Generic selectors
Exact matches only
Search in title
Search in content
Post Type Selectors
Search in posts
Search in pages
Filter by Categories
15th National Conference of the IAOMFP, Chennai, 2006
Abstract
Abstracts from current literature
Acne in India: Guidelines for management - IAA Consensus Document
Addendum
Announcement
Art & Psychiatry
Article
Articles
Association Activities
Association Notes
Award Article
Book Review
Brief Report
Case Analysis
Case Letter
Case Letters
Case Notes
Case Report
Case Reports
Clinical and Laboratory Investigations
Clinical Article
Clinical Studies
Clinical Study
Commentary
Conference Oration
Conference Summary
Continuing Medical Education
Correspondence
Corrigendum
Cosmetic Dermatology
Cosmetology
Current Best Evidence
Current Issue
Current View
Derma Quest
Dermato Surgery
Dermatopathology
Dermatosurgery Specials
Dispensing Pearl
Do you know?
Drug Dialogues
e-IJDVL
Editor Speaks
Editorial
Editorial Remarks
Editorial Report
Editorial Report - 2007
Editorial report for 2004-2005
Errata
Erratum
Focus
Fourth All India Conference Programme
From Our Book Shelf
From the Desk of Chief Editor
General
Get Set for Net
Get set for the net
Guest Article
Guest Editorial
History
How I Manage?
IADVL Announcement
IADVL Announcements
IJDVL Awards
IJDVL AWARDS 2015
IJDVL Awards 2018
IJDVL Awards 2019
IJDVL Awards 2020
IJDVL International Awards 2018
Images in Clinical Practice
In Memorium
Inaugural Address
Index
Knowledge From World Contemporaries
Leprosy Section
Letter in Response to Previous Publication
Letter to Editor
Letter to the Editor
Letter to the Editor - Case Letter
Letter to the Editor - Letter in Response to Published Article
LETTER TO THE EDITOR - LETTERS IN RESPONSE TO PUBLISHED ARTICLES
Letter to the Editor - Observation Letter
Letter to the Editor - Study Letter
Letter to the Editor - Therapy Letter
Letter to the Editor: Articles in Response to Previously Published Articles
Letters in Response to Previous Publication
Letters to the Editor
Letters to the Editor - Letter in Response to Previously Published Articles
Letters to the Editor: Case Letters
Letters to the Editor: Letters in Response to Previously Published Articles
Medicolegal Window
Messages
Miscellaneous Letter
Musings
Net Case
Net case report
Net Image
Net Images
Net Letter
Net Quiz
Net Study
New Preparations
News
News & Views
Obituary
Observation Letter
Observation Letters
Oration
Original Article
ORIGINAL CONTRIBUTION
Original Contributions
Pattern of Skin Diseases
Pearls
Pediatric Dermatology
Pediatric Rounds
Perspective
Presedential Address
Presidential Address
Presidents Remarks
Quiz
Recommendations
Regret
Report
Report of chief editor
Report of Hon : Treasurer IADVL
Report of Hon. General Secretary IADVL
Research Methdology
Research Methodology
Resident page
Resident's Page
Resident’s Page
Residents' Corner
Residents' Corner
Residents' Page
Retraction
Review
Review Article
Review Articles
Reviewers 2022
Revision Corner
Self Assessment Programme
SEMINAR
Seminar: Chronic Arsenicosis in India
Seminar: HIV Infection
Short Communication
Short Communications
Short Report
Snippets
Special Article
Specialty Interface
Studies
Study Letter
Study Letters
Supplement-Photoprotection
Supplement-Psoriasis
Symposium - Contact Dermatitis
Symposium - Lasers
Symposium - Pediatric Dermatoses
Symposium - Psoriasis
Symposium - Vesicobullous Disorders
SYMPOSIUM - VITILIGO
Symposium Aesthetic Surgery
Symposium Dermatopathology
Symposium-Hair Disorders
Symposium-Nails Part I
Symposium-Nails-Part II
Systematic Review and Meta-Analysis
Systematic Reviews and Meta-analyses
Systematic Reviews and Meta-analysis
Tables
Technology
Therapeutic Guideline-IADVL
Therapeutic Guidelines
Therapeutic Guidelines - IADVL
Therapeutics
Therapy
Therapy Letter
Therapy Letters
View Point
Viewpoint
What’s new in Dermatology
Generic selectors
