C a s e S t u d i e s

142 May • June 2007

Patients with AIDS can manifest a wide variety of skin eruptions, leading to difficulties in diagnosis. Severe psoria-

sis and crusted scabies, both known causes of generalized erythroderma, have been reported in patients infected with human immuno-deficiency virus (HIV).1–3 Crusted scabies is a particularly severe form of infestation, with Sarcoptes scabiei seen in patients with vari-ous conditions, including mental retardation, physical debilitation, and malignant tumors.4

Individuals with immunosuppression from HIV infection, leukemia, lymphoma, and lep-rosy are at risk. Occasionally infestation is seen in patients receiving systemic immunosuppres-sant drugs and rarely with topical immunosup-pressants.5 Other risk factors are alcoholism, mental disorders, neurologic diseases, Down syndrome, and sensory neuropathy. Infestation has been described in association with chronic mucocutaneous candidiasis and dystrophic epidermolysis bullosa.6 Crusted scabies has been associated with human T-lymphotrophic virus (HTLV)-I/II infection in some studies.7 In classic scabies, the average host has only 5 to 15 mites. In crusted scabies, a patient can be infected with millions of mites.

Crusted scabies in AIDS patients is manifested in both typical and atypical forms. Lesions are occasionally localized, but more frequently are widespread, with extensive thick, hyperkeratotic plaques on the extremities, back, face, scalp, and periungual region.1,8 Although hyperkeratotic,

From the Department of Dermatology, Mount Sinai

School of Medicine, New York, NY

Address for correspondence: Donald Rudikoff, MD,

Department of Dermatology, Mount Sinai School of Medicine,

1 Gustave L. Levy Place, New York, NY 10029

E-mail: rnahybrid@aol.com

C a s e S t u d i e s

A 45-year-old man with AIDS presented with extensive erythema and scaling involving the face, trunk, and upper and lower extremities, and mild nail dystrophy. The patient had been diagnosed with psoriasis 2 years previously, and at the time of presentation was using emollients and topical corticosteroid creams with little improvement. He was receiving zidovudine, lamivudine, trimethoprim/sulfamethoxazole, acyclovir, rifabutin, and hydroxyzine. Pertinent laboratory data included CD4 lymphocytes (10 cells/mm3), viral load (32,000 copies per mL) white blood cell count (3.4 × 103/µL), hemo-globin (13.5 g/dL), and platelets (204 × 103/µL). Because of the extensive eruption and lack of response to topical agents, the patient was started on acitretin 25 mg daily. The patient had shown no signs of improvement 4 weeks later and was noted to have brownish gray crusted plaques involving the beard area, neck, upper part of the back, arms, trunk, genitals, and thighs in addition to his erythroderma (Figure 1 and Figure 2). Microscopic examination of scales from the upper part of the back revealed numerous scabies mites and eggs. He was then treated with lindane shampoo on the scalp and beard area and permethrin 5% cream to the body. The patient returned 2 weeks later with some improvement after thrice-weekly applications of this regimen; however, scrapings from the trunk once again revealed live scabies mites. Microscopic examination of scales that had fallen on the examination table revealed multiple mites and eggs. The patient was then given permethrin 5% cream, which he applied 3 times a week for 2 weeks, and 1 dose of oral ivermectin, 200 μg/kg. This resulted in a marked decrease in crusting and scaling. With resolution of the scabies lesions, the patient displayed marked erythema and scaling of the trunk and extremities consistent with generalized psoriasis (Figure 3). Treatment with acitretin resulted in gradual resolution of the erythroderma. A few months later, the patient presented with nodules on the upper part of the back, which on biopsy revealed a scabies mite (Figure 4).

www.lejacq.com ID: 5723

Diagnostic Dilemma: Crusted Scabies Superimposed on Psoriatic Erythroderma in a Patient With Acquired Immunodeficiency SyndromeBrian S. Fuchs, BA; Allen N. Sapadin, MD; Robert G. Phelps, MD; Donald Rudikoff, MD

Vesna Petronic-Rosic, MD, MSc, Section Editor Section of Dermatology, University of Chicago, Pritzker School of Medicine, Chicago, IL

Figure 1. Hyperkeratotic crusting of the beard area.

