• Tinea versicolor is a common, mild, but often recurrent infection of the stratum corneum because of the lipophilic yeasts of the genus Malassezia.
• It is also termed as Pityriasis versicolor.
• Less commonly, these organisms cause serious systemic infection in low-birth-weight infants and other immune-compromised and debilitated individuals.
• Geographical distribution:
  • The disease is distributed worldwide, but is much more prevalent in tropical and subtropical regions.

What causes Tinea versicolor?

• Etiology:
  • Till now three Malassezia species were identified:
    – two lipid-dependent species, M. furfur and M . sympodialis, and one non-obligate lipophile, M. pachydermatis.
  • The genus has now been enlarged into seven species following genomic and ribosomal sequence comparisons of a large number of human and animal isolates. It comprises of the three former taxa, M. furfur, M. pachydermatis and M. sympodialis, and four new taxa, M. globosa, M. obtusa, M. restricta and M. slooffae.
  • Six of the seven Malassezia species are lipid- dependent with the exception of M. pachydermatis.
  • Molecular methods have been found to be a rapid and reliable method for the differentiation of Malassezia species.

Epidemiology of tinea versicolor:

• Malassezia species form part of the normal microbial flora of the skin of humans and other warm-blooded animals and most infections are endogenous in origin.
• The prevalence of skin colonization with these organisms depends on age, anatomical site, and, to a lesser degree, race.
• The condition of skin colonization rises from around 25% in children to almost 100% in adolescents and adults.
• In post-pubertal individuals the density of colonization is greater in anatomical sites that contain pilosebaceous glands.
•  Malassezia species have been isolated from 100% of samples from the backs of adults, but from only 75% taken from the face and scalp.
• It is assumed that colonization with Malassezia species primarily occurs at the time of puberty when the sebaceous glands become active and the concentration of lipids on the skin increases.
• The accurate conditions which results in the development of pityriasis versicolor and other forms of superficial Malassezia infection have not been defined, but host and environmental factors both seem to be essential.
• The lesions of pityriasis versicolor and seborrhoeic dermatitis have a preference for sites well supplied with sebaceous glands, such as the chest, back and upper arms.
•  It has been seen that patients with seborrheic dermatitis have higher concentrations of lipids on their skin than do other individuals.
• In-case if the non-cohabiting members of the same family have developed pityriasis versicolor it suggests a genetic pre-disposition.
• The relationship between Malassezia species and the immune system is essential.
• It is suggested by increased incidence of Malassezia folliculitis and seborrhoeic dermatitis in persons with the acquired immune-deficiency syndrome (AIDS) and those receiving corticosteroid or other immunosuppressive treatment.
• Pityriasis versicolor is worldwide in distribution, but is most prevalent in hot, humid tropical and subtropical climates, where 30-40% of the adult population may be affected.
• In temperate climates, the disease affects 14%of the adult population, but is most common during the hot summer months.
• Malassezia folliculitis is also more prevalent in tropical countries and, in temperate regions.
• It is more common during the summer months.
• Transmission of Malassezia species is occurs, either through direct contact or via contaminated clothing or bedding.
• In practice, however, infection is endogenous in most cases and transmission between persons is uncommon.

Clinical manifestations of Tinea versicolor:

• Pityriasis versicolor is a harmless condition.
• Lesions:
  • The lesions are characterized by patches of fine brown scaling, especially on the trunk, neck and upper portions of the arms.
  • The lesions may become confluent and progress to cover large areas of the trunk and limbs.
  • In the tropics the lesions are more commonly localized on the face.
  • In light-skinned subjects, the affected skin may appear darker than normal.
  • The lesions are light pink in colour but grow darker, turning a pale brown shade.
  • In dark-skinned or tanned individuals, the affected skin loses colour and becomes depigmented.
  • The same patient may have lesions of different shades, the colours depending on the thickness of the scales, the severity of the infection and the inflammatory reaction of the dermis.
  •  The amount of exposure to sunlight also affects the shade of lesions.
  • The disease is aggravated by sunlight and sweating.
  • The clinical manifestations of tinea versicolor in immunocompromised persons are alike to those observed in normal individuals.
  • However, the lesions are often more erythematous and seem to be raised.
  • In most cases the lesions show a pale yellow fluorescence under Wood’s light, allowing the extent of the disease to be examined.

Differential diagnosis of tinea versicolor:

• Hyperpigmented lesions must be differentiated from a number of conditions, including erythrasma, naevi, seborrhoeic dermatitis, pityriasis rosea and tinea corporis.
• Hypopigmented lesions can be confused with pityriasis alba and vitiligo.

Lab diagnosis of Tinea versicolor

• Specimens:
  • The scraping from the affected skin acts as material for direct microscopic examination.
• Microscopy:
  • Pityriasis versicolor lesions consists of a mixture of budding yeast cells, typical of the organism seen in normal skin sites.
  • They appear as numerous short, broad unbranched hyphae.
  • These hyphae, which are assumed to be the same organism in its pathogenic phase, are not observed at unaffected skin sites or in culture.
  • Direct microscopic examination of scrapings from lesions is enough to allow the diagnosis of pityriasis versicolor if clusters of round or oval budding cells and short hyphae are seen.
• Culture:
  • Because Malassezia species are part of the normal cutaneous flora, their isolation in culture does not contribute to diagnosis.
  • Besides, with the exception of M . pachydermatis, these organisms cannot be isolated on routine mycological media unless lipid is added.

Treatment of tinea versicolor:

• If left untreated pityriasis versicolor will remain for long periods.
• Most patients respond to topical treatment, but more than 50% relapse within 12 months.
• Oral treatment is recommended in patients with extensive or recalcitrant lesions.
• There are various topical agents which can be used to treat pityriasis versicolor.
• Selenium sulphide (2%) shampoo should be applied at night and washed off the following morning.
• The treatment should be repeated 1 and 6weeks later.
• Ketoconazole shampoo should be applied once daily for 5 days.
• It should be left in contact with the lesions for 3-5min before being rinsed off.
• Other topical imidazoles, such as bifonazole, clotrimazole, econazole, miconazole and sulconazole, should be applied morning and evening for 4-6weeks.
• Topical terbinafine should be applied to the lesions each morning and evening for 2 weeks.
• Pityriasis versicolor is often a difficult disease to clear and topical preparations may need to be reused at intervals to ensure that the infection is eradicated.
• Oral antifungal treatment should be employed for patients with extensive lesions or recalcitrant infection that is unresponsive to topical treatment.
• Both itraconazole (200mg/day for 1 week) and ketoconazole (200mg/day for 1 week) are effective treatments.
• Oral griseofulvin and terbinafine are inactive in patients with pityriasis versicolor.

Tinea (Pityriasis) versicolor: etiology, clinical manifestations diagnosis and treatment

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