eMedicine Specialties > Dermatology > Fungal Infections

Tinea Versicolor

Author: Craig G Burkhart, MD, MPH, Clinical Professor, Department of Medicine, Section of Dermatology, The University of Toledo College of Medicine; Clinical Assistant Professor, Department of Dermatology, Ohio State University College of Medicine
Coauthor(s): Lorie Gottwald, MD, Chief, Division of Dermatology, Associate Professor, Department of Internal Medicine, Medical College of Ohio at Toledo; Craig N Burkhart, MD, MSBS, Assistant Professor, Department of Dermatology, University of North Carolina at Chapel Hill
Contributor Information and Disclosures

Updated: Sep 25, 2009

Introduction

Background

Tinea versicolor is a common, benign, superficial cutaneous fungal infection usually characterized by hypopigmented or hyperpigmented macules and patches on the chest and the back. In patients with a predisposition, tinea versicolor may chronically recur. The fungal infection is localized to the stratum corneum.

Pathophysiology

Tinea versicolor is caused by the dimorphic, lipophilic organisms in the genus Malassezia, formerly known as Pityrosporum. Eleven species are recognized within this classification of yeasts, of which Malassezia globosa and Malassezia furfur are the predominant species isolated in tinea versicolor.1,2,3,4,5 Malassezia is extremely difficult to propagate in laboratory culture and is culturable only in media enriched with C12- to C14-sized fatty acids. Malassezia is naturally found on the skin surfaces of many animals, including humans. Indeed, it can be isolated in 18% of infants and 90-100% of adults.

The organism can be found on healthy skin and on skin regions demonstrating cutaneous disease. In patients with clinical disease, the organism is found in both the yeast (spore) stage and the filamentous (hyphal) form. Factors that lead to the conversion of the saprophytic yeast to the parasitic, mycelial morphologic form include a genetic predisposition; warm, humid environments; immunosuppression; malnutrition; and Cushing disease. Human peptide cathelicidin LL-37 plays a role in skin defense against this organism.

Even though Malassezia is a component of the normal flora, it can also be an opportunistic pathogen. The organism is considered to be a factor in other cutaneous diseases, including Pityrosporum folliculitis, confluent and reticulate papillomatosis, seborrheic dermatitis, and some forms of atopic dermatitis.

A basic clinical guideline summary is available from the New York State Department of Health: Dermatologic Manifestations.6

Frequency

United States

Tinea versicolor occurs more frequently in areas with higher temperatures and higher relative humidities. The national prevalence of this condition is 2-8% of the population. The exact incidence in the United States is difficult to assess because many individuals who are affected may not seek medical attention.

International

Tinea versicolor occurs worldwide, with prevalences reported to be as high as 50% in the humid, hot environment of Western Samoa and as low as 1.1% in the colder temperatures of Sweden.

Mortality/Morbidity

  • Tinea versicolor is a benign skin disease that causes scaly macules or papules on the skin. As the name implies (versi means several), the condition can lead to discoloration of the skin, with colors ranging from white to red to brown. The condition is not considered to be contagious because the causative fungal pathogen is a normal inhabitant of the skin.
  • The skin of an individual who is affected by tinea versicolor may be either hypopigmented or hyperpigmented. In the case of hypopigmentation, tyrosinase inhibitors (resulting from the inhibitory action of tyrosinase of dicarboxylic acids formed through the oxidation of some unsaturated fatty acids of skin surface lipids) competitively inhibit a necessary enzyme of melanocyte pigment formation. In hyperpigmented macules in tinea versicolor, the organism induces an enlargement of melanosomes made by melanocytes at the basal layer of the epidermis.

Race

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

Sex

Several studies have addressed the frequency of tinea versicolor based on sex, and no dominance of either sex is apparent.

Age

In the United States, tinea versicolor is most common in persons aged 15-24 years, when the sebaceous glands are more active. The occurrence of tinea versicolor before puberty or after age 65 years is uncommon.7 In more tropical countries, age frequency varies; most cases involve people aged 10-19 years who live in warmer, humid countries, such as Liberia and India.

Clinical

History

  • Most individuals with tinea versicolor report cosmetically disturbing, abnormal pigmentation.
    • The involved skin regions are usually the trunk, the back, the abdomen, and the proximal extremities. The face, the scalp, and the genitalia are less commonly involved.
    • The color of each lesion varies from almost white to reddish brown or fawn colored.
    • A fine, dustlike scale covers the lesions.
  • Tinea versicolor patients often report that the involved skin lesions fail to tan in the summer.
  • Occasionally, a tinea versicolor patient also reports mild pruritus.
  • Greater than 20% of tinea versicolor patients report a positive family history of the condition. This subset of patients records a higher rate of recurrence and longer duration of disease.8

Physical

Tinea versicolor can present in 4 forms.

