Skabies B86

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: 24.11.2024

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Synonym(s)

Acariasis; Acarodermatitis; Scabies

History
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Renucci 1835

Definition
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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.

Pathogen
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Acarus siro var. hominis or Sarcoptes scabiei hominis. See mites below. Female scabies mites are 0.3-0.5 mm in size (males 0.21-0.29 mm) and are just visible as a black dot. Mating takes place on the surface of the skin. Male mites then die. Female mites dig tunnel-like tunnels in the stratum corneum and remain viable for about 30-60 days. The mite absorbs oxygen by diffusion over the skin surface. As a result, the mites only penetrate 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 rise to > 1 million mites (picture of Scabies crustosa/S. norvegica=old term).

Occurrence/Epidemiology
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Common, 200-400 million cases/year worldwide. The prevalence depends largely on socio-economic conditions, population density and hygienic circumstances. It varies between < 1% and 30-40% and occurs epidemically. The prevalence is highest in subtropical and tropical regions, with children being affected disproportionately often. Scabies has been one of the WHO's neglected tropical diseases since 2017, but cases of scabies have also risen sharply in Europe in recent years. Exact figures on prevalence and incidence are not available due to the lack of mandatory reporting.

Etiopathogenesis
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Transmission of the mated female through close physical contact (sexual contact, bed warmth, living together in a small space, between children), less frequently via laundry, textiles or fleeting contact (exception: Scabies norvegica). Brief contact such as shaking hands, hugging or touching the skin in the medical field does not pose a risk of infection. The risk of becoming infected through bed linen in which a scabies patient has lain is < 1: 200. There is a high risk of transmission with scabies crustosa (scabies norvegica = older name), which occurs mainly in immunocompromised patients. In this highly contagious form, millions of mites are found in the infested skin or in the scales (Sunderkötter C et al. 2016).

Pathophysiology
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The number of mites rises rapidly to several hundred in the first three to four months after initial infection. The number drops again quickly to around five to fifteen mites in immunocompetent individuals as part of an immune response mediated by T helper cells type 1/-2 and as a result of mechanical removal by scratching or washing (see also the special features of Scabies crustosa). According to the classification of Coombs and Gell, post-scabies eczema is a type IV allergic reaction (late-type allergic reaction). The female itch mite lays 4-6 eggs per day in so-called mite ducts, which are located in the stratum corneum and can extend into the stratum granulosum. The characteristic itching and the typical eczema reaction are due to a cell-mediated immune reaction of the late type, which is directed against mite components and excrements. In the case of initial infestation, symptoms appear after two to five weeks, whereas in the case of reinfestation they are observed after just one to four days. Furthermore, IgE, IgM and IgG antibodies are formed, whereby the humoral immune response leaves no protective immunity against further infestations (Sunderkötter C et al. 2016).

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

Localization
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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 features
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Scabies does not become clinically symptomatic until 3-6 weeks after infection. In the case of reinfection, clinical symptoms develop after just 24 hours. This leads to the mite being literally scratched out of the skin.

The main symptom of scabies is severe itching, particularly at night. In addition, there are winding, millimetre-long, clearly palpable mite ducts with the mite visible as a dark spot at the end of the duct (mite mound). Scratching effects, 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:

  • Cultivated scabies: Clinically only isolated papules; diagnostically important is the detection of mite ducts, which, however, must be sought. The strong nocturnal itching is indicative.
  • Neglected scabies: Clinical picture of extensive "microbial eczema". It is necessary to look for duct structures, 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.
  • Scabies nodosa (persistent scabies granulomas): In young children and adults, even after sufficient antiscabial therapy, intensely itchy, 2-4 mm large, usually scratched papules may persist, probably as a hyperergic reaction to the persistent scabies allergen (late-type reaction).
  • Post-scabies itching: Persistent itching for several days to possibly 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 treatment-resistant nipple eczema.
  • Scabies in infants and small children: Face, head, neck, also genital region (!) and often (sometimes exclusively) Palmae and Plantae are affected. Efflorescences in children are often very succulent. Agonizing itching persists. Vesicles and pustules may occur. These may be clinically formative.
  • Scabies in the elderly: especially in patients with dementia, scabies is often clinically atypical, e.g. even without the typical pruritus (in a larger study in 61% of cases/especially with existing diabetes mellitus), only recognizable by therapy-resistant eczmatoid 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 microscope slide, native examination under the microscope.
  • It is also possible to visualize the mite duct by dabbing on a dye (felt-tip pen) and applying a drop of alcohol (dye is drawn into the duct by capillary forces).
  • Microscopic detection of mites using reflected light microscopy (high sensitivity) (brownish triangular outline formed by the mite's abdomen).
  • Histological detection of the mites (easily possible, especially in Scabies norwegica; otherwise mite detection is only possible in step sections, if at all).

