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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Impetigo, scabies and fungal infection

Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
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Rapidly progressive or toxin-mediated skin infection

Fever, severe pain, rapid erythematous spread, widespread bullae, skin tenderness, peeling, hypotension or reduced responsiveness can indicate cellulitis, sepsis, staphylococcal scalded skin syndrome or another invasive process.

Action: Use paediatric ABCDE and sepsis assessment, obtain cultures without delaying treatment, give prompt systemic antibiotics according to the current child and local microbiology pathway and involve paediatrics or dermatology. Admit neonates, systemically unwell children and those with widespread blistering or immune compromise.

Overview

Distinguish common contagious bacterial, mite and dermatophyte infections by morphology and distribution, use short evidence-based topical or systemic treatment, coordinate household and school advice and escalate bullous, crusted, scalp or invasive disease promptly.

Impetigo, scabies and dermatophyte infection are common but differ in organism, transmission and treatment. Describe the primary lesion before crust or scratching alters it, map distribution and ask who else is affected. Fever, pain, rapid spread, immune compromise, neonatal age, bullae, scalp bogginess or deep erythema changes urgency. Photograph with consent when it will help follow progression, but do not delay treatment of systemic illness.

Impetigo is a superficial staphylococcal or streptococcal infection. Non-bullous disease begins as vesicles or pustules that become honey-coloured crusts, often around the nose, mouth or minor trauma. Bullous disease reflects exfoliative toxin, with flaccid fluid-filled blisters, collarettes and less crust. Assess extent, fever, eczema, bites and household spread. Cellulitis, pain out of proportion, mucosal involvement or widespread peeling suggests a deeper or toxin-mediated diagnosis.

Practice

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Paediatrics and child healthOriginal SBA

Localised non-bullous impetigo

A systemically well 5-year-old has three small honey-crusted facial lesions with no bullae or cellulitis. What is the NICE first-choice treatment approach?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE NG153 impetigoHydrogen peroxide, topical and oral antibiotic choices, course length, reassessment and resistance strategy.
  • UKHSA infections in education settingsCurrent exclusion, hygiene and outbreak-control advice for impetigo, scabies and ringworm.
  • NHS scabiesWhole-household treatment, application, repeat timing, environmental actions and persistent itch.
  • BNF for ChildrenPermethrin, impetigo antimicrobials and topical and systemic antifungal child regimens.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom
For localised non-bullous impetigo, NICE recommends hydrogen peroxide 1% cream two or three times daily for 5 days. When antiseptic is unsuitable, a 5-day topical antibiotic such as fusidic acid can be used, taking resistance into account. Widespread non-bullous or bullous disease receives oral flucloxacillin, normally for 5 days and sometimes 7 when response is incomplete, using the BNFC age or weight dose. Routine topical-plus-oral combination adds resistance without benefit.

Scabies follows sensitisation to Sarcoptes scabiei. The first infestation can itch only after several weeks, allowing silent transmission; reinfestation triggers symptoms faster. Look for burrows on finger webs, wrists and sides of hands, papules at axillae, waist, buttocks, ankles and genital region and nodules on scrotum or axilla. Infants can have vesicles and pustules on palms and soles and lesions on scalp and face, distributions uncommon in healthy adults.

Successful scabies treatment is logistical. Treat every household member and close skin contact simultaneously, whether itchy or not. Apply permethrin 5% to cool dry skin over the entire body and repeat after 7 days. Include scalp, neck, face and ears for children under 2 years while avoiding eyes and mouth; include under nails and reapply after handwashing. Leave on for the product-specified interval before washing and change clothing and bedding. Follow current public-health cleaning advice rather than attempting hazardous environmental fumigation.

