Aetiology

PV is a superficial fungal infection resulting from a change to the mycelial state of dimorphic lipophilic yeasts of the genus Malassezia that colonise the stratum corneum and are normal skin flora.[1] Yeasts of this genus are found at sites rich in sebaceous lipids, including the scalp and upper trunk, as the organisms are a lipophilic fungus requiring exogenous fatty acids for growth.[1]

Originally, PV was believed to be caused by M furfur.[12] However, recent studies have demonstrated that the most common Malassezia species cultured from lesions of PV are M globosa and M sympodialis.[12][13]

PV is neither contagious nor due to poor hygiene.[1] Both exogenous and endogenous factors may lead the Malassezia organism to change from its saprophytic yeast form to the pathological mycelial form. Exogenous factors include high temperature, humidity, heavy sweating associated with athletic activity, and application of occlusive creams or lotions to the skin.[7][14][15] Endogenous factors include young adult age, hyperhidrosis, genetic susceptibility, malnutrition, pregnancy, and immunosuppression associated with corticosteroids or other immunosuppressant agents, malignant lymphoma, and HIV infection.[7]

Pathophysiology

Altered pigmentation characterises PV. Historically, the colour of these lesions was thought to vary according to sunlight exposure, chronicity of the infection, and the patients' normal pigmentation, with darker-skinned people exhibiting hypopigmented lesions and lighter-skinned people exhibiting hyperpigmentation.[14] However, one study could find no correlation between pigmentary variation in PV and duration of infection or background skin colour.[3] There are multiple theories to explain the pigmentation abnormalities for both hypopigmented and hyperpigmented lesions in PV.

Hypopigmentation has been explained by

  • Damage to melanocytes

  • Inhibition of tyrosinase by decarboxylic acid[16]

  • Lipoperoxidase produced by Malassezia species[17]​

  • Melanosomes of small size

  • Decreased numbers of melanosomes in affected skin[18]

  • Blocking of UV light by lipid-like material accumulating in the stratum corneum due to Malassezia species.[19]

However, this last theory of UV blocking does not explain the depigmentation often associated with PV in non-sun-exposed skin.[20] The theory of damage to melanocytes and inhibition of tyrosinase by decarboxylic acids is appealing as an explanation of why repigmentation can take months to years after successful treatment.[1]

Hyperpigmentation has been explained by abnormally large melanosomes,​​ a thick stratum corneum, and hyperaemia in response to infection.[18][21][22]​​​[23]

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