Exact matches only
Search in title
Search in content
Post Type Selectors
Search in posts
Search in pages
Filter by Categories
15th National Conference of the IAOMFP, Chennai, 2006
Abstract
Abstracts from current literature
Acne in India: Guidelines for management - IAA Consensus Document
Addendum
Announcement
Art & Psychiatry
Article
Articles
Association Activities
Association Notes
Award Article
Book Review
Brief Report
Case Analysis
Case Letter
Case Letters
Case Notes
Case Report
Case Reports
Clinical and Laboratory Investigations
Clinical Article
Clinical Studies
Clinical Study
Commentary
Conference Oration
Conference Summary
Continuing Medical Education
Correspondence
Corrigendum
Cosmetic Dermatology
Cosmetology
Current Best Evidence
Current Issue
Current View
Derma Quest
Dermato Surgery
Dermatopathology
Dermatosurgery Specials
Dispensing Pearl
Do you know?
Drug Dialogues
e-IJDVL
Editor Speaks
Editorial
Editorial Remarks
Editorial Report
Editorial Report - 2007
Editorial report for 2004-2005
Errata
Erratum
Focus
Fourth All India Conference Programme
From Our Book Shelf
From the Desk of Chief Editor
General
Get Set for Net
Get set for the net
Guest Article
Guest Editorial
History
How I Manage?
IADVL Announcement
IADVL Announcements
IJDVL Awards
IJDVL AWARDS 2015
IJDVL Awards 2018
IJDVL Awards 2019
IJDVL Awards 2020
IJDVL International Awards 2018
Images in Clinical Practice
In Memorium
Inaugural Address
Index
Knowledge From World Contemporaries
Leprosy Section
Letter in Response to Previous Publication
Letter to Editor
Letter to the Editor
Letter to the Editor - Case Letter
Letter to the Editor - Letter in Response to Published Article
LETTER TO THE EDITOR - LETTERS IN RESPONSE TO PUBLISHED ARTICLES
Letter to the Editor - Observation Letter
Letter to the Editor - Study Letter
Letter to the Editor - Therapy Letter
Letter to the Editor: Articles in Response to Previously Published Articles
Letters in Response to Previous Publication
Letters to the Editor
Letters to the Editor - Letter in Response to Previously Published Articles
Letters to the Editor: Case Letters
Letters to the Editor: Letters in Response to Previously Published Articles
Medicolegal Window
Messages
Miscellaneous Letter
Musings
Net Case
Net case report
Net Image
Net Images
Net Letter
Net Quiz
Net Study
New Preparations
News
News & Views
Obituary
Observation Letter
Observation Letters
Oration
Original Article
ORIGINAL CONTRIBUTION
Original Contributions
Pattern of Skin Diseases
Pearls
Pediatric Dermatology
Pediatric Rounds
Perspective
Presedential Address
Presidential Address
Presidents Remarks
Quiz
Recommendations
Regret
Report
Report of chief editor
Report of Hon : Treasurer IADVL
Report of Hon. General Secretary IADVL
Research Methdology
Research Methodology
Resident page
Resident's Page
Resident’s Page
Residents' Corner
Residents' Corner
Residents' Page
Retraction
Review
Review Article
Review Articles
Reviewers 2022
Revision Corner
Self Assessment Programme
SEMINAR
Seminar: Chronic Arsenicosis in India
Seminar: HIV Infection
Short Communication
Short Communications
Short Report
Snippets
Special Article
Specialty Interface
Studies
Study Letter
Study Letters
Supplement-Photoprotection
Supplement-Psoriasis
Symposium - Contact Dermatitis
Symposium - Lasers
Symposium - Pediatric Dermatoses
Symposium - Psoriasis
Symposium - Vesicobullous Disorders
SYMPOSIUM - VITILIGO
Symposium Aesthetic Surgery
Symposium Dermatopathology
Symposium-Hair Disorders
Symposium-Nails Part I
Symposium-Nails-Part II
Systematic Review and Meta-Analysis
Systematic Reviews and Meta-analyses
Systematic Reviews and Meta-analysis
Tables
Technology
Therapeutic Guideline-IADVL
Therapeutic Guidelines
Therapeutic Guidelines - IADVL
Therapeutics
Therapy
Therapy Letter
Therapy Letters
View Point
Viewpoint
What’s new in Dermatology
View/Download PDF

