SkabiesB86

Author:Prof. Dr. med. Peter Altmeyer

Co-Autors:Dr. med. Eva Kämmerer, Aleksandra Kulberg, Dr. med. Jeton Luzha, Dr. med. Antje Polensky, Hadrian Tran

All authors of this article

Last updated on: 16.05.2024

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Synonym(s)

Acariasis; Acarodermatitis; Scabies

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HistoryThis section has been translated automatically.

Renucci 1835

DefinitionThis section has been translated automatically.

Frequent, globally spread, highly itchy parasitic skin infection caused by Sarcoptes scabiei hominis. The reactive dermatitis induced by the infection is to be interpreted as an immunological reaction of the organism to the mite components. The skin symptoms vary considerably depending on the age of the disease, individual reaction situation and intensity of body care.

PathogenThis section has been translated automatically.

Acarus siro var. hominis o. Sarcoptes scabiei hominis. See below Mites. Female scabies mites grow to 0.3-0.5 mm (males 0.21-0.29 mm) and are just visible as a black dot. Mating occurs on the surface of the skin. Male mites then die. Female mites dig tunnel-shaped tunnels in the stratum corneum and remain viable for about 30-60 days. Oxygen uptake by the mite occurs by diffusion over the skin surface. As a result, the mites penetrate only into the stratum corneum, rarely deeper. They lay 2-3 eggs per day, from which larvae hatch after 2-3 days. Scabies mites cannot survive outside the body for more than 48 hours. In immunocompetent patients, the number of mites found is low (10-12/patient). In immunocompetent patients, the number can increase to > 1 million mites (picture of scabies norvegica).

Occurrence/EpidemiologyThis section has been translated automatically.

Frequent, 200-400 million diseases/year worldwide. The prevalence is mainly based on socio-economic conditions, population density and hygienic circumstances. It fluctuates between < 1% and 30-40% and occurs epidemically.

EtiopathogenesisThis section has been translated automatically.

The transmission of the mated female by close physical contact (sexual contact, warmth of bed, living together in a small space, between children), less often via linen, textiles or fleeting contact (exception: Scabies norvegica). The risk of getting infected through bed linen in which a scabies patient had been lying is < 1: 200.

According to the classification of Coombs and Gell, post-scabial eczema is an allergic reaction of type IV (late type allergic reaction). The female scabies mite lays 4-6 eggs a day in so-called mite ducts, which are located in the stratum corneum and can reach the stratum granulosum. The mite eggs are recognized by the body as antigens and are internalized by Langerhans cells to be presented as T-helper cells which then release pro-inflammatory cytokines and chemokines to eliminate the target cells.

Efflorescence(s)This section has been translated automatically.

Redness, linear (comma-shaped) papules, scales, blisters, itching.

LocalizationThis section has been translated automatically.

Especially interdigital wrinkles of hands and feet, elbows, anterior axillary fold, areola, navel, girdle region, penis, ankle region, contact surfaces of the glutaeen. The back is less frequently affected, head and neck as well as palmae and plantae are always free, (exception in old people with atrophic palmae and plantae; in neglected patients the palms of the hands and soles of the feet may also be affected).

With long-term (unkempt) scabies, the emphasis on the typical "scabies regions" is lost. A generalised eczema picture then appears (picture of microbial eczema).

In infants and toddlers: basically ubiquitous, also Palmae and Plantae affected; back of fingers and feet, face.

Clinical featuresThis section has been translated automatically.

In the case of initial infection, scabies does not become clinically symptomatic until 3-6 weeks after infection. In the case of reinfection, clinical symptoms develop after only 24 hours. This leads to the fact that the mite is literally scratched out of the skin.

The leading symptom of scabies is intense itching, especially at night. In addition, there are coiled, millimeter-long, clearly palpable mite ducts with the mite at the end of the duct (mite mound) recognizable as a dark dot. Scratching, eczematization and secondary bacterial infections usually characterize the clinical picture.

The maculopapular, sometimes urticarial and papulovesicular skin changes are usually an expression of an allergic reaction of the organism to the mite infection (so-called Id reaction, Scabid).

S.a.

