eMedicine Specialties > Pediatrics: General Medicine > Dermatology

Tinea Versicolor

Author: Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Contributor Information and Disclosures

Updated: Aug 5, 2009

Introduction

Background

Tinea versicolor (tin'-eah verse'-ih-color) is a common, benign, superficial, cutaneous fungal infection characterized by scaly hypopigmented or hyperpigmented macules that are located primarily on the chest and back. Patients occasionally report pruritus; otherwise, the condition is asymptomatic and is not contagious. This condition results from an overgrowth of Malassezia furfur, which is part of normal skin flora and produces color changes only when it flourishes beyond normal levels.

M furfur is a dimorphic lipophilic organism that is cultured only in media enriched with C12- or C14-sized fatty acids. Historically, the name M furfur was used to designate the fungal pathogen of tinea versicolor before it is grown in culture.

The study of Malassezia species has always been complicated. The confusion is due to different forms and different growth requirements. With the advent of DNA sequencing, much of this confusion was found to be caused by the presence of numerous very similar but different species (both pathogenic and nonpathogenic). Malassezia is able to exist in both yeast and mycelial forms, with yeast most commonly associated with normal skin. Some species 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. Studies of Malassezia are of little value unless the specific species is identified using DNA sequencing. Many of the prior studies testing therapy efficacy showed significant failure rates or recurrences. Some of these may be explained by the existence of these varied species.

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. The genus Malassezia was revised to include 7 species: Malassezia globosa, Malassezia sympodialis, M furfur, Malassezia slooffiae, Malassezia pachydermatis, Malassezia restricta, and Malassezia obtusa. Additional uncommon species have been identified using these or similar techniques. The clinical significance of each of these species continues to be studied. A study of the epidemiology of Malassezia yeasts associated with pityriasis (tinea) versicolor in Ontario, Canada, revealed the most frequently isolated species included M sympodialis, M globosa, and M furfur, accounting for 59.4%, 25.2%, and 10.8% of the isolated etiological agents, respectively.

An October 2000 study in the British Journal of Dermatology reported the spherical yeasts observed in vivo were morphologically identical to the globose yeasts characteristic of M globosa.¹ In culture, M globosa was found in 97% of cases, alone in 60% of cases, associated with M sympodialis in 29% of cases, and associated with M slooffiae in 7% of cases. 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. This strongly suggests that M globosa, in its mycelial phase, is the causative agent of tinea versicolor. This result must still be confirmed in other worldwide studies.

Because of this confusion of names, M furfur is commonly used to refer generically to the etiologic agent of tinea versicolor. Despite disagreement about the names, tinea versicolor results from a shift in the relationship between a resident yeast flora and its host.

M furfur 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. 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 rare in children younger than 12 years, tinea versicolor is common in adolescents and young adults. Beyond age 40 years, lipid levels in the skin gradually decrease, and tinea versicolor becomes uncommon.

Although M furfur is a component of normal flora, it is also an opportunistic pathogen. 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. 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.

M furfur is not a dermatophyte, does not grow on dermatophyte test media (DTM), and does not respond to griseofulvin therapy. Many treatments are effective in clearing infection and preventing recurrence. Selenium sulfide shampoo (eg, Selsun), ketoconazole shampoo, and other topical or oral therapies that contain azole antifungals are effective.

Pathophysiology

Skin lesions are either hypopigmented or hyperpigmented.² 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.

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.

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.

Mortality/Morbidity

Tinea versicolor is a benign skin disease. Morbidity results primarily 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 a number of 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.

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 all age groups, but most cases occur in individuals aged 10-19 years.

Clinical

History

Questioning the patient with tinea versicolor about skin or systemic diseases, current therapy, and drug allergies provides guidance in selecting an appropriate therapy. The following are factors that may be used to guide therapy:

• Other diseases, including renal disease, hepatic disease, and endocrine disease (eg, diabetes mellitus)
• History of HIV or other immunocompromising disorder, which can increase the severity of tinea versicolor
• Other skin disorders, including personal or family history of atopy or other eczematous conditions
• Current or recent topical or systemic therapy
• Drug allergies
• Seasonal variations in skin color
• Use of some body oils, which may supply additional nutrients to the M furfur
• Sweat associated with exercise, which may contribute to disease development and recurrence

Physical

• Lesion characteristics
  • Lesions occur in various colors and shapes, as the name implies (versi means several).
  • Lesions are either macules or very superficial papules with fine scale that may not be evident except on close examination.
  • Even when scale is not apparent, when the skin is wiped with a wet cloth and scraped for examination, it yields a surprising amount of dirty-brown keratin. If not, the areas of dyschromia may represent residual effects of previously treated tinea versicolor.
  • Occasionally, determining whether the lighter or darker skin is affected is difficult.
  • Lesions have relatively sharp margins and may be lighter or darker than the normal skin color. The lesions are frequently a light orange or tan color in light-skinned individuals.
  • The color of lesions varies from individual to individual, but each individual's lesions are approximately the same color.
  • Lesions are evenly pigmented. The inflammatory border, relative central clearing, and erythema seen in most fungal infections are lacking.
  • Small lesions are usually circular or oval.
  • Confluent patches with scattered circular or oval macules around the edges are common.
  • Other lesions may be large enough to cover most of the trunk.
  • Lesions are usually asymptomatic but may be mildly pruritic. The pruritus is more intense when the patient is excessively warm.
  • Residual hypopigmentation, without overlying scale, may remain for many months following effective treatment. These areas may become more apparent following sun exposure, causing the patient to incorrectly suspect that the infection has recurred.
• Lesion distribution
  • The upper trunk is most commonly affected, but the lesions often spread to the upper arms, antecubital fossae, neck, abdomen, and popliteal fossae.
  • Lesions in the axillae, groin, thighs, and genitalia are less common.
  • Facial, scalp, and palmar lesions occur in the tropics but are rare in temperate zones.
  • In some patients, tinea versicolor primarily affects the flexural regions, the face, or isolated areas of the extremities. This unusual pattern of tinea versicolor is seen more often in immunocompromised hosts and can be confused with candidiasis, seborrheic dermatitis, psoriasis, erythrasma, and dermatophyte infections.
  • Lesions that are imperceptible or doubtful are more visible using a Wood lamp in a darkened room.

Causes

• M furfur is now the most commonly accepted name for the organism that causes tinea versicolor. Thus, Pityrosporum orbiculare, Pityrosporum ovale, and Malassezia ovalis are synonyms for M furfur.
• Despite disagreement about the names, tinea versicolor results from a shift in the relationship between a human and a resident yeast flora.

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