Translate this page into:

Review Article
2009:75:4;340-347
doi: 10.4103/0378-6323.53128
PMID: 19584457

Crusted scabies

Kaliaperumal Karthikeyan
 Sri Manakula Vinayagar Medical College, Kalitheerthalkuppam, Pondicherry, India

Correspondence Address:
Kaliaperumal Karthikeyan
Sri Manakula Vinayagar Medical College, Kalitheerthalkuppam, Pondicherry
India
How to cite this article:
Karthikeyan K. Crusted scabies. Indian J Dermatol Venereol Leprol 2009;75:340-347
Copyright: (C)2009 Indian Journal of Dermatology, Venereology, and Leprology

Abstract

Crusted scabies is a rare manifestation of scabies characterized by uncontrolled proliferation of mites in the skin. In immunocompromised patients, this infestation is characterized by crusted lesions. The occurrence of the disease in human immunodeficiency virus-infected patients and the widespread use of immunosuppressive agents has led to a renewed interest in the disease. Early recognition and treatment is necessary to avoid an outbreak of scabies. This review highlights the pathogenesis, predisposing factors, clinical features and treatment of crusted scabies.
Keywords: Crusted, Norwegian, Scabies

Introduction

Crusted scabies was described by Boeck and Danielssen among lepers in Norway in 1848. [1] It was named as "Scabies Norvegi Boeki" by von Hebra in 1862. This severe variant of scabies occurs as widespread hyperkeratotic crusted lesions and hence the name "crusted scabies" is preferred to the eponym of "Norwegian scabies." [2]

Crusted scabies is characterized by hyperkeratosis and crusting of the skin due to the profuse proliferation of mites resulting from an altered host response to the infestation. Various cutaneous, neurologic and immunologic diseases have been described to predispose to crusted scabies [Table - 1]. [3] Most of the reports are anecdotal case reports and only a few case series of crusted scabies exist in the literature. [4],[5],[6]

Etiology

The causative agent is the scabies mite, Sarcoptes scabiei var hominis . The mite is an obligate parasite that lives in burrowed tunnels in the stratum corneum. The female mite, the chief culprit, is about 400 microns in length and has a rounded body with four pairs of legs. The front two pairs end in "suckers" and the hind two pairs in long trailing bristles. [7]

In the skin, the mite survives on a diet of dissolved human tissue but does not feed on blood. It makes burrows of about 0.5-5mm in the stratum corneum every day. The mite lives in the burrow for a period of 30 days. The female lays two-three eggs daily and the eggs hatch in 3-4 days. The young larva passes through the nymphal stage to the mature adult mite stage in 14-17 days. It is estimated that only 10% of the eggs develop into adults. The average mite in normal patient is 11. [8] However, in case of crusted scabies, the number of mites is astronomical because of uncontrolled proliferation.

The incubation period before the onset of symptoms is 3-6 weeks for primary infestation, but may be as short as 1-3 days in reinfestation.

Pathogenesis

The cutaneous manifestations of scabies are due to the burrowing of the female mite in the stratum corneum and stratum malpighi followed by humoral and delayed hypersensitivity. [9] The mite antigens that trigger the immune response are probably in the saliva. Combined with scratching, the immune system in the healthy host will reduce the mite load but rarely eliminates the mite. The failure of the immune system to suppress the proliferation of the mite is an important cause of crusted scabies development. Crusted scabies typically develops in patients with a defective T-cell immune response or decreased cutaneous sensation and reduced ability to mechanically debride the mites. Crusted scabies also develops in Australian aborigines with normal immunity. [10] The reason for the occurrence of crusted scabies in this community is unclear. Certain studies have shown an association between scabies and HLA-A11. [11],[12]

Hyperkeratosis of the skin, which is a prominent feature in crusted scabies, is probably related to increased levels of interleukin-4. [12] Recent studies have shown that skin-homing cytotoxic T cells contribute to an imbalanced inflammatory response in the dermis of crusted scabies lesional skin. This, in combination with the lack of B cells, results in failure of the skin immune system to mount an effective response, resulting in uncontrolled growth of the parasite. [13]

The presentations vary from patient to patient, depending on the degree of immunosuppression and the underlying cause. [12],[13],[14],[15]

Transmission

Scabies is a highly contagious disease. The predominant route of transmission is skin-to-skin contact. Transmission via fomites is more commonly seen in crusted scabies. The immediate environment of a patient with crusted scabies is heavily infected with mites. Patients with crusted scabies are capable of triggering an epidemic of scabies. [6]

Clinical Features

Crusted scabies is a severe variant of highly contagious scabies. Itching, which is a hallmark of scabies, is minimal or absent. It is generally believed that patients with crusted scabies do not itch. But, at least 50% of the patients have some degree of itching. [6] The itch, if present, diminishes with time.

Crusted scabies usually do not present as an acute eruption as in classical scabies. The eruption is slow in onset and insidious in progression. There are two principle components - localized horny plaques and a more distinct erythematous appearance. The plaque is composed of a parakeratotic crust that varies in thickness from about 3 to 15mm [Figure - 1],[Figure - 2],[Figure - 3]. The crusts are creamy, grey, yellow brown or yellow green in color and are adherent and firm but, when removed, they have a porous appearance resembling a pumice stone. The lesions found over the extensor surface show fissuring. When the lesions are very large and thick, the whole surface may be broken up into slabs by these fissures. On removal of the crust, the undersurface is smooth, red, moist and velvety in appearance. Such crusts are seen over the palms, on the extensor aspect of the elbows, on the scalp and ears and on the soles of the feet and the toes. [6]

Crusted scabies may also present as psoriasiform dermatitis. It can also present as warty dermatosis of the hands and feet with hyperkeratosis of the nails. The nails are dystrophic with abundant psoriasis like subungual hyperkeratosis and debris. The nails are the frequent source of relapse.