Other special forms:

  • Maintained scabies: Clinically, only isolated papules; diagnostically important is the detection of mite ducts, which, however, must be searched for. The strong nocturnal itching is indicative.
  • Neglected scabies: Clinical picture of an extensive "microbial eczema". Gait structures must be searched for, they are not in the foreground of the clinical picture. It is not uncommon for extensive verrucous plaques to form. Also weeping or pustular areas.
  • Persistent scabies granulomas: In young children and adults, even after sufficient antiscabies therapy, violently pruritic, 2-4 mm, usually scratched papules may persist, probably as a hyperergic reaction to the persistent scabies allergen (late-type reaction).
  • Post-scabies itching: Itching persisting for several days to weeks after sufficient scabies treatment.
  • Scabies incognita: Glucocorticoids, applied systemically or locally, can completely mask the clinical symptoms.
  • Localized scabies: An example of localized scabies may be therapy-resistant nipple eczema.
  • Scabies in infants and young children: face, head, neck, also genital region (!) and often (sometimes exclusively) palmae and plantae are affected. Efflorescences in children are often very succulent. There is persistent excruciating itching. Vesicles and pustules may occur. These may be clinically formative.
  • Scabies in seniors: especially in patients with dementia, scabies is often clinically atypical, e.g. without the typical pruritus (in a larger study in 61% of cases/especially with diabetes mellitus), only recognizable by therapy-resistant eczematoid lesions (Cassell JA et al. 2018).

Detection method:

  • Native detection of mites: opening of the mite duct using a fine cannula, application of the contents to a slide, native examination under a microscope.
  • It is also possible to visualize the mite duct by dabbing a dye (felt-tip pen) and applying a drop of alcohol (dye is drawn into the duct by capillary forces).
  • Microscopic detection of mites by means of reflected light microscopy (high sensitivity) (brownish triangular outline, formed by the anterior abdomen of the mite!).
  • Histological detection of the mites (easily possible especially with Scabies norwegica; otherwise mite detection is only possible in step sections, if at all).

HistologyThis section has been translated automatically.

Acanthosis, also focal spongiosis, orthokeratosis interspersed with parakeratosis mounds. Differing degrees of dermal oedema; dense, diffuse and perivascular lymphohistiocytic infiltrate penetrating the upper and middle (and often deep) dermis. Often more or less clearly pronounced histoeosinophilia. Not infrequently, mite excrement in the form of round or oval globules (skybala) can be detected in the str. corneum. In most cases, mites cannot be detected even in cut series.

Differential diagnosisThis section has been translated automatically.

Complication(s)This section has been translated automatically.

Development of post-scabial pruritus, persistent post-scabial papules or post-scabial eczema is possible. Occasional provocation of other dermatoses such as psoriasis, lichen planus or perforating, reactive collagenosis.

General therapyThis section has been translated automatically.

In older children and adults, the entire body is treated with the antiscabiosum without any gaps from the lower jaw downwards. In the case of skabies norwegica, the head must also be treated (recess of the periocular and perioral region). After rinsing or washing the product, new underwear should be applied! Beds are to be changed!

External therapyThis section has been translated automatically.

  • Adults and adolescents:
    • Permethrin 5% in a cream base (e.g. InfectoScab®) is therapy of 1st choice. Apply once for 8-12 hours, repeat after 14 days if necessary. In case of severe infestation with stationary treatment indication we recommend 3-day local treatment.
    • Alternative: Crotamiton (e.g. CROTAMITEX®) (see below).
    • Alternative: Benzyl benzoate (see below), in case of itching at the capillitium, co-treatment of the hairy scalp with Antiscabiosum 25% is possible, as this can be washed out of the hair as an emulsion.
    • Alternative: Allethrin I (e.g. Jacutin® MethylprednisolonaceponateMethylprednisolonacepona, Spregal® Spray (+ Piperonylbutoxide).
    • Alternative: 0.5% aqueous malathion lotion.
    • Alternative: 1% ivermectin lotion .
    • Notice. Additionally change outer clothing and bed linen daily. Bed linen should be washed at > 60 °C. Alternative: Store tightly in a plastic bag for 3-5 days. The mites will then die.

