Pityriasis Versicolor

Pityriasis versicolor is a chronic, recurrent superficial mycosis of the stratum corneum caused by lipophilic Malassezia yeasts. It is not a dermatophytosis, so the older name tinea versicolor is inaccurate and should be avoided. It is not contagious in the usual sense. The causative yeasts are normal skin commensals, and disease follows their conversion from the yeast to the mycelial phase in a susceptible person.

The infection is confined to the keratin layer, with minimal inflammation. The clinical problem is pigment change and scale, not tissue invasion, and invasive Malassezia disease is a separate condition caused by lipid dependent fungaemia.

Epidemiology:

• Common worldwide and most common in hot, humid tropical and subtropical climates, where prevalence can reach 30 to 40 percent in some populations.
• Peak incidence in adolescents and young adults, when sebum production is highest.
• Uncommon before puberty and after middle age.
• Affects men and women equally.
• Recurs seasonally in temperate climates.

Malassezia belongs to the Basidiomycota (class Malasseziomycetes). Species relevant to pityriasis versicolor include Malassezia globosa, the commonest in most series, Malassezia sympodialis, Malassezia furfur and Malassezia restricta. Species distribution varies geographically, and several species may coexist in one patient.

Key microbiological features:

• Lipophilic yeasts that lack fatty acid synthase and so require exogenous long chain fatty acids. Malassezia pachydermatis is the exception and grows without lipid.
• Cells are round, oval or cylindrical, 3 to 8 micrometres, with monopolar (unipolar) budding on a broad base, leaving a collarette of wall remnant at the bud scar.
• Basidiomycete biochemistry: urease positive and diazonium blue B positive, with a thick, multilayered cell wall rich in lipid.
• Species identification uses Tween assimilation patterns, catalase, beta glucosidase, MALDI TOF mass spectrometry or sequencing.
• Culture requires lipid supplementation, using modified Dixon agar or Leeming and Notman agar, or an olive oil overlay on Sabouraud agar, incubated at 32 to 35 degrees Celsius for 5 to 7 days. Colonies are cream to buff, smooth or wrinkled.

In scale from a lesion, the organism appears in two forms together: clusters of round yeast cells and short, thick, angulated hyphal elements.

Disease follows conversion of the commensal yeast to the mycelial phase. Heat, humidity, sweating and sebum favour this conversion, which explains the tropical distribution and the seasonal pattern. The host response is weak, so scale accumulates with little erythema.

Host and environmental factors:

• Hyperhidrosis and humid climate.
• Oily skin and adolescence.
• Familial predisposition, with a positive family history in a substantial minority.
• Systemic corticosteroids and Cushing syndrome.
• Pregnancy.
• Malnutrition.
• Immunosuppression, which increases extent and recurrence but does not change the superficial nature of the disease.
• Occlusion and topical oils.

Pigment change has two mechanisms:

• Hypopigmentation: Malassezia lipases hydrolyse sebum triglycerides to free fatty acids, and lipoxygenase activity oxidises unsaturated fatty acids to dicarboxylic acids, including azelaic acid. These are competitive inhibitors of tyrosinase and reduce melanin production. Tryptophan derived indole compounds, including malassezin, act on the aryl hydrocarbon receptor and are toxic to melanocytes, and the fungus also forms pityriacitrin, which absorbs ultraviolet light and reduces tanning in covered skin.
• Hyperpigmentation: larger melanosomes, thickening of the stratum corneum, and a mild inflammatory infiltrate. The mechanism is less defined than for hypopigmentation.

Ultraviolet exposure darkens normal skin but not the lesions, so the contrast increases in summer, which is a common reason for presentation.

• Well demarcated round or oval macules that coalesce into larger patches with a fine, branny (furfuraceous) scale.
• Colour varies between patients and sometimes within one patient (hence versicolor): white to pale, pink to salmon, tan, brown, or copper. Hypopigmented lesions predominate in dark skin and are the commonest presentation in the tropics.
• Distribution follows sebum rich skin: upper trunk, back, neck, proximal arms and shoulders.
• Pruritus is absent or mild.
• Scale may be subtle, and is brought out by scraping with a fingernail or slide (evoked scale, Besnier sign).

Other conditions in which Malassezia has a role should be distinguished from pityriasis versicolor:

• Malassezia folliculitis: monomorphic pruritic follicular papules and pustules on the upper trunk and shoulders, with yeasts in the follicular infundibulum, with no hyphae.
• Seborrhoeic dermatitis and dandruff: erythema and greasy scale on scalp, face and chest, with Malassezia lipase derived free fatty acids acting as irritants.
• Malassezia fungaemia: invasive infection in premature neonates and patients on parenteral lipid, unrelated to pityriasis versicolor.

The diagnosis is clinical and confirmed by direct microscopy.

• Potassium hydroxide preparation: scale scraped from the edge of a lesion, treated with 10 to 20 percent potassium hydroxide, shows short, thick, curved hyphae together with clusters of round yeasts, the spaghetti and meatballs pattern. Addition of Parker blue black ink or methylene blue improves contrast. Adhesive tape stripping stained with methylene blue is an alternative.
• Calcofluor white: fluorescence microscopy of the same preparation.
• Wood lamp: pale yellow to yellow green fluorescence of affected skin in many patients. Absence of fluorescence does not exclude the diagnosis. Hypopigmented lesions from other causes, such as vitiligo, are not fluorescent in the same way.
• Culture: not needed for routine diagnosis, and a positive culture alone does not prove disease because Malassezia is a commensal on normal skin. Culture is reserved for atypical or recurrent cases and for species identification.
• Histopathology: rarely performed. Periodic acid Schiff or Grocott methenamine silver staining shows yeasts and short hyphae in the stratum corneum, with minimal inflammation.

Interpretation: yeast cells alone on microscopy represent commensal carriage. The combination of hyphal elements with yeasts in a compatible lesion indicates disease.

Any hypopigmented patch with loss of sensation is not pityriasis versicolor until proven otherwise, because leprosy is the dangerous mimic.

Treatment aims at mycological cure, which is expected within days to weeks. Pigment normalisation takes weeks to months afterwards, and patients should be told this, because persistent pale patches after cure are not treatment failure. Retreatment is justified only if KOH remains positive or new scale appears.

Topical therapy is first line for limited or moderate disease. Because subclinical infection extends beyond visible lesions, the whole trunk, neck and upper arms are treated, not only the patches. Wash off after the stated contact time.

Selenium sulphide can irritate skin and mucosa and may discolour hair and jewellery. It should be kept away from the eyes and genitalia.

Systemic therapy is for extensive disease, frequent relapse, or failure of topical treatment:

Points that affect choice:

• Oral terbinafine and oral griseofulvin are ineffective against pityriasis versicolor.
• Oral ketoconazole is avoided because of hepatotoxicity, and its systemic use is restricted or withdrawn in many jurisdictions.
• Itraconazole is contraindicated with drugs such as simvastatin, lovastatin, triazolam, oral midazolam, dofetilide and quinidine, and needs liver tests if the course is prolonged beyond a week or if liver disease exists. It is not used in active liver disease or heart failure.
• In pregnancy and breastfeeding, topical therapy is used and oral azoles are avoided. In children, topical therapy is used.
• Sweating after a dose may increase drug delivery to the stratum corneum through sebum and sweat.

Recurrence is common, because the commensal remains on the skin and the predisposing conditions persist. Prophylaxis suits patients with frequent relapse:

• Itraconazole 200 mg twice daily for one day each month for 6 months, or
• Topical selenium sulphide 2.5% or ketoconazole 2% shampoo applied to the trunk once weekly to once monthly during warm months.