Rarely, crusted scabies may involve the entire body, including the head and the scalp. This involvement may lead on to erythroderma. Sometimes, scabies can be localized to the scalp, penis, face, finger and soles. [6]

An isolated report of crusted scabies presenting as bullous pemphigoid-like eruption exists. This patient also had crusted lesions elsewhere on the body. In such patients, an indirect immunofluorescent study is important to distinguish between scabies with blister formation and true bullous pemphigoid. [16]

Complications

Crusted scabies is complicated by secondary bacterial infection by Staphylococcus aureus . They include impetigo, ecthyma, cellulitis and lymphangitis. [6] Generalized lymphadenopathy is another important complication. Rarely, septicemia may occur in these patients.

Differential Diagnosis

Crusted scabies can mimic a variety of conditions, [17] such as:

  • Psoriasis
  • Eczema
  • Seborrheic dermatitis
  • Darier′s disease
  • Pityriasis rubra pilaris
  • Lichen planus
  • Cutaneous lymphoma

Diagnosis

Diagnosis is based on clinical findings and the demonstration of the mite. Microscopic examination of the skin scrapings from the patient is essential to demonstrate the mites. The specimen from the crusted lesion is scraped with a blunt scalpel and placed on a glass slide. A drop of mineral oil and a cover slip are placed on it. The microscopic examination reveals numerous mites, eggs and mite feces (scybala). Demonstration of mites, eggs and mite feces (scybala) is diagnostic of scabies. [5] Epiluminescence microscopy and high-resolution videodermatoscopy are noninvasive techniques that allow a detailed inspection of the patient′s skin, from the surface to the superficial papillary dermis, and can be used to visualize the mite. [34],[35]

Further, standard dermoscopy is a useful tool for diagnosing scabies, with a high sensitivity, even in inexperienced hands. [36]

Histopathology can be diagnostic if mites or parts of the mite are identified in the section. Eosinophilia is found in 58% of the affected patients. The median immunoglobulin E levels were elevated in patients with crusted scabies in contrast to scabies. [37]

The DNA finger printing system for Sarcoptes scabiei , through the polymerase chain reaction technique, is useful in crusted scabies to determine whether the patient is really cured or is getting reinfested. Further, an outbreak of scabies in the family members and close contacts gives a clue to the diagnosis.

Any crusted lesion in a moribund or debilitated patient should be examined for Sarcoptes scabiei .

Histopathology of crusted scabies

The epidermis shows marked ortho and parakeratotic acanthosis and dermal cellular infiltrate. The subcorneal layer shows burrows containing female mites. Every section shows many burrows. [38]

The mites can be seen in all stages of development: Adult, larval, nymph and egg. Foci of spongiosis, spongiform pustules and neutrophilic abscess are seen in the spinous zone.

A dense superficial and deep perivascular infiltrate of numerous plasma cells are seen in the dermis. Eosinophils and neutrophils are seen around the blood vessels at all levels of the dermis, especially the upper half. [39]

Treatment

It is important to strictly isolate patients with crusted scabies as these patients can easily trigger an outbreak of scabies. The household contacts or hospital staff should be instructed to take adequate precautions to avoid getting infested. The nails of the patients should be clipped and scabicidals should be applied as nails are the frequent source of relapse. Adequate care should be given to moribund or paralysed patients to prevent relapse. Their clothes should be laundered. The principles involved in the treatment of scabies are given in [Table - 2].

Treating crusted scabies can be very challenging due to various factors such as host′s compromised immunity, widespread nature of the eruption, the high mite burden and the limited penetration of the topical agents into the hyperkeratotic lesion. Thus, the treatment of crusted scabies not only includes scabicidals but also keratolytic agents to remove the thick crusts, which are a nidus for the mite. In crusted scabies, hyperkeratotic crusts prevent the adequate penetration of topical scabicidals. Removal of these crusts can be performed by employing a keratolytic agent such as 5-10% salicylic acid in petrolatum, 40% urea or by soaking in a hot bath. This may bring down the mite load and also enhance the efficacy of topical scabicidals. [40]

Symptomatic treatment includes antihistamines for pruritus and an emollient for dry skin. Crusted scabies can be complicated by secondary bacterial infection. If septicemia occurs, it should be aggressively treated with broad-spectrum antibiotics.

Various topical agents and oral drugs used in the treatment of classical scabies are also used in treating crusted scabies. Repeated applications are usually required and clearing is slower compared with ordinary scabies. The sequential use of two or more different agents or a combination with an oral agent may be necessary. Several drugs have been in use to treat crusted scabies, including topical sulfur compounds, benzyl benzoate, crotamiton, lindane, malathion, permethrin and ivermectin. [41] The use of lindane is contraindicated due to increased percutaneous absorption and the risk of neurotoxicity following repeated application. [42],[43]

Topical permethrin, a synthetic pyrethroid formulation in a 5% cream, is presently the preferred topical scabicidal agent. [44]

Benzyl benzoate

Benzyl benzoate is synthetically derived from the esterification of benzoic acid with benzyl alcohol. Benzyl benzoate is neurotoxic to the mites. It is used as a 25% emulsion and the contact period is 24-36 h. Because of the side effects and availability of less- toxic agents, this scabicide had fallen into disrepute. However, recent studies have found it to be effective in the management of permethrin-resistant crusted scabies and in combination with ivermectin in patients with relapses after a single treatment with ivermectin. [45],[46]