  • Tinea versicolor - Form 1
    • The most common appearance of the disease is as numerous, well-marginated, finely scaly, oval-to-round macules scattered over the trunk and/or the chest, with occasional extension to the lower part of the abdomen, the neck, and the proximal extremities.
    • The macules tend to coalesce, forming irregularly shaped patches of pigmentary alteration. As the name versicolor implies, the disease characteristically reveals a variance in skin hue. The involved areas can be either darker or lighter than the surrounding skin.
    • The condition is more noticeable during the summer months when the discrepancy in color from the normal skin becomes more apparent.
    • Light scraping of the involved skin with a scalpel blade characteristically yields a copious amount of keratin.
  • Tinea versicolor - Form 2
    • An inverse form of tinea versicolor also exists in which the condition has an entirely different distribution, affecting the flexural regions, the face, or isolated areas of the extremities. This form of tinea versicolor is more often seen in hosts who are immunocompromised.
    • This form of the disease can be confused with candidiasis, seborrheic dermatitis, psoriasis, erythrasma, and dermatophyte infections.
  • Tinea versicolor - Form 3
    • The third form of Malassezia infections of the skin involves the hair follicle. This condition is typically localized to the back, the chest, and the extremities.
    • This form can be clinically difficult to differentiate from bacterial folliculitis. The presentation of Pityrosporum folliculitis is a perifollicular, erythematous papule or pustule.
    • Predisposing factors include diabetes, high humidity, steroid or antibiotic therapy, and immunosuppressant therapy. Additionally, several reports reveal that M furfur also plays a role in seborrheic dermatitis.
  • Tinea versicolor - Form 4
    • Another clinical presentation is multiple firm, 2- to 3-mm, monomorphic, red-brown, inflammatory papules. These lesions may, or may not also demonstrate a fine white scale.
    • The lesions are usually found on the torso and are asymptomatic.
    • Histologically, the rash demonstrates not only fungal hyphae and spores in the stratum corneum, but also an interface dermatitis in the superficial dermis.9

Causes

Most cases of tinea versicolor occur in healthy individuals with no immunologic deficiencies. Nevertheless, several factors predispose some people to develop this condition. These factors include genetic predisposition; warm, humid environments; immunosuppression; malnutrition; and Cushing disease.10,11

The reason why this organism causes tinea versicolor in some individuals while remains as normal flora in others is not entirely known. Several factors, such as the organism's nutritional requirements and the host's immune response to the organism, are significant.

The organism is lipophilic, and lipids are essential for growth in vitro and in vivo. Furthermore, the mycelial stage can be induced in vitro by the addition of cholesterol and cholesterol esters to the appropriate medium. Because the organism more rapidly colonizes humans during puberty when skin lipids are increased more than that of adolescent levels and tinea versicolor is manifested in sebum-rich areas (eg, chest, back), individual variations in skin surface lipids are hypothesized to play a major role in disease pathogenesis. However, patients with tinea versicolor and control subjects do not demonstrate any quantitative or qualitative differences in skin surface lipids. Skin surface lipids are significant for the normal presence of M furfur on human skin, but they probably play little role in the pathogenesis of tinea versicolor.

Evidence has been accumulating to suggest that amino acids, rather than lipids, are critical for the appearance of the diseased state. In vitro, the amino acid asparagine stimulates the growth of the organism, while another amino acid, glycine, induces hyphal formation. In vivo, the amino acid levels have been shown to be increased in the uninvolved skin of patients with tinea versicolor in 2 separate studies.

Another significant causative factor is the patient's immune system. Although sensitization against M furfur antigens is routinely present in the general population (as proven by lymphocyte transformation studies), lymphocyte function on stimulation with the organism has been shown to be impaired in patients who are affected. This outcome is similar to the situation of sensitization with Candida albicans. In short, cell-mediated immunity plays some role in disease causation.

More on Tinea Versicolor

Overview: Tinea Versicolor
Differential Diagnoses & Workup: Tinea Versicolor
Treatment & Medication: Tinea Versicolor
Follow-up: Tinea Versicolor
References
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References

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Further Reading

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Keywords

tinea versicolor, pityriasis versicolor, chromophytosis, dermatomycosis furfuracea, tinea flava, aeromia parasitica, Kleinenflechte, Hodi-Potsy, cutaneous fungal infection, hypopigmented macules, hyperpigmented macules, Malassezia furfur, M furfur, Pityrosporon orbiculare, Pityrosporon ovale, Malassezia ovalis, Cushing disease

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Contributor Information and Disclosures

Author

Craig G Burkhart, MD, MPH, Clinical Professor, Department of Medicine, Section of Dermatology, The University of Toledo College of Medicine; Clinical Assistant Professor, Department of Dermatology, Ohio State University College of Medicine
Craig G Burkhart, MD, MPH is a member of the following medical societies: American Academy of Dermatology, Ohio State Medical Association, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Lorie Gottwald, MD, Chief, Division of Dermatology, Associate Professor, Department of Internal Medicine, Medical College of Ohio at Toledo
Lorie Gottwald, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, American Medical Association, American Medical Student Association/Foundation, and American Medical Women's Association
Disclosure: Nothing to disclose.

Craig N Burkhart, MD, MSBS, Assistant Professor, Department of Dermatology, University of North Carolina at Chapel Hill
Craig N Burkhart, MD, MSBS is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Kathryn Schwarzenberger, MD, Associate Professor of Medicine, Division of Dermatology, University of Vermont College of Medicine; Consulting Staff, Division of Dermatology, Fletcher Allen Health Care
Kathryn Schwarzenberger, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, American Dermatological Association, Dermatology Foundation, Medical Dermatology Society, and Women's Dermatologic Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Edward F Chan, MD, Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania School of Medicine
Edward F Chan, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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