cleave desmoglein-1, a desmosomal cadherin responsible for keratinocyte adhesion in the superficial epidermis. Cleavage of desmoglein-1 causes loss of cell-cell adhesion, resulting in intraepidermal blister formation at the level of the granular layer (subcorneal). This is the same molecular target as in pemphigus foliaceus (autoantibodies against desmoglein-1) and the mechanism underlying Staphylococcal Scalded Skin Syndrome (SSSS), which is essentially a generalized version of bullous impetigo when the toxin disseminates systemically."

Q2: Why doesn't bullous impetigo affect mucous membranes?

A: "Bullous impetigo spares mucous membranes due to the desmoglein compensation theory. Exfoliative toxins cleave only desmoglein-1 (not desmoglein-3). In the skin, the upper epidermis expresses predominantly desmoglein-1, so cleavage causes loss of adhesion and blistering. However, in mucous membranes, desmoglein-3 is expressed at all epithelial levels. Even when desmoglein-1 is cleaved, desmoglein-3 maintains keratinocyte adhesion, preventing mucosal blistering. This contrasts with pemphigus vulgaris, where autoantibodies target desmoglein-3, resulting in mucosal involvement."

Q3: Can antibiotics prevent post-streptococcal glomerulonephritis?

A: "No. Antibiotic treatment of impetigo does NOT prevent acute post-streptococcal glomerulonephritis (APSGN). APSGN is an immune-mediated complication caused by deposition of immune complexes (streptococcal antigen-antibody complexes) in the glomeruli. The immune response begins during the active infection, and by the time APSGN manifests (10-21 days post-infection), immune complex formation has already occurred. Antibiotics treat the active infection and reduce transmission to others, but they do not alter the host immune response or prevent immune complex deposition. This contrasts with acute rheumatic fever following pharyngitis, where prompt antibiotic treatment (within 9 days of symptom onset) can prevent the complication."

Q4: What is the difference between impetigo and ecthyma?

A:

"Ecthyma can be thought of as untreated or neglected impetigo that extends deeper into the dermis."

Q5: What is the role of nasal decolonization in recurrent impetigo?

A: "Nasal carriage of Staphylococcus aureus is present in 20-40% of the general population and increases the risk of impetigo 2-3 fold through autoinoculation (nose-to-skin transfer). In children with recurrent impetigo (≥3 episodes in 12 months), nasal S. aureus carriage is detected in 30-40% of cases.

Decolonization regimen:

• Mupirocin 2% nasal ointment applied to anterior nares BD for 5 days
• Chlorhexidine 4% body wash daily for 5 days
• Treat household contacts if recurrent transmission

Efficacy: Eradication rates of 60-70% at 3 months, though recolonization is common.

Indication: Reserve for children with ≥3 episodes per year where nasal carriage confirmed. Not for routine use after single episode."

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15. References

Primary Evidence-Based Sources

1. Cole C, Gazewood J. Diagnosis and treatment of impetigo. Am Fam Physician. 2007;75(6):859-864. PMID: 17390597.

2. Bowen AC, Mahé A, Hay RJ, et al. The global epidemiology of impetigo: a systematic review of the population prevalence of impetigo and pyoderma. PLoS One. 2015;10(8):e0136789. DOI: 10.1371/journal.pone.0136789. PMID: 26317533.

3. Hartman-Adams H, Banvard C, Juckett G. Impetigo: diagnosis and treatment. Am Fam Physician. 2014;90(4):229-235. PMID: 25250996.

4. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10-e52. DOI: 10.1093/cid/ciu296. PMID: 24973422.

5. Ladhani S, Joannou CL, Lochrie DP, et al. Clinical, microbial, and biochemical aspects of the exfoliative toxins causing staphylococcal scalded-skin syndrome. Clin Microbiol Rev. 1999;12(2):224-242. DOI: 10.1128/CMR.12.2.224. PMID: 10194457.

6. Hay RJ, Johns NE, Williams HC, et al. The global burden of skin disease in 2010: an analysis of the prevalence and impact of skin conditions. J Invest Dermatol. 2014;134(6):1527-1534. DOI: 10.1038/jid.2013.446. PMID: 24166134.

7. Public Health England. Guidance on Infection Control in Schools and other Childcare Settings. 2023. Available at: https://www.gov.uk/government/publications/health-protection-in-schools-and-other-childcare-facilities

8. National Institute for Health and Care Excellence. Impetigo: Antimicrobial Prescribing. NICE Clinical Knowledge Summaries. 2023. Available at: https://cks.nice.org.uk/topics/impetigo/

9. Koning S, van der Sande R, Verhagen AP, et al. Interventions for impetigo. Cochrane Database Syst Rev. 2012;1:CD003261. DOI: 10.1002/14651858.CD003261.pub3. PMID: 22258953.

10. Rodriguez-Iturbe B, Musser JM. The current state of poststreptococcal glomerulonephritis. J Am Soc Nephrol. 2008;19(10):1855-1864. DOI: 10.1681/ASN.2008010092. PMID: 18667731.

11. Ladhani S. Understanding the mechanism of action of the exfoliative toxins of Staphylococcus aureus. FEMS Immunol Med Microbiol. 2003;39(2):181-189. DOI: 10.1016/S0928-8244(03)00225-6. PMID: 14625103.

12. Bowen AC, Tong SYC, Chatfield MD, Carapetis JR. The microbiology of impetigo in indigenous children: associations between Streptococcus pyogenes, Staphylococcus aureus, scabies, and nasal carriage. BMC Infect Dis. 2014;14:727. DOI: 10.1186/s12879-014-0727-5. PMID: 25551178.

13. Sladden MJ, Johnston GA. Common skin infections in children. BMJ. 2004;329(7457):95-99. DOI: 10.1136/bmj.329.7457.95. PMID: 15242917.

14. Fritz SA, Hogan PG, Hayek G, et al. Household versus individual approaches to eradication of community-associated Staphylococcus aureus in children: a randomized trial. Clin Infect Dis. 2012;54(6):743-751. DOI: 10.1093/cid/cir919. PMID: 22198793.

15. David MZ, Daum RS. Community-associated methicillin-resistant Staphylococcus aureus: epidemiology and clinical consequences of an emerging epidemic. Clin Microbiol Rev. 2010;23(3):616-687. DOI: 10.1128/CMR.00081-09. PMID: 20610826.

16. Amagai M, Matsuyoshi N, Wang ZH, et al. Toxin in bullous impetigo and staphylococcal scalded-skin syndrome targets desmoglein 1. Nat Med. 2000;6(11):1275-1277. DOI: 10.1038/81385. PMID: 11062541.

17. Telfer NR, Chalmers RJ, Whale K, Colman G. The role of streptococcal infection in the initiation of guttate psoriasis. Arch Dermatol. 1992;128(1):39-42. PMID: 1739285.

18. George A, Rubin G. A systematic review and meta-analysis of treatments for impetigo. Br J Gen Pract. 2003;53(491):480-487. PMID: 12939896.

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Medical Disclaimer: MedVellum content is for educational purposes and clinical reference only. All clinical decisions should be individualized based on patient circumstances, local guidelines, and specialist consultation where appropriate. This content does not replace clinical judgment or formal medical training.