Permethrin

Permethrin is a synthetic pyrethrin derivative. It acts to disrupt the neuronal sodium channel repolarisation and cause paralysis and eventual death of the insect. Permethrin is very effective against the mites and has a low mammalian toxicity. It is reliable and rarely produces side effects. [47] Permethrin is highly toxic to insects but is less toxic to humans. Topical permethrin, a synthetic pyrethroid formulation in a 5% cream, is presently the preferred topical scabicidal agent [48] and is often used in combination with oral ivermectin. [49] Permethrin is usually applied overnight to the entire body surface, with special attention to the finger and toe creases, nails, navel and cleft of the buttocks. Permethrin is useful as a topical agent in crusted scabies. But, repeated applications are necessary to eradicate the mites.

One major problem encountered with the use of topical scabicidals is that they require repeated application. Moreover, their efficacy, tolerability and specificity for crusted scabies are not well studied. Further, in patients with crusted scabies, the skin damage clearly attenuates the barrier function and poses a major toxicity risk if lindane is used. Hence, lindane should be avoided in crusted scabies. Permethrin is a good alternative, but requires repeated application. All these problems with topical antiscabietics can be avoided by the use of oral Ivermectin.

Ivermectin

Ivermectin is an effective oral scabicidal. It is a semisynthetic antihelminthic agent derived from Streptomyces avirmitilis . It acts by inhibiting the Gamma Amino Benzoic Acid (GABA) transmission in mites. It acts by binding with a high affinity to the glutamate-gated chloride ion channels in the nerve and muscle cells.

Although it is lethal in mites, it is safe in human as it does not cross the intact blood brain barrier. The toxic effect of ivermectin appears to be insignificant. Ivermectin is contraindicated in a patient with an allergy to ivermectin and central nervous system disorders.

Ivermectin has been used successfully in crusted scabies both as monotherapy or in combination with other scabicidals. [50],[51],[52] Although a single dose may be effective, many patients require two-three doses at an interval of 1-2 weeks. [53] This is because ivermectin has no residual drug activity against the parasite and treatment should be repeated if signs and symptoms recur. [54]

Roberts et al . used a five-dose regimen to treat patients with crusted scabies. [55] Ivermectin was administered on days 1, 2, 8,9 and 15, with additional two doses on days 22 and 29 in most severe cases. With this regimen, he observed a significant decrease in patient mortality.

Combination therapy

Crusted scabies is a severe form of scabies resistant to therapy. Treatment failure is common. Concomitant oral and topical treatment is useful in patients with crusted scabies. [56] This avoids repeated dosing and ensures early cure. Combination treatment regimens used include use of topical agents such as permethrin 5% cream with oral ivermectin. [57] Alberici et al . found that topical benzyl benzoate emulsion with oral Ivermectin was successful in severe crusted scabies. [46] These applications are repeated till the mites are eradicated. Correct application must be achieved, including the subungual areas and up to edges of lower body orifices. Additionally, the hyperkeratotic crusts should be scrubbed with topical scabicidals with nail trimming. Nail taping with 40% urea has also been tried. [57]

Methotrexate was tried in the treatment of crusted scabies. [58] The use of methotrexate in crusted scabies is more of a historical interest rather than a recommended modality of treatment, with the advent of less-toxic and more-specific drugs such as ivermectin.

Environmental Decontamination

Normally, scabies does not require an environmental decontamination. But, patients with crusted scabies present a unique scenario. Their crusts, teeming with mites and laden with viable eggs, are constantly shed into the environment. A population density of 6312 mites/g was demonstrated in the dust from the linen.[59] These patients should be considered a hazard to others and appropriate isolation techniques should be adopted. It has been seen on several occasions in nursing homes that the hospital staff become infected by changing bedding and mattress. Gloves and gowns should be used while changing the bedding. Clothes and bed linen can be decontaminated by washing at 60°C. The use of insecticidal powder or aerosol should be reserved for materials that cannot be washed. [60] Prophylactic treatment of contact may involve an entire institution or visitors and family members. [59]

Crusted Scabies And an Outbreak of Scabies

Patients with crusted scabies can trigger endemic outbreaks of common scabies. Crusted scabies in elderly hospitalized patients can trigger an epidemic. Further, preexisting dermatosis, such as atopic or contact dermatitis, and use of topical steroids may mask the symptoms and promote transmission. The high potential of transmission of crusted scabies can be explained by the recovery of mites of all stages from the furnishings.

Further transmission of mites may take place by the staff in old age homes. In case of a hospital outbreak, the index case is identified and started on treatment. All other patients in the ward and the staff should be treated simultaneously. The staff attending the patient with crusted scabies should wear gloves and a gown and avoid skin-to-skin contact. In contacts, permethrin 5% cream is used as first line followed by lindane and oral Ivermectin as third line.