    • Alternative (rarely used): 5% tea tree oil.
    • Alternative (rarely used): 10% precipitated sulfur in vaseline or hydrophilic base(sulfur cream 2.5-10%): apply 2 times/day for 3-7 days each time after a soap bath.
  • Pregnancy (see below Pregnancy, Prescriptions):
    • Notice. None of the above mentioned agents is approved, therefore in pregnant women these therapy modalities are applicable in off-label use! Permethrin is listed in the Red List as a Group 4 drug, i.e. there is insufficient experience for use in humans, in animal studies there are no indications of embryotoxic/teratogenic effects.

    • Permethrin 5% in a cream base (e.g. InfectoScab) is 1st choice therapy. Apply once for 8-12 hr, repeat after 14 days if necessary.
    • Benzyl benzoate (e.g. Antiscabiosum Mago 25%; alterative NRF formulation: Benzyl benzoate emulsion 10 or 25%: apply 1 time/day, use for 3 days, then shower off.
    • Alternatively: 10% Crotamiton ointment (e.g. Crotamitex® gel/lotion/ointment)apply for 3-5 consecutive days. Cure rates vary between 50-70%.
  • Nursing mothers: therapy as for pregnant women.
    • Primarily apply permethrin and benzyl benzoate, see above. (Pyrethroids pass into breast milk; nothing is known about benzyl benzoate). According to the S1 guideline of the German Dermatological Society (as of 2016), a breastfeeding break of 5 days should be observed after treatment with permethrin and benzyl benzoates.
  • Newborns and infants:
    • Permethrin 2.5% ( R194 ), applied once over 8-12 hrs. Treatment of the entire integument including the head (excluding the mouth and eye area).
    • Alternatively: apply crotamiton ointment for 3-5 consecutive days.
    • Benzyl benzoate is not recommended; it is banned in the USA because of the so-called Gasping syndrome (severe progressive encephalopathy with metabolic acidosis and other symptoms). This syndrome occurred in infants whose catheters and infusion systems were flushed with benzyl alcohol.
  • Infants or older children:
    • Permethrin: Up to 2 years of age 2.5% ( R194 ), from 2 years of age 5% (e.g. Infectoscab 5.0% cream, not on capillitium, as not washable from hair) apply once over 8-12 hrs.
    • Alternative: Benzyl benzoate 10% (e.g. Antiscabiosum Mago 10% for children, if necessary co-treatment of the capillitium possible, because as emulsion washable out of the hair; or apply benzyl benzoate emulsion 10 or 25 % ( R027 ) 1 time/day, apply over 3 days, then shower off.

      Notice. Use of benzoyl benzoate is prohibited in neonates in the USA (deaths from use of infusion systems purified with benzyl alcohol [so-called Gasping syndrome = progressive encephalopathy, metabolic acidosis, bone marrow depression])!

    • Alternative: 2.5% precipitated sulfur in petrolatum or hydrophilic base ( R232 ): apply 2 times/day for 3-7 days each time after a soap bath (Cave: odor nuisance).
  • Immunosuppressed patients:
    • Permethrin 5% as recommended for adults. Repeat after 14 days.
    • In case of recurrence, in addition to local therapy, peroral application of ivermectin.
  • Severely eczematized patients:
    • Pretreatment with a glucocorticoid externum (e.g. 1% hydrocortisone cream) for 2-3 days; followed by classical antiscabi therapy.

Internal therapyThis section has been translated automatically.

In case of therapy resistance (frequent in patients with HIV infection), systemic therapy with ivermectin (e.g. Driponin® or Scabioral®) is recommended. Dosage: 200 µg/kg bw p.o. (max. up to 400 μg/kg bw) as a single dose, in cases of doubt always round up to whole 3 mg tablets. There is no maximum limit to the number of tablets to be taken. Calculated number of tablets to be taken all at once (with water) and 2 hours apart with a meal (empty stomach). This is usually a one-time treatment. Treatment may need to be repeated after 2-4 weeks. A return to communal facilities can take place after 24 hours according to the RKI recommendations (see source 1) if ivermectin is taken correctly.

NaturopathyThis section has been translated automatically.

Some smaller studies have been published about the alternative use of 5% tea tree oil, which prove the anti-cabiotic effect of this treatment. For further details see below. Tea Tree Oil.

AftercareThis section has been translated automatically.

