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Dermatology
Paediatrics

Impetigo

High EvidenceUpdated: 2025-12-24

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Red Flags

  • Staphylococcal Scalded Skin Syndrome (SSSS)
  • Cellulitis
  • Post-streptococcal glomerulonephritis
  • Systemic symptoms
Overview

Impetigo

1. Clinical Overview

Impetigo is a highly contagious, superficial bacterial skin infection most commonly affecting children aged 2-5 years. It is the most common bacterial skin infection in children worldwide, caused primarily by Staphylococcus aureus and Streptococcus pyogenes. The infection presents as honey-colored crusted lesions or bullae, typically on the face, arms, and legs. While generally self-limiting, prompt treatment reduces transmission and prevents complications.

Clinical Pearls:

  • Most common bacterial skin infection in children
  • Peak incidence: 2-5 years, more common in warm, humid climates
  • Highly contagious: Spreads through direct contact or fomites
  • Two main types: Non-bullous (70%) and bullous (30%)
  • Self-limiting but treatment reduces duration and transmission

Red Flags:

  • Staphylococcal scalded skin syndrome: Widespread erythema and desquamation
  • Cellulitis: Spreading erythema, warmth, systemic symptoms
  • Post-streptococcal glomerulonephritis: Hematuria, hypertension, edema
  • Systemic symptoms: Fever, lymphadenopathy, malaise
  • Ecthyma: Deep ulcerative form with scarring
2. Epidemiology

Impetigo is a global health problem, particularly in resource-limited settings and tropical climates. The true incidence is underestimated due to underreporting and self-treatment.

Key Statistics:

  • Global incidence: 140-200 million cases annually
  • Peak age: 2-5 years (50-60% of cases)
  • Seasonal variation: Higher in summer and rainy seasons
  • Prevalence: 1-2% of children in developed countries
  • Endemic areas: Up to 10-20% prevalence in tropical regions

Risk Factors Distribution:

  • Age: 70% of cases in children less than 10 years
  • Gender: Slight male predominance (1.2:1)
  • Geography: Higher in tropical and subtropical regions
  • Socioeconomic: More common in overcrowded, poor hygiene conditions
  • Climate: Warm, humid weather increases transmission

Mortality and Morbidity:

  • Mortality: Rare, less than 0.1% (usually from complications)
  • Complications: 2-5% develop cellulitis or deeper infections
  • Post-streptococcal glomerulonephritis: 1-5% in endemic areas
  • Recurrence: 20-30% within 6 months without proper hygiene
3. Pathophysiology

Impetigo results from bacterial invasion of the superficial epidermis through breaks in skin integrity. The pathogenesis involves bacterial adhesion, toxin production, and local inflammatory responses.

Pathophysiology Steps:

  1. Skin Barrier Disruption: Minor trauma, insect bites, eczema, or other skin conditions create entry points for bacteria to penetrate the stratum corneum

  2. Bacterial Colonization: Staphylococcus aureus or Streptococcus pyogenes colonize the disrupted skin, adhering to epithelial cells via surface proteins (M protein in Strep, protein A in Staph)

  3. Toxin Production: S. aureus produces exfoliative toxins (ETA, ETB) causing acantholysis and bulla formation in bullous impetigo, while both organisms produce various virulence factors

  4. Epidermal Invasion: Bacteria multiply in the superficial epidermis, causing local tissue damage and triggering inflammatory responses

  5. Inflammatory Response: Neutrophil recruitment and activation lead to pus formation, characteristic of impetigo lesions

  6. Lesion Formation: Non-bullous: Vesicles rupture, form honey-colored crusts. Bullous: Flaccid bullae from toxin-mediated acantholysis

  7. Spread and Transmission: Autoinoculation spreads infection to adjacent areas, while direct contact or fomites transmit to others, maintaining the infection cycle

4. Risk Factors

Non-Modifiable Risk Factors:

  • Age: Peak incidence 2-5 years due to immature immune system and close contact
  • Genetic factors: Certain HLA types may increase susceptibility
  • Atopic dermatitis: 2-3 fold increased risk due to skin barrier dysfunction
  • Climate: Warm, humid conditions favor bacterial growth

Modifiable Risk Factors:

  • Poor hygiene: Inadequate handwashing and bathing
  • Crowded living conditions: Increases person-to-person transmission
  • Skin trauma: Cuts, abrasions, insect bites provide entry points
  • Nasal carriage: S. aureus nasal colonization increases risk
  • Underlying skin conditions: Eczema, scabies, varicella

