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A young boy is brought to the office by his parents with a 2-year history of his skin turning white on his trunk (Figure 126-1). The boy denies any symptoms. His parents are afraid that he has the same thing that Michael Jackson had (vitiligo). The clinician does a KOH preparation of the white skin and finds the spaghetti and meatball pattern of Malassezia furfur under the microscope (Figure 126-2). His parents are relieved to receive a prescription for the tinea versicolor and to find out that it is rarely spread to others through contact.
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Tinea versicolor is a common superficial skin infection caused by the dimorphic lipophilic yeast Pityrosporum (Malassezia furfur). The most typical presentation is a set of hypopigmented macules and patches with fine scale over the trunk in a cape-like distribution.
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Pityriasis versicolor is actually a more accurate name as “tinea” implies a dermatophyte infection. Tinea versicolor is caused by Pityrosporum and not a dermatophyte.
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Etiology and Pathophysiology
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Tinea versicolor is caused by Pityrosporum (M. furfur), which is a lipophilic yeast that can be normal human cutaneous flora.
Pityrosporum exists in two shapes—Pityrosporum ovale (oval) and Pityrosporum orbiculare (round).
Tinea versicolor starts when the yeast that normally colonizes the skin changes from the round form to the pathologic mycelial form and then invades the stratum corneum.1
Pityrosporum is also associated with seborrhea and Pityrosporum folliculitis.
The white and brown colors are secondary to damage caused by the Pityrosporum to the melanocytes, while the pink is an inflammatory reaction to the organism.
Pityrosporum thrive on sebum and moisture; they tend to grow on the skin in areas where there are sebaceous follicles secreting sebum.
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Tinea versicolor consists of hypopigmented, hyperpigmented, or pink macules and patches on the trunk that ...