Histology
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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.

Diagnosis
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If symptoms typical of scabies are present (e.g. pruritus, suspicious skin florescences at the predilection sites), a suspected diagnosis can initially be made in conjunction with the epidemiological situation (infestation in the immediate vicinity). In accordance with the consensus criteria of the International Alliance for the Control of Scabies (IACS), a distinction is made between confirmed scabies, in which the mite or its products are directly visualized (level A), and clinical (level B) and suspected scabies (level C) in order to standardize the diagnosis.

A: confirmed scabies at least one point applicable

- A1: Detection of mites, eggs or feces in skin samples by light microscopy

- A2: Detection of mites, eggs or feces by imaging devicea

- A3: Detection of mites by dermoscopy

B: clinical scabies at least one point applicable

- B1: presence of mite ducts

- B2: typical lesions on the male genitalia

- B3: typical lesions with typical distribution pattern and two anamnestic criteriab

C: suspected scabies at least one point applicable

- C1: typical lesions with typical distribution pattern and one anamnestic criterionb

- C2: atypical lesions with atypical distribution pattern and two anamnestic criteriab

The diagnosis can be made at three levels (A, B or C). Clinical (B) or suspected scabies (C) should only be diagnosed if other differential diagnoses are considered less likely.

Differential diagnosis
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Complication(s)
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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 therapy
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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 therapy
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  • 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 therapy
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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.

Naturopathy
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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.

Aftercare
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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)
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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 a reduced efficacy of topical permethrin.
  • The described mutation is a non-synonymous A-to-T transversion: change of the 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 substance and a reduced effect, but no resistance. There is still no in-vivo evidence of resistance to permethrin.

Note! Studies on the evidence and efficacy of topical antiscabiosa show the best results with permethrin.

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

Literature
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  1. Agathos M (1994) Scabies. Dermatology 45: 889-903
  2. American Academy of Pediatrics (Scabies). In: Peter, G. (ed.) 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: Aristotelis opera, vol. I. De Gruyter Verlag
  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 of
  6. clinical features, epidemiology, and treatment outcomes.Lancet Infect Dis 18:894-902.
  7. Centers for Disease Control and Prevention. Parasites - Scabies. https://www.cdc.gov/parasites/scabies/index.html (2023). last accessed on 24.11.2024
  8. Chosidow O (2000) Scabies and pediculosis. Lancet 355: 819-826
  9. Chouela E et al (2002) Diagnosis and treatment of scabies: a practical guide. Am J Clin Dermatol 3: 9-18
  10. Dupuy A et al. (2006) Accuracy of standard dermoscopy for diagnosing scabies. J Am Acad Dermatol 56: 53-62
  11. 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
  12. Haas N (1987) A simple vital microscopic aid for the detection of the scabies mite. Z Hautkr 62: 1395-1398
  13. Hu S et al. (2008) Treating scabies results. Arch Dermatol 144: 1638-1641
  14. Karre S et al (1997) Steroid-induced scabies norvegica. Dermatologist 48: 343-346
  15. Madan V et al. (2001) Oral ivermectin in scabies patients: a comparison with 1% topical lindane lotion. J Dermatol 28: 481-484
  16. Müllegger RR et al (2010) Skin infections in pregnancy. Dermatologist 61: 1034-1039
  17. Paasch U, Haustein UF (2001) Treatment of endemic scabies with allethrin, permethrin and ivermectin. Evaluation of a treatment strategy. Dermatologist 52: 31-37
  18. Sunderkötter C et al. (2016) S1 guideline on the diagnosis and treatment of scabies; AWMF registry no. 013-052)
  19. Tzenow et al. (1997) Oral treatment of scabies with ivermectin. Dermatologist 48: 2-4
  20. Walton S et al. (2004) Acaricidal activity of melaleuca aternifolia (tea tree) oil. Arch Dermatol 140: 563-566

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