Persistent itch for two to four weeks can reflect immune reaction after mite death. Emollient, a mild topical corticosteroid and age-appropriate oral antihistamine for sleep may help, but antihistamine does not eradicate mites. Treatment failure usually reflects missed body areas, handwashing without reapplication, failure to repeat at 7 days or untreated contacts. Crusted scabies has heavy scale, very high mite burden and may be only mildly itchy; isolate contact risk and obtain urgent dermatology or infection-control advice for combined topical and oral therapy.

Dermatophytes infect keratin. Tinea corporis and cruris have an expanding scaly active border, sometimes with central clearing; tinea pedis affects toe webs or soles, and tinea faciei can mimic eczema. Take skin scrapings from the active edge when appearance is uncertain, treatment failed, infection is extensive or systemic therapy is considered. A topical allylamine or azole is appropriate for limited hairless skin, with duration following the selected product and continued treatment long enough to clear the active edge.

Tinea capitis usually presents with scale, broken hairs, patchy alopecia, black dots or cervical lymphadenopathy. A kerion is a tender boggy inflammatory plaque with pustules and risks permanent scarring. Topical treatment alone cannot penetrate the hair follicle: obtain plucked hairs and scalp scale for microscopy and culture and start systemic griseofulvin or terbinafine through an age-, weight-, organism- and local-prevalence-informed pathway. Household and school contact policy depends on organism and public-health guidance.

Consider mimics. Herpes simplex causes grouped painful vesicles; eczema herpeticum becomes monomorphic and systemic. Contact dermatitis follows exposure. Psoriasis has well-demarcated plaques and nail pits. Alopecia areata is smooth without scale. Bacterial scalp infection can complicate kerion. A topical corticosteroid may temporarily reduce redness in tinea while fungus extends, producing tinea incognito; ask specifically about combination creams obtained elsewhere.

Give practical infection-control advice without blame. Do not share towels, razors, hats or hair tools during active infection. Cover impetigo lesions when feasible and follow current school or nursery exclusion guidance, commonly until lesions are crusted and healed or 48 hours after effective antibiotics begin. Scabies exclusion ends after the first effective treatment, but all contacts must coordinate. Review failure early and confirm the diagnosis before repeating antimicrobial courses.

Key points

  • Non-bullous impetigo produces thin-roofed vesicles that rupture into golden crusts, often around nose and mouth; bullous impetigo forms larger flaccid blisters and is more likely to need oral treatment.
  • For localised non-bullous impetigo in a systemically well child, offer hydrogen peroxide 1% cream two or three times daily for 5 days; use a short topical antibiotic when antiseptic is unsuitable.
  • Widespread non-bullous or bullous impetigo usually needs oral flucloxacillin for 5 days using current child dosing; do not combine topical and oral antibiotics routinely.
  • Scabies causes severe nocturnal itch, burrows and papules on finger webs, wrists, axillae, waist or genital region; infants can have scalp, face, palms and soles involved.
  • Treat the child and all household or close physical contacts on the same day, even if contacts are asymptomatic, with two correctly applied permethrin 5% treatments 7 days apart unless an alternative is needed.
  • Apply scabicide to the whole body, include scalp and face in children under 2 years while avoiding eyes and mouth, cover under nails and reapply to washed hands during the treatment interval.
  • Itch can persist for several weeks after successful scabies treatment; new burrows or progressive lesions after correctly repeated household therapy suggests ongoing infestation or reinfection.

Aetiology

01

Staphylococcal or streptococcal infection

Staphylococcus aureus and group A streptococcus enter superficial damaged epidermis and produce non-bullous impetigo; toxin-producing staphylococci cause bullae.

02

Scabies mite infestation

Female Sarcoptes mites burrow into stratum corneum, while delayed hypersensitivity to mite products drives intense itch and papules.

03

Dermatophyte keratin infection

Trichophyton, Microsporum and Epidermophyton species colonise skin, hair or nails and spread through people, animals or contaminated objects.

04

Barrier and exposure risk

Eczema, minor trauma, crowding, close contact, shared equipment, contact sport and household pets increase acquisition or dissemination.

