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]

^[1]

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]

^[1]

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]

^[3]

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]

• Mupirocin 2% ointment and retapamulin 1% ointment are the recommended initial treatments for mild non-bullous and bullous impetigo.^[2]
• Retapamulin 1% ointment twice daily for 5 days is the approved regimen; it is the first pleuromutilin antibacterial, and no resistance to it had been reported at review.^[6][5]
• Fusidic acid performs as well as mupirocin in trials (RR 1.03, 95% CI 0.95 to 1.11), but heavy use drives resistance — New Zealand documented rising fusidic-acid-resistant S aureus alongside widespread topical prescribing.^[5][21]
• Hydrogen peroxide 1% cream is under trial as an antibiotic-sparing antiseptic alternative; pooled trial evidence still favours topical antibiotics over disinfectants (RR 1.15, 95% CI 1.01 to 1.32).^[22][5]

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

• Oral antibiotics for extensive or bullous disease, or for outbreaks to cut transmission: dicloxacillin or cephalexin, targeted at group A streptococci and S aureus. They are also the step up when multilesional disease fails topical therapy within 3 to 5 days.^[2]
• Suspected or confirmed MRSA — clindamycin is useful; trimethoprim-sulfamethoxazole covers MRSA but is inadequate for streptococcal infection.^[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

Decolonisation treats the reservoir, not the lesions. For recurrent staphylococcal skin infection, decolonise every household member: intranasal mupirocin plus antiseptic body washes with chlorhexidine or dilute bleach baths, alongside hygiene education and no shared towels or razors.^[19] One studied regimen runs five days.^[20] Treat the underlying atopic dermatitis, scabies, or tinea as well.^[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: impetigo is commonest in children aged two to five years.^[1][2] Neonatal disease escalates fast — SSSS can appear as early as 48 hours after birth, and treatment there runs through parenteral penicillinase-resistant penicillins plus supportive care.^[9] In recurrent or treatment-failure disease, culture the exudate and cover MRSA.^[17] Broken skin drives entry, so active atopic dermatitis needs control alongside treatment of the impetigo itself.^[1]

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]

• Where fusidic acid is heavily used, resistance follows. New Zealand documented rising fusidic-acid-resistant S aureus with widespread topical prescribing, which prompted trials of antiseptic alternatives such as hydrogen peroxide cream and simple wound care.^[21][22]
• US practice: topical mupirocin 2% or retapamulin 1% ointment first for mild disease; oral dicloxacillin or cephalexin for severe multilesional disease or outbreaks; return to work or school 12 to 24 hours after starting effective antibiotics.^[2]
• 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

^[1]

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

Stem 1 — the honey-crusted child (answer)ShowHide

A four-year-old with golden, stuck-on crusts around his nose and mouth for four days, afebrile, mildly itchy, otherwise well, after a runny nose. What is the diagnosis, the organism, and the first-line treatment? Model: This is classic non-bullous impetigo — about 70 percent of cases, caused by Staphylococcus aureus or Streptococcus pyogenes.^[1] For mild localised disease, start topical mupirocin 2% ointment or retapamulin 1% ointment after gentle crust removal.^[2] Keep him off school until 12 to 24 hours after starting effective antibiotics.^[2] Safety-net the mother: dark urine or new swelling one to three weeks after the crusts means post-streptococcal glomerulonephritis until checked — urinalysis and blood pressure at that visit.^[13]

Stem 2 — the scalded infant (answer)ShowHide

An 18-month-old is febrile, irritable, and tender to touch, with diffuse erythema and sheet-like desquamation in the flexures, with a positive Nikolsky sign. The mouth and conjunctivae are normal. A conjunctival swab grows Staphylococcus aureus; a swab of a bulla is sterile. What is the diagnosis, the mechanism, and the immediate management? Model: This is staphylococcal scalded skin syndrome (SSSS) — generalised, toxin-mediated disease of infants. Exotoxin-producing S aureus at a distant focus (here the conjunctiva) disseminates through the bloodstream, and the toxins cleave desmoglein-1; the epidermis shears in sheets.^[7][9] Bullous impetigo uses the same toxins locally, so its blistering stays confined — SSSS spreads because the toxins travel systemically.^[7] The spared mucosae separate it from toxic epidermal necrolysis.^[7] Admit for parenteral antibiotics that target S aureus — penicillinase-resistant penicillins are the backbone — plus fluids, temperature control, analgesia, and supportive skin care; monitor for hypothermia, haemodynamic instability, and relapse.^[9]