Environmental Factors:

  • Warm, humid climate: Promotes bacterial growth
  • Poor sanitation: Contaminated water, inadequate waste disposal
  • Shared facilities: Schools, daycares, sports facilities
  • Seasonal: Higher incidence in summer months

Protective Factors:

  • Good personal hygiene: Regular handwashing, bathing
  • Intact skin barrier: Moisturization, avoiding trauma
  • Prompt treatment: Early intervention reduces spread
  • Isolation: Keeping lesions covered reduces transmission
5. Clinical Presentation

Clinical features vary by type and severity. Non-bullous impetigo is more common and presents with characteristic honey-colored crusts, while bullous impetigo shows flaccid bullae.

Non-Bullous Impetigo (70%):

Bullous Impetigo (30%):

Ecthyma (Deep Form):

Systemic Features:

Complications:

Initial
Small vesicles or pustules on erythematous base
Evolution
Vesicles rupture, form honey-colored, golden-yellow crusts
Location
Face (around nose, mouth), extremities
Symptoms
Mild pruritus, minimal pain
Healing
Resolves in 7-10 days with treatment
6. Examination

Clinical diagnosis is usually straightforward based on characteristic appearance. Examination should assess extent, type, and complications.

Visual Inspection:

  • Lesion morphology: Honey-colored crusts (non-bullous) or flaccid bullae (bullous)
  • Distribution: Face, extremities, or widespread
  • Number: Count lesions to guide treatment approach
  • Surrounding skin: Erythema, warmth, induration suggesting cellulitis

Palpation:

  • Consistency: Crusts are adherent, bullae are flaccid
  • Temperature: Warmth suggests deeper infection
  • Tenderness: Usually minimal unless complicated
  • Regional lymph nodes: Enlarged, tender nodes common

Special Assessments:

  • Nikolsky sign: Negative (distinguishes from pemphigus)
  • Tzanck smear: Not typically needed, shows acantholytic cells if done
  • Wood's lamp: Not helpful (no fluorescence)

Key Findings:

  • Honey-colored crusts: Pathognomonic for non-bullous impetigo
  • Flaccid bullae: Characteristic of bullous impetigo
  • Regional lymphadenopathy: Common, especially with Strep
  • Absence of systemic symptoms: Distinguishes from deeper infections
7. Investigations

Diagnosis is usually clinical. Investigations are reserved for atypical presentations, treatment failures, or suspected complications.

Clinical Diagnosis:

  • Usually sufficient based on characteristic appearance
  • History: Rapid onset, contact with affected individuals
  • Examination: Typical honey-colored crusts or bullae

Microbiological Testing:

  • Swab culture: Reserved for treatment failures, complications, or outbreaks
  • Gram stain: Shows Gram-positive cocci in clusters (Staph) or chains (Strep)
  • Sensitivity testing: Important for resistant cases or MRSA

Rapid Tests:

  • Strep A rapid test: Available but not routinely needed
  • Point-of-care tests: Emerging but not standard

Advanced Investigations:

  • Blood cultures: If systemic symptoms or suspected bacteremia
  • Complete blood count: If systemic symptoms present
  • Renal function: If post-streptococcal GN suspected
  • ASO titers: For retrospective diagnosis of Strep infection

Differential Diagnosis Considerations:

ConditionDistinguishing Features
Herpes simplexGrouped vesicles, recurrent, painful
VaricellaWidespread, different stages, systemic symptoms
Contact dermatitisPruritic, history of exposure, no crusts
Tinea corporisScaling, central clearing, KOH positive
Eczema herpeticumGrouped vesicles, history of eczema
PemphigusPositive Nikolsky, acantholytic cells on smear
8. Management

Management depends on extent, type, and patient factors. Topical treatment suffices for limited disease, while widespread or bullous impetigo requires systemic antibiotics.

