Impetigo and ecthyma

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Impetigo is a contagious superficial bacterial infection. Examine the earliest and newest lesions, because dried crust is less specific than an intact fragile vesicle, pustule or flaccid bulla. Colour change around lesions may appear red, violet, grey or brown across skin tones; warmth, tenderness, spreading edge and depth remain important. Ask about eczema, scabies, bites, contact sport, nursery outbreaks, shared towels, recent antibiotics and household cases.

NICE separates localised non-bullous disease from widespread, bullous or systemically unwell presentations. Localised disease can avoid antibiotics with hydrogen peroxide 1% cream. When an antibiotic is necessary, choose either topical or oral treatment, not both, and set a five-day course with response-led extension to seven days. Consider antimicrobial resistance and local microbiology when MRSA is suspected.

Ecthyma is deeper than impetigo. Lift or soften a crust only when clinically safe to reveal and sample the ulcer, assess circulation and host risk, and use systemic therapy guided by likely staphylococci or streptococci and culture. Consent and analgesia matter when cleaning painful crusts. A non-healing, necrotic or unusual ulcer should be biopsied or referred rather than repeatedly labelled infection.

Key points

Non-bullous impetigo begins with thin-roofed vesicles or pustules that become honey-coloured crusted erosions, commonly around the nose, mouth and exposed limbs.
Bullous impetigo produces larger flaccid blisters, often on trunk or flexures, and warrants oral treatment because toxin-producing staphylococci are involved.
Ecthyma has an adherent dark crust over a punched-out ulcer extending into dermis; swab and use systemic treatment rather than treating it as a superficial spot.
For localised non-bullous impetigo, NICE first offers hydrogen peroxide 1% cream; a short topical antibiotic is reserved when that is unsuitable or ineffective.
Use oral flucloxacillin for bullous disease, widespread non-bullous disease when oral treatment is selected, or systemic illness; do not combine topical and oral antibiotics routinely.
A five-day course is standard, extended to seven days according to severity and response; an unreviewed repeat is not an acceptable substitute for sampling.
Advise hand hygiene, short nails, avoidance of scratching, no sharing towels or face cloths, and exclusion from school or work until lesions are crusted and healed or 48 hours after antibiotics begin.
Swab worsening, non-responsive or recurrent disease and reconsider herpes, eczema, resistance, scabies and deeper infection before changing antibiotics.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Staphylococcal infection

Staphylococcus aureus commonly enters superficial epidermis through minor trauma, eczema, insect bites or scratching and can produce non-bullous or toxin-mediated bullous disease.

Streptococcal infection

Group A streptococci cause or contribute to non-bullous impetigo and ecthyma, with transmission favoured by close contact, crowding and disrupted skin.

Autoinoculation and contact spread

Hands, shared towels and scratching transfer organisms between sites and people; impetigo is contagious even though carriage without lesions is common.

Deeper host vulnerability

Ecthyma is more likely with neglected wounds, scabies, oedema, diabetes, poor circulation, malnutrition or immune compromise and extends through the epidermis into dermis.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Superficial vesicle rupture
Bacterial proliferation beneath the stratum corneum creates fragile vesicles or pustules that rupture and dry into adherent golden or honey-coloured crust.
2
Exfoliative toxin cleavage
Bullous impetigo strains release exfoliative toxin that separates superficial epidermis, producing flaccid bullae with a thin collarette after rupture.
3
Dermal ulceration
In ecthyma, infection penetrates beneath a thick crust and destroys deeper tissue, leaving a punched-out ulcer that heals slowly and can scar.
4
Inflammatory extension
Untreated infection can spread into surrounding dermis and subcutis as cellulitis or, rarely, enter blood and cause systemic complications.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Honey-crusted erosion

A thin golden crust over a shallow moist erosion with nearby satellite lesions is characteristic of non-bullous impetigo.

Flaccid superficial bulla

A fragile clear or yellow blister that collapses to a varnish-like base and collarette supports bullous impetigo.

