Black Dot Tinea Capitis in an Immunosuppressed Man

Jane Y. Yoo, MD/MPP; Gary W. Mendese, MD; Daniel S. Loo, MD

Dr. Yoo is from Department of Dermatology, Albert Einstein College of Medicine, New York, New York. Drs. Mendese and Loo are from Department of Dermatology, Tufts Medical Center, Boston, Massachusetts.

Disclosure: The authors report no relevant conflicts of interest.

Tinea capitis is a common superficial fungal infection of the scalp primarily afflicting young children. In adults, this infection may have an atypical presentation that may lead to a delay in diagnosis. The authors present a case report of black dot tinea capitis in an immunosuppressed Asian man with psoriasis and provide a review of the literature.
(J Clin Aesthet Dermatol. 2013;6(5):49–50.)

A 63-year-old Filipino man with a history of psoriasis presented with hair loss and scalp pruritus. Longstanding use of superpotent topical steroids (clobetasol propionate 0.05% ointment) had contributed to adrenal insufficiency with undetectable morning cortisol levels. The patient was subsequently switched to cyclosporine, which he had started one month prior to his presentation.

Examination revealed diffuse alopecia with follicularly based adherent black dots with background erythema and scale admixed with erythematous papules and plaques (Figure 1). He was initially given clobetasol 0.05% solution to a small area on the scalp for pruritus, which was ineffective. Two months later, a potassium hydroxide (KOH) preparation of the persistent black dots revealed endothrix and numerous demodex mites (Figure 2). The patient was treated with oral terbinafine 250mg/day for six weeks, as the patient was on cyclosporine for psoriasis and griseofulvin is a cytochrome p450 inducer, which would have reduced serum levels of cyclosporine. At an eight-week follow-up appointment, the patient was in complete remission. Since there were no clinical signs of alopecia, erythema, papules, pustules, or scale, a follow-up scraping for demodex was not performed.

Although tinea capitis is the most common dermatophyte infection of childhood, it rarely occurs in adults due to protective factors including sweat, sebum, and colonization by Malassezia furfur.[1] It is thought that the adult scalp has higher fatty acid content and that some saturated fatty acids from adult human hair (and derived from sebum) inhibit dermatophytes.[2] The protective effect of sebaceous secretions during earlier adult life therefore predisposes elderly individuals, such as postmenopausal women, to infection.[3] However, certain risk factors, such as immunosuppression, hormonal changes, and concomitant fungal infection, can predispose individuals as well. Tinea capitis has been reported in those with a history of organ transplantation, lupus, pemphigus vulgaris, human immunodeficiency virus, and prostate cancer in the setting of systemic immunosuppressants.[4–6]

The authors also believe that the patient may have been infected with demodicosis, as there were more demodex mites per low power field than would be seen in the case of commensal demodex. This may have been an incidental finding or true infection for which the authors were not able to ascertain. Demodex mites are common commensal organisms of the pilosebaceous unit found on the scalp, face, and upper chest of older adults. Most patients are asymptomatic; however, as the density of mites increases, granulomatous reactions may occur.[7] As such, Demodex has been implicated in a number of conditions, including papulopustular rosacea, pityriasis folliculorum, blepharitis, and perioral dermatitis.[7]

Immunodeficient patients are often prone to demodicosis. Ultraviolet radiation can also lead to infection, as reported by Kulac[8] who found an increased incidence of demodicosis in patients receiving phototherapy.[8] The patient described in this case had many predisposing factors for demodicosis—age, phototherapy history, and topical steroid use for psoriasis. The diagnosis of demodex infestation was made via simple KOH preparation of one hair follicle, which demonstrated five mites. Since diagnosis of demodicosis requires demonstration of abundant mites and clearing after proper treatment, a definitive diagnosis of demodicosis could not be made.

The patient’s prolonged use of superpotent corticosteroids led to hypothalamus-pituitary-adrenal axis suppression. This, in conjunction with cyclosporine treatment, provided a favorable environment for dermatophyte and Demodex growth. Although tinea capitis is uncommon in adults, it should be included in the differential diagnosis of immunosuppressed individuals with alopecia, with or without scalp pruritus. By way of a simple KOH preparation and direct microscopy of hairs and scale from the affected area, these infections can be promptly diagnosed and treated.

The authors would like to thank Harty Ashby-Richardson, DO for her dermatopathology contribution.

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