INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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, the condition may chronically recur.  The fungal infection is localized to the stratum corneum.

Pathophysiology

Tinea versicolor is caused by the dimorphic, lipophilic organism, Malassezia furfur, which is cultured only in media enriched with C12- to C14-sized fatty acids. M furfur is now the accepted name for the organism. Pityrosporon orbiculare, Pityrosporon ovale, and Malassezia ovalis are synonyms for M furfur. M furfur is a member of normal human cutaneous flora, and it is found in 18% of infants and 90-100% of adults.

Eleven species of M furfur have been described, with Malassezia globosa being the usual form isolated in persons with tinea versicolor. 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 M furfur 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.

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 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, the disease is most common in persons aged 15-24 years, when the sebaceous glands are more active. Its occurrence before puberty or after age 65 years is uncommon. 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

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

History

• Most individuals with tinea versicolor complain of 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.

• Patients often complain that the involved skin lesions fail to tan in the summer.
• Occasionally, a patient also complains of mild pruritus.

Physical

Tinea versicolor can present in 3 forms.

• 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.

• 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.

• Form 3
• • The third form of M furfur 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.

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.

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.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Other Problems to be Considered

Confluent and reticulated papillomatosis of Gougerot and Carteaud

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Lab Studies

• The clinical presentation of tinea versicolor is distinctive, and the diagnosis is often made without any laboratory documentation.
• • The ultraviolet black (Wood) light can be used to demonstrate the coppery-orange fluorescence of tinea versicolor. However, in some cases, the lesions appear darker than the unaffected skin under the Wood light, but they do not fluoresce.
  • The diagnosis is usually confirmed by potassium hydroxide (KOH) examination, which demonstrates the characteristic short, cigar-butt hyphae that are present in the diseased state. The KOH finding of spores with short mycelium has been referred to as the spaghetti and meatballs or the bacon and eggs sign of tinea versicolor. For better visualization, ink blue stain, Parker ink, methylene blue stain, or Swartz-Medrik stain can be added to the KOH preparation.
  • Special media are required for culture. Because the diagnosis is usually clinically suspected and can be confirmed with a KOH preparation, cultures are rarely obtained.

• With blood examination, no definitive deficiencies of normal antibodies or complement are present in patients with tinea versicolor, but research continues in this area.
• • For example, although individuals who are affected reveal no specific antibody levels above those of age-matched controls, M furfur antigens do elicit a specific immunoglobulin G response in patients with seborrheic dermatitis and tinea versicolor detected by enzyme-linked immunosorbent assay and Western blotting assays.
  • M furfur does induce immunoglobulin A, immunoglobulin G, and immunoglobulin M antibodies, and it can activate complement via both the alternate pathway and the classical pathway.
  • Various studies have found defects in lymphokine production, natural killer T cells, decreased phytohemagglutinin and concanavalin A stimulation, interleukin 1, interleukin 10, and interferon gamma production by lymphocytes in patients.
  • Although these tests do not suggest an immunologic disorder, they do suggest a reduced body response to the specific fungal elements that produce tinea versicolor. Further assessment is warranted.

Histologic Findings

The organism that causes tinea versicolor is localized to the stratum corneum. M furfur can be detected by hematoxylin and eosin (H&E) alone, although periodic acid-Schiff (PAS) or methenamine silver staining are more confirmatory. On rare occurrences, the organism can approach the stratum granulosum, and it can even be found inside keratinocytes. The epidermis reveals mild hyperkeratosis and acanthosis, and a mild perivascular infiltrate is present in the dermis. An acanthosis nigricans–like epidermal change is noted in the papular variety, with dilated blood vessels observed in erythematous lesions.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Medical Care

Patients should be informed that tinea versicolor is caused by a fungus that is normally present on the skin surface and is therefore not considered contagious. The condition does not leave any permanent scar or pigmentary changes, and any skin color alterations resolve within 1-2 months after treatment has been initiated. Recurrence is common, and prophylactic therapy may help reduce the high rate of recurrence.

• Tinea versicolor can be successfully treated with various agents. Effective topical agents include selenium sulfide, sodium sulfacetamide, ciclopiroxolamine, as well as azole and allylamine antifungals. Various regimens can be used. Selenium sulfide lotion is liberally applied to affected areas of the skin daily for 2 weeks; each application is allowed to remain on the skin for at least 10 minutes prior to being washed off. In resistant cases, overnight application can be helpful. Topical azole antifungals can be applied every night for 2 weeks. Weekly application of any of the topical agents for the following few months may help prevent recurrence. In patients with widespread disease, topical antifungal therapy can be expensive. Topical allylamines have been demonstrated to be clinically and mycologically effective.
• Oral therapy is also effective for tinea versicolor and is often preferred by patients because it is more convenient and less time consuming. Of course, oral therapy can be used in consort with topical regimens. Ketoconazole, fluconazole, and itraconazole are the preferred oral agents. Various dosing regimens have been used. With ketoconazole, a 10-day 200-mg daily therapy and as a single-dose 400-mg treatment are popular, both with comparable results. Fluconazole has been offered as a single 150- to 300-mg weekly dose for 2-4 weeks. Itraconazole is usually given at 200 mg/d for 7 days.
• Oral therapy does not prevent the high rate of recurrence, and treatment with oral ketoconazole or a topical agent may need to be repeated intermittently throughout the year. Because tinea versicolor is a benign condition and oral therapy is not without risk, the decision to treat with an oral agent should be made only after a complete discussion of the risks involved. In the case of oral terbinafine, some subgroups of M furfur apparently are not clinically responsive, although in vitro studies suggest fungistatic activity. Also, a regimen of 1 tablet a month of ketoconazole, fluconazole, and itraconazole has been used successfully to prophylactically prevent recurrences.

Diet

Dietary alterations have not proved successful in the treatment of tinea versicolor.

MEDICATION

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Tinea versicolor responds well to both topical and oral antimycotic therapies. Many patients prefer oral therapy because of its convenience.

Drug Category: Antifungals

Topical antifungals temporarily eradicate the condition, although treatment may need to be intermittently repeated to prevent recurrence. Oral therapy for tinea versicolor is convenient and effective, but it does not prevent recurrences. A once-monthly (for 6 mo) oral dose of fluconazole is a popular alternative.

FOLLOW-UP

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

Further Outpatient Care

• Tinea versicolor has a high rate of recurrence, and prophylactic treatment with topical or oral therapy on an intermittent basis is necessary to prevent recurrences in most cases.

Prognosis

• Although tinea versicolor is recurrent for some patients and, therefore, a chronic disease, the condition remains treatable with the available remedies (see Medical Care and Medication). Thus, the prognosis is excellent.

Patient Education

• Patients need to realize that tinea versicolor is caused by a fungus that is normally present on the skin surface; thus, it is not considered a contagious disease. Sequelae from the disease are not permanent, and any pigmentary alterations resolve entirely 1-2 months after treatment is initiated. Treatment is needed to remedy the condition and for prophylaxis to prevent recurrences.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• References

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Article Last Updated: Nov 13, 2006