Pathophysiology

  1. 1
    Superficial epidermal invasion

    Bacteria multiply beneath the stratum corneum, creating fragile vesicles, exudate and crust while usually sparing deeper dermis.

  2. 2
    Exfoliative toxin cleavage

    Bullous staphylococcal toxin disrupts epidermal adhesion, producing large flaccid blisters and potential wider toxin-mediated skin disease.

  3. 3
    Delayed mite hypersensitivity

    Immune response to mites, eggs and faeces produces nocturnal pruritus that can persist temporarily after successful eradication.

  4. 4
    Keratin-dependent fungal growth

    Dermatophytes expand through non-living keratin, creating an active scaly margin or penetrating hair shafts where topical agents cannot reach.

Clinical features and red flags

Non-bullous impetigo

Small vesicles or pustules rupture into adherent golden crusts around the face, exposed limbs or damaged skin.

Bullous impetigo

Flaccid larger blisters leave moist erythematous bases and collarettes, often on trunk or intertriginous skin.

Classic scabies

Severe night itch, burrows and papules affect hands, wrists, axillae, waist or genitals and spread among contacts.

Infant scabies

Vesicles, pustules and burrows involve palms, soles, scalp or face as well as the trunk in young children.

Dermatophyte plaque

An enlarging annular lesion has peripheral scale and activity with relative central clearing on hairless skin.

Inflammatory kerionRed flag

A tender boggy scalp plaque with pustules, alopecia and nodes requires urgent systemic antifungal assessment to prevent scarring.

Red flags requiring action

  • Neonatal bullae, widespread tenderness or peeling can indicate staphylococcal scalded skin syndrome and needs admission.
  • Fever, severe pain, rapid spread, lymphangitis or haemodynamic change suggests cellulitis or invasive bacterial infection.
  • Thick widespread crusting in an immunocompromised or institutionalised child suggests highly contagious crusted scabies.

Investigations

  1. 01
    First-line morphology and contact assessmentFirst stepFirst line
    Why
    Distinguish bacterial crust, mite distribution and fungal border and identify symptomatic or asymptomatic close contacts.
    Interpretation and limitations
    Typical limited disease is clinical; atypical, severe or treatment-resistant morphology needs sampling or specialist review.
  2. 02
    Bacterial swab
    Why
    Identify pathogen and resistance in recurrent, widespread, MRSA-risk or non-responsive impetigo and invasive infection.
    Interpretation and limitations
    Surface colonisation can confuse results, so sample fresh exudate and interpret alongside clinical depth and response.
  3. 03
    Scabies dermoscopy or scraping
    Why
    Demonstrate mite, eggs or faecal material when diagnosis is uncertain, crusted disease is possible or outbreaks require confirmation.
    Interpretation and limitations
    A negative scraping does not exclude scabies because mite numbers can be low in ordinary infestation.
  4. 04
    Skin fungal scraping
    Why
    Sample the active scaly edge before systemic therapy or when annular lesions fail empirical topical treatment.
    Interpretation and limitations
    Microscopy can support rapid diagnosis while culture identifies species and helps explain treatment failure.
  5. 05

Differential diagnosis

01

Atopic or contact eczema

Diffuse itch, dryness and exposure-patterned inflammation can crust after scratching but lacks characteristic burrows or fungal edge.

02

Herpes simplex infection

Grouped painful vesicles or monomorphic punched-out erosions, especially with fever and eczema, require antiviral rather than antibacterial treatment.

03

Psoriasis

Sharply demarcated plaques, scalp scale and nail pitting may resemble tinea but usually lack an advancing fungal border.

04

Alopecia areata

Smooth discrete hair loss with exclamation-mark hairs has little scale or inflammation compared with tinea capitis.

05

Insect bites or papular urticaria

Grouped exposed-site papules and puncta can itch intensely but do not show burrows, household sequence or annular scale.

