Crusted scabies, also called Norwegian scabies, is a rare variant of ordinary scabies. This variant was first described in 1848 by Danielssen and Boeck, who considered the disease to be a form of leprosy endemic to Norway. [1] Unlike patients with ordinary scabies, who may be infested with only a small number of Sarcoptes scabiei mites, patients with crusted scabies harbor thousands to millions of these mites. [2,3]
While classic scabies has certain characteristic areas of involvement (e.g., the spaces between fingers, the flexor surfaces of the wrists and elbows), Norwegians scabies may occur in almost any area of the body. Crusted scabies frequently has an acral distribution, but it can also present as a generalized eruption. The infection is characterized by hyperkeratotic plaques and crusts that are far less pruritic than the typical inflammatory papules and burrows of classic scabies. [3,4]
Crusted scabies is highly contagious, often, producing outbreaks from a single case in a nursing home or on a hospital floor. [5,6] An infected patients' immediate environment, particularly his or her bedding and clothing, may be heavily infested with large numbers of mites. [6,7] Under normal conditions, the S. scabiei mite can live 24 hours off of its host, but under ideal temperature and humidity for the mite, it has been reported to live as long as 96 hours. [7]
Once considered as a possible diagnosis, crusted scabies is fairly easy to recognize. However, the infection is frequently overlooked because of its atypical presentations. In some situations, several months to a year may pass before the diagnosis is made. [6,8-10] Often, the diagnosis is discovered only after classic scabies develops in nursing staff. In patient contacts, pruritic papules without burrows typically occur on the extremities; these lesions are probably secondary to follicular irritation from immature mites or hypersensitivity to mite feces. [5,6]
Patient Populations
Patients with certain disorders or conditions may be predisposed to crusted scabies (Table 1). [2-4,7,8,11] The disease is more likely to occur in patients with cognitive deficiency and in institutionalized patients who are unable to properly interpret the pruritus associated with scabies infestation or are physically unable to respond to the itching. [3,9] Since scratching is thought to be important in the removal of mites, patients with poor cutaneous sensation due to neuropathy or systemic disease are at risk for worsening infestation.
Patients with immunodeficiency disorders have a decreased immune response to scabies infestation. Patients who are receiving immunosuppressive therapy, such as renal transplant recipients and patients who are receiving systemic or topical corticosteroid therapy, also have a decreased immune response to scabies. [3,4,6,7]
Diagnosis
Host factors are the prime determinants of the various presentations of crusted scabies. [4] Infection frequently presents as generalized dermatitis, usually associated with crusted hyperkeratosis and fissuring of the palms and soles, as well as involvement of the scalp, elbows and buttocks (Figures 1 through 5). Burrows are often obscured by the thick crusts. [4,6] The patient's nails may be dystrophic. [9] Pruritus is an inconsistent finding, most notable for its absence. [7,9]
The diagnosis of crusted scabies can be difficult to make based solely on the clinical presentation, since the disease can
TABLE 1
Predisposing Conditions
for Crusted (Norwegian) Scabies
TABLE 2
Differential Diagnosis of Crusted
(Norwegian) Scabies
mimic more common conditions such as psoriasis, eczema, drug eruption, and bacterial or fungal infections. [3,12] The wide range of manifestations of crusted scabies is reflected in its differential diagnosis (Table 2). [2,5,10,12]
Once crusted scabies is suspected, it is relatively easy to diagnose because of the large number of mites that are present. Microscopic examination of skin scrapings from crusted lesions treated with mineral oil or 10 percent potassium hydroxide reveals multiple mites [9] (Figure 6). Biopsy of the lesions, often performed when the diagnosis is unexpected, reveals mites burrowing in the stratum corneum of the epidermis [3] (Figure 7).
Treatment
LINDANE
A systematic treatment approach to crusted scabies is recommended. Lindane (Kwell, Scabene), the most widely used and most extensively studied scabicide, is a chlorinated hydrocarbon absorbed through the skin. [13,14] Peak serum levels are reached six hours after application. The half-life of this scabicide is 16 to 18 hours. Lindane is deposited in all lipid tissues, primarily the white matter of the brain. [15]
The advantages of lindane are its efficacy and the low incidence of resistance to this agent. If lindane is used strictly as directed, the potential for toxic effects may be minimuzed. [16] The use of lindane in pregnancy has not yet been studied in humans, although the scabicide has been reported to be nonmutagenic and nonteratogenic. [17]
One percent lindane cream or lotion should be applied to unbathed skin from the nexk down, and the patient should not bathe for the next eight to 12 hours. The risk of lindane ingestion, such as by children or by mentally impaired patients, may be minimized by applying lindane cream at bedtime and then washing it off in the morning. [13]
One application of lindane (or two applications spaced one week apart) is effective in patients with ordinary scabies, but patients with crusted scabies often require repeated applications of the scabicide. Consequently, care must be exercised to prevent lindane toxicity. Some authors have advocated weekly examination of skin and subungual scrapings from patients with crusted scabies before retreatment with lindane.
Daily application of lindane to localized hyperkeratotic crusts and subungual areas is recommended in crusted scabies, [13] but daily application to the entire body may result in toxicity. Therefore, in patients with extensive involvement, treatment may be spaced several days apart.
