Pediatric Tinea Versicolor

Updated: Feb 27, 2018
  • Author: Lyubomir A Dourmishev, MD, PhD; Chief Editor: Dirk M Elston, MD  more...
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Overview

Background

Tinea versicolor or pityriasis versicolor is a common superficial cutaneous fungal infection characterized by pityriasiform desquamation and hypopigmented or hyperpigmented macules formation, primarily located on the chest and back with tendency to spread. The condition is frequently asymptomatic; however, some patients occasionally report pruritus. Tinea versicolor results from an overgrowth of Malassezia furfur, which is part of normal skin flora and produces pigmentation changes when it flourishes beyond normal levels.

Historical data

The first clinical observation of pityriasis versicolor was by Willan in 1801. [1] The causative agent was isolated by Eichsted in 1846; 7 years later, the German surgeon Robin named it Microsporon furfur. Billon proposed a new family name Malassezia and subsequently proposed a new species name: Malassezia furfur. Clatelani and Chambers and, later, Gordon proposed the name Pityrosporon ovale or orbiculare and confirmed it role as a causative agent. [1]

M. furfur is a dimorphic lipophilic organism that is able to exist in both yeast and mycelial forms and does not attack the hair shaft, nails, or mucous membranes. The infection is localized to the stratum corneum and chronically recurs in predisposed patients. It is more common during warmer months and in warmer climates. Sun exposure frequently makes the lesions more apparent because affected areas become hypopigmented. In temperate climates, patients develop the disease in the spring and summer. In the tropics, patients are more likely to have tinea versicolor throughout the year.

Although M furfur is a component of normal flora, it is also an opportunistic pathogen. [2] The organism is considered a possible factor in other cutaneous diseases, including Pityrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic dermatitis, the provocation of psoriatic lesions, and some forms of atopic dermatitis. [3]

Studies also show that tinea versicolor occurs with malnutrition and various diseases, including Cushing syndrome. Pregnancy and oral contraceptives may influence susceptibility, but firm data are lacking. Patients with AIDS may present with severe seborrhea but do not have a higher incidence of tinea versicolor. Systemic infections are attributed to Pityrosporum in extremely rare cases.

Different rare clinical forms have been described as follows:

  • Papulous variant
  • Erythematous and papulous variant in children
  • Tinea versicolor with atypical localization on face
  • Tinea versicolor with atypical localization on wrists
  • Pityriasis versicolor alba
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Pathophysiology

The nutritional requirement of M furfur is one of the most important factors that affect the growth of the organism on the skin. Studies show that lesion sites have a decrease in sebaceous gland secretions and water content, along with an increase in pH value compared with normal skin. M furfur is lipophilic, and the mycelial stage of M furfur can be induced in vitro by the addition of cholesterol and cholesterol esters to the appropriate medium. However, significantly more amino acids are extracted from the skin of infected patients, suggesting that amino acids, rather than lipids, are critical for the development of the disease. In vitro, the amino acid asparagine stimulates the growth of the organism, while glycine induces hyphal formation.

Patient immune response also affects infection. Studies suggest a reduced body response to the specific fungal elements that produce tinea versicolor. In various studies, defects in lymphokine production and natural killer T cells were found; phytohemagglutinin (PHA) and concanavalin A (Con A) stimulation was decreased; and interleukin (IL)–2, IL-10, and interferon (IFN)–g production by lymphocytes was decreased in affected patients. The exact pathophysiology of this disorder remains undefined, and additional studies are needed.

In patients with hypopigmentation, tyrosinase inhibitors competitively inhibit an enzyme necessary for melanocyte pigment formation. In hyperpigmented macules, the organism induces enlargement of melanosomes made by melanocytes in the basal layer of the epidermis.

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Etiology

M furfur is now the most commonly accepted name for the etiologic agent of tinea versicolor. Thus, P orbiculare, P ovale, and Malassezia ovalis are synonyms .

