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. Note the image below.
 View Image | In patients with lighter skin color, lesions frequently are light tan or salmon colored. |
Tinea versicolor is caused by the dimorphic, lipophilic organisms in the genus Malassezia, formerly known as Pityrosporum. Fourteen species are recognized within this classification of yeasts, of which Malassezia globosa, Malassezia sympodialis, and Malassezia furfur are the predominant species isolated in tinea versicolor.[1, 2, 3, 4, 5, 6, 7, 8] 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.[9]
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; pregnancy; 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, psoriasis, and some forms of atopic dermatitis. Malassezia species have also been shown to be a pulmonary pathogen in patients with immunosuppression due to stem cell transplantation.[10]
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.[11, 12, 13] The use of bath oils and skin lubricants may increase the risk of developing tinea versicolor.[14]
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 two 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.[15]
In steroid-associated atrophying tinea versicolor, the Malassezia infecting the epidermis may impair the barrier function of skin, thus allowing improved penetration of topical corticosteroids. This may lead to enhanced corticosteroid-induced atrophy of the affected skin.[16, 17, 18] However, as atrophying tinea versicolor has been reported in patients who have not used topical steroids, it has been proposed that a T-cell–mediated immune response to the Malassezia organism may be responsible for the atrophy noted. This theory suggests that Th1 cytokines recruit histiocytes to the site of epidermal infection. These histiocytes serve as a source of elastases and they up-regulate the metalloproteinase activity, ultimately leading to atrophy of the affected epidermis.[17, 19, 20]
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.
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.
Several studies have addressed the frequency of tinea versicolor based on sex, and no dominance of either sex is apparent.
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.[21] 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.
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 contagious because the causative fungal pathogen is a normal inhabitant of the skin. Treatment leads to cessation of scaling within a few days, but discoloration may last for weeks to months. If scale cannot be provoked and new lesions are not developing, then there is no need to repeat treatment and the patient can be reassured that ongoing infection in unlikely.
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 and new treatments continue to be developed.[22]
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.
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. In patients with fair skin, the color of each lesion varies from almost white to reddish-brown or fawn colored. In darker skin types, involved areas can have varying degrees of either hypopigmentation or hyperpigmentation. A fine, dustlike scale covers the lesions.
Tinea versicolor patients often report that the involved skin lesions fail to tan in the summer and cause the affected areas to become more apparent. Conversely, affected areas may become subtler in winter months as background tan fades.
Occasionally, a tinea versicolor patient also reports mild pruritus. In most instances, the condition is asymptomatic.
Greater than 20% of tinea versicolor patients report a family history of the condition. This subset of patients records a higher rate of recurrence and longer duration of disease.[23]
Although tinea versicolor is often diagnosed by the observation of the classic hypopigmented-tohyperpigmented, centrally coalescing, oval-to-round patches with mild scale, it can occasionally be difficult to distinguish from other dermatoses. The scale on these lesions is not always immediately evident and may require scratching or stretching of the skin surface.[14]
A dermatoscope is also a useful diagnostic tool in examining affected skin. In hypopigmented lesions, dermoscopy shows a well-demarcated, white area with fine scales found largely in skin furrows. Hyperpigmented lesions under dermoscopy show fine scale in skin furrows overlying brown pigmentation.[24, 25]
Tinea versicolor can present in four forms in addition to a rare, atrophic form.
The most common appearance of the disease is as numerous, well-marginated, finely scaly, oval-to-round macules scattered over the upper trunk, with occasional extension to the lower trunk, neck, and 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.
Fine, powdery scale may be readily apparent and is uniformly provocable with light scraping of the involved skin with a scalpel blade or the edge of a glass slide. See the image below.
View Image | Hyperpigmented macules forming some confluent patches on the abdomen. While scale is not readily apparent, it is easily provoked with light scratching.... |
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.
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.
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.[26]
Atrophying tinea versicolor is a rare form that presents as atrophic, ivory-colored–to–erythematous lesions that are oval-to-round in shape. These lesions can have a wrinkled surface, and the atrophy is limited to the areas of skin affected by tinea versicolor.[16, 27]
Histologic features of these lesions include epidermal atrophy, vascular ectasia, and rarefaction of collagen and elastic fibers.[16, 19]
These lesions are often reported in patients who are either misdiagnosed or have a comorbid condition requiring an extended use of topical corticosteroids.[16, 17] However, cases of atrophying tinea versicolor have been described in patients who do not have a history of using topical corticosteroids.[19]
The clinical presentation of tinea versicolor is distinctive, and the diagnosis is often made without any laboratory documentation.