Pre- and post-treatment: Glucocorticoid-containing topical preparations such as 0.25% prednicarbate (e.g. Dermatop® cream) or methylprednisolone aceponate (Advantan® cream or lotion) are used for post-treatment and in cases of severely oozing, irritated skin prior to therapy. Since killed mites continue to act as allergens in the skin for weeks, itching often persists for some time after treatment. For open, weeping areas, moist compresses with antiseptic additives such as potassium permanganate , see also Eczema, post-scabious.

Notice. Persistent itchy eczema in treated scabies is often due to sensitization to killed mites, but occasionally due to resistance to antiscabiosa or reinfection! Scabies granulomas should be treated with topical glucorticoids (under occlusion if necessary). In some cases, local injections with glucocorticoid crystal suspensions are necessary.

In contact persons: examination, co-treatment if disease is suspected.

Note(s)This section has been translated automatically.

  • If left untreated, scabies is chronic, but can also heal spontaneously after several years.
  • Resistance has been described for permethrin, crotamiton, lindane, and benzoyl benzoate.
    • A kdr mutation (knock-down resistance mutation) in the VSSC (voltage-sensitive sodium channel) in the neuronal membranes of S. scabiei var. hominis causes reduced efficacy of topical permethrin.
    • The mutation described is a non-synonymous A-to-T transversion: change of amino acid from methionine to leucine at position 918 (M918L mutation).
    • Permethrin binds preferentially to the open/active VSSC. The kdr mutation causes a shift of the channel to the closed state, resulting in poorer binding of the active compound and reduced efficacy, but no resistance.
    • there is still no in-vivo evidence of resistance to permethrin.
  • Notice. Studies on evidence and efficacy of topical antiscabiosa show the best success with permethrin.

  • School attendance is possible again after a single application of permethrin!

LiteratureThis section has been translated automatically.

  1. Agathos M (1994) Skabies. dermatologist 45: 889-903
  2. American Academy of Pediatrics (Scabies). In: Peter, G. (eds.) 2000 Red Book: Report of the Committee on Infectious Diseases, 25th ed. Elk Grove Village, IL pp. 506-508.
  3. Aristotle (340 BC) (1960) Animalium historia. In: Aristotle's opera, Volume I. De Gruyter Publishers
  4. Bezold G et al (2001) Hidden scabies: diagnosis by polymerase chain reaction. Br J Dermatol 144: 614-618
  5. Cassell JA et al (2018) Scabies outbreaks in ten care homes for elderly people: a prospective study ofclinical
    features, epidemiology, and treatment outcomes.Lancet Infect Dis 18:894-902.
  6. Chosidow O (2000) Scabies and pediculosis. Lancet 355: 819-826
  7. Chouela E et al (2002) Diagnosis and treatment of scabies: a practical guide. At J Clin Dermatol 3: 9-18
  8. Dupuy A et al (2006) Accuracy of standard dermoscopy for diagnosing scabies. J Am Acad Dermatol 56: 53-62
  9. Folster-Holst R et al (2000) Treatment of scabies with special consideration of the approach in infancy, pregnancy and while nursing. dermatologist 51: 7-13
  10. Haas N (1987) A simple vital-microscopic aid for the detection of the scabies mite. Z Hautkr 62: 1395-1398
  11. Hu S et al (2008) Treating scabies results. Arch Dermatol 144: 1638-1641
  12. Karre S et al (1997) Steroid-induced Scabies norvegica. dermatologist 48: 343-346
  13. Madan V et al (2001) Oral ivermectin in scabies patients: a comparison with 1% topical lindane lotion. J Dermatol 28: 481-484
  14. Müllegger RR et al (2010) Skin infections during pregnancy. dermatologist 61: 1034-1039
  15. Paasch U, Haustein UF (2001) Treatment of endemic scabies with allethrin, permethrin and ivermectin. Evaluation of a treatment strategy. dermatologist 52: 31-37
  16. Tzenow et al (1997) Oral treatment of scabies with ivermectin. Dermatologist 48: 2-4
  17. Walton S et al (2004) Acaricidal activity of melaleuca aternifolia (tea tree) oil. Arch Dermatol 140: 563-566

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Last updated on: 16.05.2024