SKINmed: Dermatology for the Clinician® (ISSN 1540-9740) is published bimonthly (Jan., March, May, July, Sept., Nov.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT 06484. Copyright ©2007 by Le Jacq. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Karen Hurwitch at KHurwitch@bos.blackwellpublishing.com or 781-388-8470.

®

C a s e S t u d i e s

143May • June 2007

nonpruritic lesions are the norm, thick crust-ed plaques, red papules, psoriasiform plaques, and hyperkeratotic yellow-colored papules resembling Darier disease have been reported.9 Substantial crusting is often evident on the extremities, periungual areas, and the face.1,2 Typical burrows and pruritus are often absent.

The inflammatory lesions of scabies infestation are considered to be a delayed-type hypersen-sitivity reaction. It is thought that lesions of crusted scabies result in part from deficient cell-mediated immunity that allows massive replication of mites. In mice, immunization with scabies extract induced interferon (IFN)-γ production by splenic and lymph node lym-phocytes. In scabies-naïve mice, infestation with scabies caused increased production of interleukin (IL) 4 by lymph node cells and of IFN-γ by splenocytes.10 Infestation of previously immunized mice had a blunted IFN-γ response, suggesting that mites may produce something that inhibits IFN-γ production. A recent study of indigenous Australians with crusted scabies, none of whom were infected with HIV, found eosinophilia and significant elevation of IgE in 58% and 96% of patients.11 Increased IL-4 production by peripheral blood mononuclear cells was found in those tested. The authors suggested that perhaps this IL-4 response is inefficient at clearing mites and might, in fact, stimulate epidermal hyperkeratosis.

Crusted scabies that resemble psoriasis has previously been described in a patient with Down syndrome and longstanding psoriasis, and cases of crusted scabies with psoriasiform plaques have also been described.12,13 The demonstration of live mites and eggs in scales falling on the examination table from our patient underscore the high contagiousness of the condition. An outbreak of scabies has been reported in hospital staff exposed to a debilitated elderly woman with presumed psoriasis.14 Because patients with late-stage AIDS may be extremely debilitated, ordinary medical management may involve close con-tact with health personnel, putting them at risk for scabies infestation. Universal precau-tions and contact isolation are essential.

Another interesting aspect of our case was the development of nodules on the back, an unusual location for nodular scabies. Nodular scabies is usually considered an exuberant

reaction to mite products, but in our patient, an intact mite was found on biopsy of a nodule.

Treatment of crusted scabies should include the use of a topical keratolytic agent such as 2% salicylic acid to remove crusts and repeated applica-tions of 5% permethrin cream over a 2- to 3-week period. Topical lindane is probably less effective, and concerns have been raised about possible neurotoxicity of this agent. Oral ivermectin has been shown to be safe and highly effective in the treatment of scabies and, although not approved for this condition, has become a mainstay of

Figure 2. Brownish gray hyperkeratotic plaques and underlying erythroderma despite acitretin treatment.

Figure 3. Residual psoriatic erythroderma following treat-ment of crusted scabies.

Figure 4. Biopsy of nodule showing scabies mite.

Crusted scabies should be considered in

patients with AIDS who present with

scaly rashes.

“”

SKINmed: Dermatology for the Clinician® (ISSN 1540-9740) is published bimonthly (Jan., March, May, July, Sept., Nov.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT 06484. Copyright ©2007 by Le Jacq. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Karen Hurwitch at KHurwitch@bos.blackwellpublishing.com or 781-388-8470.