Management

01ImpetigoMatch antimicrobial route to extentFirst stepGolden crusts or flaccid bullae are present without a deeper skin emergency.+
  1. 1Use hydrogen peroxide 1% for localised non-bullous disease, or a 5-day topical antibiotic when antiseptic is unsuitable.
  2. 2AlternativeUse oral flucloxacillin for widespread non-bullous or bullous disease, selecting current child dose and allergy alternative.
  3. 3Avoid routine topical-plus-oral combination, review after the course and culture recurrent or failed infection.
02ScabiesTreat every close contact togetherNocturnal itch, burrows and compatible distribution or household spread support infestation.+
  1. 1Apply permethrin 5% correctly to the complete age-appropriate body area and repeat the entire treatment after 7 days.
  2. 2

Complications

01

Cellulitis and invasive infection

Superficial bacterial disease can extend into dermis or bloodstream, producing expanding tenderness, fever, lymphangitis and systemic deterioration.

02

Post-streptococcal glomerulonephritis

Nephritogenic streptococcal strains can trigger haematuria, oedema and hypertension after skin infection despite successful local treatment.

03

Crusted scabies outbreaks

Extremely high mite burden spreads rapidly through households and institutions and requires coordinated infection-control and specialist treatment.

04

Secondary bacterial infection

Excoriated scabies and tinea permit staphylococcal or streptococcal entry, adding crust, pain, cellulitis and occasionally sepsis.

05

Scarring alopecia

Severe inflammatory tinea capitis and delayed kerion treatment can permanently destroy follicles and leave focal hair loss.

Monitoring and follow-up

  • Review impetigo at the end of the short course or sooner for fever, pain, spread or new bullae.
  • Check for new scabies burrows after both applications and distinguish them from residual itch without active lesions.
  • Confirm every household member completed treatment on the same dates and that hands and infant scalp were not missed.
  • For tinea, measure reduction in active edge, scale and lesion size and confirm hair regrowth after scalp treatment.
  • Follow fungal culture and adjust systemic agent when species or susceptibility makes the initial choice unsuitable.
  • Ask about adverse effects, medicine interactions and adherence during multiweek oral antifungal courses.
  • Notify and coordinate infection control for institutional crusted scabies or other significant outbreaks.

Special situations

Golden crust is a stage

The fragile vesicle may be gone by presentation, leaving exudate whose colour helps recognise non-bullous impetigo.

Scabies treatment is simultaneous

An asymptomatic household member can be incubating infestation and reinfect everyone if excluded from the treatment day.

Post-scabetic itch is expected

Immune inflammation can continue after mite death, so itch alone during early weeks does not prove failure.

Scalp fungus needs oral medicine

Dermatophytes inside hair follicles are beyond topical cream reach, making systemic therapy essential for cure.

Steroid can hide tinea

Inflammation fades while fungus expands, producing less typical tinea incognito and delaying the correct diagnosis.

Common pitfalls

  1. 01

    Combining topical and oral antibiotics routinely for impetigo.

  2. 02

    Using repeated fusidic acid courses without culture or resistance review.

  3. 03

    Treating only the itchy scabies contact and leaving the household untreated.

  4. 04

    Applying permethrin once, missing hands or forgetting the 7-day repeat.

  5. 05

    Calling persistent itch treatment failure without looking for new burrows.

  6. 06

    Treating tinea capitis with shampoo or topical cream alone.

  7. 07

    Applying potent topical corticosteroid to an undiagnosed annular fungal plaque.

  8. 08

    Delaying systemic treatment of a kerion until culture is final.