Keratolytic agents, such as 20 to 40 percent urea and 6 percent salicylic acid (Keralyt Gel), can be helpful at sites of hyperkeratosis. [6,13] Hydration of the skin prior to the application of lindane can help soften crusts to improve topical penetration. To avoid toxicity, the skin should be dry before the scabicide is applied. [4,18]
Scabies-positive or symptomatic family members and nursing staff (if the patient is institutionalized) should be treated with an application of lindane. Any person who has had direct contact with an infected patient in the preceding two months should be notified, examined and treated if symptomatic. Daily laundering of the patient's bedding and a daily change of all clothing are advised. [5,13,19]
Adverse reactions to lindane usually involve misuse or gross overexposure. [17] Acute toxic reactions include nausea, vomiting, convulsions, respiratory failure with cyanosis, and death. Chronic exposure to lindane causes blood dyscrasias (such as aplastic anemia or hypoplastic bone marrow), decreased liver function, altered menses and cardiac arrhythmias. [18]
Lindane therapy is contraindicated in premature infants and in patients with seizures. [20] To avoid possible accidental ingestion of lindane, child-proof containers should be used. Gloves should be worn when the scabicide is applied.
ALTERNATIVE SCABICIDES
Alternative agents for infants and young children include crotamiton (Eurax) and 5 to 10 percent precipitated sulfur in petrolatum. Although these agents are not as efficacious or as widely studied as lindane, they have been associated with fewer adverse reactions. [17,18]
A newer topical scabicide, 5 percent permethrin cream (Elimite), has been shown to be as efficacious as 1 percent lindane in eradicating classic scabies. [21] Less than 2 percent of permethrin is absorbed percutaneously, and the drug is rapidly broken down, conjugated and excreted as inactive metabolites. [22]
Permethrin has a wide margin of safety, and a second or even third treatment over a period of one month is unlikely to result in harmful effects. [22] Although not yet studied in the management of crusted scabies, permethrin may become the agent of choice for the treatment of this disease, primarily because of the lack of toxicity with repeated applications.
SYMPTOMATIC TREATMENT
Symptomatic measures, including anti-histamines for pruritus, an emulsifying agent for dry skin and low- to medium-potency topical corticosteroids for inflammation, may be used as needed in patients with crusted scabies. [13] Since secondary infection with Staphylococcus aureaus has occurred in some patients with crusted scabies, systematic antibiotics such as erythromycin or dicloxacillin may be indicated. [10]
REFERENCES
[1] Sweitzer SE, Winer LH. Norwegian scabies. Arch Dermatol Syphilol 1941;43:678-81.
[2] Espy PD, Jolly HW Jr. Norwegian scabies: occurrence in a patient undergoing immunosuppression. Arch Dermatol 1976;112:193-6.
[3] Yarbrough GK, Iriondo M. Diabetic patient with crusted plaques. Crusted (Norwegian) scabies. Arch Dermatol 1987;123:811,814.
[4] Hall JC, Brewer JH, Appl BA. Norwegian scabies in a patient with acquired immune deficiency syndrome. Cutis 1989;43:325-9.
[5] Burns DA. An outbreak of scabies in a residential home. Br J Dermatol 1987;117:359-61.
[6] Hopper AH, Salisbury J, Jegadeva AN, Scott B, Bennett GC. Epidemic Norwegian scabies in a geriatric unit. Age Ageing 1990;19:125-7.
[7] Barnes L, McCallister RE, Lucky AW. Crusted (Norwegian) scabies. Occurrence in a child undergoing a bone marrow transplant. Arch Dermatol 1987;123:95-7.
[8] Jucowics P, Ramon ME, Don PC, Stone RK, Bamji M. Norwegian scabies in an infant with acquired immunodeficiency syndrome. Arch Dermatol 1989;125:1670-1.
[9] Frost M, Parker C. Acral hyperkeratosis with erythroderma. Norwegian scabies. Arch Dermatol 1988;124:123,126.
[10] Shelley WB, Shelley ED, Burmeister V. Staphylococcus aureus colonization of burrows in erythrodermic Norwegian scabies. A case study of iatrogenic contagion. J Am Acad Dermatol 1988;19:673-8.
[11] Suzumiya J, Sumiyoshi A, Kuroki Y, Inoue S. Crusted (Norwegian) scabies with adult T-cell leukemia. Arch Dermatol 1985;121:903-4.
[12] Keipert JA. Norwegian scabies in a girl with psoriasis. Australas J Dermatol 1986;27:29-32.
[13] O'Donnell BF, O'Loughlin S, Powell FC. Management of crusted scabies. Int J Dermatol 1990;29;258-66.
[14] Kligman AM. Percutaneous absorption and gamma benzene hexachloride agents. Cutis 1981;28(Suppl):17-9.
[15] Davies JE, Dedhia HV, Morgade C, Barquet A, Maibach HI. Lindane poisonings. Arch Dermatol 1983;119:142-4.
[16] Shacter B. Treatment of scabies and pediculosis with lindane preparations: an evaluation. J Am Acad Dermatol 1981;5:517-27.
[17] Rasmussen JE. The problem of lindane. J Am Acad Dermatol 1981;5:507-16.
[18] Solomon LM, Fahrner L, West DP. Gamma benzene hexachloride toxicity: a review. Arch Dermatol 1977;113:353-7.
[19] Karslaw RW, Dobson RM, Hood AJ, Taylor RN. Mites in the environment of cases of Norwegian scabies. Br J Dermatol 1975;92:333-7.
[20] Pramanik AK, Hansen RC. Transcutaneous gamma benzene hexachloride absorption and toxicity in infants and children. Arch Dermatol 1979;115:1224-5.
[21] Schultz MW, Gomez M, Hansen RC, et al. Comparative study of 5% permethrin cream and 1% lindane lotion for the treatment of scabies. Arch Dermatol 1990;126:167-70.
[22] Taplin D, Meinking TL. Pyrethrins and pyrethroids in dermatology. Arch Dermatol 1990;126:213-21.
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