®

C a s e S t u d i e s

144 May • June 2007

treatment for crusted scabies.15 The usual regimen consists of 2 doses of ivermectin 200 μg/kg of body weight given 2 weeks apart in conjunction with topical agents. As an inter-esting aside, methotrexate was once reported to be efficacious in crusted scabies but can also reactivate the condition.16,17

Because crusted scabies is highly contagious but completely curable, the diagnosis should

be considered in patients with AIDS who present with scaly rashes. This case points out the difficulties that may be encountered in diagnosing and treating crusted scabies in patients with psoriasis. It also underscores the contagiousness of this condition from exposure to fomites. Crusted scabies may be seen in adults, children, and infants with AIDS and has rarely been implicated as a por-tal of entry for life-threatening infection.

REFERENCES 1 Schlesinger I, Oelrich DM, Tyring SK. Crusted

(Norwegian) scabies in patients with AIDS: the range of clinical presentations. South Med J. 1994;87:352–356.

2 Portu JJ, Santamaria JM, Zubero Z, et al. Atypical scabies in HIV-positive patients. J Am Acad Dermatol. 1996;34(5 pt 2):915–917.

3 Inserra D, Bickley LK. Crusted scabies in acquired immunodeficiency syndrome. Int J Dermatol. 1990;29:287–289.

4 Wolf R, Krakowski A. Atypical crusted scabies. J Am Acad Dermatol. 1987;17:434–436.

5 Marliere V, Roul S, Labreze C, et al. Crusted (Norwegian) scabies induced by use of topical corticosteroids and treated successfully with iver-mectin. J Pediatr. 1999;135:122–124.

6 Van Der Wal VB, Van Voorst Vader PC, Mandema JM, et al. Crusted (Norwegian) scabies in a patient with dystrophic epidermolysis bullosa. Br J Dermatol. 1999;141:918–921.

7 Bergman JN, Dodd WA, Trotter MJ, et al. Crusted scabies in association with human T-cell lymphotropic virus 1. J Cutan Med Surg. 1999;3:148–152.

8 Orkin M. Scabies in AIDS. Semin Dermatol. 1993;12:9–14.

9 Anolik MA, Rudolph RI. Scabies simulating Darier disease in an immunosuppressed host. Arch Dermatol. 1976;112:73–74.

10 Lalli PN, Morgan MS, Arlian LG. Skewed Th1/Th2 immune response to Sarcoptes scabiei. J Parasitol. 2004;90:711–714.

11 Roberts LJ, Huffam SE, Walton SF, et al. Crusted scabies: clinical and immunological findings in seventy-eight patients and a review of the litera-ture. J Infect. 2005;50:375–381.

12 Gach JE, Heagerty A. Crusted scabies looking like psoriasis. Lancet. 2000;356:650.

13 Namazi MR, Barikbin B. Atypical crusted scabies in an Iranian man. Dermatol Online J. 2002;8:17.

14 Lemmon J. Scabies outbreak among nursing staff. St Vincent’s Healthcare Campus; Sisters of Charity Health Service Darlinghurst. 1998 Nursing Monograph: 30–31.

15 Meinking TL, Taplin D, Hermida JL, et al. The treatment of scabies with ivermectin. N Engl J Med. 1995;333:26–30.

16 Ward WH. Scabies norvegica. Treatment with methotrexate. Australas J Dermatol. 1971;12:44–51.

17 Burrows D, Bridges JM, Morris TC. Reactivation of scabies rash by methotrexate. Br J Dermatol. 1975;93:219–221.

SKINmed: Dermatology for the Clinician® (ISSN 1540-9740) is published bimonthly (Jan., March, May, July, Sept., Nov.) by Le Jacq, a Blackwell Publishing imprint, located at Three Enterprise Drive, Suite 401, Shelton, CT 06484. Copyright ©2007 by Le Jacq. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publishers. The opinions and ideas expressed in this publication are those of the authors and do not necessarily reflect those of the Editors or Publisher. For copies in excess of 25 or for commercial purposes, please contact Karen Hurwitch at KHurwitch@bos.blackwellpublishing.com or 781-388-8470.

®