Tinea Versicolor Mimicking Rubra Pilaris

Capt Matthew J. Darling, MC, USAF; CPT Matthew C. Lambiase, MC, USA; Capt R. John Young, MC, USAF

Tinea versicolor is a common noninvasive cuta- neous fungal disease. We recount a case of tinea versicolor that mimicked type I (classic adult) pityriasis rubra pilaris. A 54-year-old white man reported a 20-year history of a recurrent pruritic eruption that had marginally improved with use of selenium sulfide shampoo and treatment with oral antihistamines. Results of a skin examination revealed erythematous plaques; islands of spared skin; and follicular erythematous keratotic on the trunk, shoulders, and upper arms. A lesion was scraped to obtain skin scales for potassium hydroxide staining. Examination of the stained samples revealed the characteristic “spaghetti and meatballs,” confirming the diagnosis. Cutis. 2005;75:265-267.

Case Report A 54-year-old white man presented with a 20-year history of a recurrent pruritic eruption that had marginally improved with use of selenium sulfide shampoo and oral antihistamine therapy. Erythem- atous scaly plaques were noted over the trunk and extremities (Figure 1). Islands of spared skin were most notable on the trunk (Figure 2). Follicular, erythematous, keratotic papules were noted on the shoulders and upper arms (Figure 3). Results of Wood lamp examination revealed a yellow-green Figure 1. Erythematous scaly plaques and islands of fluorescence of the plaques. Results of potassium spared skin on the chest. hydroxide (KOH) staining revealed numerous yeast and hyphae. The patient was diagnosed with tinea versicolor and treated with itraconazole 200 mg/d for 2 weeks. At the follow-up visit, the eruption appeared to be 90% cleared, and the itraconazole was continued for 2 more weeks at the same dosage. Accepted for publication July 19, 2004. Dr. Darling is from the Department of Surgery, Wilford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas. Comment Drs. Lambiase and Young are from the Department of , Tinea versicolor is a common noninvasive cuta- San Antonio Uniformed Services Health Education Consortium. neous fungal disease affecting people worldwide. The opinions and assertions contained in this article are the The incidence is greater in tropical regions with private views of the authors and are not to be construed as high temperatures and high relative humidity.1 reflecting the views of the US Air Force, US Army, or the Department of Defense. Tinea versicolor is caused by the fungus Malassezia The authors report no conflict of interest. furfur, which is present on the skin of 75% to 98% Reprints not available from the authors. of healthy individuals.2,3 M furfur is a dimorphic

VOLUME 75, MAY 2005 265 Tinea Versicolor

Figure 2. Erythematous scaly plaques with islands Figure 3. Follicular erythematous keratotic papules. of sparing. lipophilic organism that converts from the yeast monophenol monooxygenase, or both may provide stage to the mycelian stage under appropriate condi- the basis for the hypopigmented lesions, whereas tions. Several factors predispose to the development inflammatory stimulation of melanocytes may lead of tinea versicolor, including high temperature, to hyperpigmented lesions.3,4,7 Patients commonly high relative humidity, greasy skin, hyperhidrosis, report that they are unable to tan in the affected hereditary factors, immunodeficiency, systemic areas. Mild pruritus may be present. Similarly, clas- corticosteroid therapy, and immunosuppressive sic adult pityriasis rubra pilaris can present as small, treatment.1,2 Because the organisms have a nutri- scaly, follicular, keratotic papules with islands of tional requirement for fatty acids, colonization normal skin; however, results of skin biopsy reveal starts soon after birth, peaking in late adolescence follicular plugs and hyperkeratosis. to early adulthood. M furfur is considered part of Tinea versicolor is primarily a clinical diagno- the skin’s normal flora.1-4 Colonization is likely due sis that can be confirmed by simply scraping the to an increase in lipids in sebum-rich areas of the lesion to obtain skin scales and staining them skin and is not a result of poor hygiene.5 M furfur is with KOH. The characteristic appearance of the generally accepted name, and Pityrosporum “spaghetti and meatballs” is seen on microscopic orbiculare and Pityrosporum ovale are synonyms.3,6 examination of the yeast and hyphal forms. Wood Tinea versicolor lesions are described as lamp illumination causes the skin to fluoresce yel- hypopigmented or hyperpigmented scaly macules low to yellow-green. Cultures are not necessary. or patches that vary in color from white to fawn. Several diseases must be considered in the differ- The lesions typically develop on the neck, chest, ential diagnosis: , , sebor- back, abdomen, or proximal upper extremities. The rheic dermatitis, secondary , pityriasis pathogenesis of the dyspigmentation is not well rosea, , , sarcoidosis, and understood. Damage to melanocytes, inhibition of pityriasis rubra pilaris.

266 CUTIS® Tinea Versicolor

Treatment for tinea versicolor includes topical 2. Ljubojevic S, Skerlev M, Lipozencic J, et al. The role of and oral agents. Topical agents such as selenium Malassezia furfur in dermatology. Clin Dermatol. sulfide 2.5% and pyrroles are the most common 2002;20:179-182. therapies. The agents must remain in contact with 3. Martin AG, Kobayashi GS. Yeast infections: candidia- the skin for a minimum of 5 to 10 minutes before sis, pityriasis (tinea) versicolor. In: Freedberg IM, the skin is washed.3,8 Frequent relapses, extensive Arthur ZE, Wolff K, et al, eds. Fitzpatrick’s Dermatology disease, or poor compliance with topical regimens in General Medicine. Vol 2. New York, NY: McGraw-Hill; may necessitate oral antifungal agents. Exercising 1999:2368-2371. one hour after oral administration of ketoconazole 4. Schmidt A. Malassezia furfur: a fungus belonging to the or fluconazole treatment and leaving the sweat in physiological skin flora and its relevance in skin disorders. contact with the skin for 8 to 12 hours may Cutis. 1997;59:21-24. increase the efficacy of systemic treatment, with 5. Sunenshine PJ, Schwartz RA, Janniger CK. Tinea versi- reported cure rates of 75% to 100%.5,8 Itraconazole, color: an update. Cutis. 1998;61:65-68, 71-72. which is secreted in the sebum, does not require 6. Elewski BE, Hazen PG. The superficial mycoses and the sweating for effectiveness.5 Unfortunately, tinea . J Am Acad Dermatol. 1989;21:655-673. versicolor has a high recurrence rate, and prophy- 7. Odom RB, James WD, Berger TG. Diseases resulting lactic or maintenance therapy may be necessary. from fungi and yeasts. In: Odom RB, James WD, Berger TG. Andrews’ Diseases of the Skin: Clinical Dermatology. 9th ed. Philadelphia, Pa: Saunders Harcourt Brace; REFERENCES 2000:388-390. 1. Faergemann J. Pityrosporum infections. J Am Acad 8. Savin R. Diagnosis and treatment of tinea versicolor. J Fam Dermatol. 1994;31(3 pt 2):S18-S20. Pract. 1996;43:127-132.

VOLUME 75, MAY 2005 267