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Scabies

SNOMED: 128870005869 wordsUpdated 03/03/2026
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Exam Tips

  • Nocturnal itch + itchy household contacts + finger-web/genital papules is a classic OSCE triad.
  • Burrow is the key specific sign; absence of visible burrows does not exclude scabies.
  • In first infestation symptoms may be delayed for weeks, so patients are infectious before obvious rash.
  • Persistent itch after treatment is common; treatment failure is more often due to missed contacts or poor application than drug resistance.
  • Think crusted scabies in immunosuppressed or neurologically impaired patients with widespread hyperkeratotic crusted rash and little itch.
  • If sexually acquired scabies is suspected, offer broader STI risk assessment and partner management.

Definition

Scabies is a contagious ectoparasitic infestation of the skin caused by the human mite Sarcoptes scabiei var. hominis, which burrows into the stratum corneum. In classical scabies the mite burden is usually low (often around 5-15 mites), whereas crusted (Norwegian) scabies is a hyperinfestation with very high mite numbers and much greater infectivity, especially in immunocompromised or neurologically impaired patients.

Pathophysiology

After skin-to-skin transmission, fertilized female mites tunnel within the superficial epidermis and lay eggs; larvae mature to adults over about 10-15 days, with a total lifecycle around 4-6 weeks. Symptoms are driven mainly by a delayed type IV hypersensitivity response to mite proteins, eggs, and faecal pellets, explaining the 3-6 week delay in first infestation and rapid itch (1-3 days) on reinfestation due to prior sensitization. Classical scabies causes intensely pruritic papules and burrows at characteristic sites, while crusted scabies reflects impaired host immune/scratch response, producing widespread hyperkeratotic crusted plaques with massive mite load and high environmental shedding. See Figure: typical interdigital burrow pattern and mite lifecycle diagram in dermatology teaching atlases.

Risk Factors

  • Close/prolonged skin contact with an infested person, including sexual contact
  • Household crowding, institutional living (care homes, prisons, barracks), and social deprivation
  • Winter season (greater crowding and longer mite survival off-host)
  • Age groups with higher transmission risk (children/adolescents) and outbreaks involving elderly people
  • Immunosuppression (e. g, HIV, lymphoma, long-term systemic corticosteroids), predisposing to crusted scabies
  • Reduced ability to scratch or perceive itch (neurological disease, cognitive impairment, physical incapacity)

Clinical Features

Symptoms

  • Generalized intense itch, classically worse at night
  • Itch in close contacts/household members
  • Earlier and often brisker symptoms on reinfestation
  • Possible minimal or absent itch in crusted scabies, infants, or sensory impairment

Signs

  • Excoriated erythematous papules in typical distribution: finger webs, wrists, axillae, waist/periumbilical area, buttocks, genitalia, breasts, extensor limbs
  • Burrows (thin grey-brown serpiginous lines, usually 0.2-1 cm) - pathognomonic when seen
  • Nodular scabies (persistent itchy nodules), especially penis/scrotum, groin, axillae, buttocks
  • In infants/young children and elderly: involvement of palms, soles, and sometimes scalp/face
  • Crusted scabies: diffuse erythematous fissured hyperkeratotic crusted plaques, including bony prominences; may be malodorous if secondarily infected

Investigations

Clinical diagnosis (history + examination):Typical nocturnal pruritus, contact history, and characteristic lesion distribution often sufficient for diagnosis
Ink burrow test:Ink tracks along burrow producing a visible dark zig-zag/linear tract
Skin scraping microscopy (from papules/burrows, multiple sites):Mites, eggs, or scybala confirms diagnosis (very high specificity if mite seen; sensitivity often limited in classical disease)
Assessment for complications:Features of secondary bacterial infection (e. g, impetigo, folliculitis, abscess) or eczematization from scratching/treatment irritation

Management

Lifestyle Modifications

  • Treat index case and all household/close contacts simultaneously, even if asymptomatic
  • Avoid close physical/sexual contact until first treatment is completed by all contacts
  • Wash clothing, bedding, and towels used in previous 3 days at >=50 degrees C; seal non-washable items for at least 72 hours (longer for crusted scabies)
  • Trim nails and clean subungual debris; reinforce adherence to full-body application instructions
  • For crusted scabies, institute infection-control measures (contact precautions, environmental decontamination, specialist input)

Pharmacological Treatment

Topical scabicides (first-line)

  • Permethrin 5% cream: apply to entire body (include scalp/face/ears in infants, elderly, and where clinically indicated), leave on 8-12 hours then wash off; repeat after 7 days

Most UK first-line treatment; ensure complete coverage including finger/toe webs, under nails, genital area, and buttocks. In infants <2 months, seek specialist advice as standard permethrin regimens may be outside routine licensing.

Topical scabicides (alternative if permethrin unsuitable)

  • Malathion 0.5% aqueous liquid: apply to whole body, leave for 24 hours, then wash off; repeat after 7 days

Use when permethrin is not tolerated or contraindicated. Can irritate skin; treat concurrent eczema to improve tolerability and treatment success.

Systemic antiparasitic (usually specialist-directed, especially crusted scabies/outbreak failure)

  • Ivermectin oral 200 micrograms/kg per dose, repeated after 7-14 days (multiple-dose regimens may be required for crusted scabies alongside topical therapy)

In UK practice often used off-label for scabies; avoid in pregnancy and usually avoid in children <15 kg unless specialist recommendation. Combine with topical treatment in crusted scabies and monitor for treatment failure/reinfestation.

Symptom and complication control

  • Emollients regularly for barrier support
  • Moderate-potency topical corticosteroid (e. g, betamethasone valerate 0.025-0.1% once or twice daily short course) for post-scabetic eczema/nodules
  • Oral non-sedating antihistamine (e. g, cetirizine 10 mg once daily) for itch; sedating option at night if needed
  • If secondary bacterial infection: oral flucloxacillin 500 mg four times daily for 5-7 days (adult typical), or clarithromycin if penicillin-allergic per local policy

Post-treatment itch can persist up to 4 weeks and does not by itself indicate failure. Reassess diagnosis, adherence, and contact treatment before repeating courses.

Complications

  • Secondary bacterial infection (impetigo, folliculitis, furunculosis, ecthyma, abscess)
  • Post-scabetic nodules and persistent pruritus
  • Secondary eczematization/lichenification from scratching or irritant treatment effects
  • Institutional and household outbreaks, particularly severe in crusted scabies
  • In vulnerable patients, crusted scabies can be extensive and difficult to eradicate

Prognosis

With correct application of therapy and simultaneous contact treatment, prognosis is usually excellent and most classical cases clear after two appropriately timed topical treatments. Itching may continue for up to 4 weeks after eradication due to persistent hypersensitivity. Crusted scabies has a higher relapse/transmission risk and often needs prolonged combined therapy plus multidisciplinary and infection-control management.

Sources & References

💊BNF Drug References(4)

NICE Guidelines(1)

📖Textbook References(9)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1656)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1656)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1655, 1656)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1829)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1656)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1617, 1618)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1489)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1655, 1656)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1828, 1829)[context]

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