Tinea versicolor is caused by Malassezia furfur, a dimorphic, lipophilic fungus. The yeast phase of the organism was previously classified as Pityrosporum orbiculare and P.ovale but they are now reclassified as being the same species as M furfur.

M. furfur is a member of the normal skin flora of  human beings. Under certain circumstances, the commensal yeast transforms into the filamentous pathogenic form.

Production of disease is related to genetic predisposition, a hot and humid climate, steroid therapy, Cushing’s disease, pregnancy and malnutrition.

The infection leads to a slightly increased epidermal turnover time resulting in visible scaling. Production of dicarboxylic acids like azelaic acid causes inhibition of tyrosine kinase resulting in hypopigmentation of the involved skin. Induction of enlargement in the size of the epidermal melanosomes is associated with the hyperpigmentation of the lesions.

M. furfur is considered to be a contributory factor in the causation of other diseases like seborrheic dermatitis, pityrosporum folliculitis, and confluent and reticulated papillomatosis as well as some cases of atopic dermatitis.

Tinea versicolor affects both sexes equally.

Typically adolescents and young adults are involved; childhood cases are more commonly seen in warm and humid climates.

The disease is usually asymptomatic, the patients presenting with the cosmetic blemish. Some patients may complain of mild pruritus or irritation.

The typical lesions of TV consist of hypopigmented to brownish, well-defined, small, round to oval macules with fine, powdery scales on their surface.

A follicular localization with coalescence to produce larger, irregularly shaped patches is characteristic.

The lesions are typically located on the upper back and chest, spreading to the adjacent areas of the arms and neck. Facial lesions are commonly seen during childhood. Less commonly, other areas of the skin may also be involved.

Tinea versicolor may rarely be localized predominantly on the flexural areas like the axillae, groins and limb flexures, causing difficulty in differentiating from seborrheic dermatitis or erythrasma.

Rarely, a follicular, itchy rash on the trunk and limbs may be caused by the fungus (pityrosporum folliculitis)

Pityriasis alba

Pityriasis rosea

Seborrheic dermatitis

Erythrasma

Vitiligo

Leprosy

Syphilis

Post-inflammatory hypopigmentation

In most cases, the clinical feature is sufficiently distinctive to permit a diagnosis.

Indistinct or doubtful lesions may be made readily visible by Wood’s lamp examination which typically shows a yellowish fluorescence of the hypopigmented patches.

Examination of skin scraping soaked in 10% potassium hydroxide helps microscopic visualization of the fungi that appear as short, thick hyphae with a large number of variously-sized spores (spaghetti and meat-ball appearance)

Selenium sulphide 2.5% in a detergent base (Selsun) is a very effective topical medication. Several recommendations for the mode of application and duration of therapy exists. Daily overnight application for a few days followed by few  weekly applications works very well. It should not be applied to the face or scrotum for severe irritation may ensue. 

Zink pyrithione in shampoo base applied as above is also effective.

Azole antifungals ( miconazole, clotrimazole, econazole, oxiconazole, bifonazole, ketoconazole etc.) is applied twice a day for a few weeks to achieve cure.  

Terbinafine and ciclopirox olamine may also be used in the same way.

Other alternatives include:

Sodium thiosulphate lotion 20%

Propylene glycol 50% in water

Tretinoin cream

In extensive involvement, where topical therapy may be impractical., systemic antifungals may be tried.

Ketoconazole 400 mg single dose repeated monthly for a few months, is a very effective systemic treatment of TV 

Fluconazole 450 mg single dose is somewhat less effective.

Itraconazole 200 mg daily for five days is an effective regimen.