Human Immunodeficiency Virus and Crusted Scabies

Scabies is commonly seen in HIV-infected patients. The defining clinical features are determined by the degree of immunosuppression. As the patients become more immunosuppressed, the more fulminant and contagious forms of scabies appear. These severe and unusual forms can be divided into papular and crusted scabies. Crusted scabies in acquired immunodeficiency syndrome (AIDS) patients can be manifested in both typical and atypical forms. Although the classic, hyperkeratotic, nonpruritic lesions are most common, reported cases have ranged in spectrum from crusting with pruritus to a pruritic, papular dermatitis to those resembling Darier′s disease or psoriasis. [61] Crusted (Norwegian) scabies usually occurs in patients with advanced HIV disease. [61],[62],[63] Although there are no definite studies to show the increase in the incidence of crusted scabies with the advent of HIV disease, a case series of crusted scabies from Dakar showed that HIV infection was the most commonly associated disease, seen in 45% of the patients. [5]

Crusted scabies superimposed on psoriatic erythroderma, particularly in patients with AIDS, can pose both diagnostic and therapeutic challenges.[64] But, the presence of atypical crusted lesions and scrapping of the lesion is always diagnostic. Further, crusted scabies should always be suspected in any crusted lesion in AIDS patients. In these patients, ivermectin and permethrin are found to be effective in treatment.

In patients with AIDS, crusted scabies can act as a portal of entry for the bacteria and lead to sepsis and death. [62]

Conclusion

Diagnosis and treatment of crusted scabies poses new challenges in the HIV era. Early diagnosis and proper treatment is the cornerstone to therapy. Ivermectin is the systemic drug of choice and repeated treatment may be required. But, no standardized protocols are available for treatment of crusted scabies. Further controlled double-blinded studies are needed to determine the best method of treatment. Future research is required to exactly understand the pathogenesis of the disease and the host-parasite interaction. Till then, crusted scabies cases will continue to occur and trigger epidemics of scabies.

