Impetigo

Meet the patient

A four-year-old is brought in with golden, stuck-on crusts around his nose and mouth that have spread over four days, after a runny nose. He is afebrile, mildly itchy, and otherwise well. His mother wants "the right cream."[1]

The two questions that decide his treatment are the two that decide every impetigo: how extensive is it? (a few lesions get topical; widespread, bullous, or systemic disease gets oral) and was it group A strep? (because one to three weeks later the kidney can pay the price). Hold those two and the rest is detail.[1]

What impetigo is — and the three faces plus the cousin

Impetigo is a highly contagious, superficial bacterial skin infection confined to the epidermis — the commonest bacterial skin infection in children worldwide. It is caused predominantly by Staphylococcus aureus and group A beta-haemolytic streptococci (Streptococcus pyogenes, GAS), alone or together. Three clinical subtypes are recognised — non-bullous (the commonest, about 70 percent), bullous (staphylococcal exfoliative-toxin-mediated), and ecthyma (a deeper ulcerative form) — and staphylococcal scalded skin syndrome (SSSS) is the related generalised toxin-mediated cousin of infants and young children.[1]

The microbiology that earns marks: S. aureus dominates in most settings and causes essentially all bullous impetigo. It produces exfoliative toxins A and B (ETA/ETB) — serine proteases that cleave desmoglein-1, a desmosomal cadherin in the superficial epidermis, producing the intra/subcorneal split of bullous impetigo and the widespread desquamation of SSSS. GAS causes non-bullous impetigo and ecthyma, and distinct nephritogenic M-protein serotypes (M49, M2, M55, M60, M57) underlie the link to post-streptococcal glomerulonephritis.[7][8][11][12]

The classic trap — bullous impetigo versus SSSS turns on where the toxin is made. In bullous impetigo the toxin is produced locally in the lesion; in SSSS it disseminates systemically from a distant focus (conjunctivitis, otitis media, nasopharyngitis, umbilical infection in a neonate), producing widespread desquamation at sites remote from the infection. That is why skin cultures of the bullae are negative in SSSS — the disease is toxin-mediated, not locally infected.[7][9]

The four faces — morphology is the whole classification

Impetigo is classified by clinical morphology, depth, and pathogenesis. Get the face right and the antibiotic, the differential, and the complication all follow.[1][3]

How common, who, and why the crust spreads

Impetigo is global but disproportionately affects children aged 2 to 5 years, with a global point prevalence of about 1 to 5 percent in paediatric populations and the highest rates in tropical, warm-humid climates and in settings of crowding, poverty, and poor hygiene. It accounts for roughly 10 percent of all childhood skin problems seen in general practice.[15]

The epidemiology that earns marks: peaks in late summer and autumn in temperate regions and persists year-round in the tropics; outbreaks in nurseries, schools, military barracks, prisons, Indigenous communities, refugee camps, and contact-sport settings (wrestling, rugby); pre-existing skin barrier dysfunction (atopic dermatitis, scabies, tinea, insect bites) is the usual portal, and secondary infection of an underlying dermatosis is called "impetiginisation."[1][16]

The global burden point examiners reward: impetigo (also called pyoderma in the public-health literature) is the commonest cutaneous manifestation of group A streptococcal disease, and the principal source of GAS exposure in Indigenous Australian, Maori, Pacific Islander, South Asian, sub-Saharan African and some Native American communities — where it feeds the pool of strains that drive both post-streptococcal glomerulonephritis and acute rheumatic fever.[10][11][14]

Why the bulla forms — desmoglein-1 and the toxin

In bullous impetigo and SSSS the mechanism is one and the same: staphylococcal exfoliative toxins A and B cleave desmoglein-1 in the granular layer, producing a superficial epidermal split. The split sits subcorneally, so the bullae are flaccid and rupture easily, and the disease heals without scarring because the basal layer is intact.[7][8]

The single mechanism-to-feature comparison examiners reward — SSSS versus toxic epidermal necrolysis (TEN):[7]

• SSSS spares mucosae and shows a superficial granular-layer split — toxin-mediated, skin cultures negative, drug trigger absent.
• TEN involves mucosae and shows full-thickness epidermal necrosis — drug-mediated (typically 1 to 8 weeks after a new drug), a medical emergency.[7]

MRSA and Panton-Valentine leucocidin (PVL) change the antibiotic. MRSA is an increasing cause, particularly in endemic regions and in recurrent or treatment-resistant disease. PVL-positive strains drive recurrent necrotic lesions and family clusters, and call for toxin-suppressing agents (clindamycin, linezolid) rather than a standard beta-lactam.[1]

Diagnosis — clinical, with a swab when it matters

The diagnosis is clinical. Useful bedside adjuncts include a Gram stain of pus or crust (Gram-positive cocci in clusters equals S. aureus; chains equals GAS — though most clinicians proceed without it), a KOH preparation to exclude tinea, a Tzanck smear or HSV PCR to exclude herpes simplex, and dermoscopy for scabies mites when secondary impetiginisation of scabies is suspected.[1][4]