Punched-out ecthyma ulcer

A thick adherent crust conceals a deeper sharply demarcated ulcer, usually on lower limbs, and may heal with a scar.

Invasive extensionRed flag

Rapidly expanding warmth, swelling and pain beyond lesions, fever or physiological instability indicates cellulitis or sepsis and needs urgent care.

Scalded-skin warningRed flag

Diffuse tenderness, fever, superficial exfoliation and widespread positive Nikolsky sign, especially in a child, suggests staphylococcal scalded-skin syndrome.

Herpetic departure

Monomorphic painful vesicles or punched-out erosions clustered on eczema, with fever or eye proximity, requires urgent viral assessment.

Red flags requiring action

Systemic toxicity, rapidly spreading pain or erythema, extensive bullae, mucosal involvement, periorbital disease, immunocompromise, neonatal infection, dehydration or suspected staphylococcal scalded-skin syndrome requires urgent assessment.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Clinical morphology and extent assessmentFirst step
Why
Classify non-bullous, bullous, ecthyma or invasive disease and choose treatment route.
Interpretation and limitations
Typical limited impetigo needs no test; depth, systemic signs and host vulnerability override lesion count.
02
Bacterial swab from a fresh lesion
Why
Guide therapy in worsening, recurrent, treatment-resistant, outbreak-associated or MRSA-risk disease.
Interpretation and limitations
Remove superficial debris, sample moist base or fresh pus before another antibiotic and interpret carriage organisms with clinical response.
03
Nasal swab for recurrent impetigo
Why
Identify a potential staphylococcal reservoir after repeated confirmed episodes.
Interpretation and limitations
Use results with local decolonisation guidance; one positive carriage swab does not prove every future rash is bacterial.
04
Blood tests and cultures for systemic illness
Why
Assess sepsis, inflammation, renal function and organ involvement when disease is severe.
Interpretation and limitations
Do not delay antibiotics in an unstable patient; dark urine, oedema or hypertension later prompts urinalysis and renal assessment.
05
Biopsy or targeted infection testing
Why
Investigate a chronic atypical ulcer, blistering disorder, herpes or travel-related mimic.
Interpretation and limitations
Select a representative active edge with consent and tell pathology or microbiology the precise differential and prior treatment.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Herpes simplex

Grouped painful vesicles or punched-out erosions, recurrent localisation and tingling favour herpes; eczema herpeticum is an urgent disseminated form.

Eczema with secondary infection

A background of itchy chronic dermatitis, lichenification and widespread flare suggests eczema; crust alone does not prove that antibiotics will treat the whole flare.

Contact dermatitis

Prominent itch, sharply exposure-shaped erythema, vesiculation and absence of progressive honey crust support allergic or irritant contact disease.

Autoimmune blistering disease

Tense bullae, mucosal lesions, widespread erosions or recurrent unexplained blistering requires urgent dermatology assessment and biopsy rather than repeated impetigo therapy.

Cutaneous ulcer mimic

Vasculitis, pyoderma gangrenosum, leishmaniasis and malignancy enter the differential when an ecthyma-like ulcer is painful, atypical, chronic or travel-associated.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Localised non-bullousMinimise antimicrobial exposureFirst stepA small area of superficial honey-crusted lesions occurs without bullae, systemic illness or high complication risk.

1Offer hydrogen peroxide 1% cream two or three times daily for five days and explain local irritation and eye avoidance.
2If unsuitable or ineffective, choose a five-day topical antibiotic according to NICE and local resistance, rather than combining products.
3EscalationReview spread or non-response, swab when indicated and escalate to oral treatment only when extent, depth or systemic state justifies it.

02Bullous or widespreadUse one systemic courseBullae, widespread non-bullous lesions or systemic symptoms make oral treatment appropriate.

1Assess hydration, temperature, pain and invasive spread, and urgently refer neonates, toxic patients or suspected scalded-skin syndrome.
2AlternativeGive oral flucloxacillin for five days, extending to seven according to response, or use a NICE allergy alternative after careful allergy assessment.
3Do not add a topical antibiotic; review within two to three days if worsening and obtain microbiology for failure or MRSA risk.

