Tinea Versicolor Clinical Presentation

  • Author: Craig G Burkhart, MD, MPH; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Feb 28, 2012
 

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]

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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]

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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; application of oily preparations; corticosteroid usage; and Cushing disease.[10, 11, 12]

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.

Oxidative stress as shown by expression of reduced glutathione contributes to the pathogenesis of this condition.[13]

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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)

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.

Specialty Editor Board

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.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

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.

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.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M 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, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

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.

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