Swab for bacterial culture and sensitivity when lesions are extensive or atypical, when there is treatment failure or recurrence within two weeks, when MRSA is suspected, in the immunocompromised host, in institutional outbreaks, and in neonatal disease. Pus swabs go onto blood agar and mannitol salt agar (or chromogenic MRSA agar in endemic settings); consider PVL PCR in recurrent or family-cluster disease.[1]

In SSSS, culture the causative focus (conjunctiva, umbilicus, wound, nasopharynx) — skin cultures of the bullae are negative. Skin biopsy is reserved for diagnostic uncertainty (distinguishing SSSS from TEN: SSSS shows a superficial split at the granular layer with normal dermis; TEN shows full-thickness epidermal necrosis with mucosal involvement).[1][7]

The non-suppurative-complication work-up after GAS impetigo: urinalysis (haematuria, RBC casts, mild proteinuria), U&E (raised urea and creatinine), complement studies (transiently low C3), ASO and anti-DNase B titres (the latter rises higher after skin infection), and blood pressure monitoring — typically at presentation and three weeks after the rash.[13]

The differential — morphology decides the list

The differential depends on the lesion morphology. Two practical axes — bullous versus non-bullous, and superficial versus generalised toxin-mediated — anchor the work-up.[3][16]

The discriminator line: mucosae involved plus full-thickness necrosis plus a drug equals TEN, not SSSS. A febrile infant with sheet-like desquamation and a positive Nikolsky but spared mucosae is SSSS — and the skin cultures will be negative.[7]

Management — topical for a few, oral for many, admit for SSSS

Treatment aims to resolve infection, reduce transmission, and prevent complications. The choice turns on extent, severity, local resistance, and host factors.[1][5][2][17]

Localised disease (few lesions, intact host) — topical first

Topical antibiotics are first-line for localised disease. Apply to the lesion after gentle crust removal (soak in warm soapy water or a moist dressing for 10 to 15 minutes), wash hands before and after, and cover with a loose dressing to limit spread. Exclude from school until 24 hours of effective treatment (UK CKS) or until lesions are crusted (US AAD).[1]

• Fusidic acid 2% ointment or cream TDS for 5–7 days — favoured in continental Europe for low resistance.
• Mupirocin 2% ointment TDS for 5 days — reserve for recurrent or MRSA-suspected disease.
• Retapamulin 1% ointment BD for 5 days — a pleuromutilin; effective for a small number of lesions.[6]
• Hydrogen peroxide 1% cream — an effective steroid- and antibiotic-free alternative endorsed by NICE CKS, relevant where antibiotic stewardship matters.[1]

Extensive, bullous, or systemic disease; SSSS — oral or IV

• Oral antibiotics for 7 days (5 to 7 for uncomplicated extensive disease): a beta-lactamase-resistant anti-staphylococcal agent — flucloxacillin 500 mg QDS (or dicloxacillin), or first-generation cephalosporin cephalexin 500 mg BD. Erythromycin 500 mg QDS or clarithromycin 500 mg BD for true penicillin allergy.[1]
• Recurrent, treatment-failure, or MRSA-suspected disease — clindamycin 300 mg QDS, doxycycline 100 mg BD (over 12 years), or TMP-SMX 960 mg BD where local resistance is low. PVL-positive strains — clindamycin or linezolid (toxin suppression) plus rifampicin 300 mg BD for the last 4 days of an anti-staphylococcal course.[1]
• SSSS — admit, fluid resuscitation, temperature control, analgesia, IV anti-staphylococcal therapy (IV flucloxacillin 1–2 g 6-hourly, or vancomycin or linezolid if MRSA); manage the skin as for a superficial scald (non-adherent dressings, bland emollients, avoid shearing forces). Most children recover within 1 to 2 weeks without scarring.[1]

Recurrent disease — decolonise the reservoir

A 5-day decolonisation cycle breaks recurrence: intranasal mupirocin 2% BD to the anterior nares PLUS chlorhexidine 4% body wash daily PLUS hot laundering of towels and bedlinen. Treat household contacts if recurrence is a family problem, and address the underlying atopic dermatitis, scabies, or tinea.[1]

General and preventive measures

Gently remove crusts with warm soapy water; keep lesions covered; wash hands and linen frequently; avoid sharing towels, flannels, and toys. Manage predisposing skin disease; bleach baths 1:100 twice weekly help when recurrent staphylococcal skin infection rides on atopic dermatitis. Treat household contacts and screen staff in nursery outbreaks.[1]

The complications that arrive later — PSGN is the one that bites

Suppurative complications — cellulitis and lymphangitis, ecthyma progression, abscess, staphylococcal bacteraemia and sepsis (uncommon in immunocompetent children; high risk in neonates and the immunocompromised), and rare haematogenous osteomyelitis or septic arthritis — are managed with systemic antibiotics and, for abscess, incision and drainage.[1]

The non-suppurative complication examiners reward — post-streptococcal glomerulonephritis (PSGN): it occurs 1 to 3 weeks after impetigo (or 1 to 2 weeks after pharyngitis), caused by nephritogenic GAS strains (M49, M2, M55, M60, M57). It presents with haematuria (smoky or tea-coloured urine), oedema, hypertension, and oliguria; biopsy shows proliferative glomerulonephritis with subepithelial humps; complement C3 is transiently low. Treatment is supportive (fluid balance, antihypertensives, diuretics, occasionally dialysis); most children resolve in 2 to 4 weeks. Antibiotics do NOT prevent PSGN once infection is established — they limit transmission only.[13]

Acute rheumatic fever (ARF) is primarily a complication of GAS pharyngitis, but skin streptococci contribute to the GAS reservoir in high-risk populations (Indigenous Australian, Maori, Pacific, South Asian, resource-limited tropical settings), and skin-derived GAS strains can be rheumatogenic. ARF typically occurs 2 to 4 weeks after pharyngitis with migratory polyarthritis, carditis, chorea, erythema marginatum, and subcutaneous nodules (revised Jones criteria).[14]

How patients come to harm — the preventable list

Impetigo is usually trivial, so the serious harms are missed complications, missed toxin-mediated disease, and iatrogenic injury:[1]

• Missing staphylococcal scalded skin syndrome in a febrile infant with diffuse erythema and a positive Nikolsky — admitted late for fluids and IV anti-staphylococcal therapy.
• Missing post-streptococcal glomerulonephritis by not checking urinalysis, U&E, BP and complement one to three weeks after GAS impetigo.
• Mislabelling SSSS as TEN (or vice versa) — the mucosae and the biopsy split settle it.
• Treating MRSA or PVL-positive disease with a beta-lactam alone and wondering why it recurs.
• Ecthyma gangrenosum missed in a neutropenic patient labelled "just ecthyma" — Pseudomonas in an immunocompromised host is an emergency.
• Acute rheumatic fever missed when carditis, polyarthritis or chorea follow streptococcal infection by 2 to 4 weeks.[1]

Prognosis, disposition, and special populations

Impetigo heals without scarring in non-bullous and bullous disease (the split is superficial to the basal layer); ecthyma scars because it reaches the dermis. Most localised disease resolves in 7 to 10 days on topical therapy, 5 to 7 days on oral therapy, and 2 to 3 weeks if untreated. SSSS in children carries an excellent prognosis with supportive care and IV anti-staphylococcal therapy, though it can be life-threatening in neonates.[1]

Special populations: neonates (high sepsis risk — admit, IV anti-staphylococcal therapy, infection-control input); children (the principal population — cephalexin 25 mg/kg/dose BD or flucloxacillin elixir 62.5 to 125 mg QDS for under 6 years); pregnancy and breastfeeding (topical fusidic acid, oral flucloxacillin, cephalexin and erythromycin are safe; avoid tetracyclines and TMP-SMX near term); atopic dermatitis (recurrent impetigo is common — aggressive emollients, treat flares early, bleach baths, decolonisation); the immunocompromised (broader differential, low threshold for culture and admission, consider MRSA and PVL).[1][17][18]

Evidence and regional deltas

The framework (topical for localised, oral for extensive, IV and supportive care for SSSS) is globally consistent, but agent choice and school-exclusion rules differ by region.[1]

• UK (BAD and NICE CKS): topical hydrogen peroxide 1% or fusidic acid for localised impetigo (to curb resistance); mupirocin reserved for recurrent or MRSA-suspected disease; flucloxacillin 500 mg QDS for 7 days for extensive disease; exclude from school until 24 hours of effective treatment.[1]
• US (AAD and IDSA 2014): topical mupirocin or retapamulin for 5 days for localised disease; oral cephalexin or dicloxacillin for extensive or bullous disease; TMP-SMX, doxycycline, linezolid or clindamycin (D-test) for confirmed MRSA; until lesions are crusted and dry before return to school.[1]
• Australia and NZ (Therapeutic Guidelines): oral flucloxacillin 500 mg QDS for 7 days; cephalexin for non-anaphylactic penicillin allergy; single-dose IM benzathine penicillin G for GAS pyoderma in mass-treatment programmes in Indigenous communities.[1]
• India and South Asia (IADVL): topical fusidic acid cost-effective first-line; oral amoxicillin-clavulanate, cephalexin or flucloxacillin for extensive disease; screen for scabies in crowded settings.[1]
• WHO and resource-limited tropical regions: impetigo is a leading cause of childhood pyoderma; single-dose IM benzathine penicillin G is the standard mass-treatment regimen for GAS pyoderma outbreaks; address crowding, water access, and skin-barrier disease.[1]

The mnemonic — the bedside checklist

The mantra: honey crust, flaccid bulla, or punched-out ulcer — topical if few, oral if many, admit if scalded — and never forget the kidney one to three weeks later.[1]

Ward-round test — three stems, thirty seconds each