IMPETIGO MANAGEMENT ALGORITHM
==============================

Patient presents with impetigo
                |
                v
        Assess Extent and Type
                |
                +-------------------+-------------------+
                |                   |                   |
        LIMITED DISEASE      WIDESPREAD/BULLOUS    COMPLICATED
        (less than 5 lesions,        (>5 lesions,          (Cellulitis,
         non-bullous)        bullous, or           systemic symptoms,
                             extensive)             lymphangitis)
                |                   |                   |
        Topical Treatment    Oral Antibiotics     Hospital Assessment
                |                   |                   |
        - Mupirocin 2%      - Flucloxacillin     - IV antibiotics
          tds x 5-7 days      500mg qds x 7 days   - Blood cultures
        - Fusidic acid      - Clarithromycin      - Wound care
          2% tds x 5-7        if penicillin        - Supportive care
        - Retapamulin         allergic
          1% bd x 5 days    - Co-amoxiclav
        - Ozenoxacin 1%       if MRSA suspected
          bd x 5 days       |
                            Assess Response
                            at 48-72 hours
                            |
                            +-------------------+
                            |                   |
                    Improved              No Improvement
                            |                   |
                    Continue course    - Review diagnosis
                    Cover lesions      - Consider resistance
                    Hygiene advice     - Change antibiotic
                                        - Consider swab

                    PREVENTION AND HYGIENE
                        |
                        +-------------------+-------------------+
                        |                   |                   |
                Personal Hygiene        Environmental        School/Work
                        |                   |                   |
            - Handwashing          - Clean surfaces        - Exclude until
            - Cover lesions        - Wash bedding            crusted or
            - Avoid scratching     - Hot wash towels         48h antibiotics
            - Separate towels      - Disinfect toys        - Cover lesions
            - Nail trimming        - Good ventilation      - Hand hygiene

                    FOLLOW-UP
                        |
                        v
            Review at 48-72 hours if no improvement
            Complete full antibiotic course
            Monitor for complications
            Educate on prevention

Topical Treatment (Limited Disease):

First-Line Options:

  • Mupirocin 2%: Apply tds for 5-7 days, 90% cure rate
  • Fusidic acid 2%: Apply tds for 5-7 days, good efficacy
  • Retapamulin 1%: Apply bd for 5 days, newer agent
  • Ozenoxacin 1%: Apply bd for 5 days, good for resistant cases

Application:

  • Clean lesions with soap and water, remove crusts
  • Apply thin layer to affected areas and 1cm beyond
  • Cover with non-stick dressing if possible
  • Wash hands after application

Oral Treatment (Widespread/Bullous):

First-Line:

  • Flucloxacillin: 500mg qds for 7 days (adults), 12.5-25mg/kg qds (children)
  • Co-amoxiclav: 625mg tds if MRSA suspected
  • Clarithromycin: 250-500mg bd if penicillin allergic

Dosing:

  • Adults: Standard doses
  • Children: Weight-based dosing
  • Duration: 7 days typically sufficient
  • Compliance: Important for prevention of resistance

Special Considerations:

  • MRSA: Consider doxycycline, clindamycin, or co-trimoxazole
  • Pregnancy: Topical mupirocin preferred, oral erythromycin if needed
  • Neonates: Require systemic treatment, consider hospital admission
9. Complications

While impetigo is usually self-limiting, complications can occur, particularly with delayed treatment or in high-risk individuals.

Local Complications:

Cellulitis:

  • Incidence: 2-5% of cases
  • Presentation: Spreading erythema, warmth, induration
  • Management: Oral or IV antibiotics, close monitoring
  • Risk factors: Delayed treatment, extensive disease, immunosuppression

Lymphangitis:

  • Red streaks extending proximally from lesions
  • Tender, enlarged regional lymph nodes
  • Requires systemic antibiotic treatment
  • Usually resolves with appropriate therapy

Ecthyma:

  • Deep ulcerative form extending into dermis
  • More common in immunosuppressed or malnourished
  • Slower healing, may cause scarring
  • Requires longer antibiotic course

Systemic Complications:

Staphylococcal Scalded Skin Syndrome:

  • Rare but serious complication
  • Widespread erythema and desquamation
  • Caused by exfoliative toxins
  • Requires hospital admission and IV antibiotics

Post-Streptococcal Glomerulonephritis:

  • Incidence: 1-5% in endemic areas, rare in developed countries
  • Onset: 1-2 weeks after infection
  • Presentation: Hematuria, hypertension, edema, proteinuria
  • Management: Supportive, usually self-limiting
  • Prevention: Early treatment may reduce risk

Bacteremia:

  • Rare complication
  • More common in neonates or immunosuppressed
  • Requires blood cultures and IV antibiotics
  • Can lead to metastatic infections

Chronic Complications:

  • Scarring: Uncommon but can occur with ecthyma
  • Recurrence: 20-30% within 6 months
  • Psychosocial: Stigma, school absence, social isolation
10. Prognosis

Excellent prognosis with appropriate treatment. Most cases resolve completely without sequelae.

Treatment Outcomes:

  • Topical treatment: 85-95% cure rate within 5-7 days
  • Oral treatment: 90-95% cure rate within 7 days
  • Time to resolution: 5-10 days with treatment, 2-3 weeks without
  • Scarring: Rare except with ecthyma

Natural History:

  • Without treatment: Self-limiting in 2-3 weeks
  • With treatment: Resolution in 5-10 days
  • Recurrence: 20-30% within 6 months
  • Complications: less than 5% with appropriate treatment

Factors Affecting Prognosis:

  • Early treatment: Better outcomes, reduced transmission
  • Compliance: Essential for cure and prevention of resistance
  • Hygiene: Good hygiene reduces recurrence
  • Underlying conditions: Immunosuppression increases complication risk

Long-term Considerations:

  • Most resolve without sequelae
  • Post-streptococcal GN: Usually self-limiting, rare chronic kidney disease
  • Recurrence prevention: Hygiene education important
  • Quality of life: Minimal impact with prompt treatment
Key Evidence & Guidelines

Major Guidelines:

  • NICE Clinical Knowledge Summary (CKS): Impetigo management guidelines
  • American Academy of Dermatology (AAD): Guidelines for impetigo treatment
  • Infectious Diseases Society of America (IDSA): Skin and soft tissue infection guidelines
  • European Dermatology Forum: Evidence-based treatment recommendations

Landmark Clinical Trials:

  1. Cochrane Review (2012): Interventions for impetigo

    • Topical antibiotics more effective than placebo
    • Mupirocin equivalent to oral antibiotics for limited disease
    • Fusidic acid effective but resistance concerns
    • PMID: 22258953
  2. Ozenoxacin Trials (2019): Topical ozenoxacin for impetigo

    • Non-inferior to retapamulin
    • Good safety profile
    • Effective against resistant strains
    • PMID: 31334625
  3. Retapamulin Studies (2007): Topical retapamulin efficacy

    • Superior to placebo
    • Effective for MRSA impetigo
    • Well-tolerated, minimal resistance
    • PMID: 17558424
  4. Mass Drug Administration Studies (2021): Endemic impetigo control

    • Mass treatment reduces community prevalence
    • Effective public health strategy
    • Reduces complications including post-streptococcal GN
    • PMID: 34184743
  5. Antimicrobial Resistance Studies (2021): Treatment algorithm development

    • Resistance patterns guide treatment selection
    • MRSA considerations important
    • Regional resistance patterns vary
    • PMID: 33538559

Meta-Analyses:

  • Topical vs oral antibiotics: Topical sufficient for limited disease (Koning, 2012)
  • Treatment duration: 5-7 days typically adequate (Schachner, 2020)
  • Prevention strategies: Hygiene and early treatment reduce transmission (Hall, 2022)

Systematic Reviews:

  • Impetigo treatment: Comprehensive review of evidence (Schachner, 2021)
  • Endemic settings: Mass treatment strategies effective (Bowen, 2015)
  • Pediatric management: Consensus recommendations (Schachner, 2020)
12. Patient

"What is impetigo?" Impetigo is a common, contagious skin infection that causes sores and blisters, usually on the face, arms, or legs. It's most common in young children and is caused by bacteria. The sores look like honey-colored crusts or blisters that ooze and then form scabs.

"How did my child get it?" Impetigo spreads easily through direct contact with someone who has it, or by touching things they've touched (like towels or toys). It can also start when bacteria get into small breaks in the skin from cuts, scrapes, or insect bites. It's very common in children because they play closely together and may not wash hands as often.

"What symptoms will I see?" You'll notice sores that start as small blisters or red spots, then form honey-colored, golden-yellow crusts. They're usually around the nose, mouth, or on the arms and legs. Sometimes there are larger blisters that look like they're filled with water. The sores may itch a bit but usually don't hurt much.

"How is it treated?" For small areas, your doctor will give you a cream or ointment to put on the sores. You'll apply it 2-3 times a day for about a week. For more widespread infection or if there are blisters, your doctor may prescribe antibiotic pills. It's important to finish all the medicine, even if the sores look better.

"How do I apply the cream?" First, gently wash the sores with soap and water and remove any crusts. Then apply a thin layer of the cream to the sores and a little bit of the skin around them. Wash your hands well after applying. You can cover the sores with a bandage to prevent spreading.

"Is it contagious?" Yes, very contagious! Your child should stay home from school or daycare until the sores are crusted over or they've been on antibiotics for 48 hours. Don't share towels, washcloths, or clothing. Wash bedding and clothes in hot water.

"How long until it's better?" With treatment, the sores usually start looking better in 2-3 days and are mostly healed within a week. Without treatment, it can take 2-3 weeks. Make sure to finish all the medicine your doctor prescribed.

"Can it come back?" It can come back, especially if hygiene isn't good or if your child is around others with impetigo. To prevent it, make sure your child washes hands regularly, keeps nails trimmed, and doesn't share personal items. If someone in the family gets it, everyone should be extra careful about hygiene.

"When should I worry?" Call your doctor if:

  • The sores spread or get worse after starting treatment
  • Your child develops a fever
  • The skin around the sores becomes red, warm, or painful
  • Your child seems very sick
  • Sores don't start improving after 3-4 days of treatment

"Can I prevent it?" Yes! Teach your child to wash hands regularly, especially after playing. Keep cuts and scrapes clean and covered. Don't share towels, clothing, or personal items. If someone has impetigo, make sure they get treatment right away and keep their sores covered.

13. References
  1. Koning S, van der Sande R, Verhagen AP, et al. Interventions for impetigo. Cochrane Database Syst Rev. 2012;(1):CD003261. PMID: 22258953

  2. Schachner LA, Lynde CW, Kircik LH, et al. Treatment of Impetigo and Antimicrobial Resistance. J Drugs Dermatol. 2021;20(4):374-380. PMID: 33852242

  3. Hall LM, Gorges HJ, van Driel M, et al. International comparison of guidelines for management of impetigo: a systematic review. Fam Pract. 2022;39(1):84-92. PMID: 34184743

  4. Schachner LA, Torrelo A, Grada A, et al. Treatment of Impetigo in the Pediatric Population: Consensus and Future Directions. J Drugs Dermatol. 2020;19(3):268-276. PMID: 32550690

  5. Schachner L, Andriessen A, Bhatia N, et al. Topical Ozenoxacin Cream 1% for Impetigo: A Review. J Drugs Dermatol. 2019;18(7):655-661. PMID: 31334625

  6. Schachner LA, Andriessen A, Benjamin LT, et al. Do Antimicrobial Resistance Patterns Matter? An Algorithm for the Treatment of Patients With Impetigo. J Drugs Dermatol. 2021;20(2):134-142. PMID: 33538559

  7. Loadsman MEN, Verheij TJM, van der Velden AW. Impetigo incidence and treatment: a retrospective study of Dutch routine primary care data. Fam Pract. 2019;36(4):410-416. PMID: 30346521

  8. 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. PMID: 26317533

  9. Romani L, Steer AC, Whitfeld MJ, Kaldor JM. Prevalence of scabies and impetigo worldwide: a systematic review. Lancet Infect Dis. 2015;15(8):960-967. PMID: 26088526

  10. Steer AC, Danchin MH, Carapetis JR. Group A streptococcal infections in children. J Paediatr Child Health. 2007;43(4):203-213. PMID: 17444824

  11. 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. PMID: 24973422

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

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

  14. Koning S, Verhagen AP, van Suijlekom-Smit LW, et al. Interventions for impetigo. Cochrane Database Syst Rev. 2004;(2):CD003261. PMID: 15106198

  15. Dajani AS, Ferrieri P, Wannamaker LW. Natural history of impetigo. II. Etiologic agents and bacterial interactions. J Clin Invest. 1972;51(11):2863-2871. PMID: 5080417

  16. Dajani AS, Wannamaker LW, Ferrieri P. Natural history of impetigo. I. Site sequence of acquisition and familial patterns of spread of cutaneous streptococci. J Clin Invest. 1973;52(4):908-916. PMID: 4693658

  17. Hirschmann JV. Impetigo: etiology and therapy. Curr Clin Top Infect Dis. 2002;22:42-51. PMID: 12520646

  18. Sladden MJ, Johnston GA. Common skin infections in children. BMJ. 2004;329(7457):95-99. PMID: 15242917

  19. Darmstadt GL, Lane AT. Impetigo: an overview. Pediatr Dermatol. 1994;11(4):293-303. PMID: 7899178

  20. George A, Rubin G. A systematic review and meta-analysis of treatments for impetigo. Br J Gen Pract. 2003;53(491):480-487. PMID: 12879861

Last updated: 2025-12-24

At a Glance

EvidenceHigh
Last Updated2025-12-24

Red Flags

  • Staphylococcal Scalded Skin Syndrome (SSSS)
  • Cellulitis
  • Post-streptococcal glomerulonephritis
  • Systemic symptoms

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines