Scabies

oPatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Sarcoptes scabiei is an obligate human parasite. Scabies has caused pruritic infestation in humans for over 2,500 years, at least back to the Roman period. The Romans used 'scabies' to describe any itchy skin disease.

It was not until the 17th century that an Italian, Giovanni Cosimo Bonomo, identified a mite as the cause of scabies.[1] It is about 0.35 mm long. The female mite tunnels into the epidermis, and deposits eggs along the burrow. The larvae hatch in a few days and create new burrows. Development from egg to adult takes about 10-15 days. Mites die after 4-6 weeks. An average host harbours ten mites, but this may be greatly increased in immunocompromised patients.

It is often difficult to diagnose due to the spectrum of associated signs and symptoms and its clinical mimicry of other conditions. There is also a period of asymptomatic infection. Pruritus develops as a hypersensitivity reaction to infection. One should maintain a high index of clinical suspicion for scabies.[2]

It is a common public health problem with an estimated 300 million cases prevalent worldwide and serious side-effects associated with some of the drugs used in its treatment. There are also concerns about increasing resistance to drugs currently available.[3]

Classical scabies is transmitted only via direct skin contact. Skin contact times have to be significant to transfer mites.

  • Scabies epidemics usually occur in institutional settings or in socially deprived groups. The more crowded the living conditions, the higher the prevalence of scabies in the population.[4]
  • Outbreaks may occur in residential or nursing homes and occasionally in schools.
  • Scabies has a cyclical rise in incidence roughly every 20 years in the UK. Reported cases have been rising in the UK since 1991. About 100 people per 100,000 of the UK population see their GP every month with scabies.[5]

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Risk factors

  • More prevalent in:
    • Urban areas, especially with overcrowding.
    • Winter months.
    • Children and sexually active adults.[1] 
  • Immunocompromised (eg, HIV infection) and the elderly are at particular risk of the crusted variant. They tend to present with clinically atypical lesions and are often misdiagnosed, causing a delay in appropriate treatment and increased risk of a local epidemic.[1]
  • Crusted scabies can also be transmitted via bedding, towels, clothes and furniture.
  • In primary infestation, signs and symptoms only develop after 3-4 weeks. Infected contacts may be asymptomatic for up to a month which is why empirical treatment of all significant contacts is suggested. Symptoms reappear within a few hours if the person is re-infested.
  • It typically presents with a papular, intensely pruritic eruption, usually involving the interdigital spaces and flexural creases. The diagnosis can be made when a burrow is detected at a typical site and the lesion causes severe itching.
    SCABIES OF THE FINGER
    Scabies of the finger
  • The rash is symmetrical, usually consisting of small, red papules, particularly obvious on the inside of the thighs, axillae, periumbilical region, buttocks, and genitals. Vesicles or nodules may also occur.
  • Scabies frequently causes severe itching. Scratching promotes secondary infection. Pruritus tends to be worse at night and after a hot bath or shower. It usually develops 2-6 weeks after the initial infestation and appears at the same time as a rash.
  • Burrows appear as fine, wavy, greyish, dark or silvery lines, 2-15 mm long, with a minute speck (the mite) at the closed end. They are most often seen in the interdigital web spaces of the hands, flexor surfaces of the wrists and elbows, axillae, ankles, feet, buttock areas, male genitalia and periareolar area in women. Thick skin is relatively resistant, so sparing is seen of the soles of the feet and upper back region in adults.
  • Some authorities describe the 'wake' sign: scabies burrows are followed by a pattern of scale similar to the 'wake' left on the surface of water by a moving bird or a boat. The 'wake' sign is specific for scabies, can be seen with the naked eye and points towards the location of the mite.[6]
    SCABIES -BURROWS ON FINGER
    Scabies - burrows on a finger
  • Young children, the elderly and immunocompromised may also have face, neck, ear and scalp involvement.
  • Even a single burrow is pathognomonic but burrows are often obliterated by bathing, scratching, crusts, or superinfection.
  • Papules are small and erythematous. They can be sparse, or numerous and close-set. Over time papules can change into vesicles and bullae.[7]
    SCABIES OF THE LEG
    Scabies of the leg
  • Papules and vesicles frequently develop into excoriations, eczema exacerbations, secondary infections and crusts.
  • Nodules may develop, especially at the elbows, anterior axillary folds, penis, and scrotum. These are firm, dull red or brownish and may persist for months. They do not necessarily indicate active infestation.
  • Crusted scabies is a hyper-infestation with thousands of mites present in exfoliating scales, due to the host's insufficient immune response. Those at risk include:
    • The immunosuppressed (eg, HIV infection, leukaemia or lymphoma).
    • Elderly patients.
    • Those with decreased peripheral sensation.
  • Hyperkeratotic crusted lesions typically affect the hands, feet, nails, scalp and ears, but all areas of skin, including the scalp and trunk, may be involved.
  • Crusted scabies is a hyperkeratotic skin disease resembling psoriasis.[8]
  • It may present with generalised lymphadenopathy and be associated with eosinophilia.
  • It often becomes secondarily infected.
  • This form of scabies is very contagious and is far more difficult to eradicate than classical scabies.

Misdiagnosis is common and other skin disorders, particularly those causing itching, should be considered, including:

  • The diagnosis is largely clinical but can be confirmed by taking a skin scraping from an affected area, placing the material on a glass slide with a drop of 10% potassium hydroxide and seeing an adult mite, egg or eggshell under light microscopy.
  • Whilst the sensitivity of skin scrapings is low, it is very specific and a mite or eggs seen under the microscope will remove any doubt.[9]
  • All members of the household, close contacts, and sexual contacts should be treated simultaneously with the index patient. It is important that all contacts apply treatment on the same day to reduce the risk of re-infestation from an untreated contact. Patients should be advised to avoid close body contact until they and their partner(s) have completed treatment.
  • The primary method of treatment for scabies is by topical application of a parasiticidal preparation overnight to the whole body from head to toe. This should be repeated a week later.
  • Apply treatment to the whole body, including the scalp, neck, face, and ears, and especially between the fingers and toes and under the nails. Treatment should not be applied after a hot bath (as this increases systemic absorption and removes the drug from its treatment site). If the hands are washed, the liquid or cream must be reapplied.
    • First-line: permethrin 5% dermal cream has been the most widely studied. It has been shown to be more effective than topical crotamiton and oral ivermectin.[12] Patients with crusted 'Norwegian' scabies may require two or three applications on consecutive days to ensure that enough penetrates the hyperkeratotic areas to kill all the mites.
    • Second-line: malathion 0.5% aqueous liquid. Malathion has only been studied in non-controlled trials.
    • Crotamiton 10% cream or lotion: less effective than permethrin and is not recommended due to its poor efficacy. It may help to relieve the itch caused by scabies.
    • Oral ivermectin (as a single oral dose of 200 micrograms/kg) is available on a named-patient basis as an adjunct to topical treatment for crusted (Norwegian) scabies. This treatment is usually initiated on specialist advice.
    Note:[5]
    • Seek specialist advice for children under 2 months old - scabies is rare in this age group.
    • Breast-feeding or pregnant women with scabies can be treated with permethrin 5% dermal cream (or malathion if permethrin is contra-indicated), although neither is specifically licensed for such; there is, however, no indication that either product is harmful to the fetus or child. Breast-feeding mothers should remove the liquid or cream from the nipples before breast-feeding, and reapply treatment afterwards.
  • Clothes, towels, and bed linen should be machine-washed (at 50°C or above) to prevent re-infestation and transmission. Items that cannot be washed can be kept in plastic bags for at least 72 hours to contain the mites until they die.
  • Outbreaks of scabies in a residential or nursing home should be referred to Public Health. All residents, staff, and their families are treated simultaneously on an agreed treatment date.
  • The risk of transmission of scabies is low in schools and children can return to school after the first application of treatment has been completed.
  • Treatment of itch:
    • Antihistamines are of little help in treating pruritus. A sedative oral antihistamine at night may help with sleeping and so reduce scratching.
    • Crotamiton cream or lotion has soothing qualities and may help to relieve the itch caused by scabies.
    • Low-dose steroid creams or simple emollients and moisturisers stored in the fridge may also ease discomfort.
  • Suspect treatment failure where:
    • Itching persists >6 weeks after the first application of an insecticide
    • Treatment was not applied as instructed or unco-ordinated between close contacts.
    • New burrows appear.
    If incorrectly applied treatment has failed, repeat, ensuring all are clear as to instructions. Where correctly applied treatment has been ineffective, give a course of a different parasiticidal preparation. This reduces the development of resistance to the medication.
  • Secondary bacterial infections should be treated with antibiotics if significant.
  • The British Association of Sexual Health and HIV (BASSH) guidelines,[11] developed for use in GUM clinics, suggest that those with scabies should be offered full STI screening, as there is anecdotal evidence that rates of other infections are similar to other attendees.
  • Scabies can cause flaring or reactivation of eczema or psoriasis.
  • Secondary infection: scabies may be associated with secondary bacterial infection, especially with staphylococci or streptococci. Scabies is a risk factor for acute post-streptococcal glomerulonephritis.[4] Crusted scabies has a high mortality rate due to secondary sepsis in the immunosuppressed.
  • Scabies nodules may require intranodular corticosteroid injection for complete resolution.
  • Those whose immunity is highly sensitive can present with extensive dermatitis or even erythroderma.
  • Scabies has social stigma and may cause psychological harm with persistent delusions of parasitosis, shame or guilt.
  • Scabies persists indefinitely unless treated. Treatment, if applied correctly, has a high chance of cure. In endemic areas, re-infestation is likely.
    Itching can persist for up to three weeks after treatment: warn patients that this does not mean treatment has failed. However, if itching is becoming more intense and persisting for more than six weeks, this is suggestive of treatment failure.
  • Crusted scabies in those with HIV may be very difficult to eliminate.

