A patient, aged 28 years, presented with complaints of lesions on the chest and back. He reported having this outbreak multiple times in his life. It usually happened in the summer months.
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Tinea versicolor is a common superficial skin infection caused by the dimorphic yeast Pityrosporum (Malassezia furfur). The typical presentation is hypopigmented or hyperpigmented, scaly macules and patches.
In the United States, the prevalence of tinea versicolor is about 2 to 8%. The infection occurs more frequently in hot and humid climates, and is thus more commonly seen in the summer. The incidence of tinea versicolor is the same in all races, however the lesions are more apparent on dark-skinned individuals due to the characteristic hypopigmentation. The infection occurs more in adolescents and young adults due to their more active sebaceous follicles.
Malassezia furur is a lipophilic yeast that is part of the normal skin flora, especially in sebum rich areas of the body. Tinea versicolor is seen when the yeast of the normal skin flora transforms into the pathologic mycelial form and invades the stratum corneum. This transformation occurs more readily under conditions such as a warm and humid climate, hyperhidrosis, oral contraceptive use, immunosuppression, systemic corticosteroid use, Cushing disease, and a malnourished state. The colonization of follicles leads to a high recurrence rate.
Tinea versicolor presents as well-demarcated, scaly macules and patches distributed over the neck, upper truck, abdomen, and upper arms. The patches occur in a variety of colors ranging from white, to pink, to brown. The lesions may also have a wrinkled appearance. Patients usually present due to cosmetic concerns about the patches and do not typically report pruritus.
The lesions are more apparent on tanned skin since the yeast filters natural sunlight and interferes with normal tanning. It is postulated that one if the compounds synthesized by Malassezia furur absorbs ultraviolet light. Another metabolite of the yeast, azelaic acid, inhibits tyrosinase in the melanin production pathway and results in hypopigmentation of the affected skin for months to weeks. The lesions may also be hyperpigmented due to hyperemia from an inflammatory response and increased melanin.
Confirmatory laboratory tests include staining scrapings of the scaling lesions with potassium hydroxide which reveals fungal spores and short hyphae, often described as “spaghetti-and-meatballs.” Additionally, examination with a Wood’s lamp will show a yellow-orange fluorescence. .
Treatment for tinea versicolor includes topical agents such as selenium sulfide shampoo or lotion which is applied to affected areas for about ten minutes and then rinsed. For more extensive infection, systemic treatment with oral ketoconazole or fluconazole may be employed.
Recurrence is common and continued use of topical or oral treatments aids in reducing reappearance. Tinea versicolor does not leave any permanent pigment changes, however it may take a few months for the lesions to completely vanish.
Megan Trainor is a medical student at Baylor College of Medicine.
Adam Rees, MD, a graduate of the David Geffen School of Medicine at UCLA, practices dermatology in Los Angeles.
- Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K. ” Chapter 189. Yeast Infections: Candidiasis, Tinea (Pityriasis) Versicolor, and Malassezia (Pityrosporum) Folliculitis.” Fitzpatrick’s Dermatology in General Medicine. New York, McGraw Hill.
- Usatine RP, Smith MA, Chumley HS, Mayeaux EJ. ” Chapter 141. Tinea Versicolor.” The Color Atlas of Family Medicine. New York, McGraw Hill.