Background
Tinea versicolor (also referred to as pityriasis versicolor) is a common and benign superficial cutaneous fungal infection that is usually characterized by hypopigmented or hyperpigmented macules and patches on the chest and the back. [1] (See the image below.) In patients with a predisposition, tinea versicolor may chronically recur. The fungal infection is localized to the stratum corneum.
In patients with lighter skin color, lesions frequently are light tan or salmon-colored.
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 lighter skin, the color of each lesion can range from almost white to reddish-brown or fawn-colored. In patients with darker skin, involved areas can have varying degrees of either hypopigmentation or hyperpigmentation. A fine, dustlike scale covers the lesions.
Patients with tinea versicolor often report that the involved skin lesions fail to tan in the summer. Thus, affected areas commonly become more visually apparent during the summer months but then may become subtler in appearance during the winter months as background tan fades.
Occasionally, a patient also reports mild pruritus. In most instances, tinea versicolor is asymptomatic.
More 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. [2]
Whereas the clinical presentation of tinea versicolor is distinctive, examination under a Wood lamp often, but not always, produces a coppery-orange fluorescence. Confirmation can be obtained through potassium hydroxide (KOH) preparation and periodic acid–Schiff (PAS) or methenamine silver staining.
Topical antifungals are the first-line treatment for tinea versicolor; oral systemic antifungals may also be employed. because tinea versicolor is often resistant to eradication, prophylactic therapy may be required to prevent recurrence. (See Treatment.)
Pathophysiology
Tinea versicolor is caused by dimorphic lipophilic organisms in the genus Malassezia (formerly Pityrosporum). More than 20 species are recognized within this genus, [3] of which Malassezia globosa, Malassezia sympodialis, and Malassezia furfur are the predominant species isolated in tinea versicolor. [4, 5, 6, 7, 8, 9, 10] Malassezia is extremely difficult to grow in laboratory culture media and is culturable only in media enriched with C12- to C14-sized fatty acids. It is naturally found on the skin surfaces of many animals, including humans (18% of infants and 90-100% of adults [11] ).
Malassezia can be found on healthy skin as well as 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 the following:
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Genetic predisposition
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Warm, humid environments
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Immunosuppression
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Malnutrition
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Pregnancy
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Cushing disease
Human peptide cathelicidin LL-37 plays a role in skin defense against this organism.
Although 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 Malassezia (Pityrosporum) folliculitis, confluent and reticulated papillomatosis, seborrheic dermatitis, psoriasis, and some forms of atopic dermatitis. Malassezia has also been shown to be a pulmonary pathogen in patients with immunosuppression due to stem cell transplantation. [12]
Etiology
Most cases of tinea versicolor occur in healthy individuals with no immunologic deficiencies. Nevertheless, several factors predispose some people to develop this condition, including the following [13, 14] :
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Genetic predisposition
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Warm, humid environments
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Immunosuppression
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Malnutrition
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Application of oily preparations
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Corticosteroid use
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Cushing disease
The use of bath oils and skin lubricants may increase the risk of developing tinea versicolor. [15]
The reason why Malassezia causes tinea versicolor in some individuals but 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.
Malassezia is lipophilic, and lipids are essential for its growth both 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 lipid levels are higher than those seen during adolescence and tinea versicolor is manifested in sebum-rich areas (eg, chest and back), individual variations in skin surface lipids have been hypothesized to play a major role in disease pathogenesis. However, patients with tinea versicolor have been shown to have any quantitative or qualitative differences in skin surface lipids as compared with control subjects. Skin surface lipids are significant for the normal presence of M furfur on human skin, but they probably are of little significance in the pathogenesis of tinea versicolor.
Evidence has been adduced 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, and another amino acid, glycine, induces hyphal formation. In vivo, amino acid levels have been shown to be increased in the uninvolved skin of patients with tinea versicolor in two separate studies. The gene MGL_3741 has been reported to play a role in amino acid biosynthesis pathways (an important source of carbon and nitrogen for yeast) in M globosa, and this gene has been proposed as potentially increasing the pathogenicity of M globosa. [16]
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. [17]
In steroid-associated atrophying tinea versicolor, 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. [18, 19]
However, atrophying tinea versicolor has also been reported in patients who have not used topical steroids. Accordingly, 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 and that the recruited histiocytes then serve as a source of elastases and upregulate metalloproteinase activity, ultimately leading to atrophy of the affected epidermis. [19, 20, 21]
A study from 2020 found a statistically significant relationship between Helicobacter pylori infection and tinea versicolor, proposing H pylori infection as an etiologic factor for this fungal infection [22] ; however, this relationship remains to be confirmed in larger studies. In addition, the control population with telogen effluvium in the 2020 study was not clearly demographically matched.
Epidemiology
US and international statistics
Tinea versicolor occurs more frequently in areas of the United States with higher temperatures and higher relative humidities. The national prevalence of this condition is 2-8% of the population. The exact US incidence is difficult to assess, because many individuals who are affected may not seek medical attention. A study using data from a large commercial insurance database cited an overall incidence of 2.8 per 1000 person-years for the United States in 2022. [23]
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.
Age-, sex-, and race-related demographics
In the United States, tinea versicolor is most common in persons aged between 15 and 24 years, when the sebaceous glands are more active; it is uncommon before puberty or after age 65 years. [24] In more tropical countries, the age frequency varies; most cases involve people aged 10-19 years who live in warmer, humid countries, such as Liberia and India.
Several studies have examined the frequency of tinea versicolor based on sex without documenting any predilection for either sex. However, the aforementioned study using data from a commercial insurance database found the condition to be more prevalent in males in the United States. [23]
Although the alteration in skin pigmentation is more apparent in darker-skinned individuals, the incidence of tinea versicolor appears to be the same in individuals of all skin types.
Prognosis
Tinea versicolor is a benign condition. As the name implies (versi- deriving from Latin vertere "to turn"), the condition can lead to altered coloration of the skin, yielding colors ranging from white to red to brown. Tinea versicolor 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 the discoloration may last for weeks to months. If scale cannot be provoked and new lesions are not developing, there is no need to repeat treatment, and the patient can be reassured that ongoing infection is unlikely.
Although tinea versicolor is recurrent in some patients and therefore can be considered a chronic disease, it remains treatable with the available remedies. The prognosis is excellent, and new treatments continue to be developed. [25]
Patient Education
It is important to explain to patients that tinea versicolor is caused by a fungus that is normally present on the skin surface and that for this reason, it is not considered a contagious disease. Sequelae from tinea versicolor are not permanent, and any pigmentary alterations typically resolve entirely within 1-2 months after treatment is initiated. Treatment is needed to remedy the condition and to provide prophylaxis against recurrences.
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In patients with lighter skin color, lesions frequently are light tan or salmon-colored.
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Hyperpigmented macules forming some confluent patches on abdomen. Scale is not readily apparent but is easily provoked with light scratching. On dark skin, affected areas may be hypopigmented or hyperpigmented.
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