The ultraviolet black light (Wood lamp) 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 lamp, 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. Contrast stain containing 1% Chicago sky blue 6B and 8% KOH (as the clearing agent) achieves the greatest sensitivity and specificity.[28]
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.
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.[29] 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.
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.[30] Effective topical agents include selenium sulfide, zinc-pyrithione, sodium sulfacetamide, ciclopirox olamine,[31] , tacrolimus,[32] as well as azole and allylamine antifungals.[33, 34, 35, 36, 37] Even if a small area of skin is involved, treating with topicals from the neck to the knees may make treatment more successful.[14] 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, some topical antifungal therapy can be expensive. Over-the-counter shampoo formulations of selenium sulfide, zinc-pyrithione, and ketoconazole are low-cost options that are widely available and can easily be used to cover large surface areas. Topical allylamines have been demonstrated to be clinically and mycologically effective. Tacrolimus 0.03% applied topically has been shown to provide a mycologically effective treatment; however, it is not effective in speeding the reduction in appearance of hypopigmentation associated with tinea versicolor.
While oral ketoconazole is contraindicated for the treatment of tinea versicolor, the topical foam may be useful in some patients.[38] The risk of serious liver damage, adrenal gland problems, and harmful drug interactions with use of oral ketoconazole outweighs it benefit for fungal skin infections.[39]
Oral therapy with other systemic antifungals is effective for tinea versicolor and is often preferred by patients because of convenience and oral administration is less time consuming than topical treatment. Of course, oral therapy can be used in consort with topical regimens. Fluconazole, and itraconazole are the preferred oral agents.[40, 41, 42] Various dosing regimens have been used. Fluconazole has been offered as a single 150- to 300-mg weekly dose for 2-4 weeks and is the safest oral agent. Itraconazole is usually given at 200 mg/d for 7 days. Pramiconazole and sertaconazole have also been used in the management of tinea versicolor.[43, 44] A review suggested the following dosing regimens: 200 mg/d for 5 or 7 days of itraconazole, 300 mg/wk for 2 weeks of fluconazole, and 200 mg/d for 2 days of pramiconazole.[45]
Oral therapy does not prevent the high rate of recurrence, and treatment with an oral or 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.[46] In the case of oral terbinafine, some subgroups of M furfur apparently are not clinically responsive, although in vitro studies suggest fungistatic activity.[47] Also, a regimen of 1 tablet a month of fluconazole or itraconazole has been used successfully to prophylactically prevent recurrences.[48]
Reports describe successful treatment of tinea versicolor with photodynamic therapy.[49, 50]
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.
Tinea versicolor responds well to both topical and oral antimycotic therapies. Many patients prefer oral therapy because of its convenience.
Clinical Context: Terbinafine topical inhibits squalene epoxidase, which decreases ergosterol synthesis, causing fungal cell death. Use this medication until symptoms significantly improve. The duration of treatment should be greater than 1 week but not greater than 4 weeks.
Clinical Context: Clotrimazole topical is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing fungal cell death. Reevaluate the diagnosis if no clinical improvement is seen after 4 weeks.
Clinical Context: Ketoconazole is an imidazole broad-spectrum antifungal agent. It inhibits the synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. Ketoconazole achieves excellent skin levels with minimal oral dosing, but oral treatment with this agent for skin infections is contraindicated because of safety concerns. M furfur is eradicated by the presence of ketoconazole in outer skin layers.
Clinical Context: Ciclopirox interferes with the synthesis of DNA, RNA, and protein by inhibiting the transport of essential elements in fungal cells.
Clinical Context: Butenafine damages fungal cell membranes, causing fungal cell growth to arrest.
Clinical Context: Naftifine is a broad-spectrum antifungal agent and synthetic allylamine derivative; it may decrease the synthesis of ergosterol, which, in turn, inhibits fungal cell growth. If no clinical improvement is seen after 4 weeks, reevaluate the patient.
Clinical Context: Econazole is effective in cutaneous infections. It interferes with RNA and protein synthesis and metabolism. It disrupts fungal cell wall membrane permeability, causing fungal cell death.
Clinical Context: Oxiconazole damages the fungal cell wall membrane by inhibiting the biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out and resulting in fungal cell death.
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.
In patients with lighter skin color, lesions frequently are light tan or salmon colored.
Hyperpigmented macules forming some confluent patches on the abdomen. While scale is not readily apparent, it is easily provoked with light scratching. On dark skin, affected areas may be hypopigmented or hyperpigmented.
In patients with lighter skin color, lesions frequently are light tan or salmon colored.
Hyperpigmented macules forming some confluent patches on the abdomen. While scale is not readily apparent, it is easily provoked with light scratching. On dark skin, affected areas may be hypopigmented or hyperpigmented.
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