References
1.
Danielsen DG, Boeck W. Treatment of Lleprosy or Greek Elephantiasis. Paris: JB Balliere; 1848.
[Google Scholar]
2.
Parish LC, Lomholt G. Crusted scabies alias Norwegian scabies. Int J Dermatol 1976;15:747-8.
[Google Scholar]
3.
Orkin M. Special forms of scabies. In: Scabies and Pediculosis. Orkin M, Maibach HI, Parish LC, and Schwartzman RM Editors. Philadelphia: Lippincott; 1977. p. 23-30.
[Google Scholar]
4.
Anbar TS, El-Domyati MB, Mansour HA, Ahmad HM. Scaly scalp associated with crusted scabies: Case series. Dermatol Online J 2007;13:18.
[Google Scholar]
5.
Dia D, Dieng MT, Ndiaye AM, Ndiaye B, Develoux M. Crusted scabies in Dakar apropos of 11 cases seen in a year. Dakar Med 1999;44:243-5.
[Google Scholar]
6.
Roberts LJ, Huffam SE, Walton SF, Currie BJ. Crusted scabies: Clinical and immunological findings in seventy-eight patients and a review of the literature. J Infect 2005;50:375-81.
[Google Scholar]
7.
Mellanby K. Biology of the parasite. In: Scabies and Pediculosis. Orkin M, Maibach HI, Parish LC, Schwartzman RM Eds. Philadelphia: Lippincott; 1977. p. 9-16.
[Google Scholar]
8.
Karthikeyan K . Scabies in children. Arch Dis Child Educ Pract Ed 2007;92:65-9.
[Google Scholar]
9.
Alexander JOD. Arthropods and skin. Berlin: Springer-Verlag, 1984:50-5.
[Google Scholar]
10.
Huffam SE, Currie BJ. Ivermectin for Sarcoptes scabiei hyperinfestation. Int J Infect Dis 1998;2:152-4.
[Google Scholar]
11.
Falk ES, Thorsby E. HLA antigens in patients with scabies. Br J Dermatol 1981;104:317-20.
[Google Scholar]
12.
Morsy TA, Romia SA, al-Ganayni GA, Abu-Zakham AA, al- Shazly AM, Rezk RA. Histocompatibility (HLA) antigens in Egyptians with two parasitic skin diseases (scabies and leishmaniasis). J Egypt Soc Parasitol 1990;20:565-72.
[Google Scholar]
13.
Walton SF, Beroukas D, Roberts-Thomson P, Currie BJ. New insights into disease pathogenesis in crusted (Norwegian) scabies: The skin immune response in crusted scabies. Br J Dermatol 2008;158:1247-55.
[Google Scholar]
14.
Karthikeyan K. Treatment of scabies: Newer perspectives. Postgrad Med J 2005;81:7-11.
[Google Scholar]
15.
Gladstone HB, Darmstadt GL. Crusted scabies in immunocompotent Child. Pediar Dermatol 2000;17:144-8.
[Google Scholar]
16.
Nakamura E, Taniguchi H, Ohtaki N. A case of crusted scabies with a bullous pemphigoid-like eruption and nail involvement. J Dermatol 2006;33:196-201.
[Google Scholar]
17.
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.
[Google Scholar]
18.
Meinking TL. Infestations. Current Problems in Dermatology 1999;11:80-103.
[Google Scholar]
19.
Mollison LC, Lo STH, Marning G. HTLV-1 and scabies in Australian aborigines (letter). Lancet 1993:342:1281-2.
[Google Scholar]
20.
del Giudice P, Sainte Marie D, Gιrard Y, Couppiι P, Pradinaud R. Is crusted (Norwegian) scabies a marker of adult T cell leukemia/lymphoma in human T lymphotropic virus type I-seropositive patients? J Infect Dis 1997;176:1090-2.
[Google Scholar]
21.
Espy PD, Jolly HW Jr. Norwegian scabies: Occurrence in a patient undergoing immunosuppression. Arch Dermatol 1976;112:193-6.
[Google Scholar]
22.
Barbosa Júnior Ade A, Silva TM, Santos MI, Garrido Mde F, Patel BN, Cavalcanti M, et al . Coexistence of an unusual form of scabies and lepromatous leprosy. A case report. Pathol Res Pract 1996;192:88-90; discussion 91-3.
[Google Scholar]
23.
Paterson WD, Allen BR, Beveridge GW. Norwegian scabies during immunosuppressive therapy. Br Med J 1973;4:211-2.
[Google Scholar]
24.
Gogna NK, Lee KC, Howe DW. Norwegian scabies in Australian Aborigines. Med J Aust 1985;142: 140-2.
[Google Scholar]
25.
Strobel M, Ball M, Moreira C, Fall M. Norwegian scabies and kwashiorkor. Ann Dermatol Venereol 1982;109:87-8.
[Google Scholar]
26.
Hissard R, Jacquet J, Villette O. Norwegian scabies and vitamin A. C R Hebd Seances Acad Sci 1955;241:1003-5.
[Google Scholar]
27.
Dourmishev A, Miteva L, Mitev V, Pramatarov K, Schwartz RA. Cutaneous aspects of Down syndrome. Cutis 2000;66:420-4.
[Google Scholar]
28.
Van Der Wal VB, Van Voorst Vader PC, Mandema JM, Jonkman MF. Crusted (Norwegian) scabies in a patient with dystrophic epidermolysis bullosa. Br J Dermatol 1999;141: 918-21.
[Google Scholar]
29.
Chutimunt N. Crusted scabies associated with systemic lupus erythematosus: Response to benzyl benzoate therapy. J Med Assoc Thai 1996;79:65-8.
[Google Scholar]
30.
Angelo C, Pedicelli C, Provini A, Annessi G, Zambruno G, Paradisi M. Successful treatment of Norwegian scabies with ivermectin in a patient with recessive dystrophic epidermolysis bullosa. Minerva Pediatr 2004;56:353-7.
[Google Scholar]
31.
Hay RJ. Norwegian scabies in a patient with a cutaneous vasculitis. Guys Hosp Rep 1974;123:177-85.
[Google Scholar]
32.
Yarbrough GK, Iriondo M. Diabetic patient with crusted plaques. Crusted (Norwegian) scabies. Arch Dermatol 1987;123:811-4.
[Google Scholar]
33.
Wolf R, Wolf D, Viskoper R, Sandbank M. Norwegian-type scabies mimicking contact dermatitis in an immunosuppressed patient. Postgrad Med 1985;78:228-30.
[Google Scholar]
34.
Haas N, and Sterry. W. The use of ELM to monitor the success of antiscabietic treatment. Epiluminescence light microscopy. Arch Dermatol 2001;137:1656-7.
[Google Scholar]
35.
Micali G, Lacarrubba F, Tedeschi A. Videodermatoscopy enhances the ability to monitor efficacy of scabies treatment and allows optimal timing of drug application. J Eur Acad Dermatol Venereol 2004;18:153-4.
[Google Scholar]
36.
Dupuy A, Dehen L, Bourrat E, Lacroix C, Benderdouche M, Dubertret L, et al . Accuracy of standard dermoscopy for diagnosing scabies. J Am Acad Dermatol 2008;59:530.
[Google Scholar]
37.
Arlian LG, Morgan MS, Estes SA, Walton SF, Kemp DJ, Currie BJ. Circulating IgE antibodies with ordinary and crusted scabies. J Med Entomol 2004;41:74-7.
[Google Scholar]
38.
Fernandez N, Torrus A, Ackerman AB. Pathological findings in human scabies. Int J Dermatol 1981;20:600.
[Google Scholar]
39.
Ackerman AB. Histopathology of human scabies. Orkin M, Maibach HI, Parish LC, and Schwartzman RM Eds. Philadelphia: Lippincott; 1977. p. 88-95.
[Google Scholar]
40.
Bitman LM, Rabinowitz AD. Hyperkeratotic plantar plaques in HIV positive patient. Crusted scabies. Localized to soles. Arch Dermatol 1998:134;1019,1022-3.
[Google Scholar]
41.
Scheinfeld N. Controlling scabies in institutional settings: A review of medications, treatment models, and implementation. Am J Clin Dermatol 2004;5:31-7.
[Google Scholar]
42.
Solomon BA, Haut SR, Carr EM, Shalita AR. Neurotoxic reaction to lindane in an HIV-seropositive patient. An old medication's new problem. J Fam Pract 1995;40:291-6.
[Google Scholar]
43.
Katsumata K, Katsumata K. Norwegian scabies in an elderly patient who died after treatment with gamma BHC. Intern Med 2003;42:367-9.
[Google Scholar]
44.
Centres for Disease Control and Prevention Sexually transmitted disease treatment guidelines2002 MMWR Morb Mort wkly Rep 2002;5:67-9.
[Google Scholar]
45.
Anderson BM, Haughen H, Rasch M. Outbreak of scabies in Norwegian nursing homes and home care patients; Control and prevention. J Hosp Infect 2000;45:160-4.
[Google Scholar]
46.
Alberici F, Pagani L, Ratti G, Viale P. Ivermectin alone or in combination with benzyl benzoate in the treatment of human immunodeficiency virus associated scabies. Br J Dermatol 2000;142:969-72.
[Google Scholar]
47.
Roos TC, Alam M, Roos S, Merk HF, Bickers DR . Pharmacotherapy of ectoparasitic infections. Drugs 2001;61:1067-88.
[Google Scholar]
48.
Burkhart CG, Burkhart CN, Burkhart KM. An epidemiologic and therapeutic reassessment of scabies. Cutis 2000;65:233-40.
[Google Scholar]
49.
Del Giudice P, Marty P. Ivermectin: A new therapeutic weapon in dermatology? Arch Dermatol 1999;135:705-6.
[Google Scholar]
50.
Del Giudice P, Chosidow O, Caumes E. Ivermectin in dermatology. J Drugs Dermatol 2003;2:13-21.
[Google Scholar]
51.
Aubin F, Humbart P.Ivermectin for crusted (Norwegian) scabies. N Eng J Med 1995;333:26-30.
[Google Scholar]
52.
Kar SK, Mania J, Patnaik S. The use of ivermectin for scabies. Natj Med J India.1994;7:15-6.
[Google Scholar]
53.
Chosidow O. Scabies and pediculosis. Lancet 2000;355:819-2I.
[Google Scholar]
54.
Cestari SC, Petri V, Rotta O, Alchorne MM. Oral treatment of crusted scabies with ivermectin: Report of two cases. Pediatr Dermatol 2000;17:410-4.
[Google Scholar]
55.
Roberts LJ, Huffam SE, Walton SF, Currie BJ. Crusted scabies: Clinical and immunological findings in seventy-eight patients and a review of the literature. J Infect 2005;50:375-81.
[Google Scholar]
56.
Meinking TL, Elgart WE. Scabies therapy for the millenium. Pediatric Dermatol 2000;2;154-6.
[Google Scholar]
57.
Bertrand R. Parasitic infections of the nails. Dermatol Online J. 2003;9:17Ct.
[Google Scholar]
58.
Ward WH. Scabies norvegica. Treatment with methotrexate. Australas J Dermatol 1971;12:44-51.
[Google Scholar]
59.
Carslaw, Zafar AB, Beidas SO et al., Control of transmission of Norwegian scabies. Infect Control Hosp Epidemiol. May 2002; 23(5): 278-9.
[Google Scholar]
60.
Schlesinger I, Oelrich DM, Tyring SK. Crusted (Norwegian) scabies in patients with AIDS: The range of clinical presentations. Crusted (Norwegian) scabies in patients with AIDS: The range of clinical presentations. South Med J 1994;87:352-6.
[Google Scholar]
61.
Rau RC, Baird IM. Crusted scabies in a patient with acquired immunodeficiency syndrome. J Am Acad Dermatol 1986;15:1058-9.
[Google Scholar]
62.
Glover A, Young L, Goltz AW. Norwegian scabies in acquired immunodeficiency syndrome: Report of a case resulting in death from associated sepsis. J Am Acad Dermatol 1987;16:396-9.
[Google Scholar]
63.
Drabick JJ, Lupton GP, Tompkins K. Crusted scabies in human immunodeficiency virus infection. J Am Acad Dermatol 1987;17:142.
[Google Scholar]
64.
Fuchs BS, Sapadin AN, Phelps RG , Rudikoff D . Diagnostic dilemma: Crusted scabies superimposed on psoriatic erythroderma in a patient with acquired immunodeficiency syndrome. Skinmed 2007;6:142-4.
[Google Scholar]

Fulltext Views
18,457

PDF downloads
3,346
Show Sections