  • Tinea corporis has an enlarging annular scaly edge with central clearing, while tinea capitis causes scale, broken hairs, alopecia, lymph nodes or an inflammatory kerion.
  • Skin dermatophyte infection usually responds to topical terbinafine or an azole for the product-specific course, but scalp and nail disease need systemic therapy and fungal sampling.
  • A boggy painful kerion needs urgent specialist treatment to prevent scarring alopecia; avoid topical corticosteroid alone on an undiagnosed annular eruption because it can mask and spread tinea.
  • A painful boggy scalp swelling with hair loss is kerion and risks permanent scarring without systemic treatment.
  • Eye, mucosal or extensive facial blistering requires consideration of herpes or severe mucocutaneous disease.
  • A child with recurrent extensive fungal infection, poor growth or unusual organisms needs immune and systemic assessment.
  • Haematuria, oedema or hypertension after impetigo suggests post-streptococcal glomerulonephritis.
  • Hair and scalp mycology
    Why
    Collect plucked hairs, brushings or scale from suspected tinea capitis or kerion before or at treatment initiation.
    Interpretation and limitations
    Species influences oral-agent choice and contact tracing, but severe kerion treatment should not await final culture.
  • 06
    Renal assessment after impetigo
    Why
    Check urine, blood pressure and renal function when oedema, dark urine or hypertension appears after skin infection.
    Interpretation and limitations
    Haematuria and proteinuria with complement changes supports post-streptococcal glomerulonephritis and needs paediatric review.
  • Treat household and close skin contacts simultaneously and coordinate clothes and bedding measures with current public-health advice.
  • 3Manage post-scabetic itch, but reassess technique, contacts and crusted disease when new lesions continue.
  • 03Tinea skinTreat the active fungal edgeA limited annular scaly lesion affects hairless skin without kerion, nail or extensive disease.+
    1. 1Use topical terbinafine or an azole for the product-specific duration, extending over the lesion and active margin.
    2. 2Keep skin dry, avoid shared towels and topical steroid monotherapy and assess pets or contact sport when relevant.
    3. 3Take scrapings and reconsider diagnosis if widespread, recurrent or not improving after a correctly completed course.
    04Tinea scalpUse systemic follicular treatmentScale, broken hairs, alopecia, nodes or kerion suggests tinea capitis.+
    1. 1Obtain hair and scale samples and assess kerion severity, pain, secondary infection and risk to household or school contacts.
    2. 2Start oral griseofulvin or terbinafine under the current weight- and organism-informed child regimen because topical therapy alone fails.
    3. 3Use adjunct antifungal shampoo to reduce shedding and review early for healing and prevention of scarring alopecia.
    Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
    Provides a topical antiseptic option that limits antibiotic exposure and resistance in small superficial infections.

    Hydrogen peroxide 1% cream

    For localised non-bullous impetigo, apply two or three times daily for 5 days, avoiding eyes and mucosa and washing hands after application.

    It may irritate eczematous skin, is unsuitable near eyes and is not enough for bullous, widespread, invasive or systemically unwell disease.

    Kills scabies mites when every body site and both lifecycle-timed applications are completed.

    Permethrin 5% cream

    Apply to the entire age-appropriate body surface, leave on for the licensed 8 to 12 hours and wash off; repeat after 7 days and treat all close contacts simultaneously.

    In children under 2 include scalp, face, neck and ears while avoiding eyes and mouth; reapply after handwashing and manage persistent itch separately.

    Eradicates limited dermatophyte infection of hairless skin by treating the advancing fungal margin.

    Topical terbinafine or azole

    Apply to clean dry affected skin and beyond the active edge at the licensed child frequency and course, commonly terbinafine once or twice daily for 1 to 2 weeks or clotrimazole two or three times daily for at least 2 weeks.

    Confirm child age licensing, continue for the full product course, avoid steroid combination misuse and use oral therapy for scalp or nail infection.

    Reaches infected hair follicles and shafts that topical creams cannot penetrate adequately.

    Oral antifungal for tinea capitis

    Use specialist-selected griseofulvin or terbinafine at the current weight-based BNFC dose and organism-appropriate duration, often several weeks, with sampling obtained before or at treatment initiation.

    Review liver disease, interactions and formulation, monitor when the chosen regimen requires it and treat kerion urgently to reduce scarring.