Pityriasis (tinea) versicolor
Pityriasis (Tinea) Versicolor
Editor: Stephanie Gallitano
Key Points
- Pityriasis versicolor (also known as tinea versicolor) is a benign superficial skin infection caused by the superficial yeast Malassezia.
- Lesions may be characterized by multiple hypopigmented or hyperpigmented round to oval macules in areas prone to sweating & oil-producing parts of the body (e.g., trunk, shoulder girdle, neck).
- Diagnosis is made clinically, but might be supported with techniques such as Wood’s lamp or bedside microscopy if the diagnosis is ambiguous.
- Treatment is typically with topical antifungals, but recurrence is common.
Background & Epidemiology
Pityriasis versicolor (PV) - also known as tinea versicolor- is a benign superficial fungal infection of the skin, caused by the superficial yeast Malassezia, which produces hypo- or hyperpigmented macules, fundamentally distributed on the trunk and shoulders. The fungus lives in the skin as a commensal organism in the form of yeast, where it colonizes hair follicles and oil drops of corneocytes. The fungus causes disease when it converts from yeast to a hyphal form, predominantly under warm and humid conditions.
Figure 1. Illustration of epidermis with fungal hyphae confined to the stratum corneum
PV is more frequent in adolescents and young adults due to increased sebum production. It has a global distribution but is more common in tropical areas where warm temperatures facilitate the conversion of the yeast into its hyphal form. Predisposing factors include:
- Warmer temperatures & humidity
- Application of oil-based products & excessive sweating
- Adolescents and young adults
- Previous antibiotic use
- Diabetes, and other forms of Immunosuppression
Clinical Presentation & Differential Diagnosis
PV is characterized by asymptomatic hypochromic macules - often covered with a fine scaly layer which can become apparent after the lesion is scratched or stretched (“evoked scale sign”). Lesions occur typically in seborrheic areas of the body, such as chest, shoulders, and neck and tend to enlarge over time and coalesce. PV may become more apparent after sun exposure. It can also form hyperpigmented, slightly erythematous lesions, or have different colors (hence the term “versicolor”). Lesions may last from weeks to months and occasionally are mildly pruritic.
You should know that there are other conditions that produce hypo- or depigmented macules - such as Pityriasis Alba, Vitiligo, Seborrheic dermatitis, or Tuberculoid Leprosy - and they are very different. If you are an experienced clinician, this comparison may be too basic for you. But if you're starting your medical training, you may want to learn how to differentiate PV from an arguably more severe condition - such as leprosy. This may come up in tropical medicine exams!
Key differences between infectious hypochromic macules in the tropics
| Pityriasis Versicolor | Tuberculoid or Boderline Tuberculoid Leprosy | Vitiligo | Pytiriasis Alba | |
| Characteristic lesions | → Many hypo- or hypercromic asymptomatic macules or patches with an inducible scale | → Typically only 1-3 asymmetric hypochromic or erythematous anesthetic macules/patches or plaques | → Well-demarcated, non-scaly, depigmented macules or patches | → Well-demarcated hypopigmented macules or patches with scaling margins |
| Body distribution | → Chest, shoulders, upper arms (serborrheic distribution) | → Any body distribution, but often more acral because of the favoring cool body sites | → Any body distribution, but more often in face, hands and genitals | → Upper parts of the body, more often the face |
| Distinguishing features | → Evoked scale sign (+) → Golden fluorescence under Wood's lamp → KOH (+) |
→ Thickened peripheral nerves Loss of sensation and/or weakness → KOH (-) | → Total loss of pigment → White hair → Lesion can develop at the site of trauma | → More common in children → Mild erythema can precede appaerance of depigmentation → Associated with atopy |
| Global distribution | → Warm/humid climates | → Tropical subclimates. Highest global burden in Brazil, India, Indonesia | → Widespread distribution | → Widespread distribution |
| Treatment options | → Topical antifungals. (zinc pyrithione, selenium sulfide, ketoconazole, clotrimazole) | → Multi drug therapy (e.g., dapsone, rifampin +/- clofazimine) | → Topical calnineurin inhibitors →Phototherapy → Topical or systemic corticosteroids or JAK inhibitors | → Emollients |
Table 1. Key differences between PV, TL/BTL, Vitiligo and PA.
Treatment & Prevention
Treatment: is offered mainly for cosmetic reasons. Topical therapy is preferred, except in extensive and more severe cases. For topical therapy, multiple preparations are available (e.g., creams, foams, shampoo, lotions, gels). Azoles and selenium sulfide may have similar efficacy. Regimens vary from a few days to 4 weeks.
Please be mindful that depigmentation may take several months to normalize! Make sure to inform your patients.
| Topical Therapy (first-line) | Non-specific topical antifungal agents | → Selenium Sulfide |
| → Zinc pyrithione | ||
| Specific topical antifungal agents | → Azoles | |
| → Ciclopirox | ||
| Systemic therapy (second-line) | - | → Azoles (ie, fluconazole, itraconazole) |
Prevention: Recurrence is common (as high as 80%). If cases are recurrent/refractory, consider medical prophylaxis with monthly doses of either topical or systemic therapy and discuss with a specialist!
Assessment: Did I Get It? (DIG-IT)
Assessment: Did I Get It? (DIG IT)
DIG ITs are online modules designed to reinforce key learning points for you! Please choose the best answer, then check all of the answer choices for more learning pearls
References
This lesson was last updated October 2 2025