tinea versicolor

Tinea versicolor is caused by the dimorphic, lipophilic yeast Malassezia furfur (formerly Pityrosporum orbiculare), which converts from its commensal yeast form to a pathogenic hyphal form under certain conditions—heat, humidity, hyperhidrosis, oily skin, immunosuppression, or use of oily skin products. The organism produces azelaic acid, which inhibits tyrosinase and disrupts melanocyte function, leading to hypopigmented lesions in dark-skinned or tanned individuals; conversely, an inflammatory response can cause hyperpigmented or erythematous lesions in lighter-skinned individuals. Clinically, patients present with well-demarcated, round-to-oval macules or thin plaques with fine scale, commonly on the upper trunk, back, neck, and proximal upper extremities. Lesions are usually asymptomatic or mildly pruritic. The condition is more common in adolescents and young adults and in tropical/humid climates. Diagnosis is clinical, supported by a positive KOH preparation revealing short hyphae and budding yeast cells described as 'spaghetti and meatballs.' Wood's lamp examination may show a yellow-green fluorescence in some cases, though this is not universal. Treatment includes topical antifungals (selenium sulfide, ketoconazole shampoo/cream, or other azoles) for localized disease, and oral antifungals (fluconazole or itraconazole) for extensive or recurrent cases. Recurrence is common due to the organism being a normal skin commensal, and pigmentary changes may take months to resolve even after successful treatment of the infection itself. It is important to distinguish tinea versicolor from vitiligo (which shows complete depigmentation and no scale), pityriasis rosea, and secondary syphilis based on clinical and microscopic findings.