Summary
Tinea versicolor (pityriasis versicolor) is a benign superficial skin infection that occurs most often in young adults during hot and humid weather and is most commonly caused by the fungi Malassezia globosa and Malassezia furfur. The infection is characterized by finely scaling, hypopigmented or hyperpigmented macules on the trunk and/or chest. Patients often become aware of the disease after sun exposure because the lesions do not tan and become more visible against the recently tanned surrounding skin. Diagnosis is commonly made clinically but can be confirmed with the spaghetti-and-meatballs pattern of the hyphae and spores on KOH preparation of skin scrapings. Antifungal topical medications such as selenium sulfide and ketoconazole are considered first-line treatment. Oral fluconazole and itraconazole may be considered for those with severe, widespread, or refractory disease. Lesions will resolve completely over time, but recurrences are common.
Tinea versicolor, despite its name, is not caused by dermatophytes. See dermatophyte infections for more information.
Epidemiology
- Occurs worldwide, with a higher incidence in tropical climates
- More prevalent in healthy individuals 21–30 years of age [1]
Epidemiological data refers to the US, unless otherwise specified.
Etiology
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Pathogens
- Malassezia spp. (previously known as Pityrosporum): most commonly Malassezia globosa and Malassezia furfur
- Dimorphic, lipophilic yeast-like fungi that are part of normal skin flora
- Not contagious
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Risk factors
- Warm and humid climates [2][3]
- Excessive sweating, seborrhea, and oily skin
- Immunosuppression
- Cushing syndrome
- Genetic predisposition
Pathophysiology
- Malassezia spp. infect the stratum corneum → lipid degradation → production of acids that inhibit tyrosinase and damage melanocytes → hypopigmentation
- Inflammatory response to pathogens → hyperpigmentation
Clinical features
- Round, well-demarcated macules that reveal a fine, subtle scale with gentle scraping that can coalesce into patches (which may have irregular shapes)
- Colors vary (hypopigmented, hyperpigmented, or erythematous skin lesions)
- Lesions do not tan in the sunlight, because of which they are more commonly noticed in the summer.
- Milder pruritus (compared to dermatophyte infections)
- Common sites are the trunk and chest, but the neck, abdomen, upper arms, and thighs may also be affected.
Patients often become more aware of the lesions after exposure to sunlight because the surrounding skin tans while the lesions do not.
Diagnostics
- Usually a clinical diagnosis
- Confirmatory test: Potassium hydroxide (KOH) preparation of skin scrapings reveals a spaghetti-and-meatballs pattern.
- Ultraviolet light (Wood lamp) may reveal a coppery-orange or yellow fluorescence (∼ 30% of cases) [2][4]
Differential diagnoses
- Vitiligo
- Seborrheic dermatitis
- Pityriasis rosea
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Pityrosporum folliculitis: an infection of hair follicles caused by Malassezia spp. that typically manifests as pruritic, papulopustular eruptions. [2][4]
- Usually occurs in immunocompromised patients (e.g., HIV, immunosuppressive therapy, stress, diabetes, steroid therapy)
- Is often difficult to distinguish from acne vulgaris (and may also occur concurrently with it)
The differential diagnoses listed here are not exhaustive.
Treatment
See “Treatment of tinea versicolor” for agents and dosages.
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Topical antifungals (first-line therapy)
- Selenium sulfide or zinc pyrithione in form of lotion or shampoo
- Azoles (miconazole; or ketoconazole; ) or allylamines (terbinafine; ) in form of creams
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Oral antifungals
- Reserved for infections that are severe, widespread, or unresponsive to topical therapy to reduce the possible risks of systemic medication (not typically used in children)
- Oral fluconazole or itraconazole are the preferred oral agents.
Prognosis
- The lesions will resolve without any permanent changes within 1–2 months of therapy.
- Recurrences are common and treatment may need to be repeated intermittently.