M furfur is a dimorphic lipophilic organism that is cultured only in media enriched with C12-sized or C14-sized fatty acids. Malassezia is able to exist in both yeast and mycelial forms, with yeast most commonly associated with saprofital form (P ovale). Historically, the name M furfur was used to designate the fungal pathogen of tinea versicolor before it is grown in culture. M furfur is not a dermatophyte, does not grow on dermatophyte test media (DTM), and does not respond to griseofulvin therapy.

With the advent of DNA sequencing, numerous pathogenic and nonpathogenic species were found. Some of them appear to be more common in certain areas of the world, and some are more likely to be pathogenic in one area and not in another. Much of the confusion was resolved with the taxonomic revision in 1996, based on sequencing of the large-subunit rRNA and nuclear DNA of more than 100 isolates of Malassezia species. [2] The genus Malassezia was revised to include 7 species: Malassezia globosa, Malassezia sympodialis, M furfur, Malassezia slooffiae, Malassezia pachydermatis, Malassezia restricta, and Malassezia obtusa. The clinical significance of each of these species is under investigation. A study of the epidemiology of Malassezia yeasts associated with pityriasis (tinea) versicolor in Canada revealed the most frequently isolated species included M sympodialis, M globosa, and M furfur.

One study found M globosa in 97% of patients with tinea versicolor; it was found alone in 60% of cases, was associated with M sympodialis in 29% of cases, and was associated with M slooffiae in 7% of cases. [2]  M sympodialis and M slooffiae were found in similar percentages on clinically uninvolved skin of the trunk, whereas M globosa was not isolated at other sites. Thus, some authors suggest that M globosa in its mycelial phase is the causative agent of tinea versicolor. [2, 3]

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Epidemiology

Frequency

United States

Depending on the method and sensitivity of sampling methods, Malassezia species may be found in as many as 18% of infants and 90-100% of adults. Clinical tinea versicolor is more common in areas with higher temperatures and higher relative humidities. The incidence of this condition is approximately 2-8% of the population. The exact incidence is difficult to assess because many affected individuals may not seek medical attention.

International

Tinea versicolor occurs worldwide, with an incidence rate of 50% in the humid, hot environment of Western Samoa and 1.1% in the colder environment of Sweden. In temperate zones, the onset occurs during the warmer months of the year, and the lesions generally fade in the cooler and drier months. In tropical countries, where heat and high humidity are more continuous, people develop more extensive and persistent disease.

Race

Although tinea versicolor is usually more apparent in darker-skinned individuals, the incidence of tinea versicolor appears to be the same in all races.

Sex

Females and males are equally affected.

Age

In temperate zones (including most of the United States), tinea versicolor is rare in children. Affected infants or children often have an atypical presentation. In temperate areas, the disorder is common in young adults aged 17-24 years. In tropical climates, tinea versicolor is more common in individuals aged about 20-30 years. Beyond age 40 years, lipid levels in the skin gradually decrease, and tinea versicolor becomes uncommon.

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Prognosis

Prognosis is excellent. Although tinea versicolor is recurrent in some patients, the condition remains treatable.

Morbidity primarily results from the discoloration. The adverse cosmetic effect of lesions may lead to significant emotional distress, particularly in adolescents. Tinea versicolor frequently recurs despite adequate initial therapy. Even with adequate therapy, residual pigmentary changes may take several weeks to resolve.

The yeasts of the genus Malassezia have been associated with numerous other diseases that affect the human skin, such as Malassezia (Pityrosporum) folliculitis, seborrheic dermatitis, atopic dermatitis, psoriasis, confluent and reticulated papillomatosis, onychomycosis, and transient acantholytic dermatosis.

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Patient Education

Tinea versicolor is caused by a fungus that is normally present on the skin surface and, therefore, is not considered a contagious disease. The disease causes no permanent sequelae, and any pigmentary alterations resolve entirely within a few months of adequate treatment. Effective therapy is available. Recurrences are common, and prophylactic therapy may be required.

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