Stem 3 — the dark urine two weeks later (answer)ShowHide

Two weeks after a course of topical fusidic acid for non-bullous impetigo, a six-year-old presents with smoky brown urine, periorbital swelling, and a blood pressure of 130/85. What has happened, and what does the work-up show? Model: This is post-streptococcal glomerulonephritis (PSGN) — the non-suppurative complication of group A streptococcal impetigo, occurring 1 to 3 weeks after the skin infection, driven by nephritogenic M-types (M49, M2, M55, M60, M57). The work-up shows haematuria with RBC casts, mild proteinuria, a raised urea and creatinine, and a transiently low complement C3; ASO and anti-DNase B titres rise (the latter higher after skin infection). Treatment is supportive — fluid balance, antihypertensives, diuretics, occasionally dialysis — and most children resolve in 2 to 4 weeks. The critical counselling point: antibiotics do not prevent PSGN once infection is established; they limit transmission only. This is why the urinalysis and BP check at three weeks matter.^[13]

References22ShowHide

1. [1]Hartman-Adams H, Banvard C, Juckett G. Impetigo: diagnosis and treatment Am Fam Physician, 2014.PMID 25250996
2. [2]Trang DT, Buck EC, Schoenherr DT. Impetigo: Rapid Evidence Review Am Fam Physician, 2026.PMID 41839109
3. [3]Pereira LB. Impetigo - review An Bras Dermatol, 2014.PMID 24770507
4. [4]Johnson MK. Impetigo Adv Emerg Nurs J, 2020.PMID 33105179
5. [5]Koning S, van der Sande R, Verhagen AP, et al. Interventions for impetigo Cochrane Database Syst Rev, 2012.PMID 22258953
6. [6]Yang LP, Keam SJ. Retapamulin: a review of its use in the management of impetigo and other uncomplicated superficial skin infections Drugs, 2008.PMID 18416589
7. [7]Brazel M, Desai A, Are A, et al. Staphylococcal Scalded Skin Syndrome and Bullous Impetigo Medicina (Kaunas), 2021.PMID 34833375
8. [8]Dollani LC, Marathe KS. Impetigo/Staphylococcal Scalded Skin Disease Pediatr Rev, 2020.PMID 32238552
9. [9]Saleh HM, Ross A, Sathe NC. Staphylococcal Scalded Skin Syndrome 2026.PMID 28846262
10. [10]Carapetis JR, Steer AC, Mulholland EK, et al. The global burden of group A streptococcal diseases Lancet Infect Dis, 2005.PMID 16253886
11. [11]Brouwer S, Rivera-Hernandez T, Curren BF, et al. Pathogenesis, epidemiology and control of Group A Streptococcus infection Nat Rev Microbiol, 2023.PMID 36894668
12. [12]Stevens DL, Bryant AE. Streptococcus pyogenes Impetigo, Erysipelas, and Cellulitis 2022.PMID 36479753
13. [13]Alhamoud MA, Salloot IZ, Mohiuddin SS, et al. A Comprehensive Review Study on Glomerulonephritis Associated With Post-streptococcal Infection Cureus, 2021.PMID 35004032
14. [14]Hirani K, Rwebembera J, Webb R, et al. Acute rheumatic fever Lancet, 2025.PMID 40484016
15. [15]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.PMID 24166134
16. [16]Empinotti JC, Uyeda H, Ruaro RT, et al. Pyodermitis An Bras Dermatol, 2012.PMID 22570033
17. [17]Zha M, Usatine R. Common Skin Conditions in Children and Adolescents: Bacterial Infections FP Essent, 2024.PMID 38896826
18. [18]Clebak KT, Malone MA. Skin Infections Prim Care, 2018.PMID 30115333
19. [19]McNeil JC, Fritz SA. Prevention Strategies for Recurrent Community-Associated Staphylococcus aureus Skin and Soft Tissue Infections Curr Infect Dis Rep, 2019.PMID 30859379
20. [20]Fritz SA, Wylie TN, Gula H, et al. Longitudinal Dynamics of Skin Bacterial Communities in the Context of Staphylococcus aureus Decolonization Microbiol Spectr, 2022.PMID 35384711
21. [21]Vogel A, Lennon D, Best E, Leversha A. Where to from here? The treatment of impetigo in children as resistance to fusidic acid emerges N Z Med J, 2016.PMID 27736855
22. [22]Primhak S, Gataua A, Purvis D, et al. Treatment of Impetigo with Antiseptics-Replacing Antibiotics (TIARA) trial: a single blind randomised controlled trial in school health clinics within socioeconomically disadvantaged communities in New Zealand Trials, 2022.PMID 35109906