03Ecthyma or recurrenceSample depth and driversA crusted ulcer extends into dermis or impetigo repeatedly returns.

1Swab a cleaned moist ulcer base, examine circulation and skin disease, and look for scabies, diabetes, immune compromise and household transmission.
2Use an oral antistaphylococcal and antistreptococcal regimen guided by severity, local policy and culture, with wound care and analgesia.
3For recurrence, review nasal carriage and decolonisation with microbiology guidance; biopsy or refer an ulcer that fails to heal or has atypical features.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

NICE first-choice topical treatment that can spare antibiotics in a small uncomplicated field.

Hydrogen peroxide 1% cream

Apply two or three times daily for five days to localised non-bullous impetigo, avoiding eyes and mucosa.

Can bleach hair and fabrics and irritate skin; unsuitable around eyes, and evidence in people with darker skin is limited.

A short topical antibiotic option for localised non-bullous impetigo when antimicrobial treatment is justified.

Fusidic acid 2% cream

Apply three times daily for five days when hydrogen peroxide is unsuitable or ineffective; extend to seven days only by clinical judgement.

Resistance can develop rapidly; avoid repeated or widespread use, do not combine with oral antibiotics routinely and follow local susceptibility advice.

NICE first-choice oral treatment for bullous or widespread impetigo and systemic illness in adults.

Flucloxacillin capsules

Take 500 mg four times daily for five days, increasing to 1 g four times daily for severe infection and extending to seven days according to response.

Check immediate and severe delayed penicillin allergy, hepatic history and interactions; take on an empty stomach and seek review for jaundice or severe diarrhoea.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cellulitis and sepsis

Extension beyond superficial skin produces spreading warmth, tenderness and swelling; fever or physiological instability demands urgent systemic assessment.

Post-streptococcal glomerulonephritis

A delayed immune nephritis can follow streptococcal skin infection, presenting with dark urine, oedema or hypertension; antibiotic treatment does not reliably prevent it.

Scarring after ecthyma

Deeper dermal destruction can leave permanent atrophic or pigmentary scars, unlike ordinary superficial impetigo that usually heals without structural loss.

Transmission and recurrence

Untreated close contacts, shared items, eczema, scabies or nasal carriage can sustain household clusters and repeated antimicrobial exposure.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review sooner than planned if fever, increasing pain, spreading inflammation, new bullae, reduced intake or eye involvement develops.
At course completion, document lesion drying and absence of new lesions rather than continuing antibiotics until every pigment mark disappears.
For non-response, verify application or dosing, obtain culture and reconsider herpes, eczema, resistance, ecthyma and invasive infection.
In recurrence, map household cases, eczema and scabies control, shared items and previous microbiology before considering decolonisation.
Safety-net dark urine, facial or leg oedema and reduced urine output after streptococcal infection for renal assessment.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Crust is an endpoint

Honey-coloured crust results from dried serum and pus; the newest lesion often gives the clearest diagnostic morphology.

Bullae change route

Toxin-mediated bullous impetigo is treated orally even when the total involved area initially appears modest.

Ecthyma destroys dermis

A punched-out ulcer beneath crust explains its slower healing, systemic treatment requirement and potential permanent scar.

Pigment is not persistence

Flat post-inflammatory colour change can remain after eradication and should not trigger antibiotic extension.

Recurrence needs ecology

Carriage, eczema, scabies, close contacts and shared textiles can matter more than choosing an increasingly broad drug.

11Common pitfallsFrequent interpretation and management errors.

01
Combining topical and oral antibiotics for routine impetigo despite NICE advice to choose one route.
02
Using repeated fusidic acid courses without culture and selecting resistant staphylococci.
03
Treating an ecthyma ulcer with superficial cream alone and missing diabetes, vascular disease or immune compromise.
04
Calling painful monomorphic erosions on eczema impetigo and delaying treatment of eczema herpeticum.
05
Extending antibiotics for residual hyperpigmentation after every active lesion has healed.