Further reading & references

  • Scabies, DermIS (Dermatology Information System)
  • Scabies; DermNet NZ
  1. Cordoro KM et al; Dermatologic Manifestations of Scabies, Medscape, Jun 2012
  2. Page TL, Eiff MP, Judkins DZ, et al; Clinical inquiries. When should you treat scabies empirically? J Fam Pract. 2007 Jul;56(7):570-2.
  3. Mounsey KE, Holt DC, McCarthy J, et al; Scabies: molecular perspectives and therapeutic implications in the face of emerging drug resistance. Future Microbiol. 2008 Feb;3(1):57-66.
  4. Heukelbach J, Feldmeier H; Scabies. Lancet. 2006 May 27;367(9524):1767-74.
  5. Scabies; NICE CKS, December 2011
  6. Yoshizumi J, Harada T; 'Wake sign': an important clue for the diagnosis of scabies. Clin Exp Dermatol. 2008 Dec 2.
  7. Wozniacka A, Hawro T, Schwartz RA; Bullous scabies: a diagnostic challenge. Cutis. 2008 Nov;82(5):350-2.
  8. Goyal NN, Wong GA; Psoriasis or crusted scabies. Clin Exp Dermatol. 2008 Mar;33(2):211-2.
  9. Heukelbach J, Feldmeier H; Ectoparasites--the underestimated realm. Lancet. 2004 Mar 13;363(9412):889-91.
  10. British National Formulary; 64th Edition (Sep 2012) British Medical Association and Royal Pharmaceutical Society of Great Britain, London
  11. Management of scabies, British Association for Sexual Health and HIV (2008)
  12. Strong M, Johnstone PW; Interventions for treating scabies. Cochrane Database Syst Rev. 2007 Jul 18;(3):CD000320.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Colin Tidy
Current Version:
Peer Reviewer:
Dr Helen Huins
Last Checked:
25/01/2013
Document ID:
2990 (v24)
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