Impetigo !
A common, contagious superficial skin infection of children that forms golden honey-coloured crusts, usually around the nose and mouth.
Updated 2026-11-01
Structures involved
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Microorganisms that cause it
In the clinical exam
Why it happens
- Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcer
- Cell junctions: tight, adherens, desmosomes, gap, hemidesmosomes
- Skin: epidermis layers, dermis, hypodermis
- Glomerulus and the filtration barrier: podocytes, mesangium, JGA
What it is
A superficial bacterial infection of the epidermis caused by Staphylococcus aureus, Streptococcus pyogenes (group A streptococcus) or both. It is the most common bacterial skin infection in children.
Who gets it
Most frequent in children aged 2–5 years, in hot and humid climates and in crowded living conditions, with peaks in warm seasons. In tropical areas of Colombia and Latin America it is common and often follows insect bites or scabies.
Causes
- Staphylococcus aureus, now the leading cause, including methicillin-resistant strains
- Streptococcus pyogenes alone or with S. aureus
- Entry through small breaks in the skin: insect bites, scratches, scabies, eczema, varicella
Risk factors
- Young age and attending nursery or school
- Hot, humid weather and poor access to water and hygiene
- Overcrowding and close-contact sports
- Pre-existing skin disease (atopic dermatitis, scabies)
- Nasal carriage of S. aureus
Pathophysiology
Bacteria colonise the skin or nose and invade minor breaks in the stratum corneum. In non-bullous impetigo, inflammation forms fragile vesicles and pustules that rupture and dry to honey-coloured crusts. In bullous impetigo, S. aureus exfoliative toxins cleave desmoglein 1 in the granular layer, producing flaccid blisters. Some nephritogenic group A strains trigger immune-complex glomerulonephritis weeks later.
Classification
- Non-bullous impetigo (about 70% of cases)
- Bullous impetigo (S. aureus exfoliative toxin)
- Ecthyma: deeper ulcerative form extending into the dermis
Symptoms and signs
- Red macules or vesicles that rupture and form golden honey-coloured crusts
- Lesions around the nose and mouth and on the limbs
- Mild itch or soreness; usually no fever
- Flaccid clear or cloudy blisters that leave a thin collarette of scale (bullous form)
- Regional lymph node enlargement, more often in the non-bullous form
Diagnosis
- Clinical
- Clinical, from the typical honey-coloured crusts or flaccid blisters in a child.
- Tests
- Gram stain and culture of exudate when lesions are extensive, recurrent, not responding to treatment, or when MRSA or an outbreak is suspected. Urinalysis and blood pressure if nephritis is suspected; complement C3 is low in post-streptococcal glomerulonephritis.
- Imaging
- Not needed.
Differential diagnosis
- Herpes simplex infection (grouped vesicles on a red base)
- Atopic or contact dermatitis with secondary crusting
- Tinea corporis
- Varicella
- Bullous pemphigoid or other blistering disease (bullous form)
Goal of treatment
Clear the infection, relieve symptoms, stop spread to others, and detect complications such as cellulitis or nephritis early.
Treatment
- Medical
- Limited lesions: topical antibiotic such as mupirocin, retapamulin or fusidic acid, after gently removing crusts with soap and water.
- Medical
- Extensive lesions, bullous impetigo, ecthyma or outbreaks: oral antibiotics active against S. aureus and streptococci (e.g. first-generation cephalosporins or penicillinase-resistant penicillins); clindamycin or trimethoprim-sulfamethoxazole when MRSA is suspected.
- Conservative
- Hygiene: handwashing, short fingernails, covering lesions, not sharing towels; children usually return to school 24 hours after starting antibiotics.
- Follow-up
- Follow-up for spread, recurrence (consider nasal carriage) and signs of nephritis such as dark urine or swelling.
Complications
- Cellulitis, lymphangitis and abscess
- Post-streptococcal glomerulonephritis (antibiotics do not prevent it)
- Staphylococcal scalded skin syndrome
- Scarlet fever, sepsis or osteomyelitis (rare)
- Scarring and pigment change after ecthyma
Prognosis
Usually resolves without scarring in 2–3 weeks untreated and faster with treatment. Post-streptococcal glomerulonephritis in children generally recovers fully.
Prevention
- Handwashing and good skin hygiene, especially in nurseries and schools
- Prompt care of cuts, bites and itchy skin disease
- Not sharing towels, clothing or razors
Test yourself
Think of the answer, then tap the question to see it.
What is the classic lesion of non-bullous impetigo?
Golden honey-coloured crusts, typically around the nose and mouth.
Which toxin causes bullous impetigo and what does it target?
Staphylococcus aureus exfoliative toxin, which cleaves desmoglein 1 in the superficial epidermis.
Which non-suppurative complication follows streptococcal impetigo, and which one classically does not?
Post-streptococcal glomerulonephritis; rheumatic fever classically follows pharyngitis, not skin infection.
What is the first-line treatment for limited impetigo?
A topical antibiotic such as mupirocin or retapamulin; oral antibiotics for extensive disease.
When can a child with impetigo usually return to school?
About 24 hours after starting antibiotic treatment, with lesions covered.
Related conditions
- Streptococcal pharyngitis
- Scabies
- Contact dermatitis (irritant and allergic)
- Cellulitis of the leg
- Acute kidney injury
- Sepsis and septic shock
Educational information, not medical advice. For any symptom, see a health professional.
Sources: Clinical Guidance for Group A Streptococcal Impetigo (Centers for Disease Control and Prevention (CDC), 2024); Impetigo (MedlinePlus (U.S. National Library of Medicine), 